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Several studies and recent patents have demonstrated that hyperhomocysteinemia (HHCY) is an independent risk factor for congestive heart failure (CHF); it is also correlated to the severity of the disease. In literature there are some data about effects of HHCY on myocardial structure and function in animal models. These studies indicate a direct effect of HCY in promoting reactive myocardial fibrosis and systolic dysfunction, promoting miocardial redox state, endothelial and mithocondryal dysfunction, negative inotropic effect. According to some authors the HHCY is a potential ethiological factor for heart failure while according to others it is just an epiphenomenon without direct effects on myocardium. Nevertheless the literature studies show the relevant involvement of HHCY in CHF and the strong relations between HHCY plasma levels and the severity and prognosis of the disease. Regarding the potential mechanistic role of HHCY in CHF, all of these studies do not provide any mechanistic insights because of their epidemiological nature. Future studies need to explore the exact pathomechanisms of HHCY in CHF.

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.

Erythropoietin is a hormone produced by the kidney, which regulates proliferation, differentiation and maturation of red cells. Recombinant human EPO (rH-EPO) is well known to correct anaemia in patients with chronic renal failure in terminal stage. However, recent studies showed the existence of several not haematopoietic effects of erythropoietin. EPO receptors have been found to be expressed in several tissues, included the cardiovascular system. An increase in cardiac systolic function has been observed in patients with chronic heart failure treated with EPO. Other beneficial effects appear to be related to the pro-angiogenic properties on endothelial cells and could be useful for treatment of ischemic heart disease. These findings suggest that EPO could provide potential therapeutic benefits in the management of cardiovascular diseases beyond anaemia correction. This review focuses its attention on the pleiotropic effects of EPO and its future promising applications in cardiovascular pathology.

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.

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.

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.