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1. MANAGEMENT OF ACUTE MYOCARDIAL INFARCTION IN PATIENTS PRESENTING WITH ST-SEGMENT ELEVATION

Author

F. Van de Werf, D. Ardissino, A. Betriu, D. Cokkinos, E. Falk, K. Fox, D. Julian, M. Lengyel, F.J. Neumann, W. Ruzyllo, C. Thygesen, R. Underwood, A. Vahanian, F. Verheugt, and W. Wijns

Subjects
Therapeutics. Pharmacology, RM1-950, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology.

Published
2015
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2. Usefulness of parahisian pacing for risk prediction of pacemaker implantation after TAVI

Author

M Notarangelo, A Dinatale, A Crocamo, R Vrenozaj, L Bearzot, G Gonzi, A Guidorossi, I Tadonio, L Vignali, G Niccoli, and D Ardissino

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Funding Acknowledgements Type of funding sources: None. Background Conduction disturbances determining pacemaker implantation are a significant concern in patients undergoing Transcatheter Aortic Valve Implantation (TAVI), a procedure that is nowadays spreading even in the low-risk population. OBJECTIVE The aim of the study was to evaluate the role of the parahisian pacing, a method to directly identify the conduction system anatomical variability, in predicting the iatrogenic damage risk conditioning pacemaker implantation after TAVI. Methods Between October 2021 and November 2022 we prospectively collected clinical features, ECG, procedural and imaging data (cardiac CT and echocardiography) of every patient who underwent electrophysiological study for pre-existing or worsening conduction disorders within 48 hours after TAVI procedures in our centre. After having recorded the HV interval, parahisian stimulation at decreasing energy output was performed (CL 600 ms, 25V to 0.5V x 2 ms) with definition of the loss of capture pattern related to the three anatomical variations of His bundle described by Kawashima (1). Fisher’s exact test was used for statistical analysis; p-value Results Out of 110 TAVI performed, a total of 31 patients with conduction disorders have been studied. Patients who developed permanent 3rd degree AV block after the procedure were excluded. Mean age was 82.6±4.4 years; 21 patients (67.7%) were males. 11 patients (35.5%) had a pre-existing conduction disorder worsened after TAVI, 13 patients (41.9%) developed newly-onset LBBB; 8 (25.8%) also developed 1st degree AV block. The total number of patients who underwent PM implantation was 16 (51.6%). The anatomical variables (membranous septum Conclusions Parahisian stimulation can be a useful tool to define the conduction system anatomical variability. It can also be helpful to predict the conduction system damage risk during TAVI, conditioning PM implantation. Our data need to be confirmed in a larger population.

Published
2023
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3. Changes of sports habits and psychological impact of pharmacologically induced Brugada type 1 pattern in young patients

Author

A Dinatale, A Crocamo, M F Notarangelo, L Bearzot, G Gonzi, F Barocelli, F Russo, G Niccoli, and D Ardissino

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Funding Acknowledgements Type of funding sources: None. Background Brugada syndrome (BrS) is an inherited disease characterized by an increased risk of sudden cardiac death (SCD). According to the latest ESC guidelines, provocation with sodium channel blocker test is less specific than previously thought, especially in asymptomatic patients(1). In these cases, in which the diagnosis of BrS itself can be controversial, management currently consists in clinical follow-up only. However, we still observe a big gap between the patient’s perception and medical recommendations of living a normal life. Objective The goal of this study was to analyze exercise habits before and after positive ajmaline testing (AT), focusing on its psychological impact on a population of low-risk young patients. Methods We enrolled all-comers patients with ajmaline-induced Brugada type 1 pattern who came to our department between 2015 and 2022. Patients were asked to rate their heart-focused anxiety using the German version of the Cardiac Anxiety Questionnaire (CAQ) (2) at last medical contact after ajmaline challenge. The intensity of habitual physical exercise was estimated in METs and divided in 3 categories: mild (6 METs). Different groups were compared using Student’s t-test for continuous variables. Significance level was set to p Results A total of 87 patients resulted positive to ajmaline challenge; among these, 16 (18.4%) underwent EPS and 4 (4.6%) of them underwent ICD implantation. Therefore, our population included 83 patients. Mean age was 45.1±13.5 years; M/F ratio was 1.4/1. 12 patients (14.5%) had family history of SCD. Mean follow-up duration was 31.6±25.3 months. After positive AT, 5 patients (5.7%) did intense physical activity (PA), 27 (31.0%) did moderate PA, 51 (58.6%) were sedentary or practiced low-intensity PA. Mean CAQ score in the overall population was 19.1±6.6 points (fig. 1A), noticeably higher than the general population (2). As shown in fig. 1B, anxiety levels were significantly lower in patients who did almost moderate PA (p=0.03), independently from previous sport habits. This suggests sport to be a protective factor against anxiety. A total of 23 people (27.7%) reduced PA (fig. 2). We compared this population to the two groups of patients whose habits were not affected by the test: respectively high-high (n=22; 25.3%) and low-low groups (n=34; 39.1%). Anxiety in high-low group patients was not significantly different from the other two (fig. 1C), although it was higher than the general population. Conclusions After positive AT, many patients lead a sedentary lifestyle. Regardless of this, anxiety after the test is higher than the normal population. Anxiety levels do not change significantly between patients who reduced PA and those who did not change their habits. Further investigation is needed to assess the trade-offs between individual arrhythmic risk and global cardiovascular risk due to sedentary lifestyle in these patients.

Published
2023
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4. Incremental value of maximum voltage and activation-guided ablation for cavotricuspid isthmus-dependent atrial flutter

Author

A Crocamo, M F Notarangelo, R Sciarroni, R Vrenozaj, A Dinatale, L Bearzot, G Gonzi, M Fioravanti, G Niccoli, and D Ardissino

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Funding Acknowledgements Type of funding sources: None. Radiofrequency (RF) catheter ablation is an effective method for treatment of typical cavo-tricuspid isthmus (CTI) dependent atrial flutter. However, despite the widespread use of contact force irrigated catheter, 11% of patients don’t achieve a first-pass CTI block, requiring additional RF applications or additional line during the same or a second procedure. From an anatomical point of view, CTI is composed of discrete bundles of muscle with intervening connective tissue, suggesting that its conduction proprieties are dependent of the anatomic architecture of the bundles. The maximum voltage-guided (MGV) ablation technique targets high-voltage electrograms along CTI to ablate the functionally active anatomic muscle bundle, without drawing a complete anatomic line. [1;2] Purpose The aim of this study was to evaluate the efficacy of maximum voltage and activation-guided ablation (MVG/LAT) for CTI atrial flutter in real-world setting. Methods This was a prospective observational study in which all patients undergoing CTI atrial flutter ablation at the Electrophysiology Laboratory of our Department from 01/2021 to 10/2022 were recruited. Patients who were undergoing the ablation procedure after having already made an unsuccessful attempt of the same were excluded from the study. Substrate and activation mapping of CTI, both during flutter and during pacing from the proximal coronary sinus (CSp), was performed in all patients, identifying the earliest activated high-voltage channels, without the use of fluoroscopy, using the Smart-Touch SF catheter (CARTO 3, V7, Biosense Webster). High-voltage channels were validate also during lateral RA pacing. CTI ablation was performed only in channels with high voltage and early activation (W 45, AI 500). Bidirectional CTI block were validate by differential atrial pacing maneuvers and activation mapping during pacing from CSp. Results Procedural data of 39 patients were evaluated (mean age 68±13 years; men 92.6%; mean right atrium volume 149 mL). The mean number of points taken per map per patient was 1151. Bipolar thresholds were customized (0.5-2.5 mV) with the aim of better visualizing high-voltage channels. In 20/39(51.2%) patients ablation was performed during atrial flutter, in 19/39(48.8%) during pacing from proximal CS. In 19/39(48.8%) patients high-voltage channels were not detected at the central isthmus line (6 o'clock, LAO). The median number of RF applications to achieve bidirectional block of the CTI were 6 (1-20) in all patients (p=NS) (Figure 1,2). During a mean follow-up of 260 days (90-531) no recurrences were documented in any patient. Conclusions MVG/LAT-guided ablation, targeting selectively conductive muscle fibers, decreases the number of RF applications and improves efficacy, mostly in patients with challenging anatomies.

Published
2023
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5. Air pollution and out-of-hospital cardiac arrest risk

Author

L. Moderato, D. Aschieri, D. Lazzeroni, L. Rossi, S. Bricoli, A. Biagi, S. Ferraro, S.M. Binno, A. Monello, V. Pelizzoni, C. Sticozzi, A. Zanni, G. Magnani, F.L. Gurgoglione, A. Capucci, S. Nani, R.A. Montone, D. Ardissino, F. Nicolini, and G. Niccoli

Abstract

BackgroundGlobally nearly 20% of cardiovascular disease deaths were attributable to air pollution. Out-of-hospital cardiac arrest (OHCA) represents a major public health problem, therefore, the identification of novel OHCA triggers is of crucial relevance. The aim of the study was to evaluate the association between air pollution (short-, mid-and long-term exposure) and out-of-hospital cardiac arrest (OHCA) risk, during a 7 years-period from a highly polluted urban area with a high density of automated external defibrillators (AEDs).Methods and resultsOHCA were prospectively collected from the “Progetto Vita Database” between 01/01/2010 to 31/12/2017; day-by-day air pollution levels were extracted from the Environmental Protection Agency (ARPA) stations. Electrocardiograms of OHCA interventions were collected from the AEDs data cards. Day-by-day particulate matter (PM) 2.5 and 10, ozone (O3), carbon monoxide (CO) and nitrogen dioxide (NO2) levels were measured. A total of 880 OHCAs occurred in 748 days. A significantly increased in OHCA risk with the progressive increase in PM 2.5, PM 10, CO and NO2 levels was found. After adjustment for temperature and seasons, a 9% and 12% increase of OHCA risk for each 10 μg/m3 increase of PM 10 (p< 0.0001) and PM 2.5 (p< 0.0001) levels was found. Air pollutants levels were associated with both asystole and shockable rhythm risk while no correlation was found with pulseless electrical activity.ConclusionsShort-term and mid-term exposure to PM 2.5 and PM 10 is independently associated with the risk of OHCA due to asystole or shockable rhythm.

Published
2023
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7. C12 MANAGING CARDIAC ARREST SECONDARY TO SPONTANEOUS CORONARY ARTERY DISSECTION: SHOULD WE ROUTINELY CONSIDER ICD IMPLANTATION? INSIGHTS FROM PARMA SCAD REGISTRY

Author

R Giacalone, M Toselli, G Pelà, M Cattabiani, A Vezzani, G Benatti, I Tadonio, M Ferretti, F Gurgoglione, M Noni, G Niccoli, D Ardissino, L Vignali, and E Solinas

Subjects
Cardiology and Cardiovascular Medicine
Abstract

Background Cardiac arrest secondary to a spontaneous coronary artery dissection (SCAD) represents a challenging scenario. It deserves specific considerations due to the dramatic presentation and the need for secondary sudden cardiac death prevention. Methods We collected clinical data of four women admitted during the last two years in the Coronary Care Unit of Parma University Hospital, whose presentation of SCAD were cardiac arrest due to ventricular fibrillation (Table1). Results Three patients survived the acute phases. One patient, being considered at high risk of SCAD recurrence, received a subcutaneous implantable cardioverter–defibrillator (S–ICD). Acute management of cardiac arrest related to SCAD deserves specific considerations. Our case series illustrates the importance of prompt resuscitation manoeuvres and early defibrillation. We propose a flow chart of management of cardiac arrest in patient with suspect of SCAD (Figure 2 A). Evaluating risk of SCAD recurrence and sudden cardiac death. The management of SCAD patients complicated by malignant ventricular arrhythmias and cardiac arrest is challenging. Looking at published registries, it appears that SCAD patients are more likely to suffer from ventricular arrythmia or sudden cardiac death than non–SCAD MI patients. The risk–benefit ratio of ICD implantation in these patients remain uncertain . Evaluation of scar burden with CMR can help stratify the global arrhythmic risk, especially as extensive myocardial scar with a residual impaired LVEF increases the risk of future arrhythmic events (Figure 2 B). In our series, only one patient underwent S–ICD implantation, and the decision was mainly driven by the finding of underlying arteriopathy affecting other vascular territories, suggesting a potentially higher rate of SCAD recurrence. For this particular subset of patients, we propose an algorithm that combines predisposing factors and myocardial injury quantification data (Figure 2 B) that could be useful for the estimate of the risk of malignant arrythmias, as well as the risk of recurrence of SCAD, but needs to be validated in larger case studies. Conclusions The acute management of cardiac arrest related to SCAD deserves specific consideration. The residual myocardial damage, predisposing and precipitants factors should be evaluated in order to estimate the SCAD recurrence and sudden cardiac death risks.

Published
2022
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8. P56 SPONTANEOUS CORONARY ARTERY DISSECTIONS: ANALYSIS OF NON TRADITIONAL RISK FACTORS

Author

R Giacalone, M Ferretti, F Gurgoglione, M Noni, G Pelà, A Vezzani, M Cattabiani, G Benatti, I Tadonio, G Magnani, F Nicolini, G Niccoli, D Ardissino, L Vignali, and E Solinas

Subjects
Cardiology and Cardiovascular Medicine
Abstract

The etiology of spontaneous coronary dissection (SCAD) is not well defined and Non traditional risk factors (NT–RF) have assumed increasing interest, but few data are available. NT–RF include three categories: Sex–related (SR–NT–FR), Sex–predominant (SP–NT–RF) and Gender–related (GR–NT–RF). (Table 1) Aim of the Study The objective of our analysis was to evaluate the incidence of NT–RF in Parma SCAD registry population. Material and methods We reviewed 62 patients with SCAD enrolled between January 2013 through November 2021 Results Traditional risk factors were less common: hypertension was the most prevalent (39 pts, 62.9%). When considering NT–RF, 51 patients (82%) had at least one of all, with at least one SR–RF (66%) or GR–RF (64,5%). Patients with NT–RF were younger at time of SCAD (mean age 53 vs 66; p = 0.027) and they were predominantly females (48 vs 7 pts, p = 0.004) (Table 2). No differences were found among NT–RF SCAD and nNT–RF SCAD patients by fibromuscular dysplasia, peripheral arterial disease and chronic kidney disease. Patients with SCAD more often presented with non ST–segment elevation myocardial infarction (43 pts, 72.6%) vs ST–segment elevation (17 pts, 27.4%). No differences in clinical presentation and angiographic characteristics were found among NT–RF and nNT–RF patients group. MACE occurred in 17.7% of patients of the overall study population, at a median follow–up of 23 (interquartile range: 11;57) months. When comparing the incidence of cardiovascular events in the 2 study groups there was a trend toward a higher prevalence of MACE in NT–RF group without statistical significance (NT–RF SCAD 19.6% – nNT–RF SCAD 9.1%; p = 0.4). (Table 3) Conclusion SCAD is an emerging cause of myocardial infarction in young and middle–aged women without the traditional cardiovascular risk profile. Although overall survival seems good, SCAD is a potentially malignant disease which can present with ventricular arrhythmias and sudden cardiac death. Risk estimation is difficult in women, due to the scarce validity of prediction models, therefore a great effort must be made by the clinical community for the widespread diffusion and use of models incorporating NT–RF. Acknowledgement of peculiar features of this disease could help clinicians and researchers to establish targeted interventions for cardiovascular primary prevention, early diagnosis and secondary prevention in women, including rehabilitation and stress management programmes.

