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Background: Atrial Fibrillation (AF) may impact adversely on mitral valve function. Transcatheter Mitral Valve Repair (TMVR) with MitraClip is considered an acceptable alternative to surgical repair in high risk patients, and the EVEREST II trial has suggested that this holds true even in patients with AF. However, there is uncertainty on the outlook of real-world patients with AF undergoing TMVR. Methods: We analyzed retrospectively collected data on patients undergoing TMVR at 3 tertiary care centers. Baseline, procedural, and outcome details were systematically sought. Patients were followed after discharge for clinical events and echocardiographic changes. Results: A total of 116 subjects were included: 61 (53%) with AF and 55 (47%) without AF. Patients with AF had worse baseline functional class and EuroSCORE II, and a higher prevalence of type II mitral regurgitation, but patients without AF had higher prevalence of dilated or ischemic cardiomyopathy and of severe mitral regurgitation (all p < 0.05). Procedural success was achieved in most patients (115 [99%]) with out any differences according to the history of AF, but multiple MitraClips were required more frequently in patients with AF (p = 0.031). Echocardiographic and clinical results at follow-up were also similarly favorable, with 4 (3%) in-hospital deaths and a total of 15 (13%) at follow-up. However, patients with AF had a higher incidence of the composite of death or rehospitalizations for heart failure (14 [34%] vs 5 [13%], p = 0.035). Differences were not especially pronounced when focusing on patients with longstanding/ permanent AF vs those with paroxysmal/persistent AF. Conclusions: Despite largely similar baseline, echocardiographic and procedural features, patients with AF undergoing TMVR with MitraClip may face a higher risk of adverse events during follow-up. Careful follow-up and medical management are thus mandatory in such patients, irrespective of the subtype of AF.

To evaluate prospectively the impact on left ventricular (LV) remodelling of an intracoronary aspiration thrombectomy device as adjunctive therapy in primary percutaneous coronary intervention (PCI) in patients with anterior ST elevation myocardial infarction (STEMI).76 consecutive patients with anterior STEMI (65.3 (11.2) years, 48 men) were randomly assigned to intracoronary thrombectomy and stent placement (n = 38) or to conventional stenting (n = 38) of the infarct related artery. Each patient underwent transthoracic echocardiography immediately after PCI and at six months. At the time of echocardiographic control, major adverse cardiovascular events (MACE) in terms of death, new onset of myocardial infarction, and hospitalisation for heart failure were also evaluated.After a successful primary PCI, patients in the thrombectomy group achieved a higher rate of post-procedure myocardial blush grade 3 (36.8% v 13.1%, p = 0.03) and effective ST segment resolution at 90 minutes (81.6% v 55.3%, p = 0.02). Six months after the index intervention, 19 patients (26.8%) developed LV dilatation, defined as an increase in end diastolic volume (EDV)or= 20%: 15 in the conventional group and four in the thrombectomy group (p = 0.006). Accordingly, at six months patients treated conventionally had significantly higher end systolic volumes (82 (7.7) ml v 75.3 (4.9) ml, p0.0001) and EDV (152.5 (18.1) ml v 138.1 (10.7) ml, p0.0001) than patients treated with thrombectomy. No differences in cumulative MACE were observed (10.5% in the conventional group v 8.6% in the thrombectomy group, not significant).Compared with conventional stenting, adjunctive aspiration thrombectomy in successful primary PCI seems to be associated with a significantly lower incidence of LV remodelling at six months in patients with anterior STEMI.

Introduction Drug-eluting stent (DES) implantation represents an important innovation in the treatment of coronary artery disease. However, inflammatory-related complications, including subacute thrombosis and in-stent restenosis, are still important limitations to percutaneous coronary intervention (PCI). The aim of this study was to compare early local release of interleukin 1β (IL-1β) and IL-6 proinflammatory cytokines after elective placement of either bare metal stents or DES. Materials and methods IL-1β and IL-6 levels were assayed in plasma obtained from the coronary sinus both before and 20 min after stent implantation in 59 patients with stable angina, who were randomly assigned to receive bare, paclitaxel-, or sirolimus-eluting stents during elective PCI. Results We found that IL-1β and IL-6 levels were significantly increased in the coronary sinus of patients receiving either bare, paclitaxel- or sirolimus-eluting stents 20 min after stent implantation as compared with basal concentrations. The variation in the level of both cytokines was comparable among the three study groups. Conclusions A local release of proinflammatory cytokines occurs shortly after coronary stent placement, including DES, which is possibly related to plaque rupture and/or endothelium traumatism following the stenting procedure. This suggests that precocious anti-inflammatory treatment could be of benefit to further improve the PCI clinical outcome.

Background: Evidences show that diabetes mellitus (DM) lead to higher risk for ischemic heart disease (IHD). Recently, we proposed that genetic polymorphisms (SNP) of coronary ion channels might be involved in IHD. We showed that the genotype distribution of SNP rs5215 for Kir6.2 subunit of ATP-dependent potassium (KATP) channels moderately deviated from the HW equilibrium and that rs5215_GG is linked to IHD susceptibility: it might have a ‘‘protective’’ role in IHD genesis. Moreover, previous studies described that SNP rs5215_GG is strongly correlated with DM and hyperinsulinism in human. Aim and methods: In the present study, we hypothesized that SNP rs5215_GG for Kir6.2 subunit for KATP channels had some influences in the susceptibility of DM to IHD. We performed a subgroup analysis about the influence of rs5215_GG in diabetic patients on our previous population, i.e. 242 patients candidates to elective or emergency coronary angiography for acute coronary syndrome or chronic angina, of which 155 with CAD, 46 with microvascular dysfunction and 41 with anatomically and functionally normal coronary arteries (control group). Results: Among 242 patients, comparing subjects with DM to those without, there was not any significant difference in the prevalence of rs5215_GG. However, among 33 subjects without DM with normal coronary arteries, SNP rs5215_GG had a higher prevalence compared to those in the CAD group (10/33; 30.3%; p= 0.0277) as well as non-diabetic patients in the microvascular dysfunction group (9/33; 27.2%; p= 0.0295). Discussion and conclusion: The variant rs5215_GG results in the substitution of isoleucine (I) residue with valine (V) in the Kir6.2 subunit of KATP channels. Our results confirm that rs5215_GG might decrease susceptibility to IHD in patients without DM. In fact, rs5215_GG was confirmed to be present more frequently in patients without DM presenting anatomically and functionally normal coronary arteries. We believe that absence of DM is protective against IHD genesis and it might be improved by coronary KATP channels expressing rs5215_GG. Taken together, our data ratify the possibility that ion channels play a key role in coronary homeostasis and that SNP encoding for ion channels are involved in IHD pathophysiology.

