22 results on '"Brunelli, C."'
Search Results
2. [Acute myocardial infarction in pregnancy].
- Author
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Rosa GM, Bauckneht M, Ferrero S, Leone Roberti Maggiore U, and Brunelli C
- Subjects
- Female, Humans, Pregnancy, Myocardial Infarction diagnosis, Myocardial Infarction physiopathology, Myocardial Infarction therapy, Pregnancy Complications, Cardiovascular diagnosis, Pregnancy Complications, Cardiovascular physiopathology, Pregnancy Complications, Cardiovascular therapy
- Abstract
Acute myocardial infarction is a rare but potential life-threatening complication of pregnancy. Its incidence is increasing because of the enlargement of the reproductive age. Treatment needs to be urgent because of the very high mortality rate. The aim of this literature review is to provide a better understanding of the available diagnostic modalities and interventional and pharmacological treatment options in the management of pregnant patients with acute myocardial infarction in order to improve the overall care provision and ensure both maternal and fetal well-being.
- Published
- 2013
- Full Text
- View/download PDF
3. A less aggressive therapeutic option for electrical storm.
- Author
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Bertero G, Agosti S, and Brunelli C
- Subjects
- Adrenergic beta-Antagonists therapeutic use, Aged, Atrial Fibrillation complications, Cardiovascular Agents therapeutic use, Catheter Ablation, Combined Modality Therapy, Electric Countershock, Humans, Male, Middle Aged, Myocardial Infarction complications, Nerve Regeneration, Percutaneous Coronary Intervention, Purkinje Fibers physiology, Recurrence, Ventricular Fibrillation etiology, Ventricular Fibrillation physiopathology, Ventricular Premature Complexes etiology, Ventricular Premature Complexes physiopathology, Cardiac Pacing, Artificial methods, Myocardial Infarction therapy, Ventricular Fibrillation therapy
- Abstract
Electrical storm (ES) describes the rapidly clustering ventricular fibrillation (VF) that requires multiple cardioversions. Emerging evidence suggests that Purkinje arborization and sympathetic nerve regeneration play a major role in initiating malignant arrhythmias. We report the case of two patients who, after having survived an acute myocardial infarction (MI), developed repetitive episodes of polymorphic ventricular tachycardia and VF one week after percutaneous revascularization, triggered by monomorphic premature ventricular contractions (PVCs). Owing to repetitive and drug-refractory VF episodes, temporary atrial overdrive pacing was attempted with complete suppression of VF. In the following month, recurrence of ventricular arrhythmia was inversely related to the atrial pacing rate. Although antiarrhythmic drugs other than beta-blockers had been discontinued, neither PVCs nor ventricular arrhythmias recurred at one-month follow-up when the lower pacing rate was set at 60 bpm. In conclusion in these patients, ES was likely related to nerve sprouting after ischemic injury. This chaotic phenomenon occurs early after tissue damage and shows a peak seven days after acute MI with degeneration of superfluous axon branches. High pacing rates can reduce early after depolarizations and suppress PVCs, thus preventing ES. On these grounds, ES patients may be treated with temporary overdrive pacing rather than early radiofrequency ablation.
- Published
- 2013
- Full Text
- View/download PDF
4. Acute myocardial infarction related to very late sirolimus-eluting stent thrombosis 6 months after discontinuation of dual antiplatelet therapy.
- Author
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Balbi M, Fedele M, Bezante GP, Brunelli C, and Barsotti A
- Subjects
- Aged, Aspirin administration & dosage, Clopidogrel, Coronary Angiography, Coronary Thrombosis diagnostic imaging, Coronary Thrombosis therapy, Drug Administration Schedule, Drug Therapy, Combination, Humans, Male, Myocardial Infarction diagnostic imaging, Myocardial Infarction therapy, Prosthesis Design, Ticlopidine administration & dosage, Ticlopidine analogs & derivatives, Time Factors, Angioplasty, Balloon, Coronary adverse effects, Angioplasty, Balloon, Coronary instrumentation, Cardiovascular Agents administration & dosage, Coronary Thrombosis etiology, Drug-Eluting Stents, Myocardial Infarction etiology, Platelet Aggregation Inhibitors administration & dosage, Sirolimus administration & dosage
- Published
- 2011
- Full Text
- View/download PDF
5. Maximal endothelial tissue plasminogen activator release is not impaired in patients with acute coronary syndromes before heparin treatment.
- Author
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Olivotti L, Spallarossa P, Piana A, Iannone A, Rossettin P, Ghigliotti G, Armani U, Barsotti A, and Brunelli C
- Subjects
- Aged, Angina, Unstable physiopathology, Anticoagulants administration & dosage, Endothelium, Vascular metabolism, Endothelium, Vascular physiopathology, Female, Heparin administration & dosage, Humans, Male, Middle Aged, Myocardial Infarction physiopathology, Angina, Unstable blood, Angina, Unstable drug therapy, Anticoagulants therapeutic use, Heparin therapeutic use, Myocardial Infarction blood, Myocardial Infarction drug therapy, Plasminogen Activators blood
- Abstract
Procoagulant and fibrinolytic disturbances are described in patients with acute coronary syndromes (ACS), but whether defective maximal tissue plasminogen activator (t-PA) release from the endothelium is also present is still controversial. Previous studies did not take into consideration the contribution of heparin, which strongly affects fibrinolysis. Accordingly, in this study, we measured maximal t-PA release in patients with ACS before, during, and after heparin treatment. Maximal t-PA release was measured by the venous occlusion test in 38 hospitalized patients with confirmed ACS (18 acute myocardial infarctions and 20 unstable anginas) before starting heparin, during heparin treatment, and 4 and 12 h after discontinuation. Plasma plasminogen activator inhibitor type 1 (PAI-1), D-dimer and prothrombin fragment F1 + 2 were also measured. Eighteen age-matched subjects with no evidence of coronary disease were used as controls. At admission, patients showed significantly higher plasma levels of t-PA, PAI-1, and F1 + 2 than controls. Before heparin, maximal t-PA release was similar in patients and controls. Heparin treatment was associated with a significant increase of plasma t-PA, while it did not affect maximal t-PA release. Coagulative and fibrinolytic disturbances are present in patients with ACS, but these do not include maximal t-PA release. Among our patients, maximal t-PA release appears stable over time and is not affected by heparin treatment.
- Published
- 2001
- Full Text
- View/download PDF
6. Detection of acute myocardial infarction by 99mTc-labeled D-glucaric acid imaging in patients with acute chest pain.
- Author
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Mariani G, Villa G, Rossettin PF, Spallarossa P, Bezante GP, Brunelli C, Pak KY, Khaw BA, and Strauss HW
- Subjects
- Aged, Angina, Unstable diagnostic imaging, Chest Pain diagnostic imaging, Female, Heart diagnostic imaging, Humans, Male, Middle Aged, Myocardial Infarction diagnosis, Radionuclide Imaging, Radiopharmaceuticals, Sensitivity and Specificity, Time Factors, Glucaric Acid analogs & derivatives, Myocardial Infarction diagnostic imaging, Organotechnetium Compounds
- Abstract
Unlabelled: Definitive diagnosis of acute myocardial infarction early in the process is often difficult. An imaging agent that localized quickly and specifically in areas of acute necrosis could provide this critical diagnostic information. To determine whether imaging with 99mTc-labeled D-glucaric acid (GLA) could provide this information, we imaged a group of patients presenting with symptoms suggestive of acute infarction., Methods: Twenty-eight patients presenting to the emergency department with symptoms highly suggestive of acute infarction were injected with 99mTC-GLA and imaged about 3 h later., Results: The sensitivity of lesion detection was remarkably time dependent. Fourteen patients with acute infarction injected within 9 h of onset of chest pain had positive scans, even in the presence of persistent occlusion. The remaining 14 patients had negative scans. Nine patients with negative scans had acute infarction but were injected more than 9 h after onset of chest pain. The final diagnosis in the remaining 5 patients was unstable angina (3 injected <9 h and 2 injected >9 h after onset of chest pain). Six patients were reinjected with 99mTc-GLA 4-6 wk after their initial study to determine whether persistent positive scans occurred with this agent. All 6 had negative scans., Conclusion: This study suggests that 99mTc-GLA localizes in zones of acute myocardial necrosis when injected within 9 h of onset of infarction.
- Published
- 1999
7. [Clarification of "DRG and PRG in infarction"].
- Author
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Bezante GP, Brunelli C, Pasdera A, Spallarossa P, Merello MR, Rossettin P, Zorzet F, and Caponnetto S
- Subjects
- Humans, Diagnosis-Related Groups, Myocardial Infarction
- Published
- 1998
8. [Cost analysis for DRG and PRG in the treatment of acute myocardial infarction in hospitalized patients].