Published
2022
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9. P466 PREDICTORS OF RECURRENT CEREBRAL ISCHEMIA AFTER PATENT FORAMEN OVALE CLOSURE: A SINGLE CENTER EXPERIENCE WITH A LONG–TERM FOLLOW–UP

Author

F Gurgoglione, M Cattabiani, L Vignali, E Solinas, C Dizdari, G Benatti, I Tadonio, F Barocelli, D Tuttolomondo, F Nicolini, D Ardissino, and G Niccoli

Subjects
Cardiology and Cardiovascular Medicine
Abstract

Aims Transcatheter patent foramen ovale (PFO) closure has been shown to lower recurrent stroke in patients with cryptogenic stroke (CS) or transient ischemic attack (TIA) with an indication for closure. However, the incidence of recurrent stroke is not negligible and underlying pathogenic mechanisms remain largely unknown. We sought to evaluate the prevalence of recurrent CS/TIA and to assess its predictors after transcatheter PFO closure. Methods We enrolled consecutive patients who underwent PFO closure for secondary prevention of neurological ischemic events at the University Hospital of Parma between 2006 and 2021. For each subject, CS/TIA index event was diagnosed after exclusion of alternative etiologies, PFO features were characterized by transesophageal echocardiography (TEE), the Risk of Paradoxical Embolism (ROPE) score was retrospectively assessed and the presence of migraine was investigated. Clinical follow–up was scheduled with outpatient visits at 3 – 12 months and yearly thereafter device implantation; the primary outcome was the recurrence of any ischemic neurological event. Results We enrolled a total of 169 patients with mean Risk of Paradoxical Embolism (ROPE) score at hospital admission of 6.4 ± 1.5. The primary indication for PFO closure was previous CS (94 [55.6%] subjects), followed by TIA (75 [44.4%]). Among patients with complete outcome data (n= 154), after a median follow–up of 112 months, recurrent cerebral ischemia occurred in 13 [8.4%], with an annualized rate of 0.92/100 patients. The presence of obesity [OR 5.268, p = 0.018], ROPE score < 7 [OR 5.991, p = 0.035] and migraine [OR = 5.932 p = 0.012] were independent positive predictors of recurrent stroke/TIA after PFO closure. Conclusion In our study, recurrent cerebral events after PFO closure were not negligible, with an annualized rate of 0.92/100 patients, consistent with prior research. Multiple heterogeneous predictors were identified: the presence of obesity, ROPE score < 7 and migraine were independent positive predictors of recurrent stroke/TIA after PFO closure

Published
2023
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10. Poster session: Aortic stenosis

Author

R. Piccolo, J. Clarke, C. A. Brambila, B. Igual Munoz, K. Hristova, M. S. Carvalho, M. Tesic, O. Azevedo, J. A. Del Prado, A. Mcculloch, O. Kaitozis, B. Popovic, S. Stankovic, H. Chamsi-Pasha, R. Abdelfatah, V. Parisi, K. Pushparajah, E. Zemtsovsky, B. Kilickiran Avci, A. Manouras, K. Takenaka, F. Parthenakis, P. Vardas, A. Goudev, M. Orii, A. Kutarski, R. De Rosa, M. Castillo Orive, A. Sahlen, H. Ahn, S. Nedjati-Gilani, G. J. King, H. Bellsham-Revell, D. Lahidheb, M. Anastasiou-Nana, F. Pereira Machado, S. Yurdakul, N. Olsen, S. Pica, A. Ebihara, T. Nakajima, P. Molina Aguilar, R. Hornsten, M. Elnoamany, M. Cramer, G. Tamborini, G. Pagano, H. Kim, S. Soderberg, A. M. Gonzalez, N. Zlatareva, E. Marangio, F. Yang, G. Cho, I. Paunovic, C. Jons, T. Tanimoto, H. Triantafyllidi, D. Gopalan, O. Ozcan, M. Norman, G. Grazioli, F. Castillo, E. Kort, R. Bruno, J. Kostic, M. Daimon, D. Kang, C. Badiu, C. Magnino, C. Bucca, I. Joao, F. Buendia Sanchez, A. Tomaszewski, M. Alasnig, J. Kisslo, T. Kawata, S. Fernandez Casares, A. Livingston, J. Silva Cardoso, S. Korkmaz, J. Rodriguez Garcia, M. Tomaszewski, Y. Motoyoshi, A. Kaneva, E. Kinova, J. Lekakis, N. Bruun, M. Elneklawy, K. Uno, K. Nour, J. M. Ferrer, T. Wada, T. Katova, E. Ermis, F. Gaita, S. Rafla, F. Macedo, S. Woo, S. Perry, M. Lonnebakken, K. Thapa, M. Banovic, C. Selton-Suty, V. Pereira, A. Lourenco, G. Dreyfus, W. Serra, M. Hedstrom, A. Hagendorff, H. Nishino, T. Filali, M. Muratori, F. De Stefano, J. Marin, B. Jedaida, I. Rangel, J. Haertel, S. Tzortzis, A. Kalogerakis, G. Galasso, P. Hoffman, L. Chen, Y. Juilliere, V. Kostova, J. Navarro Manchon, C. J. Lopez-Guarch, J L Moya Mur, J. D. J. Baguda, C. Moretti, C. Manisty, N. Hajlaoui, H. Mahfoudhi, E. Martins, F. Bourlon, Y. Choi, C. Papadopoulos, A. Santos, I. V. Vassiliadis, A. Pereira, D. Domingo Valero, P. Iacotucci, C. Fernandez-Golfin, P. Li, I. Xanthopoulou, G. Pontone, R. Tan, D. D. Valero, D. Cramariuc, D. Lovric, F. Maffessanti, V. Pehar Pejcinovic, Y. Xu, M. Gurzun, L. Mitrofanova, P. Sousa, M. Miglioranza, A. Goncalves, I. Nedeljkovic, S. Stanic, C Di Mario, Y. Shiono, Y. Bian, E. Tossavainen, N. Risum, L. Sargento, K. Hirata, K. Said, H. Park, A. M. Argudo, T. Kubo, S. Barker, A. Chetta, R. Palma Reis, E. Malev, C. Yao, I. Papadakis, R. Medeiros, J. Tong, M. Previtali, T. Yamaguchi, S.-H. Shin, M. Sitges, C. Calinescu, J. Rueda Soriano, K. Steine, R. Ichikawa, K. Farouk, S. Pedri, J. Ripsweden, S. Carillo, G. Gelbrich, P. Rees, F. Costantino, S. Hutchings, A. Bel Minguez, A. Gaspar, M. Petrovic, M. Li Kam Wa, E. Mavronasiou, R. Winter, I. Quelhas, J. Johnson, A. Gopal, H. Jurin, R. Rordorf, M. Al-Mallah, A. Kydd, M. Ezat, A. M. Duncan, A. Kyriacou, Y. Kim, D. Mihalcea, J. Lessa, L. Mont, T. Fritz Hansen, J. Separovic Hanzevacki, D. Mesa, R. Mincu, G. Pavlidis, A.D.J. Ten Harkel, L. Gabrielli, F. Civaia, B. Vujisic-Tesic, M. Lourenco, C. Cefalu, C. Alexandrescu, L. Stefani, D. Gerede, M. Bartesaghi, C. Calin, F. Alamanni, A. Giesecke, P. Fazendas, C. Sousa, C. Ginghina, J. Magne, S. Lemoine, M. Gonzalez, C. Gohlke-Baerwolf, K. H. Hirata, S. Fawzi, H. Kisacik, B. Popescu, L. Visconti, W. Brzozowski, M. Driessen, V. Schiano Lomoriello, S. Yamada, I. Machado, F. Silveira, A. Nordin, E. Velazquez, J. Simpson, D. Vasilev, R. Rimbas, R. Murphy, C. Szymanski, T. Imanishi, M. Martirosyan, E. Najjar, J. Chambers, I. Jovanovic, A. Nagorni, E. Gunyeli, M. Omelchenko, P. De Araujo Goncalves, E. Avenatti, R. Marinov, A. Rieck, C. Tribouilloy, I. Sitges, P. Navas Tejedor, N. Lousada, W. Fehri, B. Pezo Nikolic, T. Leiner, C. Lazaro Rivera, H. Pereira, M. Loeffler, R. Hural, D. Caldeira, D. Francis, M. Di Natale, P. Salgado Filho, F. Gao, C. Alm, G. Tarsia, A. Aleixo, D. Vinereanu, C. Cotrim, M. Lotfi, B. Mc Loughlin, H. Morita, S. K. Saha, A. Djordjevic-Dikic, D. Voilliot, R. Camporotondo, J. Shin, P. Pavlov, M. A. Cattabiani, G. Sekita, A. Djordjevic Dikic, K. Ishibashi, C. Pare, J. Kwan, S. Miyazaki, V. Di Tante, E. Svenungsson, V. Giga, Y. Ino, M. Rover, J. Niewiadomska, M. Florescu, I. Skjoerten, C. Wilson, P. Davlouros, M. Hazekamp, N. Moat, A. Correia, C. Tekedis, I. Ikonomidis, B. Dilekci, L. Magda, T. Le, D. Sohn, S. Hamdy, M. Cinteza, R. Enache, A. Milan, R. Dahmani, A. Lopez Granados, J. Zamorano Gomez, E. Zorio Grima, S. Ghulam Ali, B. Demirkan, A. Shehata, M. Vono, M. Chiarlo, Miguel Mota Carmo, D. Trifunovic, B. Bijnens, Y. Yatomi, J J Jimenez Nacher, B. Rogge, R. Nagai, D. Dutka, X. Shen, I. Mordi, M. Henein, F. Celeste, G. Nadais, H. El Atroush, T. Yamano, D. Andreini, B. Beleslin, H. Suzuki, L. Yan, S. Ghio, C. C. De Sousa, S. Stoebe, S. Petrovic-Nagorni, D. Leosco, T. Komori, S. El-Tobgi, S. Mihaila, A. Madureira, T. Leiria, G. Kim, H. Haouala, B. Stuart, G. Touati, K. Oleszczak, M. Ostojic, J. Song, D. Presutti, A. Fournier, H. Daida, M. Perez Guillen, I. Kuipers, H. Hwang, B. Belesiln, K. Park, Y. Guray, D. Pfeiffer, C. Reverberi, A. Lech, A. Valentini, A. Cogo, F. Piscione, S. Negrea, S. Mezghani, V. Pilosoff, P. Sogaard, N. Blom, N. Tzemos, A. Mantovani, K. Okada, A. Turco, M. Peltier, B. Lopez Melgar, U. Guray, Q. Chen, S. Chamuleau, T. Stanton, F. Baeza, S. M. Rafla, J. Roquette, I. Almuntaser, E. Picano, D. Rusinaru, R. Kalil, R. Martin Asenjo, A. Kiotsekoglou, A. Chilingaryan, B. Candemir, P. Sonecki, A. Moulias, M. Rosca, H. Marques, A. Patrianakos, S. Sahin, J. Estornell Erill, O. Enescu, J. Spratt, P. Barbier, M. Maciel, I. Ivanac Vranesic, P. Lindqvist, T. Snow, J. Silva-Cardoso, N. Koutsogiannis, D. Ardissino, L. Zhong, K. Adamyan, L. Mccormick, A. Calin, P. Innelli, S. Yokoyama, C. Erol, P. Pabari, A. Tarr, M. Galderisi, S. Govind, B. Suran, I. Simova, E. Guyeli, T. Pinho, L. Bjornadal, B. Diaz Anton, J. Hilde, R. Sicari, C. Beladan, M. Ege, A. Zacharaki, L. Ghiadoni, A. A. La Huerta, S. Zdravkovic-Ciric, O. Huttin, K. Jensen-Urstad, F. Veglio, M. Elsedi, M. Nakabachi, P. Zinzius, D. Kim, H. Dores, A. Kakkavas, H. Badran, V. Sanchez Sanchez, E. Duo, J. Carrasco, A. Almeida, M. Virdee, M. Llemit, A. Anwar, L. Pratali, J. Monmeneu Menadas, S. Nevin, L. Fusini, F. Lombera Romero, E. Despotopoulos, E. Nyktari, G. Galanti, K. Kim, A. Van Der Hulst, H. Khachab, M. Dikic, I. Cruz, M. Melsom, J. Brugada, V. Mitic, M. Landolina, S. Turhan, V. Hansteen, D Rodriguez Munoz, J. S. De Lezo, N. Gori, Z. Baricevic, S.-P. Lee, M. Arnau Vives, S. Lee, P. Gripari, S. Humerfelt, F. Huang, T. Mikami, G. Soltan, T. Akasaka, S. Kaga, G. Penney, L. Toncelli, K. Boman, B. Basnyat, E. Kowalik, A. Bartolini, S. Georgiev, K. Shahgaldi, M. Pepi, M. Ruiz Ortiz, R. Sant'anna, H. Tsutsui, P. A. Fernandez, G. Tempesti, S. Aytekin, H. Iwano, Y. Nosir, C. Raineri, J. Rasmunsson, S. Lasarov, P. Lopez Lereu, V. Persic, F. Khan, J. Hisdal, M. Gommidh, A. Alhagoly, E. Gerdts, M. Milicia, G. Rengo, K. Kimura, F. Hakansson, M. Morenate, P. Mitev, M. Yacoub, M. Satendra, B. Kusmierczyk-Droszcz, E. Romo, R. Jankovic-Tomasevic, A. Roest, J. Stepanovic, J. Schwartz, Z. Ashour, L. Klitsie, J. Giner Blasco, M. Delgado, P. Omede, S. Mayordomo Gomez, I. Paraskevaidis, J. L. Zamorano, N. Goodfield, E. Dores, S. Davies, N. Patrascu, D. Alexopoulos, L. Donate Bertolin, D. Stanojevic, E. Psathakis, M. Dobric, P. Trivilou, H. Sasmaz, A. Marinkovic, O. Mirea, G. Sieswerda, M. Maruyama, A. M. Maceira Gonzalez, T. I. Imanishi, A. Santoro, G. Festa, R. Coma Samartin, and V. Atanaskovic

Subjects
medicine.medical_specialty, Stenosis, business.industry, Internal medicine, Cardiology, medicine, Radiology, Nuclear Medicine and imaging, General Medicine, Session (computer science), Cardiology and Cardiovascular Medicine, business, medicine.disease
Published
2012
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11. Abstracts