Background: Coronary artery disease has been widely considered a “man’s disease” and not a major concern for women. However, scientists have been trying to unlock the female physiology of ischemic heart disease (IHD). In fact, women are more prone than men to microvascular coronary dysfunction. Recently, we proposed that genetic polymorphisms (SNP) of coronary ion channels may be involved in IHD susceptibility. Our published data showed that the genotype distribution of SNP rs5215 for Kir6.2 subunit of ATP-dependent potassium (KATP) channels moderately deviated from the HW equilibrium and that rs5215_GG is correlated with IHD susceptibility. In particular, we described that rs5215_GG genotype of Kir6.2 might have a ‘‘protective’’ role in IHD genesis. Aim and methods: In order to better describe the role of SNP rs5215_GG in IHD susceptibility in woman, we conducted a gender difference in term of prevalence of rs5215_GG on our previous population, i.e. 242 patients with acute coronary syndrome or stable angina, of which 155 with CAD, 46 with microvascular dysfunction and 41 with anatomically and functionally normal coronary arteries. Results: Among 242 patients, rs5215_GG was found to be more frequent in women (16/82; 19.51%; p=0.0450) compared to men. In particular, rs5215_GG was more frequent in female patients with anatomically and functionally normal coronary arteries (8/24; 33.3%; p=0.0428) compared with women with CAD, whereas there was no difference between men in normal and CAD groups. Discussion and conclusion: The polymorphism rs5215_GG is a missense SNP (ATC-GTC) that results in the substitution of isoleucine (I) residue with valine (V) in the Kir6.2 subunit of KATP channels. Our data validate the hypothesis that rs5215_GG could reduce susceptibility to IHD. In fact, rs5215_GG was confirmed to be present more frequently in woman presenting anatomically and functionally normal coronary arteries. Our results suggest that coronary KATP channels expressing rs5215_GG play a protective key role against IHD. Our data endorse the prospect of associations between SNP encoding coronary ion channels and IHD, validating the idea that ion channels play in coronary homeostasis and that their polymorphisms act in IHD genesis.

Introduction: Numerous reports suggest, among HIV+ patients (pts), an increased rate of acute coronary syndrome and cardiac death. Several data suggest that endothelial dysfunction is a major mechanisms in the development of coronary atherosclerosis in non-HIV infected patients. Hypothesis: The aim of our study is to assess coronary microvascular function using Doppler-flow wire in HIV+ patients in therapy with HAART. Methods: Thirteen HIV-infected patients were enrolled from the Department of Cardiovascular, Respiratory, Nephrology, Anesthesiology and Geriatric Sciences of the “Sapienza” University of Rome (Italy). The main inclusion criteria were: Framingham risk score Diagnostic coronary angiography was performed via percutaneous radial approach. Microvascular function was assessed by measuring coronary flow velocity reserve (CFR). Intracoronary functional tests were performed to evaluate both endothelium-dependent microvascular function [via intracoronary (IC) infusion of acetylcholine (2.5[[Unable to Display Character: –]]10 μg)] and non-endothelium-dependent microvascular function [via IC infusion of adenosine (5 μg) ]. Results: All the patients presented a Framingham risk score Conclusion: Microvascular function is not compromised in HIV + pts who presented coronary atherosclerotic plaque. Microvascular dysfunction, involved in pathophysiology of coronary artery disease in general population, seems to be not implicated in coronary atherosclerosis in HIV + pts. These data suggest a peculiar pathophysiological mechanisms for HIV related atherosclerosis.

Background: According to guidelines, implantable cardioverter defibrillator (ICD) is recommended in prevention of sudden cardiac death (SCD) in heart failure (HF) patients (pts). Guidelines have several limitations because ICD indication is based mainly on left ventricular ejection fraction (EF). Recent data showed that, independently from EF, 123-iodine metaiodobenzylguanidine imaging (123-I MIBG) could help to identify HF pts at high risk of SCD [heart/ mediastinum (H/M) ratio ≤1.6 and a summed score (SS) > 26], who may benefit of ICD. Aim: Our aim is to assess, in a real world registry, the role of 123-I MIBG for the prediction of ventricular tachyarrhythmia (VT) causing appropriate ICD therapy in HF pts. Methods: We consecutively enrolled 97 patients admitted to our hospital with diagnosis of HF, left ventricular ejection fraction (LVEF) ≤35% and indication to ICD. All patients underwent MIBG imaging. The patients were classified into two groups: Group 1 with H/M≤1.6 , SS> 26; Group2 with H/M>1.6, SS Results: 65 pts were included in group 1 and 32 pts in group 2. All baseline characteristics were similar in 2 groups apart from the etiology (table 1). In group 1, H/M ratio was 1.37±0.3 vs 1.8 ± 0.2 in group 2 (p=0.0002); SS was 37.5± 9.7 vs 16 ±6 in group 2 (p = 0.0001). At 1 year follow-up VTs causing appropriate ICD therapy in group 1 were 13.4% vs 1.28% in group 2(p=0.02); overall cardiac events were in group 1 16.4 % vs 1.92% in group 2 (p=0.02). Conclusion: Our results suggest that 123 I-MIBG can identify patients at increased risk for arrhythmic death and can be useful in the decision-making of ICD implantation independently from ejection fraction.

Introduction Asymptomatic patients with human immunodeficiency virus (HIV) infection are at increased risk of vascular disease. Whether asymptomatic HIV patients have increased prevalence or structural differences in coronary artery plaques is not clear. Methods Pubmed, Cochrane and Google Scholar were searched for articles evaluating asymptomatic HIV patients evaluated with coronary computed tomography. The prevalence of coronary stenosis (defined as >30% and >50%), of calcified coronary plaques (CCP) viewed as more ‘stable' plaques, and of non-calcified coronary plaques (NCP) viewed as more ‘vulnerable' plaques were the end points of interest. Results 9 studies with 1229 HIV patients and 1029 controls were included. No significant differences were detected about baseline cardiovascular risk profile. The prevalence of significant coronary stenosis >30% or >50% did not differ between HIV+ and HIV- patients (42% [37–44] and 46% [35–52] with an Odds Ratio [OR] of 1.38 [0.86–2.20] for >30% stenosis) and (15% [9–21] and 14% [7–22] with an OR of 1.11 [0.81–1.52]), respectively. The prevalence of calcified coronary plaques (CCP) (31% [24–32] and 21% [14–30] with an OR of 1.17 [0.63–2.16]) also did not differ among HIV+ and HIV- patients. On the contrary rates of NCP were >3-fold higher in HIV-positive patients [58% (48–60) and 17% (14–27) with an OR of 3.26 (1–30-8.18)], with an inverse relationship with CD4 cell count at meta-regression (Beta −0.20 [-0.35-0.18], p 0.04). Conclusion Asymptomatic HIV patients present a similar burden of coronary stenosis and calcified coronary artery plaques but significantly higher rates of non-calcific coronary plaques at computed tomography. The association between HIV infection, reduced CD4 cell counts and higher prevalence on non-calcific coronary artery plaques may shed light into the pathogenesis in HIV-associated coronary artery disease, stressing the importance of primary prevention in this population.

We report a case of an 81-years-old male, recently implanted with a Core Valve (CV) prosthesis and admitted to the ER for acute coronary syndrome. Coronary angiography revealed the patency of the coronary artery by-pass grafts but was impossible to cannulate the left main “imprisoned” by the CV prosthesis struts. Aortography showed an excessive gap between the CV struts and the coronary ostium. To cross the CV struts, we developed a “proboscis” catheter by cutting away the proximal end of the 7F JL 4 catheter and putting inside the 5F Heartrail catheter. The following angiograms showed a critical stenosis in the proximal obtuse marginal (branch), successfully treated with a bare-metal stent implantation. © 2012 Wiley Periodicals, Inc.

