Electrocardiogram (ECG) still remains a very useful diagnostic method in modern cardiology. Its broad availability, noninvasiveness and good sensitivity explain why it plays a capital role in the very beginning of the process of diagnosis for every patient, with or without cardiac-related complaints. For the practitioner, good training in ECG interpretation is mandatory. Sometimes, the ECG trace reveals particular aspects that may cause confusion and complicate decision-making. In this article, we present several less common situations underlying the general context and ECG features. The syndromes studied have a high pathological significance and may range from acute emergencies that call for a rapid therapeutical response to chronic syndromes that require prolonged observation, monitoring and risk stratification.

Atrial fibrillation (AF) is a supraventricular arrhythmia and the most common heart rhythm disorder in the adult population worldwide with an estimated prevalence of 2% to 4% of the population. Cases of AF have shown an increasing trend in recent decades, while its frequency is expected to rise even more. Given the significant impact on patients’ quality of life, as well as its major complications, including thromboembolic events, effective rhythm control strategies other than antiarrhythmic medication have emerged, with catheter ablation (CA) being the cornerstone of these. In recent years, CA has been upgraded to a first-line treatment for selected patients. However, complications do exist and arrhythmia-free survival is not always guaranteed. The need to better identify patients more suitable for this specific therapeutic measure is crucial in improving outcomes and preventing arrhythmia recurrences. This review aims to present currently identified predictors of AF recurrence after catheter ablation based on clinical characteristics and electrocardiographic and echocardiographic parameters, in an era of increasing interventional rhythm control approaches for the management of atrial fibrillation.

Anabolic–androgenic steroids (AASs) are synthetic derivatives of testosterone and are increasingly misused to enhance muscle growth and physical performance, particularly among athletes and recreational bodybuilders. Although AASs affect multiple organ systems, their severe and potentially life-threatening complications involve the cardiovascular system. This review summarizes current knowledge on the pathophysiological mechanisms and clinical manifestations of AAS-induced cardiomyopathy. Chronic supraphysiologic AAS use promotes cardiac injury and adverse cardiac remodeling via oxidative stress, androgen receptor overactivation, RAAS dysregulation, and pro-apoptotic signaling. These changes could lead to hypertension, dyslipidemia and atherosclerosis, myocardial fibrosis and hypertrophy, arrhythmias, heart failure, and kidney injury. Vascular dysfunction, increased arterial stiffness, and a prothrombotic state further compound the cardiovascular risks. Diagnostic approaches involve biomarker evaluation, echocardiography, and cardiac magnetic resonance imaging, revealing structural and functional cardiac abnormalities such as reduced ejection fraction, concentric hypertrophy, myocardial fibrosis, and impaired diastolic function. Although cessation of AAS use may lead to partial or complete reversal of cardiac dysfunction in some individuals, others may experience irreversible myocardial damage. The reversibility appears to depend on dosage, duration of exposure, and early intervention. This review explores the cardiovascular consequences of AAS use, with a focus on the mechanisms, diagnosis, and management of AAS-induced cardiomyopathy, and underlines the importance of education and early detection.

We performed a network meta-analysis of randomized trials comparing non-vitamin K antagonist oral anticoagulant (NOAC)-based versus vitamin K antagonists (VKA)-based regimens in patients with atrial fibrillation (AF) and acute coronary syndromes or PCI, aiming to examine the precise impact of recently established antithrombotic strategies on major bleeding as primary end-point and other safety and efficacy as secondary end-points. A literature search was conducted for randomized controlled trials. Our search took place in three major databases. The primary end point of our study was bleeding. To combine direct and indirect evidence across trials, a frequentist network meta-analysis with a random-effects model was used. Five studies were eligible for the meta-analysis enrolling a total of 11542 patients. Five studies (N=4903 patients) contributed to the network. Compared to the triple antithrombotic therapy (TAT) based VKA, only the dual antithrombotic therapy (DAT) based NOAC reduced the bleeding (RR 0.57, 95%CI 0.40-0.82). There was no difference between DAT based VKA (RR=0.66, 95%CI=0.40-1.09) or TAT based NOAC (RR=0.80, 95%CI=0.43-1.49). DAT based NOAC ranked best (P-score=0.91), followed by DAT based VKA (P-score=0.67), TAT based NOAC (P-score=0.40) and TAT based VKA (P-score=0.03). The network meta-analysis of four antithrombotic strategies, demonstrated that in patients with AF undergoing PCI the combination of DAT based NOAC is associated with a significantly lower risk of major bleeding events. This strategy does not seem to be less effective in terms of prevention of ischemic events compared to the other regimens.

Arterial hypertension is highly prevalent among individuals with chronic kidney disease (CKD), exhibiting a bidirectional association and playing a critical role in the progression of renal dysfunction. CKD affects approximately 10–12% of the global population and is often a common comorbidity in patients with true resistant hypertension. The sympathetic nervous system (SNS) plays a key role in the pathophysiological cascade of CKD-mediated hypertension. Current pharmacological therapies do not directly target SNS overactivity, highlighting the need for alternative approaches. Renal denervation (RDN), an interventional procedure that modulates both afferent and efferent renal nerve signaling, has emerged as a promising strategy for resistant hypertension with multiple pleiotropic benefits. Both preclinical and clinical trial data indicate that RDN is safe, with no significant deterioration of renal function reported in both early-stage CKD and end-stage renal disease (ESRD), as well as effective in reducing both office and ambulatory blood pressure in most studies. This review examines the pathophysiological basis for SNS overactivity in CKD, summarizes preclinical and clinical data on the safety and efficacy of RDN in this population, and discusses ongoing and future trials that may further clarify the role of RDN in CKD management and its long-term impact on renal and cardiovascular outcomes.