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O. Barthelemy, J. Silvain, D. Brieger, A. Bellemain-Appaix, G. Cayla, F. Beygui, R. Lancar, J. P. Collet, A. Mercadier, G. Montalescot, K. S. Cha, Y. H. Nam, J. H. Kim, S. Y. Park, T. H. Park, M. H. Kim, Y. D. Kim, H. C. Lee, M. S. Ahn, T. J. Hong, R. Blanco, F. Blanco, J. Szarfer, A. Garcia Escudero, G. Gigena, J. Gagliardi, A. Rodriguez, R. Sarmiento, S. Affatatto, M. Riccitelli, A. Petris, M. D. Datcu, C. Pop, M. Radoi, C. Arsenescu-Georgescu, I. Petrescu, L. Petrescu, L. Serban, E. Nechita, G. Tatu-Chitoiu, M. Dorobantu, I. Benedek, E. Craiu, C. Sinescu, D. D. Ionescu, C. Ginghina, B. Minescu, A. Izzo, P. Mantovani, L. Tomasi, L. Dall'oglio, S. Bonatti, R. Rosiello, M. Romano, F. Agostini, R. Zanini, Z. Y. Zhao, Y. J. Wu, J. J. Li, Y. J. Yany, H. Y. Qian, Y. D. Tang, A. T. Timoteo, A. Toste, A. Lousinha, R. Ramos, J. A. Oliveira, M. L. Ferreira, R. C. Ferreira, C. Cabades, J. L. Diez Gil, P. Aguar, D. Sanmiguel, A. Lopez-March, R. Marmol, L. Guerra, V. Girbes, J. Ferrando, A. Rincon De Arellano, L. Patricio, M. Blondal, T. Ainla, T. Marandi, J. Eha, M. M. Oliveira, M. N. Silva, P. S. Cunha, J. Feliciano, S. Silva, J. Kanovsky, P. Kala, J. Parenica, M. Poloczek, K. Prymusova, L. Kubkova, J. Spinar, D. Olinic, C. Homorodean, M. Ober, M. Olinic, C. Andrioaia, A. Condac, M. Masmoudi, B. Berdaoui, S. Labidi, C. Tapia Ballesteros, C. Hernandez Luis, M. G. Sandin, J. M. Vegas, R. Andion, N. Martinez, I. A. Gonzalez, M. Alvarado, I. J. Amat, J. A. San Roman, M. J. Garcia Gonzalez, E. Arroyo Ucar, C. Hernandez Garcia, M. Dorta Martin, F. Marrero Rodriguez, R. Dragu, M. Kapeliovich, H. Hammerman, D. Silva, N. Cortez-Dias, C. Jorge, J. Silva Marques, P. Carilho Ferreira, S. Robalo Martins, M. Almeida Ribeiro, C. Calisto, M. Fiuza, M. G. Lopes, P. Milicevic, M. Panic, I. Stankovic, D. Milicevic, T. Kalezic, S. Kafedzic, I. Ilic, M. Cerovic, B. Putnikovic, A. Neskovic, D. Rott, D. Leibowitz, Z. Monhart, J. Reissigova, H. Grunfeldova, P. Jansky, B. Valente, I. Villanueva Benito, I. Solla, E. Paredes, O. Diaz Castro, F. Calvo, J. A. Baz, A. Iniguez, A. Aleksova, R. Gerloni, R. Belfiore, C. Carriere, G. Barbati, E. Fabris, F. Possa, D. Nait, M. Milo, G. Sinagra, N. Marques, J. Mimoso, V. Gomes, R. M. Agra Bermejo, E. A. A. Emad Abu Assi, S. R. R. Sergio Raposeiras Roubin, P. C. G. Pilar Cabanas Grandio, C. P. G. Carlos Pena Gil, J. M. G. A. Jose Maria Garcia Acuna, J. R. G. J. Jose Ramon Gonzalez Juanatey, M. J. Daly, P. Scott, C. G. Owens, A. Tomlin, B. Smith, A. A. J. Adgey, L. R. Alvarez-Contreras, U. Juarez, A. Altamirano, A. Arias, A. Alvarez-San Gabriel, H. Gonzalez-Pacheco, C. Martinez-Sanchez, M. Rahnavardi, M. Keshtkar-Jahromi, H. Vakili, S. Gholamin, S. M. Razavi, T. Gilis-Januszewski, K.- P. Mellwig, M. Wiemer, J. Gilis-Januszewski, A. Peterschroeder, J. Koerfer, D. Horstkotte, M. Vrsalovic, B. Getaldic, N. Vrkic, H. Pintaric, S. Khan, B. Wasan, L. Moretti, P. Grossi, S. Silenzi, M. Testa, L. Candelori, L. N. Clementi, M. Forlini, L. Lando, M. L. Pezzuoli, P. Corradetti, G. Leurent, P. Y. Pennec, E. Filippi, B. Moquet, J. P. Hacot, P. Druelles, A. Rialan, G. Rouault, I. Coudert, H. Le Breton, S. Gevaert, F. Tromp, E. Vandecasteele, F. De Somer, Y. Van Belleghem, S. Bouchez, F. Martens, I. Herck, M. De Pauw, O. Ludka, M. Sepsi, R. Miklik, L. Dusek, D. Tomcikova, J. M. Garcia-Acuna, P. Aguiar-Souto, S. Raposeiras Roubin, R. Agra-Bermejo, M. Jacquet, E. Abu-Assi, J. R. Gonzalez-Juanatey, A. Ibatov, R. Labrova, R. Karlik, P. Lokaj, Q. She, S. B. Deng, S. H. Huang, L. J. Gu, J. I. A. N. Rong, Z. K. Wu, Y. Li, J. Zhang, L. Parascan, A. Campanile, L. Spinelli, G. Santulli, M. Ciccarelli, S. De Gennaro, E. Assante Di Panzillo, B. Trimarco, G. Iaccarino, E. Bobescu, G. Datcu, D. Dobreanu, B. Doka, J.- C. Charniot, C. Cosson, J. P. Albertini, R. Bittar, P. Giral, C. Cherfils, E. Guillerm, D. Bonnefont-Rousselot, A. Rusali, L. Cojocaru, I. Parepa, T. Koizumi, S. Iida, J. Sato, T. Kikutani, T. Muramatsu, S. Nishimura, N. Komiyama, W. P. Lee, B. B. Ong, K. Haralambos, D. Townsend, J. A. E. Rees, E. J. Williams, J. P. Halcox, I. Mcdowell, M. Damjanovic, G. Koracevic, D. Djordjevic-Radojkovic, M. Pavlovic, N. Krstic, S. Ciric-Zdravkovic, A. Stojkovic, Z. Perisic, S. Apostolovic, A. Faustino, L. Seca, S. Barra, F. Caetano, R. Providencia, J. Silva, P. Gomes, G. Costa, M. Costa, A. Leitao-Marques, A. L. Volkova, G. P. Arutyunov, N. A. Bylova, I. I. Dayter, Y. T. F. N. Jao, C. C. Fang, Y. Chen, C. L. Yu, S. P. Wang, J. Valencia, P. Perez-Berbel, J. M. Ruiz-Nodar, J. Pineda, P. Bordes, M. Quintanilla, V. Mainar, F. Sogorb, N. Santos, M. Serrao, H. Cafe, B. Silva, R. Oliveira, G. Caires, A. Drumond, J. Araujo, R. A. Providencia, P. L. Gomes, J. R. Pais, P. Mota, A. M. Leitao-Marques, S. Farhan, R. Jarai, I. Tentzeris, B. Vogel, M. K. Freynhofer, J. Wojta, K. Huber, M. Poli, P. Trambaiolo, F. Corsi, M. De Luca, M. Mustilli, V. Lukic, M. Simonetti, G. Ferraiuolo, M. Lettino, G. Casella, M. R. Conte, L. De Luca, G. Geraci, R. Ceravolo, A. Pani, G. Fradella, A. Schratter, H. Thiele, T. Klemm, K. Demmin, D. Lehmann, M. Mende, G. Schuler, U. Pittl, A. Chernova, S. U. Nikulina, T. Naruke, T. Inomata, T. Yanagisawa, E. Maekawa, T. Mizutani, H. Shinagawa, M. Nishii, I. Takeuchi, H. Takehana, T. Izumi, C. Paulo, J. Mascarenhas, M. Patacho, J. Pimenta, P. Bettencourt, S. Nardai, G. Y. Szabo, B. Berta, I. Edes, B. Merkely, J. Delgado Silva, R. Baptista, R. Faria, J. Trigo, P. Gago, G. Gheorghe, I. T. Nanea, A. Cristea, S. Almarichi, H. Martins, F. Saraiva, E. Jorge, P. L. Mendes, P. Monteiro, S. Costa, F. Franco, L. A. Providencia, T. Nanea, G. S. Gheorghe, S. Visan, N. Paun, R. Gaber, R. Delewi, R. Nijveldt, H. A. De Bruin, A. Hirsch, A. Van Der Laan, B. J. Bouma, J. P. G. Tijssen, A. C. Van Rossum, F. Zijlstra, J. J. Piek, H. Rus, M. Donea, C. Ciurea, G. Ifteni, G. Casolo, M. Chioccioli, M. Magnacca, J. Del Meglio, A. Comella, M. Baratto, J. Lera, L. Salvadori, C. Tessa, C. Vignali, Z. Keca, T. Momcilov Popin, G. Panic, R. White, F. Mateen, A. Weaver, Y. Agmon, E. Okisheva, D. Tsaregorodtsev, V. Sulimov, I. J. Amat Santos, C. Hernandez, C. Tapia, A. Campo, D. Fredman, L. Svensson, M. Rosenqvist, S. Tadel-Kocjancic, P. Radsel, R. Knafelj, V. Gorjup, M. Noc, E. Zima, Z. S. Jenei, E. Kovacs, I. Osztheimer, L. Molnar, A. Horvath, D. Becker, L. Geller, R. Maggi, T. Furukawa, V. Viscardi, M. Brignole, S. R. N. Leal, H. Dores, I. Rosario, J. Monge, M. J. Carvalho, I. Arroja, A. Leitao, C. Fonseca, A. Aleixo, A. Silva, S. Keuleers, P. Herijgers, M. C. Herregods, W. Budts, C. Dubois, B. Meuris, P. Verhamme, W. Flameng, F. Van De Werf, T. Adriaenssens, H. Badran, M. Elnoamany, T. Lolah, C. Olariu, C. Macarie, M. A. H. Mollik, A. I. Hassan, T. K. Paul, M. Z. Haque, R. Jahan, M. Rahmatullah, M. A. Khatun, M. T. Rahman, M. H. Chowdhury, J. Bustamante Munguira, E. Tamayo, I. Garcia-Cuenca, E. Bustamante, J. Gualis, M. L. Gomez-Martinez, S. Florez, J. I. Gomez-Herreras, R. Ramirez Rodriguez, A. M. Ramirez Rodriguez, M. A. Garcia-Bello, E. Hernadez Ortega, E. Caballero Dorta, A. Garcia Quintana, V. Piro Mastraccio, A. Medina Fernandez Aceytuno, E. Assanelli, M. De Metrio, M. Rubino, G. Lauri, A. Cabiati, J. Campodonico, M. Grazi, M. Moltrasio, I. Marana, G. Marenzi, M. Lovlien, B. Schei, R. Picon-Heras, C. Acebal, J. C. Garcia Rubira, D. Vivas Balcones, I. Nunez-Gil, B. Ruiz-Mateos, B. Ibanez, A. Fernandez-Ortiz, V. D. Vintila, O. A. Enescu, C. I. Stoicescu, C. Udroiu, M. Cinteza, G. Tatu - Chitoiu, D. Vinereanu, C. Fresco, M. De Biasio, D. Muser, R. Sappa, G. Morocutti, G. Bernardi, A. Proclemer, B. Fontanella, A. Affatato, C. Ciccarese, M. Sacchini, M. Volpini, F. Bianchetti, G. Verzura, L. Dei Cas, R. Pudil, V. Blaha, J. Vojacek, I. Paraskevaidis, I. Ikonomidis, J. Parissis, C. Papadopoulos, V. Stasinos, V. Bistola, M. Anastasiou-Nana, M. Shochat, A. Shotan, M. Kazatsker, V. Gurovich, A. Asif, E. Noiman, Y. Levy, D. Blondhaim, P. Rabinovich, S. Meisel, S. Petrovic, J. Glasnovic, M. Tomasevic, D. Sakac, S. Obradovic, O. Londono Sanchez, S. Pacreu, L. Torres, G. Mihaylov, G. M. Shaban, E. Trendafilova, V. Krasteva, T. S. Mudrov, J. P. Didon, V. Panageas, N. Vlachos, A. Pernat, I. Radan, H. Mozina, P. Pepi, F. Cionini, N. Baccaglioni, A. Viertel, J. Havers, G. Ballard, G. Groenefeld, L. M. Branco, L. Ferreira, A. Fiarresga, L. Lettieri, A. Reggiani, R. Juarez Prera, G. Blanco Palacios, A.- C. Martin, S. Manzo Silberman, A. Chaib, O. Varenne, P. Allouch, E. Salengro, A. Jegou, O. Margot, C. Spaulding, A. Diego, A. De Miguel, C. Cuellas, E. Fraile, J. Martin, B. Vega, R. Bangueses, F. Fernandez-Vazquez, A. Perez De Prado, S. Leal, M. J. Correia, J. C. Monge, J. Abecasis, C. Garcia-Garcia, I. Subirana, J. Sala, J. Bruguera, V. Valle, G. Sanz, M. Fiol, F. Aros, J. Marrugat, R. Elosua, S. N. C. Barra, A. Leitao Marques, Y. J. Yang, B. Xu, G. Y. Song, R. L. G, A. Aleksic, P. Serpytis, K. Rucinskas, A. Kalinauskas, N. Karvelyte, C. I. Santos De Sousa, S. Ferreira, J. Calaca, N. Lousada, R. Palma Reis, D. M. Gualandro, L. F. B. C. Seguro, F. G. M. Braga, O. M. Silvestre, R. L. Lage, J. Fabri, M. T. Oliveira, J. A. Urbano Moral, J. Torres Llergo, R. Solanilla Rodriguez, A. Sanchez Gonzalez, A. Martinez Martinez, C. A. Den Uil, W. K. Lagrand, M. Van Der Ent, L. S. D. Jewbali, J. M. Cheng, P. E. Spronk, M. L. Simoons, C. Mornos, D. Dragulescu, A. Ionac, J. Guardado, O. Azevedo, M. Fernandes, F. Canario-Almeida, V. Sanfins, A. Pereira, J. Almeida, V. U. Kaplunova, Y. N. Belenkov, E. V. Privalova, A. A. Fomin, A. Y. Suvorov, A. Goodkova, M. G. Rubakova, I. A. Kuznetsova, E. N. Semernin, F. Keshavarzi, J. Kojuri, V. M. Mikhailov, I. V. Vezhenkova, A. Y. A. Goodkova, I. Pavlovic, M. Schwarz, G. Jakl, P. Smetana, T. Perkmann, A. Mayr, J. Mair, G. Klug, M. Schocke, T. Trieb, W. Jaschke, O. Pachinger, B. Metzler, L. Bronze Carvalho, J. Azevedo, M. L. Andrade, M. J. Relvas, J. Coucello, G. Morais, M. Seabra, F. Afamefule, M. Luaces Mendez, R. Teijeiro-Mestre, I. J. Nunez-Gil, N. Leco-Gil, E. Madronal-Cerezo, I. Zannin, J. Ruiz, M. A. Orynchak, I. I. Vakalyuk, I. P. Vakalyuk, A. Berezin, T. Panasenko, Y. Cavusoglu, A. Cavusoglu, I. Unluoglu, M. Tek, C. Demirustu, B. Gorenek, M. Unalacak, A. Birdane, F. Yuksel, N. Ata, J. P. J. Halcox, A. Beyaztas, E. Entok, I. Uslu, A. Schaefer, U. Flierl, N. Seydelmann, J. Bauersachs, L. Calmac, S. Marinescu, G. Tatu Chitoiu, A. G. Fruntelata, S. Hamdi, Y. Maazoun, A. Neji, O. Farhat, M. Majdoub, K. Ben Hamda, F. Maatouk, S. M. Balanescu, I. Nedelciuc, D. Deleanu, F. Ortan, S. Mot, P. R. Sinnaeve, S. Moreels, M. Coosemans, T. Vydt, W. Desmet, D. Tobing, R. Rifnaldi, D. Juzar, I. Firdaus, S. Dharma, I. Irmalita, H. Kalim, R. Bejiqi, R. Retkoceri, H. Bejiqi, L. Kryeziu, M. Kelmendi, S. H. Borovci, S. M. Victor, A. Gnanaraj, R. Deshmukh, A. S. Mullasari, M. Yahalom, R. S. Kaiyal, N. Roguin, J. Bornstein, S. Atar, R. Farah, L. F. Seca, A. M. Leitao