- Author
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Bezante GP, Brunelli C, Pasdera A, Spallarossa P, Merello MR, Rossettin P, Zorzet F, and Caponnetto S
- Subjects
- Budgets, Costs and Cost Analysis, Humans, Diagnosis-Related Groups, Inpatients, Myocardial Infarction economics, Myocardial Infarction therapy
- Abstract
The cost of diagnostic and therapeutic procedures in patients with acute myocardial infarction (AMI) during hospitalization was determined using both the Diagnosis Related Group (DRG) and Process Related Group (PRG) systems. This cost-analysis system was planned and performed to estimate the cost of medical and non-medical staff involved in patient care, as well as commensurate costs. Over a three-month period, 45 patients discharged with a diagnosis of AMI, equivalent to 410 code ICD-9-CM, were enrolled in the study. The collected data were then processed and the cost for each DRG was derived. The mean cost borne for each patient with AMI was 5,864,345 Italian lire with a maximum of 17,138,300 lire for DRG 112 and a minimum of 3,332,329 lire for DRG 123. Our data suggest that in patients with AMI, there is profound discrepancy between the current DRG reimbursements and "real" cost, for example in DRG 112 (a discrepancy equivalent to 166%). The cost difference is essentially related to different procedures involved in medical care and, therefore, it follows that the overall cost of patient with AMI is primarily related to PRG cost and is largely independent of other components. These results prove that therapeutic strategies are very important in determining the cost for each DRG and that the cost for each DRG can change in relation to the PRG performed and to the progression of illness. The utilization of DRG and PRG systems appears to be an essential tool that can be used to build a system in which not only efficiency but also quality of care are evaluated.
- Published
- 1997
9. Lipoprotein (a) is increased in acute coronary syndromes (unstable angina pectoris and myocardial infarction), but it is not predictive of the severity of coronary lesions.
- Author
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Brunelli C, Spallarossa P, Bertolini S, Balbi M, Barbara C, Masturzo P, Lantieri PB, Pastorini C, and Caponnetto S
- Subjects
- Cardiomyopathies blood, Female, Heart Valve Diseases blood, Humans, Male, Middle Aged, Predictive Value of Tests, Angina, Unstable blood, Lipoprotein(a) blood, Myocardial Infarction blood
- Abstract
Lipoprotein (a) [Lp(a)] concentrations were determined in 365 patients undergoing coronary angiography for stable angina (n = 159), unstable angina (n = 99), recent myocardial infarction (n = 45), and nonischemic heart disease (cardiomyopathy or valvular disease, n = 62, non-IHD). Mean +/- SD and median Lp(a) concentrations in stable angina (29.9 +/- 29.2;22 mg/dl) did not differ from those in non-IHD (26.9 +/- 26.3; 17), but were significantly lower than in patients with unstable angina (52.7 +/- 36.6; 58) and myocardial infarction (44.8 +/- 36.4; 34) (p < 0.01). Coronary angiography revealed that 261 patients, including 4 patients in the non-IHD group, had significant (> or = 50%) coronary lesions. Lp(a) was higher in patients with (41 +/- 35; 32) than in those without (28 +/- 27; 19) angiographic evidence of significant coronary stenosis (p < 0.05) and showed a weak univariate correlation with the angiographic index (Total Score) of the severity of the disease (r = 0.106;p < 0.05). However, in the subgroup of 303 patients with stable/unstable angina or myocardial infarction, Lp(a) was predictive neither of angiographic presence nor of severity of coronary disease. Patients were then ranked according to the Total Score values. Among patients with comparable angiographic severity of coronary artery disease, Lp(a) appeared to be remarkably higher in patients with acute ischemic syndromes (unstable angina, myocardial infarction) than in patients with stable angina. In conclusion, Lp(a) was roughly twice as high in acute (unstable angina, myocardial infarction) than in chronic (stable angina) ischemic syndromes, but there was no difference between chronic stable angina and non-IHD.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1995
- Full Text
- View/download PDF
10. Perfusional and metabolic effects of nisoldipine as shown by positron emission tomography after acute myocardial infarction.
- Author
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Brunelli C, Parodi O, Sambuceti G, Corsiglia L, Rosa GM, Giorgetti A, Bezante GP, Nista N, and Caponnetto S
- Subjects
- Adult, Coronary Disease complications, Coronary Disease drug therapy, Coronary Disease physiopathology, Dobutamine, Echocardiography methods, Heart diagnostic imaging, Humans, Myocardial Infarction diagnosis, Myocardial Infarction physiopathology, Nisoldipine pharmacology, Tomography, Emission-Computed, Ventricular Dysfunction, Left drug therapy, Ventricular Dysfunction, Left etiology, Coronary Circulation drug effects, Myocardial Infarction drug therapy, Nisoldipine therapeutic use
- Abstract
After myocardial infarction, regional dysfunction can occur in viable myocardial regions because of the presence of baseline hypoperfusion. Recent evidence suggests that these areas may maintain a residual perfusion reserve. The aim of the present study was to evaluate whether oral nisoldipine can increase regional myocardial blood flow (MBF) in dyssynergic but viable myocardium after myocardial infarction. Patients with isolated left anterior descending coronary stenosis were studied 1 month after the first myocardial infarction. Patients underwent [18F]fluorodeoxyglucose imaging, and MBF was measured, using positron emission tomography and [13N]ammonia, at baseline and following dobutamine administration (10 micrograms/kg/min over 5 minutes). MBF measurements were repeated 24 hours after nisoldipine (10 mg twice daily). Preliminary results suggest that necrotic areas showed the largest reduction in baseline MBF. Dyssynergic-viable regions showed a reduced resting MBF but maintained a residual perfusion reserve in response to inotropic stimulation. Thus, nisoldipine selectively improved basal perfusion in dyssynergic-viable myocardium.
- Published
- 1995
- Full Text
- View/download PDF
11. Effectiveness and safety of a single intravenous bolus injection of tissue-type plasminogen activator in acute myocardial infarction. Bolus Dose-Escalation Study of Tissue-Type Plasminogen Activator (BEST) Investigators.
- Author
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Hackett D, Andreotti F, Haider AW, Brunelli C, Shahi M, Fussell A, Buller N, Foale R, Lipkin D, and Caponnetto S
- Subjects
- Adult, Aged, Electrocardiography, Female, Fibrinogen analysis, Humans, Injections, Intravenous, Male, Middle Aged, Myocardial Infarction blood, Myocardial Infarction physiopathology, Recurrence, Thrombolytic Therapy adverse effects, Tissue Plasminogen Activator adverse effects, Vascular Patency, Myocardial Infarction drug therapy, Thrombolytic Therapy methods, Tissue Plasminogen Activator administration & dosage
- Abstract
The efficacy of multiple intravenous bolus injections of tissue-type plasminogen activator (t-PA) in inducing rapid coronary recanalization in patients with acute myocardial infarction was previously demonstrated. In this Bolus Dose-Escalation Study of Tissue-Type Plasminogen Activator (BEST), the efficacy of 3 different doses of a single rapid intravenous bolus injection of t-PA (dute-plase, Wellcome Foundation, London) in inducing coronary patency (Thrombolysis In Myocardial Infarction perfusion grade 2 or 3) in 64 patients with acute myocardial infarction presenting less than 6 hours after onset of symptoms was investigated. At 60 minutes after administration of t-PA, the infarct-related coronary artery was patent in 9 of 17 patients (53%; 95% confidence interval [CI] 28 to 77%) after 0.3 MU/kg, in 14 of 23 (61%; 95% CI 39 to 80%) after 0.45 MU/kg and in 10 of 14 (71%; 95% CI 42 to 92%) after 0.6 MU/kg. At 90 minutes after t-PA, coronary patency was present in 9 of 17 cases (53%; 95% CI 28 to 77%) after 0.3 MU/kg, in 12 of 24 (50%; 95% CI 29 to 71%) after 0.45 MU/kg and in 10 of 13 (77%; 95% CI 46 to 95%) after 0.6 MU/kg. One patient in each dose group had a silent reoccluded infarct-related artery by 24 hours, and there were 2 clinical reinfarctions before discharge. No major bleeding events were observed. There were 5 hospital deaths, all unrelated to t-PA. A single intravenous bolus injection of 0.6 MU/kg of t-PA appears to be effective in inducing rapid coronary patency and to be safe in patients with acute myocardial infarction.
- Published
- 1992
- Full Text
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12. Hypertension as a risk factor for sudden cardiac death and nonfatal myocardial infarction. Working Group of CNR Study OD1.
