Background: Cardiovascular (CV) risk factors, causing endothelial dysfunction (ED) and left ventricular diastolic dysfunction (LVDD), contribute to an increased risk of heart failure (HF). The aim of this study was to determine the relationship between the occurrence of LVDD and ED with CV risk assessed by the Systematic Coronary Risk Evaluation2 (SCORE2) algorithm and HF. Methods: In the period from November 2019 to May 2022, a cross-sectional study that included 178 middle-aged adults was conducted. Transthoracic echocardiography (TTE) was used to assess left ventricular (LV) diastolic and systolic function. ED was assessed using the plasma values of asymmetric dimethylarginine (ADMA) and was determined using the ELISA method. Results: The majority of subjects with LVDD grades 2 and 3 had high/very high SCORE2, developed HF and all were taking medication (p < 0.001). They also had significantly lowest plasma ADMA values (p < 0.001). We found that the reduction of ADMA concentration is influenced by certain groups of drugs, or more significantly, by their combinations (p < 0.001). Conclusions: In our study, we confirmed a positive correlation between LVDD, HF and SCORE2 severity. The results showed a negative correlation between the biomarkers of ED, LVDD severity, HF, and SCORE2, which we believe is due to medication effects.

Cardiovascular diseases (CVDs) have been the most common cause of death worldwide for decades. Until recently the most affected patients were middle-aged and elderly, predominantly males, with more frequent ST elevation myocardial infarction (STEMI) caused by obstructive coronary artery disease (CAD). However, in the last two decades we have noticed an increased incidence of ischemia with non-obstructive coronary arteries (INOCA), which includes myocardial infarction with non-obstructive coronary arteries (MINOCA) and non-myocardial infarction syndromes, such as microvascular and vasospastic angina, conditions that have been particularly pronounced in women and young adults - the population we considered low-risky till than. Therefore, it has become apparent that for this group of patients conventional methods of assessing the risk of future cardiovascular (CV) events are no longer specific and sensitive enough. Heart failure with preserved ejection fraction (HFpEF) is another disease, the incidence of which has been rising rapidly during last two decades, and predominantly affects elderly population. Although the etiology and pathophysiology of INOCA and HFpEF are complex and not fully understood, there is no doubt that the underlying cause of both conditions is endothelial dysfunction (ED) which further promotes the development of left ventricular diastolic dysfunction (LVDD). Plasma biomarkers of ED, as well as natriuretic peptides (NPs), have been intensively investigated recently, and some of them have great potential for early detection and better assessment of CV risk in the future. (www.actabiomedica.it)

Background and Clinical Significance: Congenital LQTS is a life-threatening condition, resulting from a mutation of the gene encoding the cardiac ion channels, which results in prolongation of the ventricular action potential. Genetic screening of family members in symptomatic and asymptomatic patients is crucial for the prevention of sudden cardiac death. There are a number of detected mutations of congenital LQTS, of which the three forms LQT1, LQT2, and LQT3 are the best described. In addition to the described ECG morphology, the key triggers and treatment approach are described. This emphasizes even more the importance of timely screening of these patients, and the decision for therapy. It should be emphasized that the phenotypic manifestations significantly depend on the affected genes. The guidelines in the treatment approach are very clear, although it should be emphasized that beta blockers are the first and basic treatment therapy. The therapeutic choice is narrowed especially if they are not effective. Case Presentation: This is a case report of a young woman diagnosed with LQTS who was confirmed to have KCNH2 mutations through genetic analysis. The same mutation was also confirmed in her children. Changes in the therapeutic approach are described, and the use of beta blockers, depending on the symptoms and drug tolerance. Especially in the postpartum period, due to reduced progesterone levels, in this case, the patient was implanted with a cardioverter defibrillator. Conclusions: It should be emphasized that timely recognition is essential for early diagnosis, regular control, timely initiation of treatment, and prevention of adverse events.

A 67-year-old man started treatment due to frequent asymptomatic premature ventricular complexes (PVCs) accidentally being registered during a preventive examination by a specialist, because of which he was referred to cardiologist. During the initial 24-hour (h) ECG monitoring, 4.5% PVCs and one episode of asymptomatic non-sustained ventricular tachycardia (NSVT) with three PVCs in row, at a frequency of 150 beats per minute (bpm), were detected. After the introduction of beta blockers into therapy, a lower number of PVCs, without NSVT, were recorded in the control 24 h Holter ECG, while transthoracic echocardiography (TTE) showed normal left ventricular (LV) systolic function without cardiomyopathy. So, an exercise test was indicated, and it was interrupted in the third minute at 120 beats per minute (bpm) due to fatigue and pain in the hips, without malignant arrhythmias, angina or dyspneic complaints. During the rest period, a significant inferolateral depression of the ST junction was observed, which recovered in the ninth minute. Immediately after the ECG monitoring stopped, the patient lost consciousness; his pulse was not palpable, but breathing was audible, so cardiac massage was started. After he had regained consciousness, the ECG showed alternating sinus and junctional rhythm with the lowest frequency of 33 bpm, which was accompanied by marked hypotension (80/50 mmHg). The patient was immediately hospitalized; coronary angiography and repeated TTE were completely normal, while continuous ECG monitoring did not confirm malignant rhythm disorders or asystole. It was concluded that it was vasovagal syncope (VVS), most likely caused by the Bezold–Jarisch reflex (BJR).