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Diabetes mellitus is an important risk factor for a first cardiovascular event and for worse outcomes after a cardiovascular event has occurred. This situation might be caused, at least in part, by the prothrombotic status observed in patients with diabetes. Therefore, contemporary antithrombotic strategies, including more potent agents or drug combinations, might provide greater clinical benefit in patients with diabetes than in those without diabetes. In this Consensus Statement, our Working Group explores the mechanisms of platelet and coagulation activity, the current debate on antiplatelet therapy in primary cardiovascular disease prevention, and the benefit of various antithrombotic approaches in secondary prevention of cardiovascular disease in patients with diabetes. While acknowledging that current data are often derived from underpowered, observational studies or subgroup analyses of larger trials, we propose antithrombotic strategies for patients with diabetes in various cardiovascular settings (primary prevention, stable coronary artery disease, acute coronary syndromes, ischaemic stroke and transient ischaemic attack, peripheral artery disease, atrial fibrillation, and venous thromboembolism). Finally, we summarize the improvements in cardiovascular outcomes observed with the latest glucose-lowering drugs, and on the basis of the available evidence, we expand and integrate current guideline recommendations on antithrombotic strategies in patients with diabetes for both primary and secondary prevention of cardiovascular disease., Patients with diabetes mellitus have a prothrombotic status that increases the risk of cardiovascular events and worsens prognosis after these events. In this Consensus Statement, the Working Group on Thrombosis of the Italian Society of Cardiology proposes antithrombotic strategies for patients with diabetes in various cardiovascular settings.

Although the female gender is generally less represented in cardiovascular studies, observational and randomized investigations suggest that-compared with men-women may obtain different benefits from antiplatelet therapy. Multiple factors, including hormonal mechanisms and differences in platelet biology, might contribute to such apparent gender peculiarities. The thrombotic and bleeding risks, as well as outcomes after a cardiovascular event, appear to differ between genders, partly in relation to differences in age, comorbidities and body size. Equally, the benefits of antiplatelet therapy may differ in women compared with men in different vascular beds, during primary or secondary prevention and according to the type of an antiplatelet agent used. This document is an attempt to bring together current evidence, clinical practices and gaps of knowledge on gender-specific platelet function and antiplatelet therapy. On the basis of the available data, we provide suggestions on current indications of antiplatelet therapy for cardiovascular prevention in women with different clinical features; no strong recommendation may be given because the available data derive from observational studies or post hoc/subgroup analyses of randomized studies without systematic adjustments for baseline risk profiles.

Objectives: To explore the full range of right heart dimensions and the impact of long-term intensive training in athletes. Background: Although echocardiography has been widely used to distinguish the athlete's heart from pathologic left ventricular (LV) hypertrophy, only few reports have described right ventricular (RV) and right atrial (RA) adaptations to extensive physical exercise. Methods: 650 top-level athletes [395 endurance-(ATE) and 255 strength-trained (ATS); 410 males (63.1%); mean age 28.4 +/- 10.1; 18-40 years] and 230 healthy age-and sex-comparable controls underwent a transthoracic echocardiographic exam. Along with left heart parameters, right heart measurements included: RV end-diastolic diameters at the basal and mid-cavity level; RV base-to-apex length; RV proximal and distal outflow tract diameters; RA long and short diameters; and RA area. Tricuspid annular plane systolic excursion and RV tissue Doppler systolic peak velocity were assessed as indexes of RV systolic function. Pulmonary artery systolic pressure (PASP) was estimated from the peak tricuspid regurgitant velocity. Results: ATS showed increased sum of wall thickness and relative wall thickness, whereas left atrial volume, LV end-diastolic volume, LV stroke volume and PASP were significantly higher in ATE. RV and RA measurements were all significantly greater in ATE than in ATS and controls. ATE also showed improved early diastolic RV function, whereas RV systolic indexes were comparable among groups. On multivariate analysis, type and duration of training (p

Several studies have described the adaptive remodeling of the heart during exercise. In some more practiced endurance athletes, there is a disproportionate load on the right ventricle (RV), at least during exercise, and this might be the basis for a chronic pro-arrhythmic RV remodeling. Especially, in these kinds of athletes the recovery after detraining might be incomplete, in particular for RV changes. The observation of acute myocardial injury based on transient elevation of biomarkers and chronic myocardial scar, not completely reversible changes of the RV and an increased prevalence of some arrhythmias support the existence of an "exercise-induced cardiomyopathy." The aim of this paper is to review current knowledge about changes in the right heart in highly trained athletes and how these change influence cardiac function.

