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OBJECTIVE AND DESIGN: [alpha]1-Antitrypsin deficiency (AATD) is a genetic disorder that may be a pathogenic factor in vascular aneurysms and dissection. The aim of this study was to measure the diameters of the Valsalva sinuses (VS), sinotubular junction (STJ), ascending aorta (AA) and aortic arch (AAr) and elastic properties of the AA (distensibility, stiffness and tissue Doppler imaging (TDI strain)) in AATD subjects. PATIENTS: 33 AATD subjects (all Z-homozygous, 17 male, 16 female) were examined. Aortic elastic properties, namely, distensibility and stiffness index, were calculated from the echocardiographically-derived thoracic aortic diameters and TDI strain was measured on the wall of the AA 3 cm above the aortic valve. The results were compared with those obtained in healthy controls matched for age, sex and body mass index. RESULTS: AATD subjects had larger aortic diameters (VS: 3.5±0.5 vs 3.2±0.5 cm, p<0.05; STJ 2.7±0.4 vs 2.4±0.4 cm, p<0.01; AA 3.3±0.5 vs 2.9±0.4 cm, p<0.01; AAr 2.3±0.3 vs 2.1±0.3 cm, p=0.05); greater aortic stiffness 14.9±11.9 versus 7.4±4.4 (pure numbers, p<0.005); and less aortic distensibility 2.4±1.8 versus 4.0±2.6 10(-6)xcm(2)xdyne(-1), p<0.005. Peak systolic (S) and diastolic (E and A) waves of the aortic wall TDI were similar in patients and controls (S wave: 5.4±1.6 vs 5.9± 2.3 cm/s; E wave: -4.8±2.2 vs -4.5±2.2 cm/s; A wave: -6.1±2.2 vs -6.2±2.4 cm/s) while TDI strain of the aortic wall was lesser in patients than controls (-14.7±8.0% vs -28.3±7.1%, p<0.001). CONCLUSIONS: AATD subjects have a larger AA with abnormal elastic properties as compared to controls. The increase in stiffness, decrease in distensibility and abnormal strain of the aortic wall may all reflect pathological changes in its elastic tissue. [ABSTRACT FROM AUTHOR]

Treatment with inotropic agents is one of the most controversial topics in heart failure. Initial enthusiasm, based on strong pathophysiological rationale and apparent empirical efficacy, has been progressively limited by results of controlled trials and registries showing poorer outcomes of the patients on inotropic therapy. The use of these agents remains, however, potentially indicated in a significant proportion of patients with low cardiac output, peripheral hypoperfusion and end-organ dysfunction caused by heart failure. Limitations of inotropic therapy seem to be mainly related to their mechanisms of action entailing arrhythmogenesis, peripheral vasodilation, myocardial ischemia and damage, and possibly due to their use in patients without a clear indication, rather than to the general principle of inotropic therapy itself. This review will discuss the characteristics of the patients with a potential indication for inotropic therapy, the main data from registries and controlled trials, the mechanism of the untoward effects of these agents on outcomes and, lastly, perspectives with new agents with novel mechanisms of action. [ABSTRACT FROM AUTHOR]

Background: The natural evolution of signs and symptoms during acute heart failure (AHF) is poorly characterized.Methods and Results: We followed a prospective international cohort of 182 patients hospitalized with AHF. Patient-reported dyspnea and general well-being (GWB) were measured daily using 7-tier Likert (-3 to +3) and visual analog scales (VAS, 0-100). Physician assessments were also recorded daily. Mean age was 69 years and 68% had ejection fraction <40%. Likert measures of dyspnea initially improved rapidly (day 1, 0.22; day 2, 1.31; P <.001) with no significant improvement thereafter (day 7, 1.51; day 2 versus 7 P = .16). In contrast, VAS measure of dyspnea improved throughout hospitalization (day 1, 50.1; day 2, 64.7; day 7, 83.2; day 1 versus 2 P < .001, day 2 versus 7 P < .001). Symptoms of dyspnea and GWB tracked closely (correlation r = .813, P < .001). Physical signs resolved more completely than did symptoms (eg, from day 1 to discharge/day 7, absence of edema increased from 33% to 72% of patients, whereas significant improvements in dyspnea increased from 27% to 52% of patients; P < .001).Conclusions: Changes in patient-reported symptoms and physician-assessed signs followed different patterns during an AHF episode and are influenced by the measurement scales used. Multiple clinical measures should be considered in discharge decisions and evaluation of AHF therapies. [ABSTRACT FROM AUTHOR]

The International Committee of Medical Journal Editors (ICMJE) provides recommendations to improve the editorial standards and scientific quality of biomedical journals. These recommendations range from uniform technical requirements to more complex and elusive editorial issues including ethical aspects of the scientific process. Recently, registration of clinical trials, conflicts of interest disclosure, and new criteria for authorship -emphasizing the importance of responsibility and accountability-, have been proposed. Last year, a new editorial initiative to foster sharing of clinical trial data was launched. This review discusses this novel initiative with the aim of increasing awareness among readers, investigators, authors and editors belonging to the Editors´ Network of the European Society of Cardiology.