- Author
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Brunelli C, Cristofani R, and L'Abbate A
- Subjects
- Actuarial Analysis, Cause of Death, Death, Sudden epidemiology, Electrocardiography, Exercise Test, Follow-Up Studies, Humans, Hypertension mortality, Italy, Myocardial Infarction mortality, Risk Factors, Death, Sudden etiology, Hypertension complications, Myocardial Infarction etiology
- Abstract
To evaluate long-term prognosis during medical treatment of hypertension associated with angina pectoris, a total of 1083 patients with angiographically-documented coronary artery disease were followed for a mean of 66 months. At the end of the study, follow-up was complete in 98% of all patients. Of the 1083 patients, 132 (12%) had hypertension and 951 (88%) were not hypertensive. During the follow-up period, there was a total of 15 deaths (11.3%) among the hypertensive population (vs. 61 or 6.4% in the nonhypertensives) as well as a higher incidence of nonfatal myocardial infarction (9.0% in the hypertensives vs. 3.7% in the nonhypertensives) (Figure 2). Six-year cumulative survival was 84% in the hypertensive patients as compared to 92% in the nonhypertensives. Among risk factors, historical data, clinical and catheterization findings, the only noninvasively-obtainable independent predictor of prognosis using multivariate analysis was hypertension (Table 3).
- Published
- 1990
13. [The role of spasm in angina pectoris, myocardial infarction and sudden death. Indications for future research and treatment].
- Author
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Maseri A, Chierchia S, L'Abbate A, Biagini A, Distante A, Parodi O, Brunelli C, and Severi S
- Subjects
- Coronary Vasospasm physiopathology, Humans, Angina Pectoris etiology, Coronary Vasospasm complications, Death, Sudden etiology, Myocardial Infarction etiology
- Abstract
Recent concepts on the role of coronary artery spasm and other forms of vasoconstriction in coronary artery disease are studied with particular reference to episodes of transient ischemia and their therapeutic implications. The possible contribution of spasm and other obstructive mechanisms such as platelet agregation, to the different forms of angina, myocardial infarction and sudden death, is analysed in the light of clinical observations, some of which have not previously been reported. Based on these concepts and clinical considerations, new orientations for future research and treatment are suggested. In our series, long term treatment of coronary artery disease with the association of nitrate derivatives are suggested. In our series, long term treatment of coronary artery disease with the association of nitrate derivatives and calcium antagonists has led to a reduction in mortality and in the incidence of myocardial infarction over periods ranging from 2 to 4 years.
- Published
- 1982
14. Peaking time of creatine-kinase MB in patients treated with urokinase or conventionally during acute myocardial infarction: is it really a clue to reperfusion?
- Author
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Brunelli C, Spallarossa P, Ghigliotti G, Iannetti M, Fusaro MT, Tondi S, Traina M, Hoffmann E, Morgagni GL, and De Biase L
- Subjects
- Aged, Clinical Trials as Topic, Female, Humans, Isoenzymes, Male, Middle Aged, Myocardial Infarction diagnosis, Random Allocation, Clinical Enzyme Tests, Creatine Kinase blood, Myocardial Infarction drug therapy, Myocardial Reperfusion, Urokinase-Type Plasminogen Activator therapeutic use
- Published
- 1988
15. OxLDL- and HSP-60 antigen-specific CD8+ T lymphocytes are detectable in the peripheral blood of patients suffering from coronary artery disease
- Author
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Ghio, M., Fabbi, P., Contini, P., Fedele, M., Brunelli, C., Indiveri, F., and Barsotti, A.
- Published
- 2013
- Full Text
- View/download PDF
16. Effectiveness and safety of a single intravenous Bolus injection of tissue-type plasminogen activator in acute myocardial infarction
- Author
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Graham Davies, Salvatore Caponnetto, David Hackett, Nigel P. Buller, Felicita Andreotti, M Shahi, David P. Lipkin, Attilio Maseri, Agha W. Haider, Brunelli C, Anne Fussell, and Rodney A. Foale
- Subjects
medicine.medical_specialty ,Chemotherapy ,business.industry ,medicine.medical_treatment ,Thrombolysis ,medicine.disease ,Confidence interval ,medicine.anatomical_structure ,Bolus (medicine) ,Anesthesia ,Internal medicine ,medicine ,Cardiology ,Myocardial infarction ,Cardiology and Cardiovascular Medicine ,business ,Plasminogen activator ,Perfusion ,Artery - Abstract
The efficacy of multiple intravenous bolus injections of tissue-type plasminogen activator (t-PA) in inducing rapid coronary recanalization in patients with acute myocardial infarction was previously demonstrated. In this Bolus Dose-Escalation Study of Tissue-Type Plasminogen Activator (BEST), the efficacy of 3 different doses of a single rapid intravenous bolus injection of t-PA (duteplase, Wellcome Foundation, London) in inducing coronary patency (Thrombolysis In Myocardial Infarction perfusion grade 2 or 3) in 64 patients with acute myocardial infarction presenting
- Published
- 1992
17. Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin: the ASSENT-3 randomised trial in acute myocardial infarction
- Author
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Van de Werf, F., Armstrong, P. W., Granger, C., Wallentin, L., Adgey, A. A. J., Aylward, P., Binbrek, A. S., Califf, R., Cassim, S., Diaz, R., Fanebust, R., Fioretti, P. M., Huber, K., Husted, S., Lindahl, B., Lopez-Sendon, J. L., Makijarvi, M., Meyer, J., Navarro Robles, J., Pfisterer, M., Seabra-Gomes, R., Soares-Piegas, L., Sugrue, D., Tendera, M., Theroux, P., Toutouzas, P., Vahanian, A., Verheugt, F., Sarelin, H., Goetz, G., Bluhmki, E., Daclin, V., Danays, T., Houbracken, K., Kaye, J., Reilly, P., Hacke, W., von Kummer, R., Lesaffre, E., Bogaerts, K., Peeters, C., Fox, K. A. A., Brower, R., Hirsh, J., Maggioni, A., Tijssen, J., Weaver, D., Beernaert, A., Beysen, N., Broos, K., De Prins, E., D'Hollander, K., Dupon, L., Fomyna, N., Fransen, A., Genesse, D., Goffin, L., Hendrickx, R., Jansen, B., Jorissen, F., Luys, C., Luyten, A., Marschal, C., Moreira, M., Munsters, K., Salerno, R., Schoovaerts, C., Sinnaeve, P., Schildermans, C., Vandenberghe, K., Vandeschoot, K., Van Gucht, H., Van Rompaey, P., Vlassak, S., Watzeels, M., Wittockx, H., Galan, K., Humeniuk, L., Seidel, A., Molina, M., Hafley, G., Alexander, J., Pascual, A., Bestilny, S., Temple, T., Ahuad Guerrero, R., Albisu, J. P., Bassani Arrieta, C. A., Bono, J., Caccavo, A., Cagnolatti, A., Cartasegna, L. R., Castellanos, R., Chekerdemian, S., Covelli, G., Cuello, J. L., Cuneo, C. A., Fernandez, A., Ferrara, C., Ferro-Queirel, E., Gambarte, A., Garcia-Duran, R., Hasbani, E., Hrabar, A., Keller, L., Lobo Marquez, L. L., Luciardi, H., Macin, S. M., Marinig, A., Marzetti, E., Muntaner, J., Nordaby, R., Orlandini, A. D., Piombo, A. C., Pomposiello, J. C., Quijano, R. A., Amerena, J., Aroney, G., Buckmaster, N., Carroll, P., Fitzpatrick, M., Newman, R., Rowe, M., Singh, B., Thomson, A., Winter, C., Eber, B., Gaul, G. B., Klein, W., Leisch, F., Mayr, H., Mlczoch, J., Niessner, H., Pachinger, O., Pall, H., Pichler, M., Roggla, G., Schaflinger, E., Schreiber, W., Slany, J., Traindl, O., Zenker, G., Beckers, J., Bekaert, I., Berthe, C., Bodur, G., Carlier, B., Carlier, M., Carpentier, J., Celen, H., Charlier, F., Clement, A., Coenen, A., Crochelet, L., De