Background: The cholinergic nerve fibers of coronary arteries, capillaries and veins were studied in younger and older humans by staining of acetylcholinesterase and cholineacetyltransferase activities on autopsy samples of coronary vessels with the aim of investigating age-related changes. Methods: Samples of human coronary vessels were harvested and exposed to the enzymatic staining for acetylcholinesterase, immunohistochemical staining for cholineacetyltransferase and quantitative analysis of images. Morphometric values were subjected to statistical analysis of data. Results: Our results demonstrated that both acetylcholinesterase and cholineacetyltransferase are localized in the coronary vessels of younger and older humans. Staining of these two enzymes showed specific age-related changes. Structures resembling cholinergic nerve fibers were located in coronary vessels, in the extra-parenchymal (large caliber) and intraparenchymal (small caliber) branches (arteries and veins), organized in a plexus. Coronary arterioles of large caliber (diameter > 150 µm) were found to have many cholinergic nerve fibers. The quantitative analysis of images and the statistical analysis of the data demonstrated that the cholinergic neurotransmitters of coronary vessels (especially the extra-parenchymal branches of coronary arteries) strongly decrease with age. Conclusions: The age-related changes of cholinergic nerve supply of the human coronary vessels may play a role in the control of coronary circulation. Further studies are needed in order to draw definite conclusions concerning the nervous control of coronary circulation under normal and/or pathological conditions.

The relationship between catecholaminergic nerve fibers and beta-adrenergic receptors in the heart and in the coronary vessels was studied in humans. Only living tissues, harvested from brain-dead heart donors, were used in this experiment. Morphological observations and histochemical staining for norepinephrine and other catecholamines were carried out and beta-adrenergic receptors were stained by means of a beta-blocking fluorescent drug. All morphological data underwent quantitative analysis of images and statistical evaluation. This study provided direct evidence for the distribution of catecholaminergic nerve fibers and of beta-adrenergic receptors in the myocardium and in the coronary arteries. Catecholaminergic nerve fibers are located in the periadventitial tissue, in the adventitia and in the transitional zone between the intima and media. The beta-adrenergic receptors are mainly located in the more innervated part of the heart and coronary arteries but there is a major, although incomplete, overlap with related catecholaminergic nerve fibers. Moreover, using specific substrates and/or inhibitors, two types of beta-adrenergic receptors, beta(1) and beta(2), were demonstrated. Owing to the scarcity of available material (we used only four hearts), and objective difficulties in enrolling other patients, we are at this moment unable to draw general conclusions.

Levels and distribution of heart monoamine oxidases (MAOs) were studied in male Sprague-Dawley rats of 3 (young) and 24 (old) months of age using biochemical and histochemical techniques. Biochemical assay of MAOs in atria and in ventricles showed a significant increase in MAOs levels in old in comparison with young animals. MAOs histochemical staining revealed an homogeneous distribution of the enzyme within both right and left atria and/or ventricles in 3-months-old rats. In 24-months-old rats an increase of MAOs reaction in comparison with younger animals was found. This increase is more consistent in the endocardial portion of the right atrium and in the endocardial portion of the left atrium. In 3-months-old rats MAOs reaction was slightly lower in the epicardial than in the endocardial portions of both atria and/or ventricles. In 24-months-old rats MAOs reaction showed a significant increase if compared with young rats. The significance of these data is discussed in relation to the role of MAOs in rat heart.

Introduction: The European Society of Cardiology recommends cardiovascular screening to competitive athletes. In young population the execution of 12-lead ECG screening is still controversial. Hypothesis: The aim of our study is to evaluate the distribution of ECG abnormalities between competitive athletes, non competitive athletes and non athletes. Methods: From October 2010 to October 2015, we evaluated prospectively 11916 high school students (age 17.2 ± 2.4 years old; 45.9% male): 4533 (38.04 %) non athletes (G-A), 4936 (41.42 %) non competitive athletes (G-B) and 2447 (20.54%) competitive athletes (G-C). They were screened using 12-lead ECG. The statistical difference was considered significant only for p-value l this suggest that an ECG screening is recommended also in non athletes.

Aims Current guidelines give a class III recommendation to the intraprocedural use of unfractionated heparin (UFH) in patients pretreated with enoxaparin. The aim of our study was to evaluate bleeding complications in patients who underwent percutaneous coronary interventions (PCIs) performed using intraprocedural crossover of heparin therapy. Methods We retrospectively evaluated all PCIs performed at two Italian hospitals since January 2011 to December 2013. After a propensity-matched analysis, patients were divided into two groups (with a ratio 1 : 2) according to intraprocedural crossover of heparins (from enoxaparin to UFH) (Group 1) or intraprocedural UFH alone (Group 2). The primary end-point was a haemoglobin drop of at least 3 g/dl within 48 h after the procedure. Results During the 3 years analysed, 3224 patients underwent PCI, and after the propensity analysis, 309 patients were considered eligible for our study: 104 patients in Group 1 (69 ± 12 years, 78% men) and 205 patients in Group 2 (69 ± 13 years, 80% men, P = NS). There were no significant differences between the two groups for BMI, periprocedural use of antiplatelet therapy, baseline haemoglobin haematocrit or platelets levels. The primary end-point did not differ between the two groups (2.9% in Group 1 and 3.4% in Group 2, P = 0.550). Also, nadir of haematocrit or haemoglobin levels did not differ between the two groups. Finally, in hospital, major adverse cardio-cerebrovascular events did not differ between the two groups (1.9% in Group 1 and 3.9% in Group 2, P = 0.50). Conclusion In this retrospective analysis of a large PCI database, the ‘heparins crossover’ during PCI was not associated with increased bleeding risk.

Staging of heart failure represents a major issue in clinical practice. In this setting, the MOGE(S) classification was designed to be similar to the TNM classification used in oncology. Nevertheless, MOGE(S) nosology differs greatly from the key elements of the TNM classification, as well as its simplicity and clinical applicability. In fact, MOGE(S) acronym stands for morphofunctional characteristics (M), organ involvement (O), genetic or familial inheritance pattern (G), etiological information (E), and functional status (S). Recently, a new TNM-like classification for heart failure was proposed. This classification, named HLM, refers to heart damage arising from an initial stage of impaired systolic or diastolic function, without structural injury, to an advanced stage of biventricular dysfunction (H), different stages of lung involvement (L), and malfunction of peripheral organs such as the kidney, liver, and brain (M). HLM classification was influenced by the key elements of TNM staging: simplicity, clinical usefulness, efficacy for planning a therapeutic strategy, and ability to determine patient prognosis. HLM classification seems to be easily applied in the real world and valuable for balancing economic resources with the clinical complexity of patients.

Primary percutaneous coronary intervention (P-PCI) is the gold-standard treatment for ST-elevation myocardial infarction (STEMI). The main goals of a healthcare system in the setting of STEMI are two: first of all to reduce the time delays between diagnosis and P-PCI; secondly to increase the per cent of STEMI patients treated with P-PCI. The aim of this article was to propose a quality evaluation of healthcare system, identifying and defining measurable elements in the setting of P-PCI.