Definition of the optimal duration of dual anti-platelet therapy (DAPT) is an important clinical issue, given the large number of patients having percutaneous coronary intervention (PCI), the costs and risks of pharmacologic therapy, the consequences of stent thrombosis, and the potential benefits of DAPT in preventing ischaemic outcomes beyond stent thrombosis. Nowadays, the rationale for a prolonged duration of DAPT should be not only the prevention of stent thrombosis, but also the prevention of ischaemic events unrelated to the coronary stenosis treated with index PCI. A higher predisposition to athero-thrombosis may persist for years after an acute myocardial infarction, and even stable patients with a history of prior myocardial infarction are at high risk for major adverse cardiovascular events. Recently, results of pre-specified post-hoc analyses of randomized clinical trials, including the PEGASUS-TIMI 54 trial, have shed light on strategies of DAPT in various clinical situations, and should impact the next rounds of international guidelines, and also routine practice. Accordingly, the 2015 to 2016 the Board of the Italian Society of Cardiology addressed newer recommendations on duration of DAPT based on most recent scientific information. The document states that physicians should decide duration of DAPT on an individual basis, taking into account ischaemic and bleeding risks of any given patient. Indeed, current controversy surrounding optimal duration of DAPT clearly reflects the fact that, nowadays, a one size fits all strategy cannot be reliably applied to patients treated with PCI. Indeed, patients usually have factors for both increased ischaemic and bleeding risks that must be carefully evaluated to assess the benefit/risk ratio of prolonged DAPT. Personalized management of DAPT must be seen as a dynamic prescription with regular re-evaluations of the risk/benefit to the patient according to changes in his/her clinical profile. Also, in order to derive more benefit than harm from new treatments, a multi-parametric approach using several risk scores of the ischaemic and bleeding risks might improve the process of risk factor characterization. In patients with high ischaemic risk, particularly those with a history of myocardial infarction, the benefits of extended DAPT (particularly with ticagrelor up to 3 years) are likely to outweigh the risks.

Objectives: We built and validated a new heart failure (HF) prognostic model which integrates cardiopulmonary exercise test (CPET) parameters with easy-to-obtain clinical, laboratory, and echocardiographic variables., Background: HF prognostication is a challenging medical judgment, constrained by a magnitude of uncertainty., Methods: Our risk model was derived from a cohort of 2716 systolic HF patients followed in 13 Italian centers. Median follow up was 1041days (range 4-5185). Cox proportional hazard regression analysis with stepwise selection of variables was used, followed by cross-validation procedure. The study end-point was a composite of cardiovascular death and urgent heart transplant., Results: Six variables (hemoglobin, Na(+), kidney function by means of MDRD, left ventricle ejection fraction [echocardiography], peak oxygen consumption [% pred] and VE/VCO2 slope) out of the several evaluated resulted independently related to prognosis. A score was built from Metabolic Exercise Cardiac Kidney Indexes, the MECKI score, which identified the risk of study end-point with AUC values of 0.804 (0.754-0.852) at 1year, 0.789 (0.750-0.828) at 2years, 0.762 (0.726-0.799) at 3years and 0.760 (0.724-0.796) at 4years., Conclusions: This is the first large-scale multicenter study where a prognostic score, the MECKI score, has been built for systolic HF patients considering CPET data combined with clinical, laboratory and echocardiographic measurements. In the present population, the MECKI score has been successfully validated, performing very high AUC., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Rheumatoid arthritis (RA) is associated with increased mortality and morbidity because of accelerated atherosclerosis. The study assessed the prevalence of left and right ventricle diastolic and systolic dysfunction in outpatients with RA., Methods: The study included 93 outpatients with RA. In all patients and control group, echocardiographic conventional and tissue Doppler (TDI) studies were conducted., Results: In the group of RA patients, we found high prevalence of left ventricular systolic and diastolic dysfunction and right diastolic dysfunction compared with controls (13.5% vs 5.5 %, 76.3% vs 48.8% and 41.9% vs 6.6%, respectively; P < 0.001). Rheumatoid arthritis patients and controls showed significant differences about mitral, tricuspid, and pulmonary flow velocity curves; tissue Doppler curves of the lateral and the septal myocardial walls of the left ventricle; and basal myocardial free wall of the right ventricle. There were not any correlations between inflammatory and functional disease parameters and variables of systolic and diastolic function., Conclusions: Our study shows a high prevalence of left ventricular systolic and diastolic dysfunction in a population of outpatients affected by rheumatoid arthritis.

