Myocardial infarction (MI) is the leading cause of death and morbidity worldwide, with an incidence relatively high in developed countries and rapidly growing in developing countries. The most common cause of MI is the rupture of an atherosclerotic plaque with subsequent thrombotic occlusion in the coronary circulation. This causes cardiomyocyte death and myocardial necrosis, with subsequent inflammation and fibrosis. Current therapies aim to restore coronary flow by thrombus dissolution with pharmaceutical treatment and/or intravascular stent implantation and to counteract neurohormonal activation. Despite these therapies, the injury caused by myocardial ischemia leads to left ventricular remodeling; this process involves changes in cardiac geometry, dimension and function and eventually progression to heart failure (HF). This review describes the pathophysiological mechanism that leads to cardiac remodeling and the therapeutic strategies with a role in slowing the progression of remodeling and improving cardiac structure and function.

A persistent left superior vena cava (PLSVC) is the most frequent anomaly of the venous drainage system. While both a right and left superior vena cava (SVC) are usually present, a unique, left-sided SVC, also known as an isolated PLSVC, accounts for only 10–20% of cases. It is frequently associated with arrhythmias and other congenital cardiac anomalies. Though it is usually an asymptomatic condition, it may pose significant problems whenever central venous access is needed. We report a case of an isolated PLSVC that was diagnosed incidentally during pacemaker implantation for sinus node dysfunction. The venous anomaly was associated with subvalvular aortic stenosis determined by a subaortic membrane; this particular association of congenital cardiovascular anomalies is a rare finding, with only a few cases reported in the literature. We aim to highlight the clinical and practical implications of this condition, as well as to discuss the embryonic development and diagnostic methods of this congenital defect.

Background: Infective endocarditis is a severe, life-threatening condition which affects the endocardial lining of the heart. Right-sided IE typically affects the tricuspid valve and, less commonly, the pulmonary valve, often in association with intravenous drug use and intracardiac devices. Enterococcus faecalis, a significant pathogen in healthcare settings, is frequently resistant to several antibiotics, complicating treatment. Results: We present the case of a 69-year-old man diagnosed with isolated pulmonary valve endocarditis, with no identifiable risk factors, good oral hygiene, and no recent dental procedures. In our case, the E. faecalis strain, initially susceptible to ampicillin, acquired resistance during high-dose ampicillin and gentamicin therapy, leading to cardiac surgery and prolonged antibiotic treatment. Conclusions: IPE is rare, emphasizing the need for heightened clinical awareness and thorough diagnostic evaluation, especially in patients with endocarditis symptoms and known risk factors. Although ampicillin resistance in E. faecalis is uncommon, its emergence during treatment presents a challenge, necessitating careful antibiotic stewardship to improve outcomes.