Background: Thrombectomy during primary percutaneous coronary intervention (Th-PCI) improvesmyocardial reperfusion in the absence of significant changes, in the acute phase, in traditional two-dimensional (2D) echo indexes of left ventricular (LV) function. The aim of this study was to evaluatethe potential of 2D speckle tracking echocardiography (2DSTE) analysis in assessing the efficacy ofthrombectomy as compared to standard 2D echo and cardiac magnetic resonance (CMR) data. Meth-ods: Two-dimensional speckle tracking echocardiography analysis was performed in 60 anterior ST-seg-ment elevation myocardial infarction (STEMI) patients to assess global (GLS), segmental (SLS) andregional longitudinal strain (RLS). 2D echo and CMR were performed within 5 days after PCI. Patientswere divided into 2 groups according to the different methods of reperfusion used: 28 pts Th-PCI and32 pts standard PCI (S-PCI). Results: Baseline clinical and angiographic characteristics, 2D echo, andDE-CMR data before and after PCI were similar in the 2 groups, except for microvascular obstruction(MVO), significantly lower (P = 0.001) in Th-PCI group. Conversely, GLS was significantly higher inTh-PCI group (P < 0.001), and in particular in the subset of patients without MVO (P = 0.012). RLS wasalso significantly higher in Th-PCI group (P = 0.001). GLS significantly correlates with infarct size,(R = 0.47; P = 0.03) and MVO (R = 0.69, P = 0.001). Finally, SLS was significantly lower in the DEsegments (P < 0.001). Conclusions: Patients treated with Th-PCI had a more preserved microvascularintegrity resulting in a better myocardial longitudinal deformation. 2DSTE analysis adds significant infor-mation on the efficacy of thrombus aspiration as compared to standard echocardiography and it is clo-sely related to the extent of microvascular damage. (Echocardiography 2013;00:1–6)Key words: myocardial strain, myocardial infarction, strain rate imagingPrimary percutaneous coronary intervention(PCI) is the gold standard treatment in patientswith ST-segment elevation myocardial infarction(STEMI).

Aims: To assess the prevalence of anemia and iron deficiency anemia in heart failure (HF) patients, to evaluate the effectiveness of current iron deficiency treatment strategies after discharge, and to analyze hospital readmissions and mortality rates in patients with and without anemia. Patients & methods: A patient registry-based, multicenter, retrospective, observational, cohort study of 418 hospitalized HF patients in Italy, monitored from 1 March 2010 to 30 March 2011. Results: Among patients with HF, 35.9% had anemia at admission; only 51.3% were treated with current iron deficiency treatment strategies during hospitalization and then only 29% of patients who were anemic at discharge were treated with iron at home. After a 4-week follow-up, only 11% of these patients reached the hemoglobin target value (study primary end point). However, current iron deficiency treatment strategies were not significantly associated with reduced risk of rehospitalization, but with a significantly reduced mortality rate after a 6-month follow-up (study secondary end points: 11.7 vs 51.7%; p < 0.0001). Conclusion: In HF patients, there is poor attention paid to anemia, its causes and treatment. Current iron deficiency treatment strategies are mismanaged and CARMES-1 demonstrated that they appear to be insufficient at improving patient outcome in terms of rehospitalization rate reduction, generating high costs, which could be avoided through an optimized treatment strategy. Therefore, more efficacious, efficient and cost–effective treatment strategies are required in Italy for HF patients with iron deficiency anemia to meet this unmet medical need.

Cardiac pathologies are among the leading causes of mortality and morbidity in industrialized countries, with myocardial infarction (MI) representing one of the major conditions leading to heart failure (HF). Hitherto, the development of consistent, stable, and reproducible models of closed-chest MI in large animals, meeting the clinical realism of a patient with HF subsequent to chronic ischemic necrosis, has not been successful. We hereby report the design and ensuing application of a novel porcine experimental model of closed-chest chronic ischemia suitable for biomedical research, mimicking post-MI HF. We also emphasize the key procedural steps involved in replicating this unprecedented model, from femoral artery and vein catheterization to MI induction by permanent occlusion of the left anterior descending coronary artery through superselective deployment of platinum-nylon coils, as well as endomyocardial biopsy sampling for histologic analysis and cell harvesting. Our model could indeed represent a valuable contribution and tool for translational research, providing precious insights to understand and overcome the many hurdles concerning, and currently quenching, the preclinical steps mandatory for the clinical translation of new cardiovascular technologies for personalized HF treatments.

Choosing the best oral therapy for pulmonary arterial hypertension(PAH) represents a great challenge for physicians, because differentdrugs are available: exploiting antagonism of endothelin receptors likebosentanandsixtaxentan,changinginnitricoxidepathwayslikesilden-afil and tadalafil and oral analogous of prostacyclin like beraprost [1].These drugs have been validated by direct comparison to placebothrough randomized clinical trial (RCTs), offering clinical andhemodynamical improvement, while there are fewer consensusesabout effect on survival [2], especially for oral treatment. Howeverdirect head-to-head comparisons are lacking, limiting physicians intheir choices in everyday clinical practice.We searched for randomized trials in The Cochrane CollaborationCentral Register of Controlled Trials, EMBASE, and MEDLINE/PubMed.We restricted our searches to human studies, clinical trials, controlledtrials or randomized trials. We used the keywords and medical subjectheadings: “pulmonary hypertension”, “drug”, “oral drug”, “antagonist ofendothelin receptors ”, “analogous of prostacyclin”, “phosphodiesterasetype 5 inhibitor”, “bosentan”, “sildenafil”, “sixtaxentan”, “ambrisentan”,“tadalafil”,and“beraprost” as well as additional text words incombinationwithanestablishedsearchstrategyforMEDLINE/PubMed.Studies were included if they are a) reporting on a randomized clinicaltrial; b) appraising a first line oral drug; c) enrolling more than 50patients; and d) have clinical outcomes. The following outcomes,reported at the longest available follow-up according to intention-to-treat principles, were evaluated: 1) all cause mortality; 2) clinicalimprovement (according to pre-speci fied definition given in includedstudies);and3)clinicalworsening(accordingtopre-speci fieddefinitiongiveninincludedstudies).Studyvaliditywasappraisedaccordingtotherisk of bias tool recommended by The Cochrane Collaboration.Because these drugs are from the same class, and all studies com-pared active drug vs. placebo, we first pooled these studies usingpairwise meta-analysis at the class-level to estimate a common class-effect. Network meta-analysis was performed using WinBUGS 1.4.3(MRC Biostatistics Unit, Cambridge, UK) [3]. Each analysis was basedon non-informative normal priors for effect sizes, and flat uniform(0,5) priors for standard deviation parameters. Convergence waschecked using the Brooks–Gelman–Rubin diagnostic tool, and was sat-isfactory after 20,000 simulations. A further sample post burn-in of40,000 samples was taken on which all results are based. Fixed treat-ment effect models were fitted, and where possible (more than 2 stud-ies per treatment comparison) also random effect models.1500 results were first screened and finally 6 [4–9] studies wereincluded in the present analysis. Network diagrams are presented inFig. 1 showing the evidence available for each outcome.1308patientswereincluded,withanageof47(46–47.5),78%beingfemale (72.5–80), with 65.5% of them (59.5–73.5) presenting with anidiopathic etiology and 19.5% (15.25–24.75) related to collagen or vas-cular disease (all values reported as median, and 1° and 3° quartiles).46.5% (37–53) of them were in class NYHA II, with a 6 min walk-ing test of 350 m (345–379). Mean pulmonary pressure was54 mm Hg (52.5–55.25) and a pulmonary vascular resistance indexof 888 dyn s cm

Drug-eluting stents (DES) have a moderately higher incidence of stent thrombosis compared to bare metal stents (BMS) and very late DES thrombosis has been frequently described. We report a case of a 66 year-old male who experienced very late stent thrombosis at 5 years after paclitaxel-eluting stent (PES) implantation and 3 days after clopidogrel withdrawal. Intravascular ultrasound (IVUS) performed during the index procedure showed that the previously implanted PES was undersized. Since the patient could not take clopidogrel, we treated him with only a noncompliant balloon (3.0 × 15 mm) with optimal expansion as confirmed by IVUS. This case report describes a patient who continued clopidogrel treatment for 5 years and was probably protected from a procedural failure. During the current hospitalization, the patient was found to be a responder to clopidogrel after a platelet function assessment with Multiplate (Dynabyte Informationssysteme GmbH, Munich, Germany).

