Ischemia with Nonobstructive Coronary Artery Disease and Atrial Cardiomyopathy-Two Sides of the Same Story?

Ischemia with nonobstructive coronary artery disease (INOCA) is increasingly recognized as a significant cause of angina, myocardial remodeling, and eventually heart failure (HF). Coronary microvascular dysfunction (CMD) is a major endotype of INOCA, and it is caused by structural and functional alterations of the coronary microcirculation. At the same time, atrial cardiomyopathy (ACM) defined by structural, functional, and electrical atrial remodeling has a major clinical impact due to its manifestations: atrial fibrillation (AF), atrial thrombosis, stroke, and HF symptoms. Both these pathologies share similar risk factors and have a high comorbidity burden. CMD causing INOCA and ACM frequently coexist. Thus, questions arise whether there is a potential link between these pathologies. Does CMD promote AF or the reverse? Which are the mechanisms that ultimately lead to CMD and ACM? Are both part of a systemic disease characterized by endothelial dysfunction? Lastly, which are the therapeutic strategies that can target endothelial dysfunction and improve the prognosis of patients with CMD and ACM? This review aims to address these questions by analyzing the existing body of evidence, offering further insight into the mechanisms of CMD and ACM, and discussing potential therapeutic strategies.

Cardiac Reverse Remodeling in Ischemic Heart Disease with Novel Therapies for Heart Failure with Reduced Ejection Fraction.

Despite the improvements in the treatment of coronary artery disease (CAD) and acute myocardial infarction (MI) over the past 20 years, ischemic heart disease (IHD) continues to be the most common cause of heart failure (HF). In clinical trials, over 70% of patients diagnosed with HF had IHD as the underlying cause. Furthermore, IHD predicts a worse outcome for patients with HF, leading to a substantial increase in late morbidity, mortality, and healthcare costs. In recent years, new pharmacological therapies have emerged for the treatment of HF, such as sodium-glucose cotransporter-2 inhibitors, angiotensin receptor-neprilysin inhibitors, selective cardiac myosin activators, and oral soluble guanylate cyclase stimulators, demonstrating clear or potential benefits in patients with HF with reduced ejection fraction. Interventional strategies such as cardiac resynchronization therapy, cardiac contractility modulation, or baroreflex activation therapy might provide additional therapeutic benefits by improving symptoms and promoting reverse remodeling. Furthermore, cardiac regenerative therapies such as stem cell transplantation could become a new therapeutic resource in the management of HF. By analyzing the existing data from the literature, this review aims to evaluate the impact of new HF therapies in patients with IHD in order to gain further insight into the best form of therapeutic management for this large proportion of HF patients.

Left Ventricular Remodeling after Myocardial Infarction: From Physiopathology to Treatment.

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.

Role of Diphosphonates Bone Scintigraphy in Correlation with Biomarkers for a Personalized Approach to ATTR Cardiac Amyloidosis in North-Eastern Romania.

Transthyretin cardiac amyloidosis (ATTR) is a rare cardiac protein deposition disease characterized by progressive thickening of both ventricles, the inter-atrial-ventricular septum and the atrioventricular valves. The gold standard method for diagnosing this rare pathology is endomyocardial biopsy. If this method cannot be used, the alternative is a mixture of clinical and paraclinical tests. Over the course of five years, we examined 58 patients suspected of cardiac amyloidosis based on electrocardiography and ultrasonography criteria, who had been sent for bone scintigraphy in order to determine the presence of ATTR cardiac amyloidosis. However, the final diagnosis was set by correlating the bone scan with genetic testing, free light chain dosage or soft tissue biopsy. Based on the final diagnosis we analyzed the patients' predominant biomarkers in order to determine a possible correlation between them. This analysis is designed to help the general practitioner set a possible cardiac amyloidosis diagnosis.

A Rare Entity-Percutaneous Lead Extraction in a Very Late Onset Pacemaker Endocarditis: Case Report and Review of Literature.

The number of infections related to cardiac implantable electronic devices (CIEDs) has increased as the number of devices implanted around the world has grown exponentially in recent years. CIED complications can sometimes be difficult to diagnose and manage, as in the case of lead-related infective endocarditis. We present the case of a 48-year-old male diagnosed with Staphylococcus aureus device-related infective endocarditis, 12 years after the implant of a single chamber pacemaker. A recent history of the patient includes two urinary catheterizations due to obstructive uropathy in the context of a prostatic adenoma, 2 months previously, both without antibiotic prophylaxis; no other possible entry sites were found and no history of other invasive procedures. After initiation of antibiotic therapy according to antibiotic susceptibility testing, we decided to remove the right ventricular passive fixation lead along with the vegetation and pacemaker generator; because of severe lead adhesions in the costoclavicular region, and especially in the right ventricle, we needed mechanical sheaths to remove the abundant fibrous tissue that encompassed the lead. After a difficult, but successful, lead extraction along with a large vegetation and 6 weeks' antibiotic therapy, the clinical and biological evolution was favorable, without reappearance of symptoms. While very late lead endocarditis is a rarity, late lead-related infective endocarditis (more than 12 months elapsed since implant) is not an exception; this is why we find that endocarditis prophylaxis should be reconsidered in certain patient categories, our patient being proof that procedures with neglectable endocarditis risk according to the guidelines can lead to bacterial endocarditis.

Persistent Left Superior Vena Cava with Absent Right Superior Vena Cava and Discrete Subaortic Stenosis Diagnosed in a Patient with Sick Sinus Syndrome: A Case Report and Brief Review of the Literature.

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.