[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.]

[Recent advances in the care of acute myocardial infarction have resulted in more patients surviving myocardial infarction than earlier. However, heart failure is a common complication in these patients, which in turn is associated with substantial mortality, primarily due to a remodelling of the left ventricle that already starts in an early stage of the myocardial infarction. The aim of this review article is to present the pathomechanism of this remodelling and to discuss related therapeutic options. Current guidelines recommend the use of an angiotensin- converting enzyme inhibitor combined with or followed by an angiotensin receptor blocker, a beta-blocker, and an aldosterone antagonist in post-infarction patients with concomitant heart failure.]

[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. ]

[Beta-blockers are among the most widely used drugs for the treatment of cardiovascular diseases. In the mid-90’s, these drugs were recommended as first-line therapies of hypertension. With the introduction of new drugs, the list of first-choice drugs has been extended. The results of recently published major hypertension trials, which compared conventional agents (beta blockers and/or diuretics) with newer agents (angiotensin converting enzyme inhibitors, Caantagonists, angiotensin receptor blockers), raised concerns regarding the role of beta blockers in cardiovascular primary prevention. Subsequently, a metaanalysis of 13 trials has shown that compared with other drug types, beta-blocker therapy is less beneficial in patients with hypertension who do not have heart disease. Nevertheless, in cardiovascular indications other than hypertension (acute myocardial infarction, heart failure and arrhythmias), betablockers retain their dominant position.]