Cardiovascular disease is increased in HIV-infected patients. Cytokines such as osteoprotegerin are implicated in atherosclerosis. The aim of our study was to evaluate the role of osteoprotegerin in the development and progression of atherosclerosis in HIV infected subjects on suppressive antiretroviral treatment. We enrolled 76 patients; 35 HIV infected men on suppressive Highly Active Antiretroviral Therapy with Framingham score 10% as control groups. HIV positive subjects underwent echocardiography, electrocardiography, and heart multidetector computed tomography, whereas in HIV negative subjects, tomography was only performed in case of any abnormalities either in echocardiography or electrocardiography. In HIV positive patients, computed tomography showed stenosis in 51.4% of the subjects. Osteoprotegerin plasma levels were higher in HIV-infected patients than those in healthy controls but lower than in HIV negative subjects with Framingham score >10%. Higher osteoprotegerin plasma levels were found in HIV positive patients with grade I stenosis than in patients with grade II/III stenosis. In conclusion, in HIV infected subjects with Framingham score

Mechanical circulatory support by means of Intra-aortic Balloon Pump (IABP) is an established therapeutic means in high-risk patients undergoing coronary revascularization (e.g. due to severe left ventricular systolic dysfunction) or those with cardiogenic shock refractory to medical therapy. Despite its remarkable safety profile, complications during IABP deployment still occur, and may be life-threatening, especially because of the underlying risk of those receiving such device. Indeed, the IABP balloon may occasionally become entrapped in the transfemoral sheath during delivery. We hereby report a case in which IABP entrapment in a transfemoral sheath during initial delivery was successfully managed by means of retrograde wiring with an exchange-length 0.018” guide wire delivered through a transradial sheath. This clinical vignette provides evidence that a simple technical trick (i.e. retrograde tracking of 300 cm guide wire between the IABP shaft and the internal wall of the delivery sheath followed by guide wire externalization) may prove effective and safe in solving this potentially dangerous complication.

Conventionally, ischemic heart disease (IHD) is equated with large vessel coronary disease. However, recent evidence has suggested a role of compromised microvascular regulation in the etiology of IHD. Because regulation of coronary blood flow likely involves activity of specific ion channels, and key factors involved in endothelium-dependent dilation, we proposed that genetic anomalies of ion channels or specific endothelial regulators may underlie coronary microvascular disease. We aimed to evaluate the clinical impact of single-nucleotide polymorphisms in genes encoding for ion channels expressed in the coronary vasculature and the possible correlation with IHD resulting from microvascular dysfunction. 242 consecutive patients who were candidates for coronary angiography were enrolled. A prospective, observational, single-center study was conducted, analyzing genetic polymorphisms relative to (1) NOS3 encoding for endothelial nitric oxide synthase (eNOS); (2) ATP2A2 encoding for the Ca2+/H+-ATPase pump (SERCA); (3) SCN5A encoding for the voltage-dependent Na+ channel (Nav1.5); (4) KCNJ8 and KCNJ11 encoding for the Kir6.1 and Kir6.2 subunits of K-ATP channels, respectively; and (5) KCN5A encoding for the voltage-gated K+ channel (Kv1.5). No significant associations between clinical IHD manifestations and polymorphisms for SERCA, Kir6.1, and Kv1.5 were observed (p > 0.05), whereas specific polymorphisms detected in eNOS, as well as in Kir6.2 and Nav1.5 were found to be correlated with IHD and microvascular dysfunction. Interestingly, genetic polymorphisms for ion channels seem to have an important clinical impact influencing the susceptibility for microvascular dysfunction and IHD, independent of the presence of classic cardiovascular risk factors.

Background— High on-treatment platelet reactivity (HTPR) is associated with adverse outcomes. We aim to compare the novel thienopyridine prasugrel versus double-dose clopidogrel in patients with HTPR and explore the interaction between CYP2C19 genotype and both drugs. Methods and Results— Consecutive stable patients undergoing percutaneous coronary intervention were screened with the Multiplate Analyzer P2Y12 assay, defining HTPR as area under the curve >450. Those with HTPR were randomized to prasugrel (10 mg/day) or high-dose clopidogrel (150 mg/day) for 2 weeks and then crossed-over to, respectively, clopidogrel and prasugrel, repeating the P2Y12 assay at the end of each cycle. Clinical follow-up (until 3 months) and CYP2C19 genotyping was performed in all patients. The primary end point was platelet reactivity after 14 days of prasugrel versus high-dose clopidogrel. Thirty-two patients were randomized to prasugrel and then high-dose clopidogrel or to high-dose clopidogrel followed by prasugrel. Prasugrel was associated with a significantly lower platelet reactivity than high-dose clopidogrel was (325.8 versus 478.5 area under the curve, P =0.028). No patient treated with prasugrel exhibited HTPR, whereas 9 (28.1%) receiving high-dose clopidogrel still had prevalence of HTPR ( P =0.001). Similar findings were obtained changing cutoffs or considering platelet reactivity as a continuous variable. Genotyping showed the same efficacy between high-dose clopidogrel and prasugrel in the 18 (56.3%) CYP2C19*2 noncarriers (HTPR in 12.5% versus 0, P =0.274), whereas it was significantly worse in the 14 (43.7%) carriers (HTPR in 43.7% versus 0, P =0.003). Conclusions— HTPR is successfully abolished by therapy with prasugrel irrespective of CYP2C19 genotype. Conversely, high-dose clopidogrel can address HTPR only in CYP2C19*2 noncarriers. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01465828.

Background: Percutaneous coronary intervention (PCI) is the main treatment in patients with acute coronary syndromes (ACS). Current guidelines recommend the administration of a loading dose of clopidogrel, ticagrelor or prasugrel during the procedure. Ticagrelor and prasugrel have proven to overcome some limitation related to clopidrogrel administration as of pharmacological resistance. P2Y12 antagonists increase adenosine concentration by inhibiting red blood cells reuptake and induces adenosine triphosphate release from human red blood cells, which is further degraded to adenosine. Ticagrelor has been demonstrated to increase the coronary blood flow velocity more than prasugrel, as assessed by transthoracic Doppler echocardiography after incremental doses of adenosine administration. Currently, no data are available on comparison between prasugrel and clopidrogrel in term of vasodilation effect evaluated invasively. Methods/Design: This prospective, single-center, investigator-initiated, randomized controlled trial will compare the adenosine induced coronary dilatation after the treatment with ticagrelor (180 mg) versus prasugrel (60 mg) in patients with ACS undergoing PCI. A total of 90 patients, aged ≥ 18 and ≤ 75 years, admitted with ACS, treated by PCI with stent implantation and with a second intermediate non-culprit lesion will be included and randomized 1:1 to prasugrel (60 mg) or ticagrelor (180 mg). Coronary flow reserve (CFR), the study endpoint, will be recorded before the stent implantation on the intermediate lesion, then immediately after the stent implantation and during the adenosine intravenous administration at incremental doses of 50, 80, 110 and 140 μg/kg/min with 2-minute interval between infusions. Discussion: Our clinical trial, for the first time, will evaluate the supposed adenosine induced effect of the ticagrelor in terms of coronary vasodilatation calculated by CFR. Currently, CFR represents the gold standard to assess the ability of the myocardium to increase blood flow in response to maximal exercise. Furthermore, this trial will be the first to compare the effects of ticagrelor versus prasugrel on patients ACS. This trial will allow to better understand the physiological pathway of coronary vasodilatiation induced by ticagrelor versus prasugrel using invasive methods. Trial registration: ClinicalTrials.gov identifier: NCT02032303; registered on December 18, 2013. Ethics: The study was approved by the Ethics Committee of Policlinico Umberto I Rome Hospital (approval No. 2322/15) and will be performed in accordance with the ethical standards of the responsible committee on human experimentation and the Declaration of Helsinki. Informed consent: A signed informed consent will be given by each patient with ACS before undergoing angiography.