Marques, R. Margato, P. Sousa, H. Ribeiro, L. Rocha, A. Correia, J. I. Moreira, H. C. Carvalho, M. Afifi, N. Abed, A. Suarez-Barrientos, D. Vivas, F. Castro-Ferreira, E. Franco, J. C. Garcia-Rubira, V. Fuster, C. Macaya, B. Ibanez Cabeza, S. Salinger, D. Milic, T. Stanojlovic, T. Kostic, M. A. Khan, F. Vrapi, K. Naeem, J. Davar, K. Hristova, G. Pencheva, R. Radeva, S. Milanov, A. Fareed, M. Oraby, G. M. Nasr, F. Maklady, P. Dupouy, J. T. Sorensen, C. J. Terkelsen, J. F. Lassen, S. Trautner, E. F. Christensen, T. T. Nielsen, H. E. Botker, H. R. Andersen, K. A. Thygesen, L. Checco, T. Usmiani, P. L. Sbarra, M. Boffini, R. Saviolo, C. Grasso, F. Conrotto, M. Marchetti, M. Rinaldi, S. Marra, F. Moscoso Costa, J. Ferreira, L. Raposo, C. Aguiar, M. Trabulo, J. A. Silva, V. Marques, A. Swiatkowski, J. Kowalczyk, R. Lenarczyk, P. Chodor, G. Honisz, T. Was, M. Swierad, B. Sredniawa, L. Polonski, Z. Kalarus, A. S. Postadzhiyan, H. Velinov, V. Velchev, D. Hazarbasanov, M. Apostolova, B. Finkov, M. Petrovic, A. Jovelic, T. Canji, I. Srdanovic, T. Popov, M. Golubovic, K. Pavlovic, N. Cemerlic-Adjic, J. Bro-Jeppesen, J. Kjaergaard, M. C. Wanscher, S. L. Nielsen, L. S. Rasmussen, C. Hassager, M. Khan, E. Crolla, H. Morley, L. Akeroyd, Y. Beaini, C. Morley, R. H. Bekeredjian, U. Krumsdorf, W. Rottbauer, H. A. Katus, S. Pleger, A. Botelho, N. Quintal, P. Faria, S. Gomes, J. C. Roussel, T. Senage, C. Perigaud, O. Habash, M. Michel, M. Treilhaud, P. Despins, J. N. Trochu, O. Baron, D. Duveau, A. N. Kitsiou, K. Giannakopoulos, G. Papadimitriou, S. Karas, Z. Babic, V. Nikolic Heitzler, D. Milicic, M. Bergovec, M. Raguz, J. Mirat, M. Strozzi, Z. Plazonic, L. Giunio, R. Steiner, M. Freynhofer, I. Brozovic, V. Bruno, L. Leherbauer, M. Djurkovic, M. Willheim, W. Huebl, S. Hahne, I. Kozanli, K. Kalla, A. Geppert, G. Unger, A. F. Simoes Marques Assuncao Caetano, C. Faustino, A. Ariza Sole, J. C. Sanchez Salado, V. Lorente Tordera, V. Martinez Garcia, J. Salazar Mendiguchia Y Garcia, J. A. Gomez Hospital, J. Maristany Daunert, F. J. Berdejo Gago, E. Esplugas Oliveras, A. Brzozowska-Czarnek, A. Urbanik, N. Kakouros, S. Kakouros, J. Lekakis, J. Rizos, D. Kokkinos, J. Venevtseva, A. Melnikov, M. Valiahmetov, T. Gomova, I. Perelomova, J. J. Ferrer Hita, F. Bosa-Ojeda, A. Sanchez-Grande-Flecha, G. Yanes-Bowden, M. J. Vargas-Torres, A. Rodriguez-Gonzalez, C. Rubio-Iglesias-Garcia, A. Dominguez-Rodriguez, C. Enjuanes-Grau, F. Marrero-Rodriguez, A. I. Suceveanu, A. Suceveanu, L. Mazilu, L. Alexandrescu, E. Dumitru, V. Miu, V. Jitari, F. L. Voinea, K. P. Balachandran, R. Schofield, R. Sankaranarayanan, K. Helm, C. Crowe, R. Singh, J. Mcdonald, M. J. Chuen, M. Kobusiak-Prokopowicz, M. Preglowska, A. Mysiak, T. Doi, T. Sakoda, T. Akagami, T. Naka, T. Tsujino, T. Masuyama, M. Ohyanagi, N. Kume, H. Mitsuoka, K. Hayashida, M. Tanaka, L. M. Biasucci, R. Della Bona, G. Biasillo, M. Leo, M. Zaninotto, M. Plebani, F. Crea, R. Dellabona, B. Gok, A. Unalir, B. Timuralp, N. Nikulina, S. S. Yakushin, G. I. Furmenko, S. A. Akinina, R. Ingrid, L. Bronze, S. Djambazov, A. Zhivkov, I. Maznev, M. Ingeliev, R. Slavov, N. Cvetkova, V. Patarinski, L. Groch, J. Horak, N. Dimitrov, H. G. Hayrapetyan, P. Cabanas-Grandio, C. Pena-Gil, N. A. Mc Keag, C. J. Mc Cann, C. Cardwell, I. S. Young, N. Mikhalchikova, N. Burova, M. Zaccaria, P. Palmisano, V. Palumbo, M. M. Ciccone, S. Favale, K. C. Chen, W. H. Yin, J. H. Liu, S. Goncalves, J. F. Santos, P. Amador, L. N. Soares, K. Zahidova, F. Guliyev, N. Zahidov, P. Carrilho-Ferreira, J. S. Marques, J. Carvalho De Sousa, H. Uthoff, C. Thalhammer, M. Potocki, T. Reichlin, M. Noveanu, M. Aschwanden, D. Staub, N. Arenja, T. Socrates, C. Mueller, Y. Zhao, X. Wu, Q. Xue, L. Gao, H. Lin, S. Wang, K. Watanabe, A. Kawamura, T. Seko, A. Omura, S. Sakabe, A. Kasai, A. V. Starodubova, G. Storozhakov, O. Kisliak, F. Hautieva, M. Tursheva, N. Fedotova, R. C. Di Maio, J. Mclaughlin, J. D. Allen, J. M. C. Anderson, H. Khaled Nagi, O. Tayeh, W. Farok, A. Mousa, P. Neuzil, J. Skoda, J. Petru, L. Sediva, S. Kralovec, F. Holy, K. Holdova, P. Jehlicka, P. Plasil, V. Y. Reddy, S. Alabakovska, D. Labudovic, S. Jovanova, K. Tosheska, M. Alabakovski, K. Jeevaratnam, S. P. Tee, Y. Zhang, L. Guzadhur, I. S. Gurung, R. Duehmke, A. A. Grace, M. Lei, C. L. Huang, Y. Ishibashi, M. Yamauchi, Y. Akashi, H. Musha, F. Miyake, T. Hnatek, L. Kamenik, P. Sedlon, J. Luxova, B. Steuerova, J. Skvaril, M. Cernohous, M. Zavoral, N. Ratkovic, N. R. Nemanja Djenic, A. J. Aleksandra Jovelic, S. O. Slobodan Obradovic, B. G. Branko Gligic, E. Kletsiou, M. Giannakopoulou, E. Bozas, E. K. Iliodromitis, E. D. E. Papathanassoglou, M. Anton, G. Anton, M. Muraru, S. Salinger Martinovic, M. Radosavljevic, D. Stanojevic, M. Zivkovic, T. Pessoa, N. Aspromonte, C. Ronco, M. Tubaro, M. Santini, F. Colivicchi, A. Aiello, D. Cruz, A. Anzoletti Boscolo, G. Vianello, R. Valle, A. Parspour, S. Watkins, D. Datta, A. G. Nikishin, M. M. Pirnazarov, T. A. Nurbaev, Z. Motovska, M. Fischerova, P. Osmancik, M. Maly, P. Widimsky, E. Pavli, A. Dibra, J. Mehilli, L. Dibra, A. Schoemig, A. Kastrati, P. Carmo, M. Almeida, R. Teles, P. Goncalves, J. Brito, F. D'ascenzo, A. Gonella, G. Longo, A. Pullara, C. Moretti, F. Sciuto, P. Omede', G. Biondi Zoccai, G. P. Trevi, I. Sheiban, H. M. Cafe, D. Pereira, D. Freitas, D. Ortiz Berbel, J. M. Rabasa Baraibar, A. M. Leone, A. De Caterina, A. Aurelio, A. Sciahbasi, E. Lioy, C. Trani, F. Burzotta, I. Porto, A. G. Rebuzzi, K. Trusinskis, D. Juhnevica, K. Strenge, D. Sondore, I. Kumsars, S. Jegere, I. Narbute, A. Grave, I. Zakke, A. Erglis, C. Ferrari, A. L. Bartorelli, M. Saeed, D. Cozma, S. Pescariu, S. I. Dragulescu, H. S. Kamal, A. Abdelfattah, A. M. Abdelbary, H. Elassar, A. Naggar, M. Khaled, A. M. Fareed, J. M. Pernes, J. C. Gaux, M. W. Prull, B. Sasko, H. Wirdemann, A. Bittlinsky, T. Butz, H. J. Trappe, M. Perazzolo Marra, L. Cacciavillani, A. Marzari, M. De Lazzari, R. Turri, P. China, F. Corbetti, S. Iliceto, L. L. Stazhadze, E. A. Spiridonova, N. A. Bulanova, A. A. Ermolaev, L. Savic, I. Mrdovic, G. Krljanac, J. Perunicic, M. Asanin, R. Lasica, M. Matic, Z. Vasiljevic, M. Ostojic, M. Tichy, C. Andrys, A. Conti, C. Poggioni, G. Viviani, F. Bulletti, V. Boni, M. Luzzi, S. Vicidomini, M. Donati, B. Del Taglia, R. Pini, O. Sousa, R. Fontes-Carvalho, D. Caeiro, N. Dias Ferreira, G. Silva, E. Pereira, J. Ribeiro, A. Albuquerque, V. Gama Ribeiro, M. Murai, Y. Takeda, T. Shinmyo, J. Tanigawa, H. Hazui, T. Nakakohji, Y. Ohishi, M. Hoshiga, T. Ishihara, T. Hanafusa, J. Belohlavek, V. Rohn, J. Kunstyr, M. Lips, M. Semrad, F. Mlejnsky, J. Tosovsky, A. Linhart, J. Lindner, Z. Sablik, A. Samborska-Sablik, J. Drozdz, W. Gaszynski, M. M. Izquierdo-Gomez, R. Juarez-Prera, G. Blanco-Palacios, R. Lakhdar, M. Drissa, B. Jedaida, H. Drissa, F. Sampaio, H.- T. Hsin, J.- H. Huang, K.- M. Chiu, Z.- S. Chen, P.- C. Lin, L.- Y. Chen, S.- H. Chu, I. Efthimiadis, P. Skendros, A. Sarantopoulos, P. Boura, A. M. Van Der Laan, P. A. Van Der Vleuten, M. Klees, J. G. P. Tijssen, B. E. Backus, A. J. Six, J. H. Kelder, A. Mosterd, E. G. Mast, T. P. Mast, R. Braam, R. Tio, R. Veldkamp, P. A. Doevendans, N. Paarup Dridi, L. Holmvang, T. Engstroem, S. Rekik, J. Brunet, F. X. Hager, G. Bayet, L. Meille, J. M. Quatre, J. Sainsous, P.- H. Chu, C.- H. Tang, N. Pogosova, I. E. Koltunov, I. D. Sapunova, V. A. Vigodin, R. Uhliar, A. Schmidt, B. Brockmeyer, A. Suzuki, Y. Eki, H. Higuchi, A. Yukawa, R. Yamauchi, Y. Sato, Y. Endo, J. Salazar Mendigucha Garcia, S. Homs Vila, A. Cequier Fillat, R. Andion Ogando, M. Sandin Fuentes, J. M. Vegas Valle, I. A. Gonzalez Garcia, I. A. Duro Aguado, A. J. Palomino Doza, I. Gomez Salvador, J. A. San Roman Calvar, T. M. Mamarasulov, L. Todorovic, Z. C. H. Cherneva, S. D. Denchev, K. Heltai, A. Boytsov, N. N. Nikulina, D. Zanna, V. Marangelli, C. Caiati, R. Picon Heras, M. J. Loureiro, I. Urazovskaya, D. Vinogradova, E. Vasilieva, A. Shpektor, E. Conti, M. B. Musumeci, F. M. Lauri, E. Dito, M. De Giusti, A. Lallo, D. Fusco, M. Davoli, M. Volpe, C. Autore, H. Gamra, Z. Dridi, M. Hassine, F. Addad, I. Gherissi, A. Reda, M. Mahjoub, S. Bouraoui, M. Abdennadher, F. Betbout, P. M. F. P. Mota, J. D. Silva, R. Jankovic Tomasevic, V. Djordjevic, D. Djordjevic Radojkovic, A. Scafa Udriste, A. Fruntelata, E. Gainoiu, S. Bogdan, D. Zamfir, C. Teodorescu, M. Guran, D. Constantinescu, A. Konopka, M. Banaszewski, I. Wojtkowska, J. Stepinska, J. V. Vidergold, I. V. Osipova, T. V. Tavrovskaya, J. V. Galkina, A. V. Timofeev, R. I. Vorobyov, E. N. Vorobyova, L. Matos, A. C. C. Carvalho, W. Oliveira, F. Cintra, D. Poyares, M. Andersen, R. Martins, S. Tufik, P. Ostadal, J. Brada, S. Horakova, M. Mlcek, V. Hrachovina, O. Kittnar, I. V. Gorudko, I. V. Buko, S. N. Cherenkevich, L. Z. Polonetsky, V. Y. Plotkin, M. A. Timoshina, S. V. Azanchevskaya, N. N. Chromov-Borisov, A. Vorlat, L. Snoep, M. J. Claeys, C. J. Vrints, A. Palazzuoli, M. Caputo, I. Quatrini, A. Calabro, G. Antonelli, M. S. Campagna, B. Franci, R. Nuti, A. Maisel, M. Negrini, T. Minora, P. Marino, R. Seregni, E. Tavlueva, O. Barbarash, L. Barbarash, T. Janota, J. Kudlicka, K. Malik, D. Wichterle, J. Hradec, R. Body, S. D. Carley, G. Mcdowell, M. Nuttall, C. Wibberley, M. France, J. K. Cruickshank, K. Mackway-Jones, M. Leon, C. Cozma, F. Mitu, D. R. Almeida, C. B. Dias, I. Burazor, M. Burazor, M. Krstic, M. Lazovic, M. Vukmanovic, J. Djordjevic, Z. Radovanovic, D. Ilic, P. Bosnjakovic, A. C. Ferreira, P. S. Mateus, P. Fontes, T. Teixeira, G. Conte, A. Menozzi, E. Solinas, M. G. Bolognesi, I. Tadonio, F. Mantovani, A. Cattabiani, L. Vignali, D. Ardissino, O. Tautu, A. Alexandrescu, R. Niculescu, R. Jankovic, N. Bozinovic, C. Santos, F. Costa, G. Cardoso, I. Correia, K. Fountoulaki, S. Kastellanos, E. Voltirakis, A. Kokotos, C. Michalakeas, K. Kontsas, K. Hasioti, E. T. Iliodromitis, M. G. Sandin Fuentes, E. Zatarain Nicolas, N. Martinez Uruena, M. Alvarado Montes De Oca, V. Dytrych, T. Kovarnik, O. Smid, A. Kral, A. G. Aroutunov, S. Intwala, I. Jegere, H. S. H. Shaalan, Z. Pagava, R. Agladze, R. Shakarishvili, N. Sharashidze, L. Gujejiani, G. Saatashvili, T. Z. Katova, V. Kostova, Y. Simova, S. Vukotic, S. Rafajlovski, R. Romanovic, N. Antonijevic, B. Gligic, M. Hutyra, T. Skala, D. Horak, D. Vindis, M. Taborsky, A. Contine, M. Del Pinto, F. Angeli, P. Verdecchia, F. Borgognoni, E. Grikstaite, P. Pantano, G. Ambrosio, C. Cavallini, C. Bonanad, J. Sanchis, V. Bodi, J. Nunez, X. Bosch, M. Heras, M. Pellicer, A. Llacer, L. Adao, M. Oliveira, H. Goncalves, J. Primo, V. Gama, C. Lombardi, M. Metra, S. Bugatti, E. Pasotti, F. Quinzani, M. Adamo, C. Villa, R. Rovetta, A. Manerba, M. Mariani, A. Dushpanova, M. Baroni, E. Cerone, A. Nardelli, J. Gianetti, S. Berti, F. Feliciano, R. Soares, S. Santos, A. Kruger, D. Vondrakova, J. Herget, C. Navarro, N. A. Cromie, J. A. A. Adgey, D. Caeiro Pereira, P. Braga, R. Fontes Carvalho, A. Rodrigues, M. Goncalves, L. Simoes, and K. V. Borisov