Keyser, F., De Man, F., de Meester, A., Dendale, P., Dhondt, E., Dhooghe, G., El Allaf, D., Elshot, S., Emmerechts, C., Foret, F., Gatera, E., Geraedts, J., Gerardy, A. C., Gysbrechts, M., Hallemans, R., Hellemans, S., Herssens, H., Huygens, L., Janssens, L., Lalmand, J., Maamar, R., Marechal, P., Mertens, D., Michel, P., Morandini, E., Nannan, M., Nguyen, D., Odeurs, W., Peerenboom, P., Pirenne, B., Quinonez, M., Raymenants, E., Renard, M., Silance, P. G., Standaert, A. M., Striekwold, H., Thiels, H., Valadi, D., van Brabandt, H., Van Dormael, M., Van Iseghem, P., Van Walleghem, U., Vanden Bosch, H., Vandenbossche, J. L., Vermylen, J., Verstraete, S., Vo Ngoc, P., Willems, P., Zenner, R., Campos de Albuquerque, D., Coutinho, M., de Camargo Carvalho, A. C., Fernandes Manenti, E. R., Ferreira Azevedo, A., Golin, V., Gun, C., Marin Neto, J. A., Marino, R. L., Miranda Abrantes, J. A., Nicolau, J. C., Porto Alegre Dancini, E. M., Rabelo, A., Ramos, R. F., Rizzi Coelho, O., Alexander, D., Bata, I. R., Bhargava, R. K., Bogaty, P., D'Amours, G., Darcel, I., Finnie, K. J. C., Fowlis, R., Gupta, M. K., Henderson, M., Howlett, M. K., Javier, J. J., Kieu, C. V., Kumar, G., Lebouthillier, P., Leduc, F., Lepage, S., Mcavinue, T., Mcgillen, J. E., Mcmeekin, J. D., Morse, J. W., Pistawka, K., Raimondo, E. F., Sandrin, F., Smith, H., Smylie, P. C., Tran, K., Turabian, M., Wagner, K. R., Winkler, L. H., Woo, K. S., Falstie-Jensen, N., Lind Rasmussen, S., Lomholt, P., Markenvard, J., Nielsen, H., Petersen, J., Romer, F., Ahonen, J., Huttunen, M., Kokkonen, L., Luukkonen, J., Mantyla, P., Melin, J., Mustonen, J., Valli, J., Voutilainen, S., Agraou, B., Allam, S., Baradat, G., Battistella, P., Bazin, P., Bouvier, J. -M., Destrac, S., Fouche, R., Fournier, P. -Y., Funck, F., Garnier, H., Grall, J. -Y., Gully, C., Lallement, P. -Y., Loiselet, P., Mycinsky, C., Page, A., Parisot, M., Range, G., Rocher, R., Tafani, C., Thisse, J. -Y., Tibi, T., Tissot, M., Wahl, P., Backenkohler, U., Bavastro, P., Beckmann-Hiss, H., Behnke, M., Bermes, M., Bernsmeier, R., Bethge, K. P., Bethge, H., Block, M., Burkhardt, W., Cieslinski, G., Claus, G., Deetjen, A., Diefenbach, A., Diehm, C., Dietz, A., Dippold, W. G., Eichner, A., Erckenbrecht, J. F., Gawlick, L., Gerber, V., Goppel, L., Gottwik, M., Grosch, B., Hammer, B., Hanheide, M., Hanrath, P., Haspel, J., Hennersdorf, F., Hermanns, M., Hoffmeister, H. M., Holzapfel, P., Hubner, H., Jansen, W., Jung, S., Kaddatz, J., Kienbock, H., Klein, H. H., Konz, K. H., Kulschbach, M., Leschke, M., Liebau, G., Linnartz, M., Lockert, G., Loesbrock, R., Lollgen, H., Ludwig, N., Mudra, H., Munzer, K., Nebel, B., Nellessen, U., Neu, C., Olbrich, H. G., Pfeffer, A., Pfeiffer, P., Plate, V., Pollock, B., Rapp, H., Rommele, U., Sauer, K., Scheffler, N., Schlotterbeck, K., Schmidt-Salzmann, A., Schnitzler, G., Schumann, H., Schuster, C. J., Schuster, P., Schweizer, P., Seitz, K., Simon, R., Spes, C., Szabo, S., Terhardt-Kasten, E., Theuerkauf, B., Tigges, R., Tinnappel, J., Topp, H., Trockel, P., Unland, N., Veth, V., Vom Dahl, J., Vossbeck, G., Weindel, K., Weib, D., Wiewel, D., Wirtz, P., Zipp, C., Apostolou, T., Chalkidis, C., Exadaktylos, N., Foussas, S., Hatseras, D., Karas, S., Karydis, K., Lambrou, S., Louridas, G., Manolis, A., Nanas, J., Novas, I., Panagiotidou, T., Papadopoulos, C., Papakonstantinou, D., Papasteriadis, E., Pavlidis, P., Pyrgakis, V., Skoufas, P., Stavrati, A., Tyrologos, A., Vardas, P., Vrouchos, G., Zacharoulis, A., Zarifis, J., Brown, A., Daly, K., Fennell, W., Horgan, J., Mccann, H., Mcdonald, K., O'Reilly, M., Sullivan, P., Altamura, G., Ambrosio, G., Auteri, A., Aveta, P., Azzarito, M., Badano, L. P., Barbiero, M., Barletta, C., Biscosi, C., Boccanelli, A., Bottero, M., Brizio, E., Brunazzi, M. C., Brunelli, C., Bugatti, U., Capozi, A., Capucci, A., Carfora, A., Caronna, A., Carrone, M., Casazza, F., Cauticci, A., Ceci, V., Ciconte, V., Circo, A., Ciricugno, S., Comito, F., Cornacchia, D., Corsini, G., D'Andrea, F., De Rosa, P., De Simone, M., Del Citerna, F., Del Pinto, M., Dell'Ali, C., Della Casa, S., Della Monica, R., Delogu, G., Di Biase, M., Di Chiara, A., Di Guardo, G., Di Marco, S., Di Mario, F., Di Napoli, T., Di Palma, F., Fadin, B. M., Fazzari, M., Ferraiuolo, G., Fiaschetti, R., Fontanelli, A., Fresco, C., Gambelli, G., Gasbarri, F., Gemelli, M., Giani, P., Gigantino, A., Giomi, A., Giorgi, G., Greco, C., Gregorio, G., Guagnozzi, G., Guiducci, U., Guzzardi, G., Izzo, A., La Rosa, A., Leone, F., Leone, G., Lo Bianco, F., Locuratolo, N., Maggiolini, S., Malinconico, M., Mancone, C., Mangiameli, S., Marchi, S. M., Maresta, A., Mauri, F., Mazzini, C. A., Michisanti, M., Miracapillo, G., Modena, M. G., Morgagni, G. L., Mossuti, E., Nascimbeni, F., Negrelli, M., Notaristefano, A., Pardi, S., Peci, P., Pettinati, G., Pietropaolo, F., Pirelli, S., Pretolani, M., Prinzi, D., Proietti, F., Raganelli, L., Rapino, S., Re, F., Ricci, R., Rinaldi, G., Rusticali, G., Severi, S., Spallarossa, P., Tartagni, F., Terrosu, P., Tortorella, G., Tota, F., Tritto, I., Tuccilo, B., Turco, V., Uscio, G., Valagussa, F., Vergoni, W., Verzuri, M. S., Vetrano, A., Villani, R., Zanini, R., Boisante, L., Niclou, R., Alcocer, L., Castro, A., Fragoso, J., Gonzalez, V., Gonzalez-Pacheco, H., Hernandez-Santamaria, I., Huerta, R., Huerta, D., Martinez, A., Mendoza, M., Moguel, R., Navarro, J., Portos, J. M., Rodriguez, I., Sierra, L., Valencia, S., Vazquez, A., Arnold, A. E. R., Boehmer, A. G., de Graaf, J. J., Funke Kupper, A. J., Gobel, E. J. A. M., Janus, C. L., Linssen, G. C. M., Sedney, M. I., Slegers, L. C., Spierenburg, H. A. M., Strikwerda, S., Tans, J. G. M., Twisk, S. P. M., van der Heijden, R., van Kalmthout, P. M., Verheugt, F. W. A., Holt, E., Skogsholm, A., Thorshaug, R., Thybo, N. K., Wang, H., Maciejewicz, J., Piotrowski, W., Pluta, W., Ruminski, W., Skura, M., Smielak-Korombel, W., Carranca, J., Carvalho, M., Catarino, C., Cunha, D., Ferreira, D., Ferreira, J., Ferreira da Costa, A. F., Lopes de Carvalho, J., Martins, L., Mourao, L., Oliveira Carrageta, M., Prazeres de Sa, E., Puig, J., Ramalho Dos Santos, M. J. J., Resende, M., Seabra Gomes, R., Baig, M. M. E., Bayat, J., Benjamin, J. D., Ranjith, N., Routier, R., Wittmer, H., Abizanda Campos, R., Alonso Garcia, M. A., Amaro Cendon, A., Arboleda Sanchez, J. A., Blanco Varela, J., Bruguera I Cortada, J., Carpintero Avellaneda, J. L., Caturla Such, J., Civeira Murillo, E., Fernandez Aviles, F., Fernandez Fernandez, R., Figueras Bellot, J., Fiol Sala, M., Froufe Sanchez, J., Garcia Calabozo, R., Garcia Palacios, J. L., Gonzalez Maqueda, I., Kallmeyer Martin, C., Lopez Sendon, J. L., Manzano Ramirez, A., Marine Rebull, J., Monton Rodriguez, A., Pique Gilart, M., Reina Toral, A., Rodriguez Llorian, A., Ruano Marco, M., Sanchez Miralles, A., Sanjose Garagarza, J. M., Santalo Bel, M., Torres Ruiz, J. M., Valentin