Long-term intensive exercise training programs lead to numerous progressive cardiac adaptations, which are collectively termed "athlete's heart." Noninvasive diagnostic techniques, such as color Doppler echocardiography, have been widely used in the analysis of the athlete's heart. Initial experiences focused mainly on left heart adaptations to training. However, in recent years, substantial structural and functional adaptations of the right heart have been documented. The present review article focuses on recent data defining right heart adaptation to short- and long-term periods of exercise training. Right ventricular (RV) morphology and function may be more profoundly affected by intense exercise and, in some cases, functional recovery may be incomplete. Moreover, there is speculation that such changes may represent a substrate for proarrhythmic RV remodeling in some highly trained athletes, even in the absence of a known familial redisposition.

To test whether two-dimensional longitudinal strain (2DSE) performed after revascularization by percutaneous coronary intervention (PCI) could predict left ventricular (LV) remodeling in patients with recent non-ST elevation myocardial infarction (NSTEMI).In 70 patients (62.7 ± 8.7 years) with recent NSTEMI (between 72 hours and 14 days), undergoing coronary angiography for recurrent angina, myocardial deformation parameters were measured by 2DSE before and 24 hours after reperfusion therapy. Strain in all LV segments was averaged to obtain a global value (Global longitudinal Strain--GLS). Infarct size was estimated by clinical parameters and cardiac markers. After 6 months from intervention, LV negative remodeling was defined as lack of improvement of LV function, with increase in LV end-diastolic volume of greater than or equal than 15%.At follow-up, patients were subdivided into remodeled (n=32) and non-remodeled (n = 38) groups. Patients with negative LV remodeling had significantly lower baseline LV ejection fraction (44.8±6.9 vs. 48.7 ± 5.5 %; p0.05), higher peak troponin I (p0.001) and reduced GLS (- 10.6±6.1 vs - 17.6 ± 6.7 % p0.001) than those without LV remodeling. GLS showed a close correlation with peak troponin I after PCI (r = 0.64, P0.0001) and LV WMSI (r = 0.42, p0.01). By multivariable analysis, diabetes mellitus (P0.005), peak of Troponin I after PCI (P0.0005), GLS at baseline (OR: 4.3; p0.0001), and lack of improvement of GLS soon after PCI (OR: 1.45, P0.01) were powerful independent predictors of negative LV remodelling at follow-up. In particular, a GLS ≤ 12 % showed a sensitivity and a specificity respectively of 84.8% and 87.8% to predict negative LV remodelling at follow-up.in patients with recent NSTEMI, longitudinal LV global and regional speckle-tracking strain measurements are powerful independent predictors of LV remodeling after reperfusion therapy.

BACKGROUND: The aim of this study was to define the range of left ventricular (LV) velocities and deformation indexes in highly trained athletes, analyzing potential differences induced by different long-term training protocols. METHODS: Standard echocardiography, pulsed-wave tissue Doppler echocardiography, and two-dimensional strain echocardiography of the interventricular septum and lateral wall were performed in 370 endurance athletes and 280 power athletes. Using pulsed-wave tissue Doppler, the following parameters of myocardial function were assessed: systolic peak velocities (S(m)), early (E(m)) and late (A(m)) diastolic velocities, and the E(m)/A(m) ratio. By two-dimensional strain echocardiography, peaks of regional systolic strain and LV global longitudinal strain were calculated. RESULTS: LV mass index and ejection fraction did not significantly differ between the two groups. However, power athletes showed an increased sum of wall thicknesses (P < .01) and relative wall thickness, while LV stroke volume and LV end-diastolic diameter (P < .001) were greater in endurance athletes. By pulsed-wave tissue Doppler analysis, E(m) and E(m)/A(m) at both the septal and lateral wall levels were higher in endurance athletes. By two-dimensional strain echocardiography, myocardial deformation indexes were comparable between the two groups. E(m)/A(m) ratios ≥ 1 were found in the overall population, while 90 % of athletes had an E(m) ≥ 16 cm/sec, S(m) ≥ 10 cm/sec, and global longitudinal strain ≤ -16%. Multivariate analyses evidenced independent positive association between Em peak velocity and LV end-diastolic volume (P < .001) and an independent correlation of global longitudinal strain with the sum of LV wall thicknesses (P < .005). CONCLUSIONS: This study describes the full spectrum of systolic and diastolic myocardial velocities and deformation indexes in a large population of competitive athletes.

Exercise causes changes in the heart in response to the hemodynamic demands of increased systemic and pulmonary requirements during exercise. Understanding these adaptations is of great importance, since they may overlap with those caused by pathological conditions. Initial descriptions of athlete's heart focused mainly on chronic adaptation of the left heart to training. In recent years, the substantial structural and functional adaptations of the right heart have been documented, highlighting the complex interplay with left heart. Moreover, there is evolving evidence of acute and chronic cardiac damage, mainly involving the right heart, which may predispose subjects to atrial and ventricular arrhythmias, configuring an exercise-induced cardiomyopathy. The aim of this article is to review the current knowledge on the physiologic and pathophysiologic changes in the right heart in highly trained athletes.