Subjects
Cardiology and Cardiovascular Medicine
Published
2010
Full Text
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12. Genetic studies in complex disease

Author

P, Merlini and D, Ardissino

Subjects
Polymorphism, Genetic, Genetic Linkage, Research Design, Statistics as Topic, Myocardial Infarction, Humans, Genetic Predisposition to Disease, Hematology
Published
2004
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13. Genetic predisposition to atorvastatin-induced myopathy: a case report

Author

M, Francesca Notarangelo, N, Marziliano, M, Antonietta Demola, F, Pigazzani, A, Guidorossi, P, Angelica Merlini, and D, Ardissino

Subjects
Male, Polymorphism, Genetic, Muscular Diseases, Heptanoic Acids, Liver-Specific Organic Anion Transporter 1, Atorvastatin, Humans, Organic Anion Transporters, Genetic Predisposition to Disease, Pyrroles, Coronary Artery Disease, Middle Aged, Aged
Abstract

The major clinical complication of statins is a variety of muscle complaints ranging from myalgia to rhabdomyolysis. There is growing evidence that carriers of genetic polymorphisms in the enzymes and transporters implicated in statin disposition, particularly the SLCO1B1 gene, are at increased risk of myotoxicity. Our objective is to report on two cases of statin-induced myopathy occurring in a family with two patients who are carriers of the loss of function SLCO1B1 genetic variant and to briefly review the related literature.Patient 1, a 48-year-old man with history of coronary artery disease, experienced rapidly evolving muscle pain and weakness of the extremities during treatment with atorvastatin 40 mg. Patient 2, a 65-year-old man, father of patient 1, had symptoms similar to those of his son after 2 weeks' treatment with the same statin. Atorvastatin was stopped in both cases, and symptoms resolved. On the basis of family relationship between the two patients, it was possible to hypothesize a genetic basis for the myopathy. Genotyping showed the patients to be carriers of the rs4363657 polymorphism of SLCO1B1 gene.The two cases reported here and the brief literature review emphasize the impact of genetic factors on the risk of myopathy with statins. Although genotyping all patients before initiating therapy is not recommended at present, pharmacogenetic testing may be useful for new patients who have a family history of statin-induced myopathy.

Published
2012

14. Long-term mortality in patients unsuitable for surgical revascularization undergoing elective left main coronary artery angioplasty

Author

L, Vignali, G, Talanas, A, Menozzi, M A, Cattabiani, E, Solinas, E, Aurier, and D, Ardissino

Subjects
Aged, 80 and over, Male, Drug-Eluting Stents, Coronary Artery Disease, Kaplan-Meier Estimate, Middle Aged, Severity of Illness Index, Survival Analysis, Italy, Elective Surgical Procedures, Myocardial Revascularization, Feasibility Studies, Humans, Female, Stents, Angioplasty, Balloon, Coronary, Coronary Artery Bypass, Aged, Retrospective Studies
Abstract

Elective percutaneous coronary intervention (PCI) of left main coronary artery disease remains an important challenge in interventional cardiology. Nonetheless, this procedure is useful for patients with significant left main stenosis who are candidates for revascularization but unsuitable for coronary artery bypass graft. In this study the Authors sought to evaluate the safety and long-term mortality of PCI of left main coronary artery disease. Secondary endpoints were to analyse long-term mortality in various categories (patients75 years vs patients75 years, males vs females, drug eluting stents [DES] vs bare metal stents [BMS]).Between January 2003 and December 2006, 131 patients who consecutively under-went PCI on left main stem were reviewed. The mean follow-up time was 14.0+/-10.8 months. Survival curves were plotted with the Kaplan-Meier method and compared with the Log-rank test.The Kaplan-Meier curves did not show statistically significant differences in terms of all-cause mortality at follow-up between protected and unprotected left main coronary disease (12% vs 14% respectively, P=0.67). In the protected left main group, there was a significantly higher use of DES compared with unprotected left main group (59% vs 43%, P=0.02).The data show that PCI for left main coronary disease is feasible, safe and with an acceptable long-term mortality rate in patients at high-surgical risk unsuitable for surgical revascularization.

Published
2008

16. Use of digitalis in the treatment of heart failure: data from the Italian Network on Congestive Heart Failure (IN-CHF)

Author

Camerini, A, Griffo, R, Aspromonte, N, Ingrilli', F, Lucci, D, Naccarella, F, Maggioni, Ap, IN-CHF INVESTIGATORS- Piemonte Borgomanero (M. Zanetta, A. M. Paino), Casale Monferrato (M. Ivaldi, A. Giusti), Uslenghi, Cuneo (E., Milanese, U., Deorsola), A., Greco Lucchina, Orbassano (P., Pozzi, R., Rabajoli), F., Veruno (P. Giannuzzi, E. Bosimini), Valle d’Aosta Aosta (M. De Marchi, G. Begliuomini), Richichi, Lombardia Belgioioso (I., Ferrari, A., Barzizza), F., Bergamo Riabilitazione Cardiologica (A. Gavazzi, F. Dadda), Bergamo U. O. Cardiologia Cardiovascolare (A. Gavazzi, A. Fontana), Brescia (C. Rusconi, P. Faggiano), Cogo, Cassano D’Adda (R., Castiglioni, G., Gibelli), G., Chiari (F. Bortolini, A. L. Turelli), Como (G. Ferrari, R. Jemoli), Pirelli, Cremona (S., Bianchi, C., Emanuelli), C., De Martini), Desio (M., Erba (G. Maggi, D. Agnelli), Ferrara), Esine (E., Rovelli, Garbagnate Milanese (G., Lureti, G., Cazzani), E., Giordano, Gussago (A., Zanelli, E., Domenighini), D., Legnano (S. De Servi, C. Castelli), Mariano Comense (G. Bellati, E. Moroni), Milano Fondazione Don Carlo Gnocchi IRCCS (M. Ferratini, E. Gara), Malliani, Milano Sacco (A., Muzzupappa, S., Turiel, M., Guzzetti, S., Cappiello), E., Milano Niguarda (S. Klugmann, F. Recalcati), Milano Pio Albergo Trivulzio (S. Corallo, D. Valenti), Cobelli), Montescano (F., Monza (A. Grieco, A. Vincenzi), Schweiger, Passirana-Rho (C., Rusconi, F., Palvarini), M., Ferrari, Pavia IIAARR S. Margherita (E., Carbone), M., Tavazzi, Pavia IRCCS Policlinico San Matteo (L., Campana, C., Serio), A., Croce, Saronno (A., Nassiacos, D., Meloni), S., Seriate (P. Giani, T. Nicoli), Sondalo (G. Occhi, P. Bandini), Sondrio (S. Giustiniani, M. Moizi), Tradate Fondazione S. Maugeri (R. Pedretti, M. Paolucci), Onofri, Tradate Ospedale di Circolo Galmarini (M., Amati, L., Ravetta), M., Venco, Varese Medicina Interna Azienda Ospedaliera e Universitaria (A., Bertolini, A., Saggiorato), P., Salerno Uriarte, Varese U. O. Cardiologia Azienda Ospedaliera e Universitaria (J., Morandi, F., Provasoli), S., Vizzolo Predabissi (M. Lombardo, P. Quorso), P. A. Trento Rovereto Cardiologia Ospedale Civile (G. Vergara, A. Ferro), Rovereto Medicina Ospedale Civile (M. Mattarei, C. Pedrolli), Catania, Veneto Belluno (G., Tarantini, L., Russo), P., Castelfranco Veneto (L. Celegon, G. Candelpergher), Conegliano Veneto (P. Delise, C. Marcon), Guarnerio, Feltre (M., De Cian, F., Agnoli), A., Montebelluna (G. Neri, M. G. Stefanini), Iliceto, Padova (S., Boffa, G. M., Tiso), E., Pieve di Cadore (J. Dalle Mule, A. Stefania), San Bonifacio (R. Rossi, E. Carbonieri), Treviso (P. Stritoni, G. Renosto), Fontanelli, Vicenza (A., Ottani, F., Varotto), L., Perini), Villafranca (G., Friuli Venezia Giulia Gorizia (D. Igidbashian, G. Giuliano), Monfalcone (T. Morgera, E. Barducci), San Vito al Tagliamento (M. Carone, G. Pascottini), Fioretti, Udine A. O. S. Maria della Misericordia (P., Albanese, M. C., Fresco), C., Udine Casa di Cura Città di Udine (P. Venturini, F. Picco), Liguria Arenzano (R. Griffo, A. Camerini), Chierchia, Genova Ospedali Civili (S., Mazzantini, S., Torre), F., Spirito, Genova Ospedali Galliera (P., Derchi, G., Delfino), L., Genova-Sestri Ponente (S. Domenicucci, L. Pizzorno), Località S. Caterina-Sarzana (G. Filorizzo, D. Bertoli), Rapallo (G. Gigli, S. Orlandi), Gentile), Sestri Levante (A., Emilia Romagna Bentivoglio (G. Di Pasquale, R. Vandelli), Bologna Cardiologia Tiarini-Corticella (F. Naccarella, M. Gatti), Forlì (F. Rusticali, G. Morgagni), Modena Medicina d’Urgenza Ospedale Civile S. Agostino (S. Zucchelli, M. Pradelli), Modena U. O. Cardiologia Ospedale Civile S. Agostino (G. R. Zennaro, G. Alfano), Modena, Modena Ospedale Policlinico (M. G., Reggianini, L., Coppi), F., Parma (D. Ardissino, W. Serra), Piacenza (A. Capucci, F. Passerini), Riccione (L. Rusconi, P. Del Corso), Piovaccari, Rimini (G., Bologna, F., Caccamo), L., Gambarati), Scandiano (G., Bernardi, Toscana Castelnuovo Garfagnana (D., Mariani, P. R., Volterrani), C., Cosmi), Cortona (F., Empoli (V. Mazzoni, F. Venturi), Firenze Divisione di Cardiologia A. O. Careggi (D. Antoniucci, G. Moschi), Zuppiroli, Firenze U. O. Cardiologia 3 A. O. Careggi (A., Pieri, F., Beligni), C., Firenze U. O. Cardiologia 2 A. O. Careggi (M. Ciaccheri, G. Castelli), Santoro, Firenze Nuovo Ospedale San Giovanni di Dio (G. M., Minneci, C., Sulla), A., Firenze P. O. di Camerata (F. Marchi, G. Zambaldi), Fucecchio (A. Zipoli, A. Geri Brandinelli), Grosseto (S. Severi, G. Miracapillo), Pesola, Lido di Camaiore (A., Comella, A., Magnacca), M., Lucca (E. Nannini, A. Boni), Mantini, Montevarchi (G., Bongini, M., Palmerini), L., Vergoni, Pescia (W., Italiani, G., Di Marco), S., Pisa A. O. Pisana (M. De Tommasi, A. M. Paci), Pontedera (G. Tartarini, B. Reisenhofer), Umbria Città di Castello (M. Cocchieri, D. Severini), Foligno (L. Meniconi, U. Gasperini), Ambrosio, Perugia (G., Alunni, G., Murrone), A., Spoleto (G. Maragoni, G. Bardelli), Mocchegiani, Marche Ancona Centro Cardiologia Ambulatoriale G. M. Lancisi (R., Pasetti, L., Budini), A., Ancona Divisione di Cardiologia G. M. Lancisi (G. Perna, D. Gabrielli), Russo, Ancona Geriatrico Sestilli-INRCA IRCCS (P., Testarmata, P., Antonicelli), R., Camerino (R. Amici, B. Coderoni), Lazio Albano Laziale (G. Ruggeri, P. Midi), Frascati (G. Giorgi, F. Comito), Frosinone (G. Faticanti, F. Qualandri), Grottaferrata (D. Galileo Faroni, C. Romaniello), Roma INRCA (F. Leggio, D. del Sindaco), Majid Tamiz, Roma C. Forlanini (A., Avallone, A., Suglia), F., Roma Cristo Re (V. Baldo, E. Baldo), Roma I U. O. Cardiologia San Camillo (E. Giovannini, G. Pulignano), Roma II Divisione di Cardiologia con UTIC San Camillo (S. F. Vajola, E. Picchio), Tanzi, Roma Serv. Centr. Cardiologia-PS Cardiologico San Camillo (P., Pozzar, F., Terranova), A., Santini, Roma San Filippo Neri (M., Ansalone, G., Magris), B., Boccanelli, Roma San Giovanni (A., Cacciatore, G., Bottero), G., Palamara, Roma Sandro Pertini (A., Valtorta, C., Salustri), A., Roma S. Andrea (M. Volpe, L. De Biase), Gaspardone, Roma S. Eugenio (A., Amaddeo, F., Barbato), G., Ceci, Roma Santo Spirito (V., Aspromonte, N., Chiera), A., Scabbia, Viterbo (E. V., Pontillo, D., Castellani), R., Abruzzo Popoli (C. Frattaroli, A. Mariani), De Simone, Vasto (G., Levantesi, G., Di Marco), G., Molise Larino Medicina Generale-U. O. Geriatria (F. Porfilio, A. Pasquale Potena), Staniscia, Termoli (D., Colonna, N., Montano), A., Mininni, Campania Napoli Divisione di Cardiologia A. O. V. Monaldi (N., Miceli, D., Scherillo), M., Napoli I Divisione Med-Centro Diagnosi e Cura SCC A. O. V. Monaldi (P. Sensale, O. Maiolica), Napoli Medicina Incurabili (M. Visconti, A. Costa), Napoli Cardiologia San Gennaro (P. Capogrosso, A. Somelli), Vergara, Nola U. O. Cardiologia e UTIC P. O. Maria della Pietà (G., Napolitano, F., Provvisiero), P., Oliveto Citra (G. D’Angelo, P. Bottiglieri), Puglia Bari (G. Antonelli, N. Ciriello), Ignone, Brindisi (G., Angelini, E., Andriulo), C., Casarano (G. Pettinati, F. De Santis), Francavilla Fontana (V. Cito, F. Cocco), Galatina (F. Daniele, A. Zecca), Gallipoli (F. Cavalieri, C. Picani), Lecce Vito Fazzi (F. Magliari, A. De Giorgi), Santoro), Mesagne (V., San Pietro Vernotico (S. Pede, A. Renna), Scorrano (E. De Lorenzi, O. De Donno), Baldi, Taranto S. S. Annunziata (N., Polimeni, G., Russo), V. A., Tricase (A. Galati, R. Mangia), Basilicata Policoro (B. D’Alessandro, L. Truncellito), Calabria Belvedere Marittimo (F. P. Cariello, F. Rosselli), Catanzaro U. O. Cardiologia Policlinico (G. Borrello, M. Affinita), Catanzaro U. O. Malattie Cardiovascolari Policlinico (F. Perticone, C. Cloro), Sollazzo, Cetraro (G., Matta, M., Lopresti), Venneri, Cosenza Cardiologia Annunziata (N., Misuraca, G., Caporale), R., Cosenza Medicina Annunziata (A. Noto, P. Chiappetta), Tassone), Reggio Calabria E. Morelli (F., Salituri), Rossano (S., Iannopollo, Siderno (M., Errigo, C., Marando), G., Trebisacce (L. Donnangelo, G. Meringolo), Canonico), Sicilia Avola (G., Carini, Catania Cannizzaro (V., Coco, R., Franco), M., Catania Cardiochirurgia Ferrarotto (M. Abbate, G. Leonardi), Messina Papardo (R. Grassi, G. Di Tano), Consolo), Messina Piemonte (G., Coglitore, Messina (S., Cento, D., De Gregorio), C., Palermo Casa del Sole Lanza di Trabia (V. Sperandeo, M. Mongiovì), Palermo Buccheri La Ferla FBF (A. Castello, A. M. Schillaci), Palermo Civico e Benfratelli (E. D’Antonio, U. Mirto), Di Pasquale), Palermo G. F. Ingrassia (P., Palermo V. Cervello (A. Canonico, M. Floresta), Battaglia, Palermo P. O. Villa Sofia (A., Ingrillì, F., Cirrincione), V., Piazza Armerina M. Chiello (B. Aloisi, A. Cavallaro), Braschi, Trapani (G. B., Ledda, G., Rizzo), C., Sanna, Sardegna Cagliari San Michele Brotzu (A., Porcu, M., Salis), S., Lai, Cagliari SS. Trinità (C., Pili, G., Piras), S., Iglesias (E. Spiga, G. Pes), Nuoro (G. Mureddu, I. Maoddi), and Sassari SS. Annunziata (P. Terrosu, F. Uras).