We report a case of an 81-years-old male, recently implanted with a Core Valve (CV) prosthesis and admitted to the ER for acute coronary syndrome. Coronary angiography revealed the patency of the coronary artery by-pass grafts but was impossible to cannulate the left main "imprisoned" by the CV prosthesis struts. Aortography showed an excessive gap between the CV struts and the coronary ostium. To cross the CV struts, we developed a "proboscis" catheter by cutting away the proximal end of the 7F JL 4 catheter and putting inside the 5F Heartrail catheter. The following angiograms showed a critical stenosis in the proximal obtuse marginal (branch), successfully treated with a bare-metal stent implantation.

Objectives The aim of this study is to assess the efficacy of the high-dose rosuvastatin preadministration in reducing periprocedural myocardial necrosis and major adverse cardiovascular and cerebrovascular events (MACCE) in patients undergoing elective percutaneous coronary intervention (PCI). Background Elective PCI may be complicated with an elevation of cardiac biomarkers. Several studies suggested that pretreatment with statins may be associated with a reduction in periprocedural myocardial necrosis. Methods One hundred and sixty patients with stable angina who underwent elective PCI were randomly assigned to receive either a preprocedural loading dose (40 mg) of rosuvastatin group (RG, n = 80) or a standard treatment [control group (CG), n = 80].The primary endpoint was the incidence of periprocedural myocardial necrosis. The secondary endpoint was the assessment of MACCE [cardiac death, all-myocardial infarction (MI), stroke, and target vessel revascularization (TVR)] at a 30-day and 12-month follow-up, as well as the rate of periprocedural rise of Troponin T-serum levels >3× upper limit of normal. Results Twelve and 24-hr post-PCI creatinine kinase MB isoform elevation >3× occurred more frequently in the CG than in the RG (22.7 vs. 7.1; P = 0.034 and 26.4 vs. 8.7; P = 0.003). At the 30-day and 12-month follow-up, the incidence of cumulative MACCE was higher in CG than in the RG (30.0% vs. 8.7%; P = 0.001 and 35.0% vs. 12.5%; P = 0.001).The difference between the groups was mainly due to the periprocedural MI incidence (26.4% vs. 8.7%; P = 0.003).The rate of cardiac death, spontaneous MI, TVR, and stroke were similar in the two groups. Conclusions High loading dose of rosuvastatin within 24 hr before elective PCI seems to decrease the incidence of periprocedural myocardial necrosis during a period of 12-months compared to the standard treatment. © 2012 Wiley Periodicals, Inc.

Transradial approach (TRA) for percutaneous coronary interventions (PCIs) is a common alternative to transfemoral approach associated with lower complications. However, a limitation of TRA is the use of large caliber guiding catheters due to the small size of the radial artery. The sheathless guiding catheter system that is in diameter 1-2 French (Fr) smaller than the corresponding introducer sheath may overcome these difficulties.From January 2010 through December 2010 in 5 Italian high-volume hospitals, 213 consecutive patients who underwent TRA-PCIs using the sheathless Eaucath guiding catheter system because of small radial artery caliber (Group 1) or undergoing bifurcation PCIs (Group 2) were enrolled in this registry. In patients of Group 1 (n = 79), a 6.5-Fr sheathless guiding catheter was employed, whereas in patients of Group 2 (n = 134) a 7.5 Fr was used.Among the 213 patients enrolled, 270 vessels were treated for 316 lesions. No procedures required conversion to a conventional guiding catheter system. There were significantly more female patients in Group 1, and they were, older, shorter, and thinner than patients in Group 2. No cases of major vascular complications were observed in either groups. During procedures, adjunctive devices employed included intravascular ultrasound, thrombectomy catheters, and distal protection systems.The use of the sheathless guiding catheter system is feasible for TRA-PCIs in case of small radial artery caliber or intended coronary bifurcation intervention.

Objectives: The aim of our study is to evaluate the safety and efficacy of DES implantation in an unselected, “real world,” high-risk population. Background: Several clinical trials showed that drug-eluting stents (DESs) implantation is safe and effective in selected population. In spite of these encouraging results, there are some concerns about “real world” utilization of these stents. Methods: One thousand four hundred and fifty-five off-label patients have been included in our registry. Primary end-points were: long-term clinical incidence of major adverse cardiac and cerebrovascular events (MACCE) and thrombosis (ST). We detected the difference between uniDES vs. multiDES implantation in terms of MACCE, death, nonfatal-MI, the composite of death/nonfatal-MI and target lesion revascularization (TLR) and the difference between DES type in term of MACCE. Results: At 36 months follow-up we found: cardiac death occurred in 20 patients (1.6%); 33 patients (2.6%) had a nonfatal MI and 81 patients (6.3%) had a TLR. We observed one (0.1%) acute, 9 subacute (0.6%), 6 late (0.6%), and 1 (0.5%) very late definite ST. No difference were found in terms of overall MACCE, MI, death and composite of death/nonfatal-MI between uni- and multiDES implantation but multiDES group had a higher incidence of TLR. No difference between DES type in term of MACCE was detected. Conclusions: DES utilization shows their safety and efficacy in off-label patients with complex clinical and angiographic profile in terms of long-term incidence of MACCE. MultiDES implantation is associated with a higher risk of long-term TLR. No difference between DES type was found. © 2011 Wiley Periodicals, Inc.

Highly active antiretroviral therapy has greatly reduced AIDS-related morbidity and mortality; however, its widespread use has been associated with a marked rise in the frequency of cardiovascular diseases in patients with HIV. Moreover, HIV infection is associated with accelerated coronary atherosclerosis and vasculopathy, although the mechanisms underlying these findings have not been determined. We describe the case of a 45-year-old woman with HIV/HCV coinfection, irritable bowel syndrome, and accelerated progression of coronary atherosclerosis after execution of percutaneous coronary intervention (PCI). In this case, the rapidity of progression of atherosclerosis seems linked principally to chronic inflammation and excess immune activation that can depend by a concourse of factors (chronic C hepatitis, irritable bowel syndrome, PCI execution) not directly associated with traditional risk factors. Caregivers following HIV-infected patients should be aware of the increased risk of accelerated atherogenesis in these subjects, principally in case of presence of causes of intense immune activation.

Staging of heart failure represents a major issue in clinical practice. In this setting, the MOGE(S) classification was designed to be similar to the TNM classification used in oncology. Nevertheless, MOGE(S) nosology differs greatly from the key elements of the TNM classification, as well as its simplicity and clinical applicability. In fact, MOGE(S) acronym stands for morphofunctional characteristics (M), organ involvement (O), genetic or familial inheritance pattern (G), etiological information (E), and functional status (S). Recently, a new TNM-like classification for heart failure was proposed. This classification, named HLM, refers to heart damage arising from an initial stage of impaired systolic or diastolic function, without structural injury, to an advanced stage of biventricular dysfunction (H), different stages of lung involvement (L), and malfunction of peripheral organs such as the kidney, liver, and brain (M). HLM classification was influenced by the key elements of TNM staging: simplicity, clinical usefulness, efficacy for planning a therapeutic strategy, and ability to determine patient prognosis. HLM classification seems to be easily applied in the real world and valuable for balancing economic resources with the clinical complexity of patients.