Segura, V., Ahlstrom, P., Ahremark, U., Bandh, S., Bellinetto, A., Dahlberg, A., Hansen, O., Hurtig, U., Jonasson, L., Karlsson, J. E., Larsson, L. E., Moller, B., Ohlin, H., Persson, H., Sandstedt, L., Soderberg, S., Svennberg, L., Swahn, E., Tygesen, H., Broccard, A. F., Estlinbaum, W., Follath, F., Frutiger, A., Hess, N., Maggiorini, M., Marti, D., Muller, P., Rickenbacher, P., Schaller, M. D., Weinbacher, M., Abdulali, S., Ahmad, G., George, S., Ghazi, A., Rao, K. N., Bishop, A., Bridges, A., Canepa-Anson, R., Cave, M., Clarck, R., Cooper, I., de Belder, A., Farrer, M., Kendall, J. M., Ludman, P., Mattu, R., Mcglinchey, P., Moriarty, A. J., Muthusamy, S., Nee, P. A., Nolan, J., Papouchado, M., Rose, E. L., Shahi, M., Stephens, J., Trevelyan, J., Abdul-Karim, A., Adler, L., Arunasalam, S., Avington, D., Baron, S., Beel, T., Bellamy, B., Bennett, J., Berndt, T., Berrick, A., Bersin, R. M., Bethala, V., Bharath, S., Bouchard, A., Boulet, J. E., Bowerman, R., Boyek, T., Brar, R. S., Brodell, G., Bryant, B., Buckner, J. K., Cage, J., Cannon, J. D., Carducci, B., Carr, K., Chang, M., Chelliah, N., Chin, W. L., Chin, J., Church, D. H., Clark, R., Coulis, L., Dadkhah, S., Dearing, B., Defranco, A., Dharawat, M., Dharawat, R., Dhruva, N., Dicola, J., Dykstra, G., Eisenberg, S., El-Bialy, A., Fera, S., Ford, K., Foreman, R. D., Friedman, S., Friedman, V., Garibian, G., Gelormini, J., Geninatti, M. R., Genovese, R., Ghazi, F., Gilchrist, I., Gitler, B., Glover, R., Gonzalez, J., Goulah, R., Graham, B., Gray, R., Grodman, R., Habib, G. B., Hack, T., Hamroff, G., Hanna, G., Hart, M., Haught, H., Hawkins, J., Hempel, R., Hiremath, Y., Hiser, W., Holland, E., Jaffe, N., Jamal, N., James, K. F., Kalla, S., Kates, M., Kemper, A. J., Kennedy, J. J., Kerut, E. K., Killpack, M., King, J., T. Y., Ko, Kollar, K., Kontos, M., Kugelmassluu, A., Kumar, A., Kutscher, A. H., Lambrecht, C., Lancaster, L., Layden, J., Lazar, A., Lebow, M., Lee, C., Lee, A. B., Lehr, J., Levin, F. L., Levitt, R., Levy, R. M., Lieberman, A., Litman, G. I., Lui, H., Luu, M. Q., Macdonald, G., Madyoon, H., Mancherje, C., Marmulstein, M., Mclaurin, B. T., Mcnellis, M., Mendelson, R., Micale, P. J., Miller, M. J., Miller, M. S., Miller, J., Millman, A., Millsaps, R., Minor, S., Modica, J., Morse, H., Moskovits, N., Nester, B. A., Newton, A. S., Niazi, I., Niederman, A., Oatfield, R., Painter, J. A., Pamfilis, S. M., Pamulapati, K. M., Patel, N., Payne, R., Pearson, C., Peizner, D. S., Petrovich, L., Piriz, J., Pollack, M., Pollock, S., Popkave, A., Puma, J. A., Quesada, R., Quigley-Malcolm, D., Raby, K., Ravindran, K., Rees, A. P., Reiner, J., Rivera, E., Rogers, F., Rosenthal, A., Rowe, W. W., Ryan, P. F., Ryman, K., Salacata, A., Santolin, C., Saucedo, J., Savage, R., Savage, W., Schumacher, R., Segarra, S., Sharkey, S., Shonkoff, D., Silver, M., Silver, S. L., Singh, G., Sinyard, R. D., Sporn, D., Srivastava, N. K., Stomel, R., Suresh, D. P., Tallman, M., Togioka, T., Varma, S., Verant, R. P., Wallach, R., Weinberg, M., Weinberg, D., Weinstein, J. M., Wesley, G., Westerman, J. H., Wheeling, J., Whitaker, J., Widmer, M., Yasin, M., and Zakrzewski, M. J.
- Subjects
Male ,medicine.medical_specialty ,Abciximab ,Ischemia ,Myocardial Infarction ,Tenecteplase ,Injections ,Immunoglobulin Fab Fragments ,Reperfusion therapy ,Fibrinolytic Agents ,Recurrence ,Internal medicine ,medicine ,Humans ,Myocardial infarction ,Enoxaparin ,Aged ,Intention-to-treat analysis ,Chi-Square Distribution ,business.industry ,Heparin ,Antibodies, Monoclonal ,General Medicine ,Middle Aged ,medicine.disease ,Survival Analysis ,Regimen ,Treatment Outcome ,Anesthesia ,Tissue Plasminogen Activator ,Cardiology ,Drug Therapy, Combination ,Female ,business ,Platelet Aggregation Inhibitors ,medicine.drug - Abstract
BACKGROUND: Current fibrinolytic therapies fail to achieve optimum reperfusion in many patients. Low-molecular-weight heparins and platelet glycoprotein IIb/IIIa inhibitors have shown the potential to improve pharmacological reperfusion therapy. We did a randomised, open-label trial to compare the efficacy and safety of tenecteplase plus enoxaparin or abciximab, with that of tenecteplase plus weight-adjusted unfractionated heparin in patients with acute myocardial infarction. METHODS: 6095 patients with acute myocardial infarction of less than 6 h were randomly assigned one of three regimens: full-dose tenecteplase and enoxaparin for a maximum of 7 days (enoxaparin group; n=2040), half-dose tenecteplase with weight-adjusted low-dose unfractionated heparin and a 12-h infusion of abciximab (abciximab group; n=2017), or full-dose tenecteplase with weight-adjusted unfractionated heparin for 48 h (unfractionated heparin group; n=2038). The primary endpoints were the composites of 30-day mortality, in-hospital reinfarction, or in-hospital refractory ischaemia (efficacy endpoint), and the above endpoint plus in-hospital intracranial haemorrhage or in-hospital major bleeding complications (efficacy plus safety endpoint). Analysis was by intention to treat. FINDINGS: There were significantly fewer efficacy endpoints in the enoxaparin and abciximab groups than in the unfractionated heparin group: 233/2037 (11.4%) versus 315/2038 (15.4%; relative risk 0.74 [95% CI 0.63-0.87], p=0.0002) for enoxaparin, and 223/2017 (11.1%) versus 315/2038 (15.4%; 0.72 [0.61-0.84], p
- Published
- 2001
18. PREAMI: Perindopril and remodelling in elderly with acute myocardial infarction: Study rationale and design
- Author
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Battaglia, A., Ferraro, L., Lo Monaco, M., Palumbo, A., Mariani, M., Biadi, O., Boccalatte, A., Polimeno, S., Rosa, V., Liguori, L., Cuomo, S., Boccanelli, A., Morosetti, P., D Angelo, G., Bottiglieri, P., Brunelli, C., Spallarossa, P., Rolandi, A., Rossettini, Pf, Campa, P., Francesco BARILLA', Biase, L., Biscosi, C., Zampino, D., Capponi, E., Buccolieri, M., Gattobigio, R., Capucci, A., Passerini, F., Piepoli, M., Castello, A., Chiariello, M., Betocchi, S., Ciampi, Q., Losi, M., Corsini, G., Melorio, S., Dalle Mule, J., Mazzella, M., Cristinziani, Gr, Mario, L., Luca, I., Fusco, F., Del Salvatore, B., Sorino, M., Delise, P., Mozzato, Mg, Bilardo, G., Coro, L., Fantinel, M., Zasso, A., Fedele, F., Di Donato, D., Romano, S., Pascale, F., Giasi, M., Ciarcia, L., Lizzardo, A., Mastursi, M., Giordano, A., Benigno, M., Zanelli, E., Campana, M., Giovannini, E., Lacche, A., Pulignano, G., Giuffrida, G., Montana, G., Licciardello, G., L Abbate, A., Carpeggiani, C., Morales, A., Leghissa, R., Mandorla, S., Del Pinto, M., Borgioni, C., Mininni, N., Petrillo, Me, Moretti, G., Bonaglia, M., Zoni, A., Piscicelli, C., Orlandi, M., Panciroli, C., Oddone, A., Caizzi, V., Tartarini, G., Lattanzi, F., Reisenhofer, B., Pascotto, P., Zanocco, A., Dabizzi, Rp, Bini, L., Mondanelli, D., Frascarelli, F., Pitscheider, W., Erlicher, A., Rauhe, W., Bonsante, E., Polimeni, M., Catananti, F., Guerrisi, G., Magnani, B., Rapezzi, C., Ferlito, M., Amati, S., Di