Objective and Design: α1-Antitrypsin deficiency (AATD) is a genetic disorder that may be a pathogenic factor in vascular aneurysms and dissection. The aim of this study was to measure the diameters of the Valsalva sinuses (VS), sinotubular junction (STJ), ascending aorta (AA) and aortic arch (AAr) and elastic properties of the AA (distensibility, stiffness and tissue Doppler imaging (TDI strain)) in AATD subjects., Patients: 33 AATD subjects (all Z-homozygous, 17 male, 16 female) were examined. Aortic elastic properties, namely, distensibility and stiffness index, were calculated from the echocardiographically-derived thoracic aortic diameters and TDI strain was measured on the wall of the AA 3 cm above the aortic valve. The results were compared with those obtained in healthy controls matched for age, sex and body mass index., Results: AATD subjects had larger aortic diameters (VS: 3.5 ± 0.5 vs 3.2 ± 0.5 cm, p<0.05; STJ 2.7 ± 0.4 vs 2.4 ± 0.4 cm, p<0.01; AA 3.3 ± 0.5 vs 2.9 ± 0.4 cm, p<0.01; AAr 2.3 ± 0.3 vs 2.1 ± 0.3 cm, p=0.05); greater aortic stiffness 14.9 ± 11.9 versus 7.4 ± 4.4 (pure numbers, p<0.005); and less aortic distensibility 2.4 ± 1.8 versus 4.0 ± 2.6 10(-6)×cm(2)×dyne(-1), p<0.005. Peak systolic (S) and diastolic (E and A) waves of the aortic wall TDI were similar in patients and controls (S wave: 5.4 ± 1.6 vs 5.9 ± 2.3 cm/s; E wave: -4.8 ± 2.2 vs -4.5 ± 2.2 cm/s; A wave: -6.1 ± 2.2 vs -6.2 ± 2.4 cm/s) while TDI strain of the aortic wall was lesser in patients than controls (-14.7 ± 8.0% vs -28.3 ± 7.1%, p<0.001)., Conclusions: AATD subjects have a larger AA with abnormal elastic properties as compared to controls. The increase in stiffness, decrease in distensibility and abnormal strain of the aortic wall may all reflect pathological changes in its elastic tissue.

Objectives: Aortic valve replacement (AVR) is recommended in patients with symptomatic aortic stenosis (AS). However a large number of elderly patients remain untreated because of a high operative risk. The aim of this study was to assess the risk profile of a group of AS patients, evaluating the prevalence of comorbidities and associated cardiac diseases and their impact on therapeutic decisions., Methods: Two-hundred forty consecutive AS patients underwent complete clinical evaluation, in order to define the stenosis severity, the prevalence of several associated cardiac conditions and comorbidities. Furthermore, the treatment choices based on this approach were recorded., Results: Mean age was 78.6 ± 8.93 years, 75.5% was ≥ 75 years old, 60% females; 226 patients (94.2%) had symptoms and 54.2% was in NYHA classes III-IV. Valve area <1cm(2) was detected in 81.6% of patients. Both comorbidities and associated cardiac diseases were common; particularly, renal dysfunction was detected by estimated glomerular filtration rate in 52.7%, chronic obstructive lung disease in 25.4%, cerebrovascular/peripheral artery disease in 30.8% and 11.6%, respectively, diabetes in 30%, malignancies (current or previous) in 26.6% of patients. Among associated cardiac diseases, coronary artery disease was detected in 43.7%, LV systolic dysfunction in 28.7%, pulmonary hypertension in 67%, at least moderate mitral regurgitation in 32.5% and porcelain aorta in 7.5% of patients. Fourteen asymptomatic patients (pts) (5.9%) remained in follow-up, 77 (32%) underwent surgical AVR, 64 (26.7%) underwent transcatheter valve implantation, 28 (11.6%) underwent balloon valvuloplasty and 57 (23.8%), despite symptoms, remained on medical therapy alone., Conclusions: Comorbidities and coexisting cardiac diseases are very common in AS and may strongly influence the decision-making process., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Background: There are conflicting data on the role of a patent foramen ovale (PFO) in the pathogenesis of cryptogenic stroke. The aim of this study was to evaluate the incidence of cerebrovascular events associated with PFO in a large population of patients during mid-term follow-up., Methods and Results: We prospectively investigated 446 consecutive patients (58% female, age 50 ± 14 years) in whom PFO was detected by contrast echocardiography following cryptogenic stroke (30.5%), transient ischemic attack (TIA, 23.7%), migraine(10.5%) or evaluation for other cardiac diseases(35%). Prevalence of other clinical conditions potentially associated with cerebral embolism, such as mitral valve disease, atrial fibrillation and aortic atherosclerosis were 31%, 12.5%, 11.2%, respectively; 99 out of 446 patients (22%, group 1) underwent PFO closure, shortly after diagnosis, while 347 (78%, group 2) received only medical therapy (antiplatelet drugs and vitamin K antagonists). During 54 months (range 12-96) of average follow-up few events had been observed: one fatal stroke (1%) in group 1 and 3 nonfatal strokes (0.86%) in group 2 (not significant); there were more TIAs in group 1 than in group 2 (5, 5% versus 3, 0.86%, p=0.02): 8/12 new cerebrovascular events occurred in patients with previous cerebral ischemia and in 7/12 there were other cardioembolic sources. Kaplan-Meier survival free from cerebrovascular events showed a slightly better prognosis in unclosed PFO patients compared to closed PFO ones, statistically significant (p=0.004)., Conclusions: New cerebrovascular events are rare in unselected subjects with PFO, even in those with previous cerebral ischemia and those who have not undergone PFO closure, with an event rate similar to that observed in the general population., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