The present study first time detected D1-D5 dopamine receptor subtypes in the native human heart simultaneously, found presence of D1, D2, D4, and D5 in cardiac tissues, and revealed distribution features of dopamine receptor subtypes in the epicardium, myocardium, and endocardium. Samples from four native hearts coming from young brain-dead donors, which for technical reason were not used for transplants, were studied. Dopamine receptors were revealed by immunochemistry technique and immunoblot analysis. Morphometrical quantification of the density of each receptor subtype was performed by an image analyzer. Our results demonstrate that only four subtypes of dopamine receptors can be found in cardiac tissues: D1, D2, D4, and D5. These dopamine receptors have been detected in endocardium, myocardium, and epicardium. D1 receptors were stored primarily in the epicardial layer. Dopamine receptors are distributed in the wall of both atria and ventricles, and its transmural gradient can be described in the wall of the human heart. Sections of atria and ventricles exposed to antidopamine receptor antibodies showed fluorescent-positive reaction in the epicardium, myocardium and endocardium. D4 receptor immune reactivity was remarkably less intense than D2 receptor immune reactivity. All the subtypes of dopamine receptors are in close relationships with all cardiac structures. Our findings provide a favorable basis for researching the role of dopamine receptors in controlling functions of the human heart and in the pathogenesis of cardiovascular diseases.

Background Percutaneous coronary intervention (PCI) is a highly effective therapy for acute ST-elevation myocardial infarction. Adjunctive therapy with platelet glycoprotein (GP) IIb/IIIa inhibitor can result in increased vessel patency and improved outcomes in ST-elevation myocardial infarction patients undergoing PCI. The investigation of novel dosing and delivery strategies of this therapy may help to further improve outcomes. Methods IC-Clearly is a randomized, open-label, multicenter trial, with the purpose of evaluating the effectiveness of an intracoronary bolus dose of abciximab delivered using the ClearWay RX catheter vs. an intravenous bolus of abciximab for ST-elevation myocardial infarction with angiographically visible thrombus (thrombus grade >or=2). A total of 150 patients will be randomized 1: 1 to treatment of the culprit artery with intracoronary abciximab (75 patients) or intravenous abciximab (75 patients) in addition to a maintenance infusion regimen of abciximab administered intravenously for 12 h after PCI. The number of patients included in this study is based on the estimation of sample size needed to identify a statistically significant difference in the primary endpoints between the two groups. The primary endpoint chosen to evaluate this hypothesis is infarct size assessed by cardiac magnetic resonance. Clinical outcomes will be assessed for each patient through hospital discharge and at 30-day follow-up. Conclusion The purpose of this study is to evaluate whether an intracoronary bolus of abciximab delivered with the ClearWay RX catheter prior to the 12 h post-PCI intravenous infusion regimen of abciximab will result in significant additional clot resolution in vivo and improved myocardial perfusion when compared with an intravenous bolus of abciximab on top of the 12 h post-PCI intravenous infusion regimen of abciximab as per standard practice. The primary endpoint chosen to evaluate this hypothesis is infarct size as assessed by cardiac magnetic resonance.

We investigated the extent and nature of myocardial damage by using cardiovascular magnetic resonance (CMR) in relation to different time-to-reperfusion intervals.Previous studies evaluating the influence of time to reperfusion on infarct size (IS) and myocardial salvage in patients with ST-segment elevation myocardial infarction (STEMI) have yielded conflicting results.Seventy patients with STEMI successfully treated with primary percutaneous coronary intervention within 12 h from symptom onset underwent CMR 3 +/- 2 days after hospital admission. Patients were subcategorized into 4 time-to-reperfusion (symptom onset to balloon) quartiles:or =90 min (group I, n = 19),90 to 150 min (group II, n = 17),150 to 360 min (group III, n = 17), and360 min (group IV, n = 17). T2-weighted short tau inversion recovery and late gadolinium enhancement CMR were used to characterize reversible and irreversible myocardial injury (area at risk and IS, respectively); salvaged myocardium was defined as the normalized difference between extent of T2-weighted short tau inversion recovery and late gadolinium enhancement.Shorter time-to-reperfusion (group I) was associated with smaller IS and microvascular obstruction and larger salvaged myocardium. Mean IS progressively increased overtime: 8% (group I), 11.7% (group II), 12.7% (group III), and 17.9% (group IV), p = 0.017; similarly, MVO was larger in patients reperfused later (0.5%, 1.5%, 3.7%, and 6.6%, respectively, p = 0.047). Accordingly, salvaged myocardium markedly decreased when reperfusion occurred90 min of coronary occlusion (8.5%, 3.2%, 2.4%, and 2.1%, respectively, p = 0.004).In patients with STEMI treated with primary percutaneous coronary intervention, time to reperfusion determines the extent of reversible and irreversible myocardial injury assessed by CMR. In particular, salvaged myocardium is markedly reduced when reperfusion occurs90 min of coronary occlusion.

Primary percutaneous coronary intervention is the standard treatment in patients with ST-segment elevation myocardial infarction achieving a TIMI 3 flow in more than 90% of patients. However, despite a brisk epicardial coronary flow in the infarct-related artery, frequently post-ischemic microvascular damage limits the efficacy of primary PCI. Recent studies suggest that thrombectomy during primary PCI, in patients with intracoronary angiographically visible thrombus, represents a useful adjunct to pharmacotherapy able to prevent distal embolization.

Background: The myocardial blush grade (MBG) during primary-PCI predicts long-term recovery of left ventricular function. Tissue Doppler imaging (TDI) quantitatively assess regional myocardial function by measuring systolic strain (SS). No data are available on the correlation between MBG and the infarcted segmental systolic function by TDI in STEMIpts. Methods: We evaluated 40 STEMI pts, divided in four groups (MBG 0; MBG 1; MBG 2; MBG 3) 10 pts for each goup. Primary PCI was performed according to current standard guidelines. Coronary angiograms were analyzed off-line by two expert interventional cardiologists in a blinded manner. MBG were estimated visually. Sixteen-segments model was applied and regional myocardial function was evaluated, immediately after primary PCI, by measuring SS by TDI . Only SS value in infarcted segments was correlated with the MBG. Results: No significative difference was observed between groups except for family history of CAD that was higher in MBG 2 group. Mean ejection fraction (39,1 ± 8,8%) and mean symptoms to balloon time(4.3 ± 1.6 h ) was similar in the population. 136 infarcted segments were studied by TDI. A significant direct correlation between the MBG and the SS (r=0.79; p ). We also observed a significative difference (p Conclusions: Abnormal values of SS was observed in infarcted segments. The significant correlation observed between the MBG and SS may demonstrate that MBG represent an important predictive index not only of good reperfusion but also of rapid segmental function recovery; similarly an evaluation of SS after primary PCI could be useful to evaluate if primary percutaneus reperfusion has been effective or not.