Subjects
Adult, Heart Failure, Male, Dose-Response Relationship, Drug, Digitalis Glycosides, Middle Aged, Prognosis, Risk Assessment, Severity of Illness Index, Survival Analysis, Drug Administration Schedule, Drug Utilization, Treatment Outcome, Italy, Atrial Fibrillation, Heart Function Tests, Multivariate Analysis, Ambulatory Care, Confidence Intervals, Odds Ratio, Humans, Female, Registries, Aged, Retrospective Studies
Abstract

Since the large multicenter DIG trial has shown no effects of digitalis on the all-cause mortality of patients with chronic heart failure (HF), the broad prescription of this drug in patients with HF appears to be at the very least, questionable. The aims of this study were: to analyze prescription patterns of digitalis, from 1995 to 2000, in a large group of outpatients with HF; to analyze the independent predictors of digitalis prescription and to evaluate the impact of the results of the DIG trial on the prescription rate of this drug.From 1995 to 2000, 11 070 HF outpatients (mean age 64 +/- 12 years, ejection fraction 35 +/- 12%) were enrolled in a large Italian database.Out of 11 070 patients, 7198 (65%) were treated with digitalis. At multivariate analysis, the following variables were independently associated with digitalis prescription; atrial fibrillation (odds ratio [OR] 3.3, 95% confidence interval [CI] 2.9-3.8), ejection fraction30% (OR 1.7, 95% CI 1.5-1.9), NYHA class III-IV vs II-III (OR 1.3, 95% CI 1.2-1.5), admission for HF during the previous year (OR 1.4, 95% CI 1.2-1.5). After the publication of the DIG trial, there was a significant reduction in the rate of digitalis prescription: the percentage of patients taking digitalis fell from 68% in 1996-1997 to 61% in 1998-1999 (p0.001).Over 60% of Italian outpatients with HF were treated with digitalis; as expected, patients with a low ejection fraction, atrial fibrillation and in a more advanced stage of HF are more likely to receive this drug. Finally, after the publication of the DIG trial, the rate of digitalis prescription significantly decreased.

Published
2004

17. Identification of differentially expressed genes in coronary atherosclerotic plaques from patients with stable or unstable angina by cDNA array analysis

Author

Merlini Pa, D. Ardissino, Eugenia Biguzzi, S. Blakemore, S. Lucreziotti, Elena M. Faioni, Francesco Falciani, A. M. Randi, E. Bramucci, M. Lennon, and Pier Mannuccio Mannucci

Subjects
Regulation of gene expression, Inflammation, Pathology, medicine.medical_specialty, Unstable angina, Gene Expression Profiling, Thrombosis, Hematology, Coronary Artery Disease, Biology, medicine.disease, Angina Pectoris, Coronary artery disease, Gene expression profiling, Angina, Tissue factor, Gene Expression Regulation, Complementary DNA, Gene expression, medicine, Cluster Analysis, Humans, Oligonucleotide Array Sequence Analysis
Abstract

The composition of atherosclerotic plaques is a crucial factor in determining rupture, thrombosis and clinical events. In this study, we analyzed gene expression in coronary plaques from patients with stable or unstable angina using gene arrays. Total RNA was extracted from eight plaques collected by therapeutic directional coronary atherectomy. cDNA probes, generated by amplification, were hybridized to nylon arrays containing 482 genes. Here we report the results for the inflammation, adhesion and hemostasis subsets. Many genes not previously associated with atherosclerosis, such as the lymphocyte adhesion molecule MadCAM, were expressed in the plaques. anova analysis showed higher tissue factor (TF) expression in unstable angina samples. Five genes were expressed at lower levels in unstable angina samples: anticoagulant protein S, cyclooxygenase (COX)-1, interleukin (IL)-7 and chemokines monocyte chemotactic protein (MCP)-1 and -2. Gene arrays provide a new approach to study plaque composition and identify candidate markers of plaque instability.

Published
2003

18. [Restenosis: mechanisms]

Author

V, Cucci, G, Gonzi, and D, Ardissino

Subjects
Coronary Restenosis, Hyperplasia, Humans, Thrombosis, Prognosis, Tunica Intima
Published
2002

19. Effect of hirudin vs heparin on haemostatic activity in patients with acute coronary syndromes; the GUSTO-IIb haemostasis substudy

Author

K, Kottke-Marchant, M C, Bahit, C B, Granger, P, Zoldhelyi, D, Ardissino, L, Brooks, J H, Griffin, R F, Potthoff, F, Van de Werf, R M, Califf, and E J, Topol

Subjects
Male, Hemostasis, Heart Diseases, Heparin, Thrombin, Syndrome, Hirudins, Middle Aged, Treatment Outcome, Double-Blind Method, Fibrinolytic Agents, Hirudin Therapy, Acute Disease, Humans, Female, Blood Coagulation, Aged
Abstract

We compared the effects of hirudin and heparin on thrombin generation and activity among 350 patients with acute coronary syndromes enrolled in the GUSTO-IIb trial.We obtained blood at baseline; at 4, 8, and 24h into infusion; at drug termination; and 6 and 24h after termination. We assayed for thrombin activity (fibrinopeptide A, activated protein C, thrombin-antithrombin complex), thrombin generation (prothrombin fragment 1.2), and platelet activation (platelet factor 4). Median baseline fibrinopeptide A and platelet factor 4 levels were elevated. Thrombin formation tended to increase with hirudin and decrease with heparin; by 8h into infusion, thrombin formation was significantly less for heparin (P0.01). Most patients showed reduced thrombin activity and platelet activation during infusion of either agent. Hirudin-assigned patients had significantly lower fibrinopeptide A levels during infusion. Six h post-termination, both groups had increased thrombin activity. Thrombin formation was increased in heparin patients (P0.0001), significantly more than with hirudin (P=0.005). Higher values of haemostasis markers tended to be associated with poorer 30-day outcomes.Although hirudin did not prevent generation of new thrombin, it appeared to inhibit thrombin activity more than did heparin and produced slower increases in thrombin formation after discontinuation. The reelevation of thrombotic markers after stopping intravenous antithrombin therapy and the tendency toward increased thrombotic events with post-treatment increases in marker levels suggest an ongoing, clinically significant prothrombotic state. These results raise the possibility of improving on current antithrombotics by preventing thrombin generation and thrombin activity and by sustained suppression of the prothrombotic state.

Published
2002

21. [New strategies in the treatment of acute myocardial infarction]

Author

G, Gonzi and D, Ardissino

Subjects
Clinical Trials as Topic, Fibrinolytic Agents, Microcirculation, Angioplasty, Myocardial Infarction, Animals, Humans, Thrombosis, Platelet Glycoprotein GPIIb-IIIa Complex
Abstract

A number of experimental and clinical studies have recently underlined the importance, in acute myocardial infarction, of platelet adhesion and aggregation after plaque rupture. During clot resolution, platelet-rich thrombi are relatively resistant to fibrinolytic agents, mainly due to the release of plasminogen inhibitor-1 by platelets which are activated as a result of the increase in thrombin generation induced by plasminogen activator therapy despite heparin administration. Platelet glycoprotein (GP) IIb/IIIa integrin receptor blockers prevent platelet aggregation by blocking the final pathway of platelet activation. Thus, they also prevent the formation of an intraluminal white thrombus without affecting adhesion. Animal and human studies have shown that the potent inhibition of platelet GP IIb/IIIa receptors can lead to modest reperfusion rates even without exogenous fibrinolytic therapy. This suggests that combining the "dethrombotic" effects of a GP IIb/IIIa antagonist with lower fibrynolytic doses may result in a synergistic effect. Preclinical studies including patients with myocardial infarction have shown that such combined treatment increases the incidence, speed and durability of reperfusion. It has also been proved to be useful in improving the microcirculatory coronary flow and in facilitating subsequent percutaneous coronary interventions. In the phase III GUSTO V trial, abciximab combined with 5 + 5 U of reteplase and low-dose weight-adjusted heparin led to a 30-day mortality rate that was similar to that obtained with full-dose reteplase (10 + 10 U) and standard heparin therapy, without causing a significant increase in the incidence of intracranial hemorrhage. The results of this trial offer a rationale for alternative reperfusion therapy, although further analyses, including a 1-year follow-up, are needed to define the patient groups that are most likely to benefit from such a new regimen.

Published
2001

23. Prothrombotic genetic markers

Author

M L, Rossi, P A, Merlini, and D, Ardissino

Subjects
Genetic Markers, Risk Factors, Coronary Thrombosis, Mutation, Fibrinogen, Humans, Prothrombin, Platelet Glycoprotein GPIIb-IIIa Complex, Factor VII
Abstract

The last decade has been characterized by an explosion of research studies on genetic epidemiology. In particular, as far as ischemic heart disease is concerned, a lot of research was focused on prothrombotic genetic risk factors. Unfortunately, the success of this approach in the field of venous thrombosis has not been replicated in the field of myocardial infarction. In the present editorial, a comment on the studies already available is provided and the possible limitations of the present approach are analyzed.

Published
2001

24. Laboratory markers of hypercoagulability

Author

M L, Rossi, P A, Merlini, and D, Ardissino

Subjects
Myocardial Infarction, Humans, Thrombophilia, Enzyme-Linked Immunosorbent Assay, Thrombosis, Angina, Unstable, Syndrome, Biomarkers, Blood Coagulation Factors
Abstract

Investigations carried out over the last 40 years have demonstrated that coronary artery thrombosis is the critical event underlying myocardial infarction and unstable angina. The existence of a prolonged hypercoagulable state preceding the thrombotic event has been postulated for some time and significant associations have been established between the plasma concentrations of a number of hemostatic variables and the frequency of myocardial infarction. High plasma fibrinogen, factor VII/VIIa, tissue-type plasminogen activator and plasminogen activator inhibitor levels have been associated with at least as great a risk of developing myocardial (re)infarction or sudden death as high cholesterol levels, especially in the young. In the last year more sensitive assays have been developed, and they should allow a precise biochemical definition of hypercoagulable states. The significance of these new assays and their role in defining a hypercoagulable state in different conditions are analyzed.

Published
2001

25. Reactivation of ischemic events in acute coronary syndromes: results from GUSTO-IIb. Gobal Use of Strategies To Open occluded arteries in acute coronary syndromes

Author

M C, Bahit, E J, Topol, R M, Califf, P W, Armstrong, D A, Criger, V, Hasselblad, A, Betriu, J, Hirsh, D, Ardissino, and C B, Granger

Subjects
Male, Heparin, Myocardial Infarction, Thrombosis, Middle Aged, Antithrombins, Recombinant Proteins, Isoenzymes, Survival Rate, Electrocardiography, Hirudin Therapy, Recurrence, Risk Factors, Creatine Kinase, MB Form, Humans, Female, Thrombolytic Therapy, Creatine Kinase, Aged, Randomized Controlled Trials as Topic
Abstract

We sought to determine the incidence of and risk factors for thrombotic events early after discontinuing antithrombin therapy in patients with acute coronary syndromes.Discontinuation of treatment with heparin and other thrombin inhibitors in patients with unstable coronary syndromes has related to clinical and biochemical evidence of early reactivation of thrombosis.We studied 8,943 of the 12,142 patients with acute coronary syndromes enrolled in the Global Use of Strategies To Open occluded arteries in acute coronary syndromes trial of hirudin versus heparin. We excluded patients who received no study drug, lacked timing data, died or had myocardial (re)infarction [(re)MI] during study-drug infusion, or began heparin treatment within 2 h after treatment with the study drug was stopped. We assessed the incidence and timing of (re)MI by type and timing of antithrombin treatment.In all, 215 patients (2.4%) suffered (re)MI, 49 within 12 h of antithrombin therapy discontinuation and 166 between hour 12 and hospital discharge. The duration of infusion did not differ between the hirudin and heparin groups. The rate of early re(MI) after drug therapy discontinuation was significantly higher in patients given heparin versus hirudin (0.8% vs. 0.3%, p = 0.002). Patients with (re)MI had higher mortality at 30 days (23.6% vs. 2.4%, p = 0.001) and 1 year (35.2% vs. 6.7%, p = 0.001) compared with patients without (re)MI.The incidence of (re)MI was clustered within 12 h of heparin therapy discontinuation, with the greatest risk within 4 h. There was no evidence of early reactivation of thrombotic events after hirudin. Patients who had (re)infarction had worse outcomes. Better understanding of the mechanism and possible prevention of recurrent thrombosis is needed.

Published
2001

26. Influence of diabetes mellitus on clinical outcomes across the spectrum of acute coronary syndromes. Findings from the GUSTO-IIb study. GUSTO IIb Investigators

Author

D K, McGuire, H, Emanuelsson, C B, Granger, E, Magnus Ohman, D J, Moliterno, H D, White, D, Ardissino, J W, Box, R M, Califf, and E J, Topol

Subjects
Male, Heparin, Myocardial Infarction, Comorbidity, Hirudins, Middle Aged, Risk Assessment, Diabetes Mellitus, Type 1, Treatment Outcome, Double-Blind Method, Reference Values, Confidence Intervals, Odds Ratio, Humans, Female, Aged, Follow-Up Studies, Probability
Abstract

We examined the characteristics, outcomes, and effects of hirudin vs heparin treatment of diabetic patients across the spectrum of acute coronary syndromes.We studied the 12,142 patients enrolled in the randomized GUSTO-IIb study. Diabetic patients (n=2175) were older, more often female, more often had prior cardiovascular disease, hypertension, and hyperlipidaemia, and less often were current smokers. Diabetic patients had a higher overall incidence of death or (re)infarction at 30 days (13.1% vs 8.5%, P=0.0001), whether they presented with ST-segment elevation (13.9% vs 9.9%, P=0.0017) or not (12.8% vs 7.8%, P=0.0001), and at 6 months (18.8% vs 11.4%, P=0.0001). Among diabetic patients, hirudin was associated with a tendency toward a lower risk of death or (re)infarction at 30 days (12.2% vs 13.9% with heparin) and 6 months (17.8% vs 20.2%). Diabetic patients had more major bleeding, stroke, heart failure, shock, atrioventricular block, and atrial arrhythmias, but no increased risk for ocular bleeding.Diabetic patients with acute coronary syndromes had worse 30-day and 6-month outcomes, particularly those without ST-segment elevation. The statistically non-significant trend toward improved outcomes with hirudin was similar among patients with and without diabetes, with a greater point estimate for the absolute difference in patients with diabetes.

