[Acute heart failure may develop in previously healthy hearts. Nevertheless, structural abnormalities can facilitate its development and also, chronic heart failure can progress into acute stage. Considering the total cost of care in the patient's life, this is the most expensive heart disease. The clinical signs and physical abnormalities are usually of diagnostic power, however, instrumental investigations are necessary to recognize complications and to guide therapy. Patients should be monitored in well equipped coronary care units. Therapy consists of medications, coronary revascularization and use of mechanical assist devices.]

[INTRODUCTION - The protein complex coenzyme Q10 (CoQ10) has a role in ATP production as a mitochondrial electron transport molecule, and it also has a strong antioxidant effect. Several studies have proved the correlation between the decrease in CoQ10 level and the severity of heart failure. Heart failure is a multifactorial syndrome, the development of which is greatly influenced by an abnormal energy metabolism. CASE REPORT - The 61-year-old woman developed heart failure after a myocardial infarction. She complained of fatigue, dyspnoea and reduced physical endurance even with optimal treatment. When her therapy was completed by CoQ10, her endurance and life quality significantly improved and her symptoms ameliorated. CONCLUSIONS - Medical treatment of chronic heart failure is an evidence-based, complex therapy. Despite the complex management, morbidity and mortality of this condition remain high. A number of studies have shown that CoQ10 substitution can improve the clinical and haemodynamical parameters of patients with heart failure. On the basis of these results, the use of CoQ10 as an adjuvant therapy to complex treatment has an increasing role.]

[Endothelial cells - under autocrine and paracrine control - may have a central role in the regulation of vascular tone. Endothelial dysfunction is a very early sign of heart failure but the clinical consequence is not well understood. Recent evidence suggests that upregulation of the neuro-endocrine-, and the renin-angiotensin-aldosterone system would lead to increased tissue- and circulating angiotensin-II levels. Elevated concentration of angiotensin-II provides a mechanism by which vasomotor responses to nitric oxide, prostaglandins are blunted, while the effects of vasoconstrictors such as thromboxans, endothelin and chatecholamins are enhanced. The higher basal vascular tone leads to the degeneration and atrophy of skeletal muscle, moreover to the the ischaemic damage of myocardial cells. Because renin-angiotensinaldosterone system is under genetic control, the deleterious effects of angiotensin-II depends on the angiotensin-converting enzyme gene. Pharmacological attempts to counteract endothelial dysfunction in heart failure may include the angiotensin-converting enzyme inhibitor, which can potentially improve the endothel dependent vasodilatation response. The importance of measuring endothelial function by non-invasive techniques is yet unknown, thus, before we introduce the widespread testing of patients for endothelial function, more research has to be done.]

[The rennin-angiotensin system plays a major role in cardiovascular diseases. In the past decade, extensive research investigated the possible clinical benefit of the use of angiotensin-converting enzyme inhibitors in various clinical conditions. Their benefits have been clearly demonstrated in many cardiovascular conditions and agreement as to their potential usefulness has been established in chronic heart failure, asymptomatic left ventricular dysfunction, acute myocardial infarction and hypertension, and in the primary prevention in patients with high risk for cardiovascular events. Numerous randomised clinical trials over the past two decades established their efficacy in reducing adverse outcomes (mortality, hospitalitazion, and physical limitation) in patients with heart failure and left ventricular systolic dysfunction. Based on these results, angiotensin-converting enzyme inhibitors are indicated in all patients with left ventricular systolic dysfunction regardless of etiology, in the absence of intolerance or a contraindication. Despite the recent improvements in the treatment of heart failure, mortality remains high, with approximately 50% patients dead at five years. Although angiotensinconverting enzyme inhibitors decrease mortality, they incompletely suppress angiotenzin-2 when used chronically. Since angiotensin receptor blockers block the biologic effects of angiotenzin-2 more completely than angiotensin-converting enzyme inhibitors, they may be beneficial in the treatment of heart failure. In comparison trials, angiotensin receptor blockers were found to have no benefit over angiotensin-converting enzyme inhibitor therapy. Thus, angiotensin-converting enzyme inhibitors should remain first-line treatment for heart failure. However, in case of intolerance, angiotensin receptor blocker therapy is a reasonable substitute and provides excellent tolerability.]

[SGLT-2-inihibitors are considered as a new class among oral antidiabetic drugs. The first derivatives of this class became available in the last couple of years in Hungary. According to the requirements from regulatory bodies, randomized, controlled clinical trials have been initiated in order to evaluate the cardiovascular safety of nearly all new antidiabetic drugs in patients with type 2 diabetes. Among SGLT-2-inhibitors, only one trial with empagliflozine has been completed so far. Based on the endpoints of the EMPA-REG OUTCOME trial a significant decrease in different cardiovascular events and total mortality was observed in type 2 diabetic patients with elevated cardiovascular risk. The exact pathomechanism of this beneficial effect has not been clearly understood. Currently, the position statements and scientific guidelines clearly describe the place of SGLT-2-inhibitor drugs in the treatment algorithm; the beneficial effect of empagliflozine on cardiovascular events should seriously be considered when making therapeutic decision. Together with the results of ongoing studies with SGLT-2-inhibitors (dapagliflozine: DECLARE, canagliflozine: CANVAS), these data will provide a more robust evidence about the cardiovascular safety of this new class of oral antidiabetic drugs. ]