Obstructive sleep apnea (OSA) is an increasingly relevant cause of cardiovascular morbidity worldwide. Although the association between OSA and the cardiovascular system is well-known, the extent of its effects is still a topic of interest, including pathophysiologic mechanisms, cardiovascular sequelae, and OSA therapies and their effects. Commonly described mechanisms of cardiovascular etiologies revolve around sympathetic activation, inflammation, and intermittent hypoxia resulting from OSA. Ultimately, these effects lead to manifestations in the cardiovascular system, such as arrhythmias, hypertension, and heart failure, among others. The resulting sequelae of OSA may also have differential effects based on gender and age; several studies suggest female gender to have more susceptibility to cardiovascular mortality, as well as an increase in age. Furthermore, several therapies for OSA, both established and emerging, show a reduction in cardiovascular morbidity and may even reduce cardiovascular burden. Namely, the establishment of CPAP has led to improvement in hypertension and cardiac function in patients with heart failure and even reduced the progression of early stages of atherosclerosis. Effective management of OSA decreases abnormal neural sympathetic activity, which results in better rhythm control and blood pressure control, both in waking and sleep cycles. With newer therapies for OSA, its effects on the cardiovascular system may be significantly reduced or even reversed after long-term management. The vast extent of OSA on the cardiovascular system, as well as current and future therapeutic strategies, will be described in detail in this review.

Atherosclerosis, a condition characterized by the accumulation of lipids and a culprit behind cardiovascular events, has long been studied. However, in recent years, there has been an increase in interest in its initiation, with researchers shifting focus from traditional pathways involving the vascular infiltration of oxidized lipids and towards the novel presence of chronic inflammatory pathways. The accumulation of pro-inflammatory cytokines, in combination with the activation of transcription factors, creates a positive feedback loop that drives the creation and progression of atherosclerosis. From the upregulation of the nod-like receptor protein 3 (NLRP3) inflammasome and the Notch and Wnt pathways to the increased expression of VEGF-A and the downregulation of connexins Cx32, Cx37, and Cx40, these processes contribute further to endothelial dysfunction and plaque formation. Herein, we aim to provide insight into the molecular pathways and mechanisms implicated in the initiation and progression of atherosclerotic plaques, and to review the risk factors associated with their development.

Non-pharmacological therapies play an essential role in the management of heart failure, complementing pharmacological treatments to mitigate disease progression and improve patient outcomes. This review provides an updated perspective on non-pharmacological interventions with a focus on lifestyle modifications, device therapies, and the management of heart failure in special populations, such as the elderly, women, and patients with comorbid conditions like renal dysfunction and diabetes. Key lifestyle interventions, including sodium and fluid restriction, dietary changes, and physical activity, are explored for their impact on symptom reduction, hospital readmissions, and quality of life. Device therapies like cardiac resynchronization therapy (CRT) and implantable cardioverter defibrillators (ICD) are also evaluated for their effectiveness in reducing mortality in patients with advanced HF. Special attention is given to vulnerable populations, emphasizing the need for individualized approaches tailored to specific pathophysiological mechanisms and socioeconomic factors. By integrating these strategies, healthcare providers can optimize care and enhance patient adherence, reducing the overall burden of heart failure.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by structural abnormalities, arrhythmias, and a spectrum of genetic and clinical manifestations. Clinically, ARVC is structurally distinguished by right ventricular dilation due to increased adiposity and fibrosis in the ventricular walls, and it manifests as cardiac arrhythmias ranging from non-sustained ventricular tachycardia to sudden cardiac death. Its prevalence has been estimated to range from 1 in every 1000 to 5000 people, with its large range being attributed to the variability in genetic penetrance from asymptomatic to significant burden. It is even suggested that the prevalence is underestimated, as the presence of genotypic mutations does not always lead to clinical manifestations that would facilitate diagnosis. Additionally, while set criteria have been in place since the 1990s, newer understanding of this condition and advancements in cardiac technology have prompted multiple revisions in the diagnostic criteria for ARVC. Novel discoveries of gene variants predisposing patients to ARVC have led to established screening techniques while providing insight into genetic counseling and management. This review aims to provide an overview of the genetics, pathophysiology, and clinical approach to ARVC. It will also focus on clinical presentation, ARVC diagnostic criteria, electrophysiological findings, including electrocardiogram characteristics, and imaging findings from cardiac MRI, 2D, and 3D echocardiogram. Current management options—including anti-arrhythmic medications, device indications, and ablation techniques—and the effectiveness of treatment will also be reviewed.

West Nile Virus (WNV) myocarditis is nearly fatal, according to the current medical literature. We report a previously healthy 37-year-old Caucasian male who presented to our facility with two days of progressive lower extremity weakness, fever, edema, and shortness of breath found to have left ventricular global hypokinesis with an ejection fraction of less than 25%, consistent with acute viral myocarditis. He also has concomitant WNV meningoencephalitis due to his altered mentation. He was found to have a positive serum WNV IgM suggestive of a diagnosis of WNV myocarditis. He was intubated and was placed on vasoactive pressors for supportive care due to evidence of mixed cardiogenic and septic shock. After two weeks of hemodynamic support, we discovered a near-complete cardiac recovery, as shown on a repeat transthoracic echocardiography (TTE) and a normalized mean arterial blood pressure. This is a unique case report because near fatality is often associated with WNV myocarditis secondary to tachyarrhythmia, and there are currently no documented cases that are suggestive of cardiac recovery from the current literature.

Cardiogenic shock (CS) remains a significant clinical challenge with persistently high mortality rates. Defined by impaired cardiac output resulting in end-organ hypoperfusion, CS commonly arises from acute myocardial infarction (AMI-CS) or acute exacerbations of heart failure (HF-CS). The severity of CS is classified by the Society for Cardiovascular Angiography and Interventions (SCAI) into stages A (at risk) through E (extremis), which informs treatment strategies, including pharmacotherapy and mechanical circulatory support (MCS). Recent advancements in percutaneous mechanical circulatory support devices, including intra-aortic balloon pumps (IABPs), Impella devices, TandemHeart, Protek-Duo, and veno-arterial extracorporeal membrane oxygenation (VA-ECMO), have transformed management paradigms by offering targeted hemodynamic support. While DanGer-SHOCK, a pivotal randomized trial, demonstrated improved outcomes with early Impella use in anterior STEMI-associated CS, the trial’s focus population and center expertise suggest that its findings should be interpreted in the context of broader AMI-CS and HF-CS presentations. Device selection is guided by shock severity, anatomical considerations, comorbidities, and institutional capabilities. This review synthesizes current evidence, evaluates the clinical utility and efficacy of existing and emerging percutaneous MCS technologies, and highlights ongoing clinical trials and future directions in optimizing CS management. Emphasis is placed on individualized patient selection, evidence-based deployment of MCS devices, and multidisciplinary team collaboration, which collectively represent a critical transition towards improving clinical outcomes in CS.