Published
2000

27. Death and nonfatal reinfarction within the first 24 hours after presentation with an acute coronary syndrome: experience from GUSTO-IIb. Global Utilization of Strategies for Total Occlusion

Author

N S, Kleiman, C B, Granger, H D, White, P, Armstrong, D, Ardissino, F V, de Werf, P, Zoldeyhi, T D, Thompson, R M, Califf, and E J, Topol

Subjects
Male, Heparin, Myocardial Infarction, Hirudins, Middle Aged, Survival Analysis, Disease-Free Survival, Recombinant Proteins, Treatment Outcome, Fibrinolytic Agents, Hirudin Therapy, Recurrence, Multivariate Analysis, Humans, Female, Aged
Abstract

A large proportion of deaths among patients with myocardial infarction occurs within the first 24 hours after presentation. It is not clear whether this phenomenon is also true of patients without ST-segment elevation who may or may not have infarction at the time of presentation. Thrombin activity may also be greatest during the first 24 hours after plaque rupture. Accordingly, this study was designed to examine the pattern of early ischemic events among patients with acute coronary syndromes and to determine whether the direct thrombin inhibitor desirudin (r-hirudin) would be most effective during this period.Among the 11,142 patients enrolled in GUSTO-II, death or (re)infarction occurred within 24 hours in 210 patients (1.7%), representing 19% of the 1135 deaths that had occurred by 30 days. Death or (re)infarction occurred within 24 hours in 113 patients (2. 7%) with ST-segment elevation and in 97 patients without ST-segment elevation (1.2%, P.001), representing 26% and 14% of the 30-day event rates, respectively, for the 2 enrollment strata. Among patients with ST-segment elevation, most of these events were deaths, whereas among patients without ST-segment elevation, most events were (re)infarctions. Death or (re)infarction by 24 hours occurred in 80 (1.3%) patients treated with desirudin and 130 (2.1%) patients treated with heparin (P =.01). This finding predominantly consisted of prevention of death among patients with ST-segment elevation and of (re)infarction among patients without ST-segment elevation.These findings have important implications for early triage of patients with acute coronary syndromes and for the development of new therapies directed at stabilizing the unstable atherosclerotic plaque.

Published
1999

29. Sirolimus-eluting vs. uncoated stents for prevention of restenosis in small coronary arteries: A randomized trial

Author

D. Ardissino, C. Cavallini, and E. Bramucci

Subjects
medicine.medical_specialty, business.industry, medicine.disease, law.invention, Coronary arteries, medicine.anatomical_structure, Restenosis, Randomized controlled trial, law, Sirolimus, Internal medicine, medicine, Cardiology, Cardiology and Cardiovascular Medicine, business, General Nursing, medicine.drug
Published
2005
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30. Activation of the hemostatic mechanism during thrombolysis in patients with unstable angina pectoris

Author

P A, Merlini, D, Ardissino, K A, Bauer, L, Oltrona, A, Spinola, P, Diotallevi, R D, Rosenberg, and P M, Mannucci

Subjects
Male, Hemostasis, Heparin, Fibrinolysis, Middle Aged, Peptide Fragments, Cohort Studies, Fibrinolytic Agents, Risk Factors, Humans, Female, Prothrombin, Streptokinase, Thrombolytic Therapy, Angina, Unstable, Prospective Studies, Aged, Fibrinopeptide A
Abstract

In patients with myocardial infarction, thrombolytic therapy induces a paradoxical activation of the hemostatic mechanism. In patients with unstable angina, the effect of thrombolysis on the coagulation cascade is unknown. We prospectively measured the plasma concentrations of prothrombin fragment 1 + 2 and fibrinopeptide A in consecutive patients with unstable angina randomized to receive placebo alone (n = 23), streptokinase 1,500,000 IU over 1 hour followed by a 48-hour placebo infusion (n = 21), or streptokinase 250,000 over 1 hour followed by a continuous infusion of 100,000 IU per hour over 48 hours (n = 20). All the patients received intravenous heparin for 72 hours. The plasma levels of the different markers were measured at baseline, 90 minutes, 24 hours, and 48 hours after the start of therapy. The median baseline plasma concentrations of prothrombin fragment 1 + 2 and fibrinopeptide A were similar in the three treatment groups. In comparison with placebo, an increase in plasma prothrombin fragment 1 + 2 and fibrinopeptide A, was observed after 90 minutes in the two groups receiving thrombolysis. After 24 and 48 hours, the prothrombin fragment 1 + 2 levels remained significantly higher only in the patients receiving the 48-hour streptokinase infusion. In patients with unstable angina, thrombolytic therapy induces an activation of the hemostatic mechanism, despite concomitant heparin administration; in those receiving a prolonged streptokinase infusion, the activation of coagulation persists for as long as the drug is administered.

Published
1995

31. Humoral factors in thrombus formation

Author

P A, Merlini and D, Ardissino

Subjects
Hemostasis, Heart Diseases, Atrial Fibrillation, Humans, Thrombolytic Therapy, Thrombosis, Blood Coagulation, Biomarkers
Published
1994

32. [95] EFFECTS OF RADIOLOGY CONTRAST MEDIA ON CULTURED HUMAN ENDOTHELIAL CELL MORPHOLOGY AND FUNCTION AND PROTECTIVE ACTION OF N-ACETYLCYSTEIN AND ROSUVASTATIN

Author

Nicoletta Ronda, Rita Gatti, E. Fiaccadori, D. Ardissino, G. Orlandini, Francesco Potì, and A. Palmisano

Subjects
Pathology, medicine.medical_specialty, Nutrition and Dietetics, Morphology (linguistics), Chemistry, Endocrinology, Diabetes and Metabolism, Radiology contrast, Medicine (miscellaneous), Endothelial stem cell, medicine, Rosuvastatin, Cardiology and Cardiovascular Medicine, Function (biology), medicine.drug
Published
2009
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36. New generation of EP catheter: Single catheter for EP study and internal defibrillation in ventricle and atrium

Author

A. Sammali, D. Ardissino, S. Sermasi, Giovanni Quinto Villani, A. Carboni, M. Marconi, Alessandro Capucci, and P. Accorti

Subjects
medicine.medical_specialty, Atrium (architecture), business.industry, Defibrillation, medicine.medical_treatment, Catheter, medicine.anatomical_structure, Ventricle, Physiology (medical), Internal medicine, Cardiology, Medicine, Cardiology and Cardiovascular Medicine, business
Published
2001
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37. [Changes in left ventricular function induced by isometric exercise in coronary disease]

Author

S, De Servi, G, Spécchia, D, Ardissino, L, Angoli, A, Mussini, E, Bramucci, G, Marinoni, C, Montemartini, and P, Bobba

Subjects
Male, Time Factors, Diastole, Heart Rate, Heart Ventricles, Isometric Contraction, Muscle Relaxation, Physical Exertion, Humans, Coronary Disease, Female, Middle Aged
Abstract

The effects of isometric exercise on left ventricular function in 16 patients with chronic coronary heart disease were assessed by measuring left ventricular pressures and volumes under basal conditions and during a sustained effort of 2 minutes 30 seconds at 50% of the maximal effort. In 7 patients (Group I) with abnormal elevation of left ventricular end diastolic pressure (LVEDP) (over 4 mmHg) the end diastolic volume remained unchanged and the diastolic pressure-volume curve was displaced upwards. The ejection fraction fell together with the percentage filling during the first part of diastole with 50% filling occurring after 61% instead of 45% of diastole. The time constant T also increased showing abnormal relaxation. In 9 patients without abnormal elevation of LVEDP on exercise no changes in the other parameters studies were observed. Our results show that pathological elevation of LVEDP during isometric exercise is associated with a decreased ejection fraction and an abnormality of left ventricular relaxation with a reduced rate of filling during protodiastole and an upward displacement of the diastolic pressure-volume curve. The LVEDP alone is therefore an important index of the haemodynamic behaviour of the left ventricle during isometric exercise.

Published
1980

38. Variable threshold exertional angina in patients with transient vasospastic myocardial ischemia. Repeat exercise test results and therapeutic implications

Author

S, de Servi, G, Specchia, C, Falcone, A, Gavazzi, A, Mussini, L, Angoli, E, Bramucci, D, Ardissino, L, Vaccari, J, Salerno, and P, Bobba

Subjects
Adult, Male, Radiography, Electrocardiography, Exercise Test, Coronary Vasospasm, Humans, Female, Middle Aged, Coronary Vessels, Blood Flow Velocity, Angina Pectoris, Veins
Abstract

Thirty-five of 70 patients with vasospastic angina at rest complained of chest pain during exercise or during usual daily activity. In 22, the angina threshold was described as variable during exercise: that is, the amount of exertion that induced angina was not always the same. In 12 patients with variable threshold exertional angina, 3 exercise tests performed in the morning on different days yielded different results, because chest pain and ischemic electrocardiographic changes occurred at different work loads with a wide range in heart rate-systolic pressure product. Two patients, in whom great cardiac vein flow was measured during exercise before and after taking nifedipine, tolerated heavier work loads after receiving the drug, with a more marked increase in flow during exercise. It is concluded that variable threshold exertional angina can be objectively demonstrated by repeat exercise tests in patients with vasospastic angina. Variability of the angina threshold may be due to a functional mechanism that causes myocardial ischemia in addition to the increased myocardial metabolic requirements provoked by exercise. Because in such patients fluctuations in coronary arterial tone play an important role in determining the response to exercise, calcium antagonistic drugs, which lower coronary tone and prevent the occurrence of coronary spasm, are effective in increasing exercise capacity.

Published
1983

39. [Angina at rest. Clinical, electrocardiographic and angiographic observations in 107 patients]

Author

P M, Casali, S, De Servi, D, Ardissino, L, Martinelli, A, Mussini, E, Bramucci, C, Falcone, G, Minzioni, M, Viganò, G, Specchia, and P, Bobba

Subjects
Adult, Male, Nifedipine, Myocardial Infarction, Arrhythmias, Cardiac, Coronary Disease, Middle Aged, Coronary Angiography, Angina Pectoris, Electrocardiography, Nitroglycerin, Postoperative Complications, Humans, Female, Coronary Artery Bypass, Aged
Abstract

107 patients suffering from angina at rest associated with ST segment changes underwent coronary arteriography. 46 patients showed ST segment elevation during ischemic attacks (group I) while 61 patients exhibited ST segment depression during chest pain (group II). Non-significant coronary artery disease was more frequent in group I patients (group I 15%, group II 5%) as well as one vessel disease (group I 33%, group II 15%) while multivessel disease and left main involvement were more frequent in group II patients (group I 28%, group II 60%). Depression of left ventricular function was found in similar percentage of cases in both groups. During hospitalization all patients were treated with calcium antagonists (Nifedipine 10/20 mg every six hours) and/or nitrates (2% nitroglycerin ointment 2 inches every six/four hours) with one death (occurring after coronary arteriography) and eleven non-fatal myocardial infarctions. 50 patients underwent coronary bypass grafting with four perioperative deaths and six nonfatal myocardial infarctions. Most of the surgically treated patients were poorly responsive to medical treatment and had multivessel disease or left main involvement. Since these features are known to be related to a poor prognosis with medical treatment, surgical results in such patients seem satisfactory.

Published
1980

41. [Positive exercise test in the absence of pain. Characteristic of a high-risk population?]

Author

A, Gavazzi, C, Falcone, D, Ardissino, S, De Servi, G, Specchia, and P, Bobba

Subjects
Adult, Male, Exercise Test, Humans, Coronary Disease, Female, Middle Aged, Angina Pectoris
Abstract

157 consecutive patients (pts) with suspected coronary artery disease and an ischemic ecg response during exercise test (ET) were studied. During ET 61 of them (group I) had neither chest pain nor anginal equivalent, while 96 (group II) experienced angina. There were no significant differences between the two groups in regard to age, sex, prior myocardial infarction, history of angina or hypertension. During ET pts of group I tolerated a higher work load (group I 3467 Kpm, group II 2594 Kpm, P less than 0,05) and had a higher maximal heart rate (group I 128,3 b/min, group II 120,4 b/min, P less than 0,05) with a more marked ST segment depression (group I 2,4 mm, group II 1,8 mm, P less than 0,01) and with a more elevated incidence of arrhythmias (group I 18%, group II 7%, P less than 0,05). The coronary angiography showed significant obstruction (greater than or equal to 75%) in 91,7% of group I and in 91,6% of group II (prevalence of single vessel disease in group I and multiple vessel disease in group II). No significant difference was found between group I and II in regard to left ventricular ejection fraction (group I 51%, group II 53%), left ventricular end-diastolic pressure (group I 12,9 mmHg group II 13,6 mmHg) and left ventricular end-diastolic volume (group I 102,3 ml/m2, group II 104,2 ml/m2). We conclude that ST segment depression during ET in asymptomatic pts at risk for cardiovascular disease is predictive of coronary artery disease as in symptomatics. These subjects have, compared with symptomatics, a higher work load tolerance but with more marked ecg ischemic changes and more frequent arrhythmias during ET, thus representing a group of coronary population at potentially higher risk.

Published
1980

42. [Silent myocardial ischemia]

Author

G, Specchia, C, Falcone, R, Rondanelli, S, De Servi, C, Opasich, D, Ardissino, S, Codega, G, Corsico, M T, La Rovere, and R, Tramarin

Subjects
Exercise Test, Humans, Coronary Disease, Cardiomyopathies, Angina Pectoris, Follow-Up Studies
Published
1986

43. Phenotype commitment in vascular smooth muscle cells derived from coronary atherosclerotic plaques: differential gene expression of endothelial Nitric Oxide Synthase

Author

ML Rossi, N Marziliano, PA Merlini, E Bramucci, U Canosi, P Presbitero, E Arbustinie, PM Mannucci, and D Ardissino

Subjects
Biology (General), QH301-705.5
Abstract

Unstable angina and myocardial infarction are the clinical manifestations of the abrupt thrombotic occlusion of an epicardial coronary artery as a result of spontaneous atherosclerotic plaque rupture or fissuring, and the exposure of highly thrombogenic material to blood. It has been demonstrated that the proliferation of vascular smooth muscle cells (VSMCs) and impaired bioavailabilty of nitric oxide (NO) are among the most important mechanisms involved in the progression of atherosclerosis. It has also been suggested that a NO imbalance in coronary arteries may be involved in myocardial ischemia as a result of vasomotor dysfunction triggering plaque rupture and the thrombotic response. We used 5’ nuclease assays (TaqMan™ PCRs) to study gene expression in coronary plaques collected by means of therapeutic directional coronary atherectomy from 15 patients with stable angina (SA) and 15 with acute coronary syndromes (ACS) without ST elevation. Total RNA was extracted from the 30 plaques and the cDNA was amplified in order to determine endothelial nitric oxide synthase (eNOS) gene expression. Analysis of the results showed that the expression of eNOS was significantly higher (p

Published
2009
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44. Polygenic Prediction of Recurrent Events After Early-Onset Myocardial Infarction.