The question whether to anticoagulate patients with cardiomyopathy or not is over 50 years old. Multiple clinical trials have demonstrated the superior therapeutic effect of warfarin compared with placebo in the prevention of thromboembolic events amongst patients with nonvalvular atrial fibrillation. The purpose of our work is to review literature about the role of anticoagulation in the main cardiomyopathies., (Copyright © 2011 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Chronic stable angina affects 6-7 million Americans and contributes to a significant reduction in quality of life and life expectancy. Current pharmacotherapy for reducing episodes of exertional angina includes β-blockers, calcium channel blockers and long-acting nitrates. Patients may have contraindications to the use of one or more of these agents or be unable to tolerate initial or larger therapeutic doses. As a result of the inability of current management strategies to optimally control episodes of chronic angina, new therapies have been investigated that do not have some of the limitations of current therapies. New therapies for chronic stable angina are based on a mechanism involving membrane current such as the funny current and the late Na current. Ranolazine (Ran) is an antianginal drug acting on I(Na). After its current indication in the chronic stable angina, the role of this molecule is still being studied for prophylaxis of certain arrhythmias and treatment of heart failure. Moreover, have been recently developed new interesting patents of novel pharmaceutical effects and derivates of Ran.

Inotropic agents are administered to improve cardiac output and peripheral perfusion in patients with systolic dysfunction and low cardiac output. However, there is evidence of increased mortality and adverse effects associated with current inotropic agents. These adverse outcomes may be ascribed to patient selection, increased myocardial energy expenditure and oxygen consumption, or to specific mechanisms of action. Both sympathomimetic amines and type III phosphodiesterase inhibitors act through an increase in intracellular cyclic adenosine monophoshate and free calcium concentrations, mechanisms that increase oxygen consumption and favor arrhythmias. Concomitant peripheral vasodilation with some agents (phosphodiesterase inhibitors and levosimendan) may also lower coronary perfusion pressure and favor myocardial damage. New agents with different mechanisms of action might have a better benefit to risk ratio and allow an improvement in tissue and end-organ perfusion with less untoward effects. We have summarized the characteristics of the main inotropic agents for heart failure treatment, the data from randomized controlled trials, and future perspectives for this class of drugs., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Introduction: Dyspnoea and peripheral oedema, caused by fluid redistribution to the lungs and/or by fluid overload, are the main causes of hospitalization in patients with heart failure and are associated with poor outcomes. Treatment of fluid overload should relieve symptoms and have a neutral or favorable effect on outcomes., Areas Covered: We first consider the results obtained with furosemide administration, which is still the mainstay of treatment of congestion in patients with heart failure. We then discuss important shortcomings of furosemide treatment, including the development of resistance and side effects (electrolyte abnormalities, neurohormonal activation, worsening renal function), as well as the relationship of furosemide - and its doses - with patient prognosis. Finally, the results obtained with potential alternatives to furosemide treatment, including different modalities of loop diuretic administration, combined diuretic therapy, dopamine, inotropic agents, ultrafiltration, natriuretic peptides, vasopressin and adenosine antagonists, are discussed., Expert Opinion: Relief of congestion is a major objective of heart failure treatment but therapy remains based on the administration of furosemide, an agent that is often not effective and is associated with poor outcomes. The results of the few controlled studies aimed at the assessment of new treatments to overcome resistance to furosemide and/or to protect the kidney from its untoward effects have been mostly neutral. Better treatment of congestion in heart failure remains a major unmet need.

Introduction: Nitrates are used in the treatment of coronary heart disease and heart failure. The major drawback of their therapeutic use is the rapid development of tolerance., Aim of the Study: To investigate the effect of different nitrates on isolated rabbit hearts and aortic strips and the mechanism responsible for nitrate tolerance, using nitroglycerine (NTG), isosorbide dinitrate (ISDN), 5-mononitrate (5MN) and 2-mononitrate (2MN)., Materials and Methods: Preparations were stimulated by different spasmogenic agents: KCl, angiotensin II and noradrenaline; nitrates were administered on the plateau contraction, at the concentration of maximum inhibitory effect. In another series of experiments, preparations were preincubated with the maximum inhibitory concentration of each nitrate to evaluate the induction of tolerance., Results: Nitrates produced the following maximum inhibitions on noradrenaline-induced contraction: NTG 90% (10(-6) mol/l), ISDN 60% (10(-4) mol/l), 5MN 55% (10(-4) mol/l) and 2MN 80% (10(-4) mol/l). After incubation a loss of vasodilator effect of nearly 50-60% was observed for all the nitrates considered except 2MN, whose loss of effect was significantly lower (36%). The cyclic guanosine monophosphate (cGMP) levels measured in the preparations were lower in the presence of 2MN than the other compounds., Conclusion: These data suggest that 2MN is able to induce a lower cGMP increase and less tolerance induction; since these observations seem to be correlated, the vasodilator effect of 2MN probably also involves mechanisms other than stimulation of guanylate cyclase.