Atherosclerosis represents the most common pathological substrate of coronary heart disease (CHD), and the characterization of the disease as a chronic low-grade inflammatory condition is now largely accepted. A number of mediators of inflammation have been widely studied, both as surrogate biomarkers and as causal agents, in the pathophysiological network of atherogenesis and plaque vulnerability. The epidemiological observation that biomarkers of inflammation are associated with clinical cardiovascular risk supports the theory that targeted anti-inflammatory treatment appears to be a promising strategy in reducing residual cardiovascular risk on the background of traditional medical therapy. A large number of randomized controlled trials have shown that drugs commonly used in cardiovascular disease (CVD), such as statins, may be effective in the primary and secondary prevention of cardiovascular events through an anti-inflammatory effect. Moreover, several anti-inflammatory drugs are being tested for their potential to reduce residual cardiovascular risk on the background of validated medical therapy for atherosclerotic disease. In this paper, we review relevant evidence with regard to the relationship between inflammation and CVD, from pathogenesis to therapeutic strategies.

Obesity has become an important public health issue in Western and developing countries, with well known metabolic and cardiovascular complications. In the last decades, evidence have been growing about the active role of adipose tissue as an endocrine organ in determining these pathological consequences. As a consequence of the expansion of fat depots, in obese subjects, adipose tissue cells develope a phenotypic modification, which turns into a change of the secretory output. Adipocytokines produced by both adipocytes and adipose stromal cells are involved in the modulation of glucose and lipid handling, vascular biology and, moreover, participate to the systemic inflammatory response, which characterizes obesity and metabolic syndrome. This might represent an important pathophysiological link with atherosclerotic complications and cardiovascular events. A great number of adipocytokines have been described recently, linking inflammatory mileu and vascular pathology. The understanding of these pathways is crucial not only from a pathophysiological point of view, but also to a better cardiovascular disease risk stratification and to the identification of possible therapeutic targets. The aim of this paper is to review the role of Adipocytokines as a possible link between obesity and vascular disease.

Natriuretic peptides (NPs) counter the effects of volume overload or adrenergic activation of the cardiovascular system. They are able to induce arterial vasodilatations, natriuresis and diuresis, and they reduce the activities of the renin–angiotensin–aldosterone system and the sympathetic nervous system. However, in addition to wall stress, other factors have been associated with elevated natriuretic peptide levels. Since 2000, because of their characteristics, NPs have become quantitative plasma biomarkers of heart failure. Nowadays, NPs play an important role not only in the diagnosis of heart failure, but also for a prognostic purpose and a guide to medical therapy. Finally, a new drug that modulates the NP system or recombinant analogs of NPs are now available in patients with heart failure.

Background Our objective was to explore the right ventricular (RV) dimensions and function and the effect of long-term intensive training in a large population of top level athletes using real-time three-dimensional (3D) echocardiography. Methods A total of 430 top-level athletes (220 endurance-trained athletes [ETAs] and 210 strength-trained athletes; 265 men [61.6%]; mean age 27.4 ± 10.1 years, range 18–40) and 250 healthy controls underwent a transthoracic echocardiographic examination. Three-dimensional RV measurements included serial short-axis reconstructions of the RV volumetric data sets, and the RV endocardial contour was traced with cross-reference to the long-axis images for identification of the tricuspid annulus. The end-diastolic and end-systolic RV volumes and ejection fraction were calculated off-line using the method of the summation of discs. Results The strength-trained athletes had a greater heart rate, body surface area, and systolic blood pressure at rest than the ETAs and controls. All RV diameters and 3D volumes and all transmitral and transtricuspid Doppler indexes were greater in the ETAs. Also, the left ventricular stroke volume, cardiac index, and pulmonary artery systolic pressure were greater in the ETAs, and all two-dimensional and 3D RV systolic indexes were comparable. On univariate analysis, the 3D RV end-diastolic volume was significantly associated with advanced age, male gender, duration of training, endurance training, increased left ventricular stroke volume, and pulmonary artery systolic pressure. On multivariate analysis, in the overall study population, the type and duration of training ( P P P Conclusions The results of the present study have delineated the upper limits of the RV dimensions in highly trained athletes as measured by real-time 3D echocardiography. The RV end-diastolic volume was significantly greater in the ETA than in the strength-trained athletes and controls.