Leo, L., Manzo, M., Baldi, C., Cristofaro, M., Citro, R., Raviele, A., Turiano, G., Zuin, G., Rengo, F., Furgi, G., Papa, A., Rotiroti, D., Rosato, G., Siano, F., Pagliuca, MR, Rovelli, G., Heyman, J., Locati, I., Sanguinetti, M., Tomassini, F., Mantovani, R., Sanna, A., Marras, L., Crabu, E., Locci, G., Moio, N., Scilla, C., Tavazzi, L., Magrini, G., Bersano, C., Laudisa, Ml, Trimarco, B., Argenziano, L., Silvestri, S., Valagussa, F., Ciro, E., Cantu, E., Trocino, G., Rossillo, A., Valagussa, L., Finocchi, G., Benvenuto, Gm, Bonanno, C., Ometto, R., Risica, G., Gualandi, G., Facchin, L., Tenderini, P., Nicolosi, Gl, Burelli, C., Macor, F., Bellone, E., Laiso, D., Carvalho, P., Peila, C., Fagiano, A., Gardiol, S., Ganci, B., Presutto, P., Fontanelli, A., Morgera, T., Scarpino, L., Barbuzzi, S., Capogrosso, V., Terrosu, Pf, Contini, Gm, Sabino, G., Pes, R., Uneddu, F., Mecca, D., Tommaso, I., Rusconi, C., Brunazzi, Mc, Codeluppi, P., Pasqualini, M., Gorni, R., Negrelli, M., Paparoni, S., Core, A., Pecce, P., Petrella, L., Zennaro, Rg, Garuti, W., Alfano, G., Bacca, F., Petrucci, G., Paci, Am, Bigalli, G., Mangiameli, S., Gulizia, M., Cardillo, R., Ferrari, G., Tettamanti, F., Butti, E., Picchione, N., Sulla, A., Stroder, P., Perna, Gp, Ricci, S., Generali, Ca, Adornato, E., Ghisio, A., Tidu, M., Ferrari, R., Mele, D., Cicchitelli, G., Merli, E., Russa, O., Azcarate, Jma, Gonzales, Pz, Vilchez, F., Alonso, Lfi, Montero, Jmm, Zarzosa, Cd, Martin, Es, Ros, Jo, Martinez, Mh, Palau, Vm, Carranza, Mst, Mayor, Djlb, Cocina, Eg, Valderrama, Jc, Jimenez, Rp, Pardo, Jam, Cortada, Jb, Lorente, Lj, Guerrero, Jjg, Martinez, A., Coronado, Jlb, Casado, Rs, Cendon, Aa, Cokkinos, D., Maounis, T., Karatasakis, G., Kremastinos, D., Iliodromitis, S., Karatzas, D., Georgiadis, M., Paraskevaidis, I., Toutouzas, P., Antoniadis, P., Angeli, C., Vadas, P., Kaleboubas, M., Stamatelopoulos, S., Nanas, I., Kanakakis, A., Dalianis, A., Zacharoulis, A., Fotiadis, I., Pyrgakis, V., Liata, O., Mazen, B., Kardaras, F., Kardara, D., Krokos, V., Sioras, H., Fousas, S., Stefanidis, A., Papadopoulos, G., Papadopoulos, C., Papagiannis, I., Karidas, I., Zobolos, S., Preami, Investigators, A., Battaglia, L., Ferraro, M. L., Monaco, A., Palumbo, M., Mariani, O., Biadi, A., Boccalatte, S., Polimeno, V. D., Rosa, L., Liguori, S., Cuomo, A., Boccanelli, P., Morosetti, G., D'Angelo, P., Bottiglieri, C., Brunelli, P., Spallarossa, A., Rolandi, P. F., Rossettini, P., Campa, F., Barilla, L. D., Biase, C., Biscosi, D., Zampino, E., Capponi, M., Buccolieri, R., Gattobigio, A., Capucci, F., Passerini, M., Piepoli, A., Castello, M., Chiariello, Betocchi, Sandro, Q., Ciampi, Losi, MARIA ANGELA, G., Corsini, S., Melorio, J. D., Mule, M., Mazzella, G. R., Cristinziani, L., Mario, I. D., Luca, F., Fusco, B. D., Salvatore, M., Sorino, P., Delise, M. G., Mozzato, G., Bilardo, L., Coro', M., Fantinel, A., Zasso, F., Fedele, D. D., Donato, S., Romano, F. D., Pascale, M., Giasi, L., Ciarcia, A., Lizzardo, M., Mastursi, A., Giordano, M., Benigno, E., Zanelli, M., Campana, E., Giovannini, A., Lacche, G., Pulignano, G., Giuffrida, G., Montana, G., Licciardello, A., L'Abbate, C., Carpeggiani, A., Morale, R., Leghissa, S., Mandorla, M. D., Pinto, C., Borgioni, N., Mininni, M. E., Petrillo, G., Moretti, M., Bonaglia, A., Zoni, C., Piscicelli, M., Orlandi, C., Panciroli, A., Oddone, V., Caizzi, G., Tartarini, F., Lattanzi, B., Reisenhofer, P., Pascotto, A., Zanocco, R. P., Dabizzi, L., Bini, D., Mondanelli, F., Frascarelli, W., Pitscheider, A., Erlicher, W., Rauhe, E., Bonsante, M., Polimeni, F., Catananti, G., Guerrisi, B., Magnani, C., Rapezzi, M., Ferlito, S., Amati, L. D., Leo, M., Manzo, C., Baldi, M. D., Cristofaro, R., Citro, A., Raviele, G., Turiano, G., Zuin, F., Rengo, G., Furgi, A., Papa, D., Rotiroti, G., Rosato, F., Siano, M. R., Pagliuca, G., Rovelli, J., Heyman, I., Locati, M., Sanguinetti, F., Tomassini, R., Mantovani, A., Sanna, L., Marra, E., Crabu, G., Locci, N., Moio, C., Scilla, L., Tavazzi, G., Magrini, C., Bersano, M. L., Laudisa, Trimarco, Bruno, L., Argenziano, S., Silvestri, F., Valagussa, E., Ciro, E., Cantu, G., Trocino, A., Rossillo, L., Valagussa, G., Finocchi, G. M., Benvenuto, C., Bonanno, R., Ometto, G., Risica, G., Gualandi, L., Facchin, P., Tenderini, G. L., Nicolosi, C., Burelli, F., Macor, E., Bellone, D., Laiso, P., Carvalho, C., Peila, A., Fagiano, S., Gardiol, B., Ganci, P., Presutto, A., Fontanelli, T., Morgera, L., Scarpino, S., Barbuzzi, V., Capogrosso, P. F., Terrosu, G. M., Contini, G., Sabino, R., Pe, F., Uneddu, D., Mecca, I. D., Tommaso, C., Rusconi, M. C., Brunazzi, P., Codeluppi, M., Pasqualini, R., Gorni, M., Negrelli, S., Paparoni, A., Core, P., Pecce, L., Petrella, R. G., Zennaro, W., Garuti, G., Alfano, F., Bacca, G., Petrucci, A. M., Paci, G., Bigalli, S., Mangiameli, M., Gulizia, R., Cardillo, G., Ferrari, F., Tettamanti, E., Butti, N., Picchione, A., Sulla, P., Stroder, G. P., Perna, S., Ricci, C. A., Generali, E., Adornato, A., Ghisio, M., Tidu, R., Ferrari, D., Mele, G., Cicchitelli, E., Merli, O., Russa, J. M., A., P. Z., Gonzale, F., Vilchez, L. F. I., J. M. M., C. D., Zarzosa, E. S., Martin, J. O., De, M. H., Martinez, V. M., Palau, M. S. T., D. J. L., E. G., Cocina, J. C., Valderrama, R. P., Jimenez, J. A., M., J. B., Cortada, L. J., Lorente, J. J., G., A., Martinez, J. L., B., R. S., Casado, A. A., Cendon, D., Cokkino, T., Maouni, G., Karatasaki, D., Kremastino, S., Iliodromiti, D., Karatza, M., Georgiadi, I., Paraskevaidi, P., Toutouza, P., Antoniadi, C., Angeli, P., Vada, M., Kalebouba, S., Stamatelopoulo, I., Nana, A., Kanakaki, A., Daliani, A., Zacharouli, I., Fotiadi, V., Pyrgaki, O., Liata, B., Mazen, F., Kardara, D., Kardara, V., Kroko, H., Siora, S., Fousa, A., Stefanidi, G., Papadopoulo, C., Papadopoulo, I., Papagianni, I., Karida, and S., Zobolos
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Male ,Ventricular Remodeling ,Myocardial Infarction ,Angiotensin-Converting Enzyme Inhibitors ,Electrocardiography ,ace inhibitors ,elderly ,heart rate variability ,left ventricular remodeling ,myocardial infarction ,perindopril ,Double-Blind Method ,Echocardiography ,Research Design ,Perindopril ,Electrocardiography, Ambulatory ,Humans ,Female ,Aged - Abstract
Angiotensin-converting enzyme (ACE) inhibitors reduce mortality, the development of remodeling, left ventricular (LV) dysfunction, and ischemic events, both when administered alone as long-term treatment in patients with impaired LV function and/or heart failure (HF) and as short-term treatment, early after acute myocardial infarction (AMI) and/or HF. The few data available on the use of ACE inhibitors in the elderly after AMI are conflicting. Nothing is known about the effects of ACE inhibitors in elderly postinfarction patients with preserved LV function: these patients have a remarkable medium- to long-term mortality and HF incidence after infarction. The aim of this study is to evaluate, in patients with AMI agedor =65 years, the effects of Perindopril on the combined outcome of death, hospitalization for HF, and heart remodeling, considered to be aor =8% increase in LV end-diastolic volume (LVEDV). Secondary objectives include the same factors listed in the primary end points but considered separately. In addition, safety of the drug, ventricular remodeling, and adaptation are being evaluated. A total of 1100 patients with AMI (first episode or reinfarction), agedor =65 years, and preserved or only moderately depressed LV (LV ejection fractionor =40%), are to be enrolled and randomly assigned to treatment (8 mg for 12 months of Perindopril or placebo, in double-blind conditions). Clinical assessment is performed at fixed times, and periodic evaluations of (1) ventricular shape, dimensions, and function by quantitative 2-D echocardiography, and (2) heart rate variability and arrhythmias by ambulatory electrocardiographic monitoring are anticipated. The results and conclusions will be available by 2002 year.