Background: Many echocardiographic parameters have been proposed for the assessment of the patients with heart failure (HF). Recently, the myocardial performance index (MPI) has been shown to be an accurate index of myocardial function. We assessed the correlation with other clinical and echocardiographic measurements and the prognostic value of MPI in patients with HF., Methods and Results: The MPI was assessed in 112 consecutive patients with persistent symptoms of HF (II-III NYHA class), sinus rhythm, LV systolic dysfunction (defined by an ejection fraction 0.55 (median value) and medium to severe mitral regurgitation were associated with a relative risk of cardiovascular events of 18.7 (95% confidence interval [CI], 16.6-20.7; P < 0.005) and of 3.03 (95% CI, 2-4.1; P = 0.035), respectively., Conclusions: In our patients with HF, MPI was the best predictor of cardiovascular events. Mitral regurgitation was the only other variable which had an additive prognostic value at multivariate analysis.

Myxomas are the most frequent benign primary cardiac tumours (50% of benign heart tumours). This kind of tumour is most likely to be localized in the left atrium, followed by the right atrium, right ventricle and left ventricle. Quite exceptional is the presence of a myxoma originating from the tricuspid valve or from the Eustachian valve. We describe the case of a woman with moderate dyspnoea of unknown origin and the presence of tricuspid myxoma who underwent tricuspid valve curettage.

Caseous calcification of the mitral annulus is a rare form of periannular calcification that generally appears as a calcified mass with a central echolucent area that may lead to diagnostic errors. The case is reported of a 65-year-old woman in whom a suspicious mass was detected with transthoracic echocardiography performed for dyspnea.

Introduction: The diastolic function of the left ventricle is a main point of the physiological adaptations of the cardiovascular system to the various situations., Aim of the Study: Evaluation of left atrium diameter change during diastole and left atrial volume and their possible correlation with different left ventricular diastolic filling pattern., Material and Methods: Ninety patients with echocardiographically determined diastolic dysfunction and eighty healthy volunteers were included in the study. We measured left atrium emptying fraction (LAEF), defined as ratio of end-diastolic left atrial diameter to end-systolic diameter and left atrial volume. Mitral flow pulsed wave velocities were recorded. E, A, E/A, deceleration time of early diastolic filling, isovolumetric relaxation time were measured. Pulmonary vein S, D and atrial reversal velocities and tissue Doppler imaging of E' and A' mitral anular velocities were obtained., Results: LAEF was found 0.6 +/- 0.4 (mean SE) in the control group, 0.81 +/- 0.04 in pseudonormal pattern (P < 0.05, control vs pseudonormal group), 0.89 +/- 0.01 in the greater A wave than E wave (P < 0.001, control vs restrictive pattern group), and 0.78 +/- 0.2 in the A > E group (P < 0.05, control vs A > E pattern group)., Conclusions: LAEF and atrial volume are a new and practical methods for the differentiation of the normal-pseudonormal mitral flow pattern, in particular in setting without new ultrasound technologies.

We describe a case of a man, 42 years old, submitted to successful fibrinolitic strategy with rTPA in acute mitralic prosthesis valve thrombosis and ipomobility of one emidisk. There aren't a consensus agreement in therapeutic strategy but we may support the approach of some authors that employ fibrinolisis in patients without absolute or relative controindications and if thrombus dimension is less than 1 cm otherwise they make use of heparin therapy in non obstructive thrombosis with successive transesophageal echocardiography evaluation for the efficacy and the later indication for thrombolisis or surgery treatment.

We describe the case of a 50-year-old woman who was admitted to a pheriferal department for heart failure. The echocardiography revealed a small mass measuring about 1.3 x 1.0 cm adhering to the non-coronary cusp of the aortic valve, mild dilated cardiomiopathy and severe biventricular dysfunction. This mass had erroneously been considered a thrombotic lesion, so the patient was treated with thrombolysis and heparin e.v. Only after a transoesophageal echocardiography a tumour cardiac mass was suspected. The diagnosis of fibroelastoma was confirmed by MRI and then from the anatomic and histoligical definition after surgery.

Diabetes mellitus is a worldwide epidemic whose incidence and prevalence have significantly increased in recent decades. Diabetic patients have an increased mortality and morbidity related to ischemic heart disease and are more likely to develop multivessel coronary artery disease than non-diabetic patients. An acute coronary event is the leading cause of death among diabetics. These patients have an increased risk of complications after an acute coronary syndrome both during the acute phase and in the post-infarction period. Experimental evidences showed an increased prevalence of atherosclerosis as well as platelet and coagulation abnormalities in patients with diabetes, even after data adjustment for other risk factors. Both hyperglycemia and insulin resistance play a role in the pathogenic link between diabetes and atherosclerosis. Diabetic patients, therefore, could derive a greater benefit from therapies shown to be effective in treating and preventing ischemic heart disease. An aggressive correction of cardiovascular risk factors and accurate risk stratification of patients with diabetes are needed.