BACKGROUND: Although the physiologic range of pulmonary artery systolic pressure (PASP) has been reported, data on how it is manifested in athletes are limited. The aim of the present study was to explore the full spectrum of PASP and the long-term training impact in a large population of highly trained athletes. METHODS: Six hundred fifteen consecutive athletes (370 endurance-trained athletes [ATEs] vs 245 strength-trained athletes [ATSs]; 28.4 ± 10.1 years old) and 230 healthy control subjects (27.5 ± 11.3 years old) underwent transthoracic echocardiography. PASP was estimated by measuring maximal tricuspid regurgitant jet velocity (TRV) with the modified Bernoulli equation. The ratio of TRV to right ventricular outflow tract time-velocity integral (TRV/RVOTTVI) was obtained as a correlate of pulmonary vascular resistance (PVR). RESULTS: Left ventricular (LV) mass index and ejection fraction did not differ significantly between the two groups of athletes. Conversely, ATSs showed an increased sum of wall thickness and relative wall thickness, whereas LV end-diastolic diameter, LV stroke volume, peak TRV, and PASP were significantly higher in ATEs. The ratio between transmitral E wave and tissue Doppler e' wave was not different among the three groups. The ratio TRV/RVOTTVI was ≤ 0.2 (ie, normal PVR) in all subjects. A TRV value > 2.5 m/s was observed in 76 athletes (12.3%). By multivariable analysis, age (P < .01), type and duration of training (P < .01), and LV stroke volume (P < .001) were the only independent predictors of PASP in athletes. CONCLUSIONS: This study delineates the full range of resting TRV and derived PASP in highly trained athletes. The upper physiologic limit of PASP in endurance athletes may reach 40 mm Hg, in line with the greater increase in stroke volume. This should be considered a "physiologic phenomenon" when evaluating athletes for sports eligibility.

AIMS: To analyse right ventricular (RV) myocardial deformation in patients with left ventricular (LV) hypertrophy secondary to either hypertrophic cardiomyopathy (HCM) or athlete's competitive endurance training. METHODS AND RESULTS: Standard Doppler echo, exercise stress echo, and 2D speckle-tracking strain echocardiography (2DSE) of RV longitudinal deformation in RV septal and lateral walls were performed in 50 top-level endurance athletes and in 35 patients with HCM, all men, having evidence of LV hypertrophy. Right ventricular global longitudinal strain (GLS) was calculated by averaging local strains along the entire right ventricle. The two groups were comparable for age and blood pressure, whereas athletes showed lower heart rate and increased body surface area than HCM. Interventricular septal thickness was higher in HCM, whereas both LV and RV end-diastolic diameters (LVEDD and RVEDD) and LV stroke volume were increased in athletes. Right ventricular tricuspid annulus systolic excursion was comparable between the two groups. Conversely, RV GLS and regional peaks of RV myocardial strain were significantly impaired in patients with HCM (all P < 0.001). Multiple linear regression models detected an independent association between RV GLS and LVEDD (beta-coefficient = -0.68, P < 0.0001) in athletes, as well as an independent correlation of the same RV GLS with septal thickness (beta = 0.63, P < 0.0001) in HCM. An RV GLS cut-off value of -0.16% differentiated athletes and HCM with an 86% sensitivity and a 92% specificity. Furthermore, in the overall population, RV GLS (beta = 0.51, P < 0.0001) was a powerful independent predictor of maximal workload during exercise stress echo. CONCLUSION: Right ventricular myocardial systolic deformation is positively influenced by preload increase in athletes and negatively associated with increased septal thickness in HCM. Therefore, 2DSE may represent a useful tool in the differential diagnosis between athlete's heart and HCM, underlining the different involvement of RV myocardial function in either physiological or pathological LV hypertrophy.

Cardiotrophin-1 (CT-1), a member of interleukin (IL)-6 family, was originally isolated for its ability to induce a hypertrophic response in neonatal cardiac myocytes. This cytokine mediates a pleiotropic set of growth and differentiation activities through a unique receptor system, consisting of IL-6 receptor (IL-6R) and a common signal transducer, the glycoprotein 130 (gp130). Both in humans and in mice, CT-1 mRNA has been detected in several tissues, such as liver tissue, adipose tissue, and tissues in the respiratory and nervous systems; in each of these tissues it performs different functions. Predominant actions of CT-1 are on the heart, where it is synthesized and where it provides first myocardial protection by promoting cell survival and proliferation, it carries on its haemodynamic effects and endocrine properties, and finally, it predisposes the heart to pathological conditions. The aim of this review is to describe the pathophysiological mechanisms through which CT-1 carries out its activities, especially on the heart, and its potential contribution as a disease marker in clinical cardiology. Recent studies have confirmed its active role in promoting structural changes typical of most common cardiovascular disease, such as hypertension, valve diseases, congestive heart failure, and coronary artery disease. In fact, CT-1 induces myocyte hypertrophy and collagen synthesis, thereby participating in the progression of ventricular remodelling, which results in cardiac muscle failure at the latest stage. CT-1 plasma levels are elevated in patients with hypertension and coronary artery diseases, and they are also correlated with the severity of valve diseases and heart failure. Therefore, CT-1 may represent a diagnostic, staging, and prognostic biomarker of cardiovascular diseases.