- Published
- 2000
19. OxLDL- and HSP-60 antigen-specific CD8+ T lymphocytes are detectable in the peripheral blood of patients suffering from coronary artery disease.
- Author
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Ghio, M., Fabbi, P., Contini, P., Fedele, M., Brunelli, C., Indiveri, F., and Barsotti, A.
- Subjects
CORONARY disease ,LOW density lipoproteins ,CD8 antigen ,LYMPHOCYTES ,INFLAMMATION ,ATHEROSCLEROTIC plaque ,T cells ,CHEST pain ,PATIENTS - Abstract
Abstracts: Inflammatory and immunologic mechanisms are important for the initiation and the progression of atherosclerotic lesions. OxLDL and HSP-60 antigens are involved in the pathogenesis of atherosclerotic disease by triggering immune cells within the plaques. Through the MHC pentamer assays, we investigated the presence of OxLDL- and HSP-60-specific CD8
+ T lymphocytes in twenty HLA-A2-positive patients suffering from coronary artery disease (10 NSTEMI and 10 stable angina). Similarly, 10 age- and sex-matched healthy subjects were enrolled as controls. Biological samples were collected within 6 h of admission to hospital, at 30 days and at 180 days. OxLDL- and HSP-60-specific CD8+ T lymphocytes were never detectable in the peripheral blood from all the healthy controls. On the contrary, at each scheduled time point, both of these specific cells could be detected in peripheral blood from all enrolled patients. More in detail, the flow cytometric analysis of MHC-1 pentamer OxLDL-specific CD8+ T lymphocytes revealed a sharp and significant increase at the hospital admission, within 6 h from the chest pain onset, followed by an evident decline to lower levels at 30 days and at 180 days from the enrollment in the study. On the contrary, although MHC-1 pentamer HSP-60 CD8+ T lymphocytes were detectable in enrolled patients, almost no variance could be detectable during the follow-up scheduled evaluations. On the whole, this finding indicates that HSP-60- and OxLDL-specific CD8+ T lymphocytes could play a role in the maintenance or worsening of the atherosclerotic coronary disease. [ABSTRACT FROM AUTHOR]- Published
- 2013
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20. Long-term survival in medically treated patients with ischemic heart disease and prognostic importance of clinical and electrocardiographic data (the Italian CNR Multicentre Prospective Study ODI)
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Cristofani R, Brunelli C, and A L'Abbate
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medicine.medical_specialty ,education.field_of_study ,medicine.diagnostic_test ,business.industry ,Cross-sectional study ,Mortality rate ,Population ,Infarction ,medicine.disease ,Clinical trial ,Internal medicine ,Cardiology ,medicine ,Myocardial infarction ,Cardiology and Cardiovascular Medicine ,education ,business ,Prospective cohort study ,Electrocardiography - Abstract
In order to study long-term survival in medically treated patients with ischaemic heart disease in our country and to evaluate the prognostic significance of clinical variables, 1083 patients less than 65 years old were followed up for a mean period of 66 months (min 36, max 93). All patients performed an exercise stress test and had coronary angiography. Vital status was known for 98.3% of the patients. The great majority were treated with calcium antagonists and nitrates. In the overall population, the annual cardiac mortality rate was 1.54%. On the basis of clinical variables, groups with a tenfold difference in mortality could be identified. The annual cardiac mortality was 0.29% in patients without myocardial infarction and effort ischaemia and reached 3.12% in those with extensive infarction and/or severe reduction of exercise tolerance. Among risk factors, only arterial hypertension was an independent predictor of mortality. According to angiographic variables, the highest mortality rate was 5.7% in patients with three-vessel disease and poor left ventricular function. When multivariate analysis was applied to clinically stratified subgroups, angiographic variables gave additional prognostic information on survival only in the subgroup with an intermediate prognosis. In conclusion (1) the annual cardiac mortality in our medically treated patients is low; (2) patients with very different prognoses may be identified on a clinical basis; (3) coronary angiography adds prognostic information only in moderately severe disease.
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- 1989
21. Major Role of Coronary Spasm in the Pathogenesis of Myocardial Infarction at Young Age
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M. Marzilli, A. Biagini, Attilio Maseri, Brunelli C, A. L’Abbate, S. Severi, M. G. Mazzei, and M. G. Trivella
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medicine.medical_specialty ,Transient ischemia ,business.industry ,medicine.disease ,Angina ,Pathogenesis ,Young age ,Internal medicine ,Coronary vasospasm ,cardiovascular system ,medicine ,Cardiology ,cardiovascular diseases ,Myocardial infarction ,business - Abstract
The role of coronary vasospasm in the genesis of angina, postulated many years ago, has been recently documented both in resting angina [6, 8] and in some cases of angina on effort [14]. Conversely, the role of coronary vasospasm in the genesis of myocardial infarction (MI), although postulated and even demonstrated in some cases, is still unclear [9]. Therefore, to discuss the role of spasm at young age is difficult.
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- 1981
22. Efficacy of perindopril in reduction of cardiovascular events among patients with stable coronary artery disease: randomised, double-blind, placebo-controlled, multicentre trial (the EUROPA study)
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Fox, K. M., Bertrand, M., Ferrari, Roberto, Remme, W. J., Simoons, M. L., Simoons, M., Bassand, J. P., Aldershvile, J., Hildebrandt, P., Cokkinos, D., Toutouzas, P., Eha, J., Erhardt, L., Erikssen, J., Grybauskas, P., Kalnins, U., Karsch, K., Sechtem, U., Keltai, M., Klein, W., Luscher, T., Mulcahy, D., Nieminen, M., Oto, A., Ozsaruhan, O., Paulus, W., Providencia, L., Riecansky, I., Ruzyllo, W., Ferrari, R., Santini, U., Tavazzi, L., Soler Soler, J., Widimsky, P., Julian, D., Dargie, H., Murray, G., Kubler, W., Thygesen, K., Duprez, D., Steg, G., Drexel, H., Gombotz, G., Heyndrickx, G. H., Legrand, V., Materne, P., Van Mieghem, W., Bocek, P., Branny, M., Cech, M., Charouzek, J., Drazka, J., Fabik, L., Florian, J., Francek, L., Groch, L., Havranek, P., Hradec, J., Jansky, P., Jirmar, R., Jokl, I., Krejcova, H., Kvasnak, M., Maratka, T., Marcinek, G., Moravcova, J., Nedbal, P., Peterka, K., Povolny, J., Rosolova, H., Semrad, B., Sochor, K., Spacek, R., Spinar, J., Stipal, R., Stuchlik, K., Sulda, M., Ulman, J., Vaclavicek, A., Vojtisek, P., Bjerregaard Andersen, H., Kristensen, K., Madsen, J. K., Markenvard, J., Meibom, J., Norgaard, A., Scheibel, M., Leht, A., Teesalu, R., Vahula, V., Itkonen, A., Juvonen, J., Karmakoski, J., Kilkki, E., Koskela, E., Melin, J., Nieminen, M. S., Savola, R., Terho, T., Voipio Pulkki, L. M., Apffel, F., Attali, P., Barjhoux, C., Baron, B., Berthier, Y., Dambrine, P., Decoulx, E., Deshayes, P., Fouche, R., Genest, M., Godard, S., Guillot, J. P., Hanania, G., Khattar, P., Leroy, F., Mansourati, J., Piquemal, R., Quiret, J. C., Raynaud, P., Rondepierre, D., Roynard, J. L., Sudhibhasilp, S., Van