Acute heart failure (HF) is the most common diagnosis at discharge in patients aged > 65 years. It carries a dismal prognosis with a high in-hospital mortality rate and very high post-discharge mortality and rehospitalization rates. It is a complex clinical syndrome that is challenging to define as it may vary widely with respect to underlying pathophysiological mechanisms and clinical presentations. Different clinical scenarios have prognostic significance and may influence therapeutic options. Amongst the main clinical presentations, we may include the following: de novo HF vs acutely decompensated chronic HF, HF caused, and/or worsened, by myocardial ischemia, acute HF with low, normal, or high systolic blood pressure, acute HF caused by hydrosaline retention or fluid redistribution to the lungs, acute HF with comorbidities (diabetes, anemia, renal insufficiency, etc.). Different pathophysiological mechanisms and clinical presentations may coexist in the same patient. Identification and, whenever possible, treatment of underlying pathophyisiological mechanisms should be a primary objective of acute HF management.

Behçet's disease (BD) is a multisystemic, chronic, inflammatory disease of unknown origin characterized by alternation of exacerbation and quiescence phases. Cardiac involvement in BD is infrequent. We report a case of a young man with BD with right ventricular thrombus and pulmonary thromboembolism. A 20-year-old man was admitted to our hospital with a 6-month history of dyspnea at rest, asthenia, and fever. Transthoracic echocardiography showed right wall thickened and presence of floating masses in the right outflow tract. Transesophageal echocardiography confirmed the presence of diffuse thrombosis in the right ventricle, with mobile ramifications in its outflow tract. Cardiovascular magnetic resonance and computed tomography of heart confirmed the presence of thrombi, the increased thickness of endocardiac tissue, and altered cardiac wall signal transmission. Computed tomography scan showed multiple pulmonary thrombi. Myocardial biopsy specimen showed diffused subendocardial thrombosis with damage of cardiac myocytes and presence of granulocytes. Six months after discharge, no cardiac masses were detected by transthoracic echocardiography. However, a few weeks after this last echocardiogram, the patient was again hospitalized for a new episode of acute pulmonary embolism. The patient was discharged with increasing dose of oral anticoagulant, with no evidence of cardiac masses at transthoracic echocardiography and thrombosis at computed tomography. The patient is still healthy on anticoagulant, immunosuppressive, and steroid therapy. This case provides a rare example of BD, in which we found-at the same time-heart and pulmonary manifestations, with the presence of right ventricular thrombus and pulmonary thrombi in situ.

Peripartum cardiomyopathy (PPCM) is a rare disorder in which left ventricular dysfunction and symptoms of heart failure occur in the peripartum period in previously healthy women. Incidence of PPCM ranges from 1 in 1300 to 1 in 15,000 pregnancies. The etiology of PPCM is unknown, but viral, autoimmune, and idiopathic causes may contribute. The diagnostic criteria are onset of heart failure in the last month of pregnancy or in the first 5 months postpartum, absence of determinable cause for cardiac failure, and absence of a demonstrable heart disease before the last month of pregnancy. Risk factors for PPCM include advanced maternal age, multiparity, African race, twinning, gestational hypertension, and long-term tocolysis. The clinical presentation of patients with PPCM is similar to that of patients with dilated cardiomyopathy. Echocardiography is central to diagnosis. Early diagnosis and initiation of treatment are essential to optimize pregnancy outcome. Treatment is similar to medical therapy for other forms of dilated cardiomyopathy. About half the patients of PPCM recover without complications. The prognosis is poor in patients with persistent cardiomyopathy. Persistence of disease after 6 months indicates irreversible cardiomyopathy and portends worse survival.

Arsenic trioxide is an effective treatment for patients with acute promyelocytic leukaemia (APL) who have relapsed from or are refractory to all trans-retinoic acid and anthracycline chemotherapy. Cardiac effects observed include electrocardiographic changes such as QTc prolongation, T-wave abnormalities, torsades de pointes and sudden death. We describe a case of a man, 76 years old, who was admitted to our department for dyspnoea in APL in treatment with arsenic trioxide. Chest radiograph illustrated an enlarged cardiac silhouette and bilateral pleuric effusion and the ECG evidenced QT prolongation. The patient was also submitted to transthoracic echocardiography that revealed moderate pericardial effusion without signs of cardiac tamponade and a normal biventricular function. This condition was considered to be associated with arsenic trioxide polyserosit and the drug therapy was immediately discontinued and steroid drugs started. After 2 weeks of arsenic trioxide therapy suspension there was evidence of complete resolution of pericardial and pleuric effusion and the ECG showed normal QT interval.

Coronary artery spasm can cause both brady- and tachyarrhythmia, through induction of AV block (usually linked to coronary spasm of the right coronary artery) or ventricular tachycardia/fibrillation linked to extensive myocardial ischemia. The electrocardiographic aspect of coronary artery spasm is an ST segment elevation. We describe the case of patient implanted with an implantable cardioverter defibrillator (ICD) for unexplained syncope which, during coronary artery spasm, received an inappropriate device firing due to ST segment elevation, leading to a double count of the QRS by the ICD.

We report the case of a patient admitted to the hospital on two different occasions, separated by a time interval of 12 years, with the same clinical picture: acute anterior myocardial infarction complicated by early ventricular fibrillation. The patient was successfully resuscitated because, in both circumstances, he was 'lucky' to arrive at hospital within a few minutes of the onset of chest pain, and to have ventricular fibrillation in the Emergency Department. The issue of intracardiac defibrillator implantation, despite this situation is not contemplated in the current guidelines (left ventricular ejection fraction was preserved), is discussed here.