Author

Ardissino M, Paraboschi EM, Lambert SA, Kim LG, Kelemen M, Maglietta G, Crocamo A, Magnani G, Bricoli S, Vignali L, Niccoli G, Tubaro M, Pastika L, Sau A, Ng FS, de Marvao A, Honigberg MC, Natarajan P, Nelson AJ, Inouye M, Di Angelantonio E, Asselta R, Ardissino D, and Butterworth AS

Subjects
Humans, Male, Female, Adult, Middle Aged, Risk Factors, Age of Onset, Proportional Hazards Models, Cohort Studies, Hyperlipoproteinemia Type II genetics, Follow-Up Studies, Genetic Predisposition to Disease, Coronary Artery Disease genetics, Myocardial Infarction genetics, Recurrence, Multifactorial Inheritance
Abstract

Background: Myocardial infarction (MI) is a complex disease caused by both lifestyle and genetic factors. This study aims to investigate the predictive value of genetic risk, in addition to traditional cardiovascular risk factors, for recurrent events following early-onset MI., Methods: The Italian Genetic Study of Early-Onset Myocardial Infarction is a cohort study enrolling patients with MI before 45 years. Monogenic variants causing familial hypercholesterolemia were identified, and a coronary artery disease polygenic score (PGS) was calculated. Ten-fold cross-validated Cox proportional hazards models were fitted sequentially including all clinical variables, the PGS, and monogenic variants on the composite outcome of cardiovascular death, recurrent MI, stroke, or revascularization., Results: During a 19.9-year follow-up, 847 (50.7%) patients experienced recurrent events. Each 1-SD higher PGS was associated with a 21% higher hazard of recurrent events (hazard ratio, 1.21 [95% CI, 1.13-1.31]; P =4.04×10 -6 ). Except for secondary prevention, PGS was the strongest determinant of recurrent event risk (C index, 0.56 [95% CI, 0.54-0.58]) compared with clinical risk factors. Overall, predictive performance of clinical risk factors (C index, 0.69 [95% CI, 0.67-0.71]) improved after adding the PGS (C index, 0.69 [95% CI, 0.68-0.71]; P =0.006). When dividing the population by PGS quintiles, the highest fifth had a 57% higher hazard of recurrent events than the lowest fifth (hazard ratio, 1.57 [95% CI, 1.26-1.96]; P =5.57×10 -5 )., Conclusions: When compared with other clinical risk factors, PGS was the strongest predictor of event recurrence among patients with an early-onset MI. Though the discriminative power of recurrent event prediction in this cohort was modest, the addition of PGS significantly improved discrimination., Competing Interests: Dr Natarajan reports research grants from Allelica, Amgen, Apple, Boston Scientific, Genentech/Roche, and Novartis; personal fees from Allelica, Apple, AstraZeneca, Blackstone Life Sciences, Creative Education Concepts, CRISPR Therapeutics, Eli Lilly & Co, Foresite Labs, Genentech/Roche, GV, HeartFlow, Magnet Biomedicine, Merck, and Novartis; scientific advisory board membership of Esperion Therapeutics, Preciseli, and TenSixteen Bio; scientific cofounder of TenSixteen Bio; equity in MyOme, Preciseli, and TenSixteen Bio; and spousal employment at Vertex Pharmaceuticals, all unrelated to the present work. Dr Honigberg reports consulting fees from CRISPR Therapeutics and Comanche Biopharma, advisory board service for Miga Health, and grant support from Genentech, all unrelated to the present work. Dr Inouye is a trustee of the Public Health Genomics Foundation, a member of the Scientific Advisory Board of Open Targets, and has a research collaboration with AstraZeneca PLC, which is unrelated to this study. Dr Butterworth reports institutional grants from AstraZeneca, Bayer, Biogen, BioMarin, Bioverativ, Novartis, Regeneron, and Sanofi. The other authors report no conflicts.

Published
2024
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45. Health-related quality of life in elderly cardiac patients undergoing cardiac rehabilitation and the association with exercise capacity: the EU-CaRE study.

Author

Kjesbu IE, Sibilitz KL, Petersen J, Houben VJG, Wilhelm M, Pena-Gil C, Iliou MC, Zeymer U, Ardissino D, Van't Hof AWJ, van der Velde AE, de Kluiver EP, and Prescott E

Subjects
Humans, Male, Female, Aged, Europe, Anxiety psychology, Treatment Outcome, Age Factors, Time Factors, Aged, 80 and over, Exercise Test, Mental Health, Recovery of Function, Heart Diseases rehabilitation, Heart Diseases physiopathology, Heart Diseases psychology, Heart Diseases diagnosis, Quality of Life, Cardiac Rehabilitation methods, Exercise Tolerance, Depression psychology, Depression diagnosis, Exercise Therapy methods
Abstract

Aims: The ability to be physically active is pivotal to the quality of life in elderly patients. This study aims to describe the association between exercise capacity and health-related quality of life (HRQoL), anxiety, and depression following an exercise-based cardiac rehabilitation (CR) programme in elderly cardiac patients., Methods and Results: Patients aged ≥65 years with acute and chronic coronary syndrome or heart valve surgery were consecutively included from eight CR centres in seven European countries. Exercise capacity [VO2peak(mL/kg/min)] was assessed with a cardiopulmonary exercise test (97%) or a 6-min walk test. Outcome variables included HRQoL [36-item Short-Form Health Survey physical and mental component scores (PCS and MCS)], anxiety (Generalized Anxiety Disorder-7), and depression (Patient Health Questionnaire-9). Mixed models were used to address the association between baseline and the development in VO2peak, and outcome variables stratified on sex, and adjusted for baseline values, age, and CR centre. A total of 1633 patients were included (T0), 1523 (93%) completed end-of-CR assessment (T1), and 1457 (89%) were available for 1-year follow-up (T2). Women had higher percentage of predicted VO2peak but poorer scores in HRQoL, anxiety, and depression at all time points. All scores improved in both sexes at follow-up. We found significant associations between VO2peak at baseline as well as development in VO2peak and all outcome variables at T1 and T2 in men (all P < 0.001). In women, VO2peak was only associated with PCSs (P < 0.001)., Conclusion: Improvements in exercise capacity were strongly associated with improvements in HRQoL and mental health, however, with stronger associations in men. The results highlight the importance of physical fitness for HRQol and mental health. The findings from this study might be useful to better target individual CR programmes., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Published
2024
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46. Sudden cardiac death after early-onset myocardial infarction: a multicentre longitudinal cohort study with a 20-year follow-up.

Author

Bricoli S, Magnani G, Ardissino M, Maglietta G, Celli P, Ferrario M, Canosi U, Cernetti C, Negri F, Merlini PA, Tubaro M, Berzuini C, Manzalini C, Moschini L, Ponte E, Pozzi R, Buratti S, Botti A, Barocelli F, Biagi A, Bonura R, Bearzot L, Moccetti T, Crocamo A, Notarangelo MF, Moscarella E, Calabrò P, Niccoli G, and Ardissino D

Subjects
Humans, Male, Female, Follow-Up Studies, Italy epidemiology, Middle Aged, Risk Factors, Adult, Longitudinal Studies, Age of Onset, Death, Sudden, Cardiac epidemiology, Death, Sudden, Cardiac etiology, Myocardial Infarction complications, Myocardial Infarction mortality, Myocardial Infarction epidemiology
Abstract

Aims: Sudden cardiac death (SCD) is a serious consequence of a myocardial infarction (MI), but identifying patients at risk of developing SCD remains a major clinical challenge, especially in the case of juvenile MI. The aim of this study is to identify predictors of SCD after early-onset MI using long-term follow-up data relating to a large nationwide patient cohort., Methods and Results: The Italian Genetic Study on Early-onset MI enrolled 2000 patients experiencing a first MI before the age of 45 years, who were followed up for a median of 19.9 years. Fine-Gray proportional hazard models were used to assess the associations between their clinical, demographic, and index event data and the occurrence of SCD. Sudden cardiac death occurred in 195 patients, who were more frequently males, were hypertensive and/or diabetic, had a history of previous thrombo-embolic events with a greater atherosclerotic burden, and had a lower left ventricular ejection fraction (LVEF) after the index event. A multivariable analysis showed that the independent predictors of SCD were diabetes, hypertension, previous thrombo-embolic events, a higher SYNTAX score, and a lower LVEF. There was no clear evidence of the clustering of SCD events during the follow-up. Sudden cardiac death was the first post-MI clinical event in 101 patients; the remaining 94 experienced SCD after a non-fatal MI or hospitalization for coronary revascularization., Conclusion: Sudden cardiac death frequently occurs during the 20 years after early-onset MI. The nature of the identified predictors and the absence of clustering suggest that the pathophysiological basis of SCD may be related to progressive coronary atherosclerosis., Competing Interests: Conflict of interest: none declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Published
2024
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47. Population Heterogeneity and Selection of Coronary Artery Disease Polygenic Scores.

Author

Debernardi C, Savoca A, De Gregorio A, Casalone E, Rosselli M, Herman EJ, Di Primio C, Tumino R, Sieri S, Vineis P, Panico S, Sacerdote C, Ardissino D, Asselta R, and Matullo G

Abstract

Background/objectives: The identification of coronary artery disease (CAD) high-risk individuals is a major clinical need for timely diagnosis and intervention. Many different polygenic scores (PGSs) for CAD risk are available today to estimate the genetic risk. It is necessary to carefully choose the score to use, in particular for studies on populations, which are not adequately represented in the large datasets of European biobanks, such as the Italian one. This work aimed to analyze which PGS had the best performance within the Italian population., Methods: We used two Italian independent cohorts: the EPICOR case-control study (576 individuals) and the Atherosclerosis, Thrombosis, and Vascular Biology (ATVB) Italian study (3359 individuals). We evaluated 266 PGS for cardiovascular disease risk from the PGS Catalog, selecting 51 for CAD., Results: Distributions between patients and controls were significantly different for 49 scores ( p -value < 0.01). Only five PGS have been trained and tested for the European population specifically. PGS003727 demonstrated to be the most accurate when evaluated independently (EPICOR AUC = 0.68; ATVB AUC = 0.80). Taking into account the conventional CAD risk factors further enhanced the performance of the model, particularly in the ATVB study ( p -value = 0.0003)., Conclusions: European CAD PGS could have different risk estimates in peculiar populations, such as the Italian one, as well as in various geographical macro areas. Therefore, further evaluation is recommended for clinical applicability.

Published
2024
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48. Prognostic role of coronary artery ectasia in patients with nonobstructive coronary artery disease.

Author

Gurgoglione FL, Benatti G, Vignali L, Tadonio I, Magnani G, Denegri A, Lazzeroni D, Tuttolomondo D, De Gregorio M, Indrigo E, Signoretta G, Abbati V, Nicolini F, Ardissino D, Solinas E, and Niccoli G

Subjects
Humans, Prognosis, Coronary Vessels diagnostic imaging, Dilatation, Pathologic complications, MINOCA, Coronary Angiography adverse effects, Risk Factors, Angina Pectoris, Coronary Artery Disease complications, Coronary Artery Disease diagnostic imaging, Coronary Artery Disease epidemiology, Myocardial Infarction diagnostic imaging, Myocardial Infarction epidemiology, Myocardial Infarction etiology, Coronary Aneurysm
Abstract

Aims: Coronary artery ectasia (CAE) has been linked to the occurrence of adverse events in patients with ischemia/angina and no obstructive coronary arteries (INOCA/ANOCA), while the relationship between CAE and myocardial infarction with nonobstructive coronary arteries (MINOCA) has been poorly investigated. In our study we aimed at assessing differences in clinical, angiographic and prognostic features among patients with CAE and MINOCA vs. INOCA/ANOCA presentation., Methods: Patients with angiographic evidence of CAE were enrolled at the University Hospital of Parma and divided into MINOCA vs. INOCA/ANOCA presentation. Clinical and quantitative angiographic information was recorded and the incidence of major adverse cardiovascular events (MACE) was assessed at follow-up., Results: We enrolled a total of 97 patients: 49 (50.5%) with MINOCA and 48 (49.5%) with INOCA/ANOCA presentation. The presentation with MINOCA was associated with a higher frequency of inflammatory diseases ( P  = 0.041), multivessel CAE ( P  = 0.030) and thrombolysis in myocardial infarction (TIMI) flow < 3 ( P  = 0.013). At a median follow-up of 38 months, patients with MINOCA had a significantly higher incidence of MACE compared with those with INOCA/ANOCA [8 (16.3%) vs. 2 (4.2%), P  = 0.045], mainly driven by a higher rate of nonfatal MI [5 (10.2%) vs. 0 (0.0%), P  = 0.023]. At multivariate Cox regression analysis, the presentation with MINOCA ( P  = 0.039) and the presence of TIMI flow <3 ( P  = 0.037) were independent predictors of MACE at follow-up., Conclusion: Among a cohort of patients with CAE and nonobstructive coronary artery disease, the presentation with MINOCA predicted a worse outcome., (Copyright © 2024 Italian Federation of Cardiology - I.F.C. All rights reserved.)

Published
2024
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50. Predictors of recurrent cerebral ischemia after patent foramen ovale closure: A single center observational study.

Author

Gurgoglione FL, Vignali L, Cattabiani MA, Solinas E, Benatti G, Tadonio I, Barocelli F, Dizdari C, Tuttolomondo D, Ardissino D, Nicolini F, and Niccoli G

Subjects
Humans, Treatment Outcome, Cerebral Infarction complications, Secondary Prevention, Obesity complications, Ischemic Attack, Transient diagnosis, Ischemic Attack, Transient epidemiology, Ischemic Attack, Transient etiology, Foramen Ovale, Patent complications, Foramen Ovale, Patent diagnostic imaging, Foramen Ovale, Patent epidemiology, Embolism, Paradoxical diagnostic imaging, Embolism, Paradoxical epidemiology, Embolism, Paradoxical etiology, Stroke diagnosis, Stroke epidemiology, Stroke etiology, Ischemic Stroke complications, Migraine Disorders
Abstract

Objectives: Transcatheter patent foramen ovale closure lowers recurrent stroke in patients with cryptogenic stroke or transient ischemic attack with an indication for closure. However, the incidence of recurrent stroke is not negligible and underlying pathophysiology remains largely unknown. We sought to evaluate the prevalence of recurrent ischemic neurological events and to assess its predictors after transcatheter patent foramen ovale closure., Methods: We enrolled consecutive patients who underwent patent foramen ovale closure for secondary prevention of neurological ischemic events at the University Hospital of Parma between 2006 and 2021. Clinical and procedure-related features were collected for each patient. The incidence of recurrent ischemic neurological events was assessed at follow-up., Results: We enrolled a total of 169 patients with mean Risk of Paradoxical Embolism score at hospital admission of 6.4 ± 1.5. The primary indication was previous cryptogenic stroke (94 [55.6 %] subjects), followed by transient ischemic attack (75 [44.4 %]). Among patients with complete outcome data (n= 154), after a median follow-up of 112 months, recurrent cerebral ischemia occurred in 13 [8.4 %], with an annualized rate of 0.92/100 patients. The presence of obesity [OR 5.268, p = 0.018], Risk of Paradoxical Embolism score < 7 [OR 5.991, p = 0.035] and migraine [OR = 5.932 p = 0.012] were independent positive predictors of recurrent stroke/ transient ischemic attack after patent foramen ovale closure., Conclusions: The presence of obesity, Risk of Paradoxical Embolism score < 7 and migraine were independent positive predictors of recurrent ischemic neurological events after patent foramen ovale closure., Competing Interests: Declaration of Competing Interest The authors declare that there is no conflict of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Published
2024
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