Belle, E., Bilbal, A., Lauer, B., Rettig Sturmer, G., Riessen, R., Rutsch, W., Sigel, H. A., Simon, R., Von Schacky, C., Winkelmann, B. R., Avgeropoulou, C., Christakos, S., Feggos, S., Floros, S., Fotiadis, I., Goudevenos, I., Kardara, D., Karidis, C., Koliopoulos, N., Kremastinos, D., Lekakis, I., Manolis, A., Pyrgakis, V., Papanikolaou, C., Papasteriadis, E., Skoufas, P., Stravrati, A., Stavridis, A., Syribeis, S., Vardas, P., Vassiliadis, I., Voudris, V., Zobolos, S., Berenyi, I., Edes, I., Janosi, A., Kalo, E., Karpati, P., Kornel, S., Pap, I., Polak, G., Reiber, I., Rusznak, M., Tarjan, J., Timar, S., Toth, K., Barton, J., Crean, P., Daly, K., Kearney, P., Meany, T. B., Quigley, P., Antolini, R., Azzolini, P., Bellone, E., Branzi, A., Brunelli, C., Capponi, E., Capucci, A., Casaccia, M., Cecchetti, E., Ceci, V., Celegon, L., Colombo, A., Corsini, G., Cucchini, F., Dalla Volta, S., De Caterina, R., De Luca, I., De Servi, S., Di Donato, M., Di Giacomo, U., Di Pasquale, G., Fiorentini, C., Gaddi, O., Giannetto, M., Giannuzzi, P., Giordano, A., Giovannini, E., Guarnierio, M., Iacono, A., Inama, G., Leghissa, R., Lorusso, R., Marinoni, G., Marzilli, M., Mauri, F., Mosele, G. M., Papi, S., Pela, G., Pettinati, G., Polimeni, M. R., Portaluppi, Francesco, Proto, C., Renaldini, E., Riva, S., Sanguinetti, M., Santini, M., Severi, S., Sinagra, G., Tantalo, L., Vajola, S. F., Volterrani, M., Ansmite, B., Gailiss, E., Gersamija, A., Ozolina, M. A., Baubiniene, A., Berukstis, E., Grigoniene, L., Kibarskis, A., Kirkutis, A., Marcinkus, R., Milvidaite, I., Vasiliauskas, D., Aalders, J. C. A., Bruggeling, W. A. J., De Feyter, P. J., De Leeuw, M. J., De Waard, D. E. P., De Weerd, G. J., De Zwaan, C., Dijkgraaf, R., Droste, H. T., Freericks, M. P., Hagoort Kok, A. W., Hillebrand, F., Jap, W. T. J., Jochemsen, G. M., Kiemeney, F., Kuijer, P. J. P., Mannaerts, H. F. J., Piek, J. J., Saelman, J. P. M., Slob, F. D., Smits, W. C. G., Suttorp, M. J., Tan, T. B., Van Beek, G. J., Van den Merkhof, L. F. M., Van der Heyden, R., Van Hessen, M. W. J., Van Langeveld, R. A. M., Van Nierop, P. R., Van Rey, F. J. W., Van Straalen, M. J., Vos, J., Werner, H. A., Westendorp, J. J. C., Achremczyk, P., Adamus, J., Baska, J., Bolinska Soltysiak, H., Bubinski, R., Ceremuzynski, L., Cieslinski, A., Dariusz, D., Drozdowski, P., Dubiel, J. S., Galewicz, M., Halawa, B., Janion, M., Jaworska, K., Kaszewska, I., Kleinrok, A., Kornacewicz Jach, Z., Krawczyk, W., Krynicki, R., Krzciuk, M., Krzeminska Pakula, M., Kuch, J., Kuzniar, J., Liszewska Pfejfer, D., Loboz Grudzien, K., Musial, W., Opolski, G., Pasyk, S., Piwowarska, W., Pulkowski, G., Rynkiewicz, A., Sinkiewicz, W., Skura, M., Slowinski, S., Smielak Korombel, W., Targonski, R., Templin, W., Tendera, M., Tracz, W., Trusz Gluza, M., Wodniecki, J., Zalewski, M., Zinka, E., Carrageta, M., Gil, J. C., Ferreira, R., Marques, A. L., Andrade, C. M. S., Seabra Gomes, R., Bada, V., Belicova, M., Dukat, A., Kaliska, G., Kamensky, G., Micko, K., Mikes, Z., Palinsky, M., Pella, D., Renker, B., Sefara, P., Sojka, G., Sulej, P., Szakacs, M., Salcedo, J. M. A., Orcajo, N. A., Garcia, P. A., Sanpera, J. M. A., Azcarate, J. A., Mayor, J. L. B., Martinez, V. B., Coronado, J. L. B., Ojeda, F. B., Caimari, R. B., Cortada, J. B., Valderrama, J. C., Ligorit, A. D., Caliani, J. S. E., Aviles, F. F., Guerrero, J. J. G., Lopez, D. G., Cocina, E. G., Urena, C. G., Lorente, L. J., Garcia Aranda, V. L., De Miguel, C. M., Montero, J. M., Romero, P. M., Benito, I. M., Lopez, F. N., Peiro, F. N., De Ros, J. O., Mas, J. O., Bermejo, M. A. P., Peralta, L. J. P., Padial, L. R., Sanz, A. S., Bonnin, J. S., Martin, E. S., Belsue, F. V., Ekdahl, S., Forslund, L., Ohlin, H., Pieper, M., Moccetti, T., Acarturk, E., Guzelsoy, D., Turkoglu, C., Adgey, A. A. J., Ahsan, A., Al Khafaji, M., Ball, S. G., Birkhead, J., Boon, N., Brack, M., Bridges, A., Buchalter, M., Calder, B., Cooke, R. A., Corr, L., Cowell, R., Curzen, N. P., Davidson, C., Davies, J., De Belder, M. A., Dhiya, L., Doig, J. C., Findlay, I. N., Francis, C. M., Glancy, J. M., Greenwood, T. W., Groves, P., Hall, A. S., Hamilton, G., Haq, I., Hillman, R., Hubbard, W., Hudson, I., Hutton, I., Ilsley, C., Innes, M., James, M., Jennings, K., Johnston, G., Jones, C. J. H., Joy, M., Keeling, P., Kooner, J., Lawson, C., Levy, R. D., Lip, G., Mclachlan, B., Montgomery, H. E., Morley, C. A., Murdoch, D. L., Muthusamy, R., Oakley, G. D. G., Penny, W., Percival, R., Purvis, J., Pye, M. P., Ramsdale, D., Roberts, D. H., Rozkovec, A., Salmassi, A. M., Saltissi, S., Sardar, S., Shapiro, L. M., Schofield, P. M., Stephens, J., Shakespeare, C., Srivastava, S., Swan, J. W., Tildesley, G., Travill, C., Wilkinson, P. R., Fratacci, M. D., Lerebours, G., and Deckers, J.
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Relative risk reduction ,Male ,medicine.medical_specialty ,Myocardial Infarction ,Angiotensin-Converting Enzyme Inhibitors ,Coronary Disease ,Coronary artery disease ,Double-Blind Method ,Internal medicine ,Cause of Death ,Clinical endpoint ,Perindopril ,Medicine ,Humans ,Myocardial infarction ,Heart Failure ,Ejection fraction ,business.industry ,General Medicine ,Middle Aged ,medicine.disease ,Heart Arrest ,Treatment Outcome ,Cardiovascular Diseases ,Heart failure ,ACE inhibitor ,Cardiology ,Female ,business ,circulatory and respiratory physiology ,medicine.drug ,Follow-Up Studies - Abstract
Background Treatment with angiotensin-converting-enzyme (ACE) inhibitors reduces the rate of cardiovascular events among patients with left-ventricular dysfunction and those at high risk of such events. We assessed whether the ACE inhibitor perindopril reduced cardiovascular risk in a low-risk population with stable coronary heart disease and no apparent heart failure. Methods We recruited patients from October, 1997, to June, 2000. 13655 patients were registered with previous myocardial infarction (64%), angiographic evidence of coronary artery disease (61%), coronary revascularisation (55%), or a positive stress test only (5%). After a run-in period of 4 weeks, in which all patients received perindopril, 12218 patients were randomly assigned perindopril 8 mg once daily (n=6110), or matching placebo (n=6108). The mean follow-up was 4.2 years, and the primary endpoint was cardiovascular death, myocardial infarction, or cardiac arrest. Analysis was by intention to treat. Findings Mean age of patients was 60 years (SD 9), 85% were male, 92% were taking platelet inhibitors, 62% beta blockers, and 58% lipid-lowering therapy. 603 (10%) placebo and 488 (8%) perindopril patients experienced the primary endpoint, which yields a 20% relative risk reduction (95% CI 9-29, p=0.0003) with perindopril. These benefits were consistent in all predefined subgroups and secondary endpoints. Perindopril was well tolerated. Interpretation Among patients with stable coronary heart disease without apparent heart failure, perindopril can significantly improve outcome. About 50 patients need to be treated for a period of 4 years to prevent one major cardiovascular event. Treatment with perindopril, on top of other preventive medications, should be considered in all patients with coronary heart disease.
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