Urocortins and the corticotropin releasing hormone have a long evolutionary history. In the nervous system the corticotropin releasing hormone is responsible of anxiogenic effects associated with stress, while urocortins are concerned with adaptive behavior. Urocortins are also expressed in the heart, where they may play an autocrine/paracrine role binding to corticotropin releasing hormone-R2 receptors. The expression of endogenous cardiac urocortin is increased by in vitro ischemia-reperfusion damage, and the addiction of exogenous urocortins is associated with reduction of myocardial cell death during ischemia-reperfusion damage in vitro, ex vivo and in vivo. In isolated perfused heart urocortin enhances cardiac contractility and decreases high energy phosphates reduction after ischemia-reperfusion damage. Urocortin is also associated with peripheral and coronary vasodilation and with positive inotropic effect. There are experimental data which suggest a beneficial effect of urocortins in subjects with heart failure and a possible beneficial role of urocortin in preventing the iatrogenic ischemia-reperfusion damage caused by cardioplegic arrest during cardiac surgery. These early observations suggest that assessment of the clinical use of urocortin in heart failure and for the prevention of ischemia-reperfusion damage in cardiac surgery should be actively pursued.

A novel syndrome with transient asynergy of the apical segments of the left ventricle, also known as tako-tsubo cardiomyopathy, has been recently described and presents characteristics and effects similar to acute myocardial infarction. We report the case of a 69-year-old woman presenting with chest pain typical of myocardial ischemia, electrocardiographic abnormalities typical of antero-lateral transmural myocardial infarction, and unstable clinical and hemodynamic condition. Trans-thoracic echocardiography showed a left ventricular dysfunction with a markedly decreased ejection fraction. The patient received heparin and abciximab bolus but coronary angiography demonstrated the absence of coronary stenoses, thrombi, and coronary spasm. Due to impaired neurological conditions the patient underwent brain tomography that showed subarachnoid haemorrhage secondary to a right vertebral artery aneurysm rupture. The possible occurrence of a reversible cardiomyopathy mimicking an acute coronary syndrome in presence of intracranial bleeding should be always considered.

Over the last years a growing interest for the biochemical abnormalities detectable in heart failure has become evident. In particular, large scientific evidence has been provided on hormones (catecholamines, renin-angiotensin-aldosterone system, natriuretic peptides) and cytokines (tumour necrosis factor, interleukins, etc.). Quite recently the attention of clinicians and researchers has also been directed towards high serum levels of tumour markers in this syndrome. Carbohydrate antigen 125 has been observed to increase in patients with congestive heart failure, to correlate with haemodynamic and clinical parameters of severity, and to show significant changes after adequate treatment. The aim of this paper is to review the data currently available on serum levels of tumour markers in patients with chronic heart failure, focusing the attention on the potential clinical use of carbohydrate antigen 125.

The abnormalities of aortic valve morphology and function represent the most common cardiac-valve lesion particularly in elderly. The etiology of aortic stenosis is degenerative-calcific in the majority of patients. Many risk factors seems to be linked to the calcification and the stenosis of the aortic valve but they must be confirmed. In this review the etiology and the possible physiopathology of the aortic valve stenosis is discussed.

Beta-blockers are not an homogeneous group of agents. Only three beta-blockers, carvedilol, bisoprolol and metoprolol succinate, have had favorable effects on prognosis in controlled clinical trials in the patients with chronic heart failure. However, pharmacological differences exist between them. Metoprolol and bisoprolol are selective for beta(1)-adrenergic receptors while carvedilol blocks also beta(2)-, and alpha(1)- adrenergic receptors, and has associated antioxidant, anti-endothelin and antiproliferative properties. In COMET carvedilol was associated with a significant reduction in mortality compared to metoprolol tartrate further showing that different beta-blockers may have different effects on the outcome. These differences may be related to the ancillary properties of carvedilol or to its broader antiadrenergic profile. However, also more effective and prolonged blockade of beta1 adrenergic receptors may occur with carvedilol compared to metoprolol.

Objective: The aim of the study was to evaluate the mid-term results of total arterial myocardial revascularization (TAMR) with composite grafts in patients older than 70 years when compared to standard CABG technique, since the usefulness of TAMR in the elderly has not been demonstrated yet., Methods: A prospective randomized study was designed with the following end-points: post-operative complications, death, recurrence of angina, graft occlusion, any cardiac event and reinterventions. One hundred and eighty-eight patients older than 70 years were enrolled and assigned to Group 1(G1)=94 pts, for total arterial revascularization or Group 2(G2)=94 pts, for standard CABG (LITA on LAD plus additional saphenous veins). The groups were comparable in terms of pre-operative characteristics and Euroscore (mean: G1=8.4 vs. G2=8.2)., Results: No differences between the groups were observed in terms of mean number of grafted vessels (G1=2.1 vs. G2=2.3), mean aortic cross-clamping time (G1=34+/-8 vs. G2=33+/-6min), mechanical ventilation time (G1=23+/-4 vs. G2=22+/-4hr), ICU stay (G1=40+/-10 vs. G2=39+/-9hr), post-operative complications and hospital mortality (G1=5.3% vs. G2=4.2%). At a mean follow-up of 12+/-4 months, cumulative incidence of angina recurrence was 2.1% in G1 vs. 11% in G2 (P=0.021). Angiographic evaluation showed 98.2% arterial patency in G1 vs. 86% saphenous vein graft patency in G2 (P<0.001). Multivariate analysis identified conventional CABG surgery as independent predictor of angina recurrence, graft occlusion and late cardiac events., Conclusions: Total arterial revascularization with composite grafts proved to be a safe and effective procedure also in the elderly. Composite arterial grafts provided superior clinical outcome with a lower rate of angina recurrence, graft occlusion and late cardiac events when compared to conventional CABG strategy.

