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.

Hypertrophic cardiomyopathy (HCM) is characterized by excessive growth of myocardial tissue, most commonly due to genetic mutations in sarcomere proteins. This can lead to complications such as heart failure, mitral regurgitation, syncope, arrhythmias, sudden cardiac death, and myocardial ischemia. While we have come a long way in our understanding of the pathophysiology, genetics, and epidemiology of HCM, the past 10 years have seen significant advancements in diagnosis and treatment. As the body of evidence on hypertrophic cardiomyopathy continues to grow, a comprehensive review of the current literature is an invaluable resource in organizing this knowledge. By doing so, the vast progress that has been made thus far will be widely available to all experts in the field. This review provides a comprehensive analysis of the scientific literature, exploring both well-established and cutting-edge diagnostic and therapeutic options. It also presents a unique perspective by incorporating topics such as exercise testing, genetic testing, radiofrequency ablation, risk stratification, and symptomatic management in non-obstructive HCM. Lastly, this review highlights areas where current and future research is at the forefront of innovation in hypertrophic cardiomyopathy.

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.

Hypertrophic cardiomyopathy is the most prevalent inherited cardiac condition, distinguished by an autosomal dominant inheritance pattern. Diagnosis can be achieved through echocardiography, cardiac magnetic resonance imaging, and genetic testing. Recently, significant advancements have occurred in pharmacological and invasive therapies that are transforming the management of hypertrophic cardiomyopathy, including the introduction of cardiac myosin inhibitors, radiofrequency ablation, and gene editing. Additional trials are being conducted on investigational therapies, with the results anticipated in the near future. This review aims to provide a concise overview of both currently approved and investigational treatments for hypertrophic cardiomyopathy.

Remdesivir is an antiviral drug recommended for the treatment of COVID-19. The therapeutic benefits of remdesivir remain under investigation, with further literature emerging regarding its cardiac side-effect profile. The objective of this study was to investigate the association of remdesivir with bradycardia using a propensity score-matched analysis. Secondary outcomes included assessing in-patient mortality and hospital length of stay following remdesivir treatment for COVID-19. A single-institution retrospective study investigating treatment with and without remdesivir in 645 patients admitted for COVID-19 management was performed. Following treatment with remdesivir, patients were analyzed for episodes of bradycardia, defined in this study as 2 consecutive episodes of a heart rate <60 beats per minute. Matched cohorts were generated after controlling for potential confounders associated with remdesivir exposure. Subsequently, a propensity score-matched analysis was conducted to minimize selection bias and to account for the characteristics between the 2 comparison groups. In a sample of 645 COVID-19 patients, 58% were in the treatment group (Remdesivir+) and 42% were in the control group (Remdesivir-). 59% were males with a mean age of 57 ± 14.5 years. After propensity score matching, the remdesivir + group had a higher incidence of bradycardia (48.5% vs 30.7%, P = .028). The remdesivir + group was found to have a lower rate of in-patient mortality (1.0% vs 3.0% P < .001) and longer in-patient length of stay (13.7 vs 6.3 days, P < .001) compared to the remdesivir- group. Patients with COVID-19 had a greater prevalence of bradycardia following treatment with remdesivir. For these patients, remdesivir reduced in-patient mortality compared with untreated COVID-19 patients.

Although arrhythmogenic right ventricular cardiomyopathy (ARVC) has been a well-described entity, the condition still remains a growing topic in research. 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 nonsustained ventricular tachycardia to sudden cardiac death. Its prevalence has been estimated to range between 1 in every 1000-5000 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. Known and newer discoveries of gene variants predisposing patients to ARVC have led to established screening techniques while providing insight into genetic counseling and management. This review will cover important information regarding the genetics and pathophysiology of 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.