Background: In patients with ST-elevatrion myocardial infarction (STEMI), impairment of microcirculatory function is a negative independent predictor of myocardial function recovery. Compared with conventional stenting, thrombectomy during primary percutaneous coronary intervention (PCI) seems to improve the parameters of myocardial tissue perfusion. We sought to evaluate the impact of thromboaspiration on procedural outcomes and microascualr damage and infarct size by contrast enhanced-MRI (ce-MRI) as compared to conventional primary PCI. Methods:We randomized 75 patients (mean age 64.3±10.2, 55 male) referred to our Hospital with a STEMI ( Results: No differences on baseline, clinical and angiographic preprocedural findings were observed between the two groups. After trombectomy, a TIMI II flow was present in in 38.6 vs 19.6% (p=0.054) and TIMI III was 30.7 vs 72.5% (for group 1 and 2, respectively, p Conclusion:Compared with conventional stenting, a pretreatment with thrombectomy during primary PCI, improves epicardial flow and procedural outcomes. The long term ce-MRI evaluation suggests a reduction in microvascular damage and infarct size compared with the acute evaluation in the thrombectomy group.

Drug-eluting stents (DES) present a slightly higher incidence of stent thrombosis compared to bare metal stents and some cases of DES thrombosis are described in the literature. Therefore, there is consensus in recommending treatment with clopidogrel for at least 6 months in addition to life-long aspirin administration. We describe a case of very late paclitaxel-eluting stent thrombosis despite 21 months of clopidogrel treatment, which occurred just 2 weeks after its withdrawal, causing an acute coronary syndrome that was promptly resolved with an urgent invasive strategy. In our experience, paclitaxel-eluting stent thrombosis can occur several months after stent implantation despite prolonged clopidogrel treatment.

T lymphocytes play an important role in the induction and progression of acute coronary syndromes (ACS). To gain insight into how different T cell subsets can influence ACS, we analyzed the frequencies of circulating CD4+T cells producing either pro-inflammatory interferon(IFN)-γ or anti-inflammatory interleukin (IL)-10 in subjects presenting with ST-elevation myocardial infarction (STEMI). The effect of coronary bare metal (BS) and paclitaxel-eluting stent (PES) on the balance between CD4+IFN-γ+ and CD4+IL-10+ lymphocytes was also investigated. Peripheral blood mononuclear cells (PBMC) were isolated from 38 consecutive patients with STEMI before and 48 hrs or 6 days after implantation of either BS or PES. Twenty patients with no history of coronary artery disease were included as basal controls. PBMC were stimulated in vitro with anti-CD3/anti-CD28 monoclonal antibodies, and CD4+IFN-γ+ or CD4+IL-10+ T cells were detected by flow cytometry intracellular staining. The frequency of peripheral CD4+IL-10+ T cells was significantly higher in STEMI patients as compared with controls. Conversely, the frequency of CD4+IFN-γ+ T lymphocytes did not differ between STEMI and subjects without history of coronary artery disease. Six days after the revascularization procedure, the percentage of CD4+IL-10+ T cells was significantly decreased in BS but not in the PES group, whereas the relative percentage of CD4+IFN-γ+ T lymphocytes were diminished in both groups as compared with baseline levels. Our data indicate that STEMI is associated with a peripheral expansion of CD4+IL-10+T lymphocytes, and that primary coronary revascularization with implantation of either BS or PES is followed by a reduction in circulating CD4+IFN-γ+ T lymphocytes. PES implantation, however, appears to inhibit the relative decrease of the IL-10 producing lymphocyte as observed in BS implanted patients, shifting the balance between pro-inflammatory and anti-inflammatory T cell populations in favor of the latter.

Implantable cardioverter defibrillator (ICD) is recommended for the prevention of sudden cardiac death (SCD) in patients with heart failure, basing mainly on ejection fraction (EF). However, the latter has low sensibility and specificity. 123-iodine metaiodobenzylguanidine (123-I MIBG) imaging

Background Naturally-occurring regulatory T cells (Treg) constitute a mature T-cell population characterized phenotypically by co-expression of CD4 and CD25 high surface molecules. We investigated here the frequency of circulating Treg in patients presenting with STEMI in comparison with subjects without coronary artery disease (CAD). The effect of primary percutaneous coronary intervention (PCI) with implantation of a bare (BS) or paclitaxel-eluting stent (PES) on peripheral Treg distribution was also examined. Methods Peripheral blood mononuclear cells were isolated from 30 consecutive patients presenting with STEMI and from 30 age-matched control subjects with angiographically normal coronary arteries. Treg were detected by flow cytometry according to their characteristic CD4 + CD25 high membrane phenotype, and their frequency was assessed before PCI and at 48 h and at 6 days after PCI. CD27 expression identifying a highly suppressive Treg subset was also analysed. Results The percentages of both CD27+ Treg and CD27- Treg were significantly lower in patients with STEMI in comparison with controls. In addition, the CD27+ Treg/ CD27- Treg ratio was skewed toward the CD27 − population. The frequency of both Treg subsets significantly increased 48 h after either BS or PES implantation, remaining elevated for up to at least 6 days after PCI. Conclusions Our data suggest that the percentage of circulating Treg is significantly reduced in patients with STEMI, suggesting that this immunosuppressive T-cell subset is compartmentalized within the acutely ischemic myocardium to limit the ongoing inflammation associated with this condition, and that coronary revascularization is associated with partial reconstitution of peripheral Treg pool.

Objective To assess the diagnostic accuracy of troponin I (TnI) elevation in patients with acute coronary syndrome (ACS) in the emergency department (ED). Methods We retrospectively studied 166 patients with elevated TnI and electrocardiographic (ECG) change consistent with non-ST-segment elevation myocardial infarction. They were transferred from the ED to our coronary care unit (CCU) to undergo coronary angiography. Results Significant coronary stenosis were identified in 101 (61%) of patients. The other 65 patients were found to have different cardiac diseases (n=52) and in 13 patients diagnoses were not even related to the cardiovascular system. Wall motion abnormalities were assessed by echocardiographic wall motion score index (WMSI). Positive predictive value (PPV) of TnI varied from 53 to 65% for higher progressive values of the biomarker. The following PPVs were then calculated: PPV(TnI+CK-MB)=64%; PPV(TnI+WMSI)=72%, PPV(TnI+CK-MB+WMSI)=74%. Conclusions Abnormal values of TnI were detected in a variety of diseases not related to ACS. Even if troponin release indicates myocardial injury, it is not always synonymous with infarction or ischemia. A misinterpretation of TnI elevation may give rise to a diagnostic dilemma and cause unnecessary morbidity. An integration of biomarkers (TnI and CK-MB), ECG and WMSI will help identify false-positive ACS patients and avoid inappropriate admissions to CCU.

Background: Age-related changes of catecholaminergic nerve fibers supplying the myocardium and the coronary vessels were studied in adult and in old rats. Objective: The purpose of this study was to investigate whether there are quantitative changes in myocardial and/or coronary catecholaminergic nerve fibers and related neurotransmitters. Methods: Samples of myocardium and/or coronary vessels were studied by means of glyoxylic acid induced fluorescence, aldehyde-induced fluorescence, and neuropeptide Y immunoreactivity. All morphological results were submitted to quantitative analysis of images. Biochemical dosage of proteins and of norepinephrine was also performed, and morphological data were compared with biochemical ones. Finally, all data were subjected to statistical analysis. Results: Our findings are indicative of an age-related decrease of all types of fluorescent sympathetic nerve fibers in rat heart and coronary arteries. Moreover, our data show that aging induces a strong decrease of norepinephrine levels in tissue homogenates of rat heart and coronary vessels. The majority of the catecholaminergic nerve fibers that show strong age-related changes are not contiguous with contractile cells of myocardium and/or of vascular wall. In fact, these fibers are located in adventitial (or epicardial) and in endothelial (or endocardial) layers. Conclusion: The decrease of the catecholaminergic innervation of heart and coronary vessels of old rats can be in close relationships to the poor cardiac and/or coronary functions observed in old animals.