Coronary angiography is still the first choice method for the diagnosis of coronary artery disease in patients with dilated cardiomyopathy. The diagnosis of coronary artery disease is, in its turn, essential as patients with associated coronary artery disease have a worse prognosis, compared to patients with idiopathic dilated cardiomyopathy, and, more importantly, coronary revascularization may significantly improve left ventricular function, clinical symptoms and prognosis, when performed in the presence of a significant amount of viable myocardium. The favorable effects on the left ventricular function are greater when a contractile reserve is shown. However, revascularization of viable myocardium may have other beneficial effects like a reduction in left ventricular remodeling and in the incidence of recurrent ischemic events and malignant arrhythmias. The detection of viable myocardium should, however, be preceded by the detection of coronary artery disease through coronary angiography. The clinical history and the results of the non-invasive evaluation, with the possible exception of coronary calcium detection by electron beam computed tomography, do not, in fact, allow the diagnosis of coronary artery disease. Coronary angiography is thus indicated in all the patients with suspected coronary artery disease (e.g. males > 35 years, with coronary risk factors, a history of chest pain and/or regional wall motion abnormalities and/or perfusion defects at stress scintigraphy) in whom the age and general conditions warrant a coronary revascularization procedure. Coronary angiography is also indicated in all the patients who are candidates to heart transplantation or whose symptoms are secondary to a mechanical complication of myocardial infarction.

Controlled clinical trials, performed in more than 16,000 patients to date, have consistently shown the beneficial effects of long-term beta-blocker therapy in patients with chronic heart failure. However, it is not clear whether this represents a class effect or it is specific only to some agents. Beneficial effects on the prognosis of the patients with mild to moderate heart failure have been shown with metoprolol, bisoprolol, and carvedilol. However, these beta-blockers differ in their pharmacological characteristics. Metoprolol and bisoprolol are selective for beta 1-adrenergic receptors and are devoid of ancillary properties. Carvediol, at doses of 50 mg daily, blocks all beta 1-, beta 2-, and alpha 1- adrenergic receptors, and has associated antiproliferative and antioxidant activities. These differences cause a different acute hemodynamic response with a reduction in cardiac output and a tendency to a rise in pulmonary wedge pressure with selective agents and no change in cardiac output and a slight decrease in pulmonary pressures with carvedilol. Accordingly, when the therapy is started, the most frequent side effects are worsening heart failure with metoprolol and bisoprolol and hypotension and dizziness with carvedilol. It is still controversial whether these differences may also influence the long-term effects of therapy. Differently from selective beta-blockers, carvedilol does not upregulate beta 1-receptors, blocks all adrenergic receptors, decreases cardiac norepinephrine release, thus providing a more comprehensive blockade of the cardiac adrenergic drive. These properties have caused a larger increase in LV function and a lack of improvement in maximal exercise capacity with carvedilol, compared to selective beta-blockers. It is however, unclear whether these differences may also influence the patients' outcome.

Background: Inflammation is an important component of ischemic heart disease. PTX3 is a long pentraxin whose expression is induced by cytokines in endothelial cells, mononuclear phagocytes, and myocardium. The possibility that PTX3 is altered in patients with acute myocardial infarction (AMI) has not yet been tested., Methods and Results: Blood samples were collected from 37 patients admitted to the coronary care unit (CCU) with symptoms of AMI. PTX3 plasma concentrations, as measured by ELISA, higher than the mean+2 SD of age-matched controls (2.01 ng/mL) were found in 27 patients within the first 24 hours of CCU admission. PTX3 peaked at 7.5 hours after CCU admission, and mean peak concentration was 6.94+/-11.26 ng/mL. Plasma concentrations of PTX3 returned to normal in all but 3 patients at hospital discharge and were unrelated to AMI site or extent, Killip class at entry, hours from symptom onset, and thrombolysis. C-reactive protein peaked in plasma at 24 hours after CCU admission, much later than PTX3 (P<0.001). Patients >64 years old and women had significantly higher PTX3 concentrations at 24 hours (P<0.05). PTX3 was detected by immunohistochemistry in normal but not in necrotic myocytes., Conclusions: PTX3 is present in the intact myocardium, increases in the blood of patients with AMI, and disappears from damaged myocytes. We suggest that PTX3 is an early indicator of myocyte irreversible injury in ischemic cardiomyopathy.