Brugada syndrome (BrS) is an inherited cardiac channelopathy with variable expressivity that can lead to sudden cardiac arrest (SCA). Studies worldwide suggest that BrS and Brugada pattern (BrP) have low prevalences in general. However, studies also note that BrS is most prevalent among certain Asian populations. Among the different global regions, the highest prevalence is believed to be in Southeast Asia, followed by the Middle East, South Asia, East Asia, Europe, and North America. It is not only important to recognize such varying degrees of BrS prevalence within Asia but also to understand that there may be significant differences in terms of presenting symptoms, occult risk factors, and the impact on clinical outcomes. The importance of identifying such differences lies in the necessity to develop improved risk assessment strategies to guide secondary prevention and treatment for these patients. Specifically, the decision to pursue placement of an implantable cardiac defibrillator (ICD) can be lifesaving for high-risk BrS patients. However, there remains a significant lack of consensus on how to best risk stratify BrS patients. While the current guidelines recommend ICD implantation in patients with spontaneous Type 1 ECG pattern BrS who present with syncope, there may still exist additional clinical factors that may serve as better predictors or facilitate more refined risk stratification before malignant arrhythmias occur. This carries huge relevance given that BrS patients often do not have any preceding symptoms prior to SCA. This review seeks to delineate the differences in BrS presentation and prevalence within the Asian continent in the hope of identifying potential risk factors to guide better prognostication and management of BrS patients in the future.

Acute myocardial infarction remains a significant cause of mortality worldwide and its burden continues to grow. Its pathophysiology is known to be complex and multifactorial, with several acquired and inherited risk factors. As advances in technology and medical therapy continue, there is now increasing recognition of the role that genetics play in the development and management of myocardial infarction. The genetic determinants of acute coronary syndrome are still vastly understudied, but the advent of whole-genome scanning and genome-wide association studies has significantly expanded the current understanding of genetics and simultaneously fostered hope that genetic profiling and gene-guided treatments could substantially impact clinical outcomes. The identification of genes associated with acute myocardial infarction can help in the development of personalized medicine, risk stratification, and improved therapeutic strategies. In this context, several genes have been studied, and their potential involvement in increasing the risk for acute myocardial infarction is being investigated. As such, this article provides a review of some of the genes potentially related to an increased risk for acute myocardial infarction as well as the latest updates in gene-guided risk stratification and treatment strategies.

Infective endocarditis (IE) is an uncommon but life-threatening condition characterized by infection and inflammation of the endocardial surface of the heart, most commonly affecting native or prosthetic valves. Recent data indicate in-hospital mortality rates ranging from 15% to 25%, with evidence of increasing mortality even in high-income countries. Beyond its fatal potential, IE poses a major public health burden, accounting for over 1.7 million disability-adjusted life years (DALYs) globally in 2019. This review aims to discuss recent advancements in the diagnosis and management of IE given the shifting epidemiology and pathogen profile of the disease. There is a rising incidence of healthcare-associated IE and an expanding population of vulnerable patients, including the elderly and those with prosthetic material or indwelling catheters. Diagnostic capabilities have rapidly advanced with the adoption of modalities such as 18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT), cardiac CT, and cardiac magnetic resonance (CMR), particularly in patients with prosthetic valve endocarditis or culture-negative presentations. Additionally, the expanding indications for surgical intervention and increasing antimicrobial resistance have added complexity to management decisions. These developments underscore the need for a comprehensive review to support healthcare providers in navigating the modern diagnostic and therapeutic landscape of IE.

Patients with a clinical indication for aortic valve replacement can either undergo surgical aortic valve replacement (SAVR) or Transcatheter Aortic Valve Implantation (TAVI). There are many different factors that go into determining which type of replacement to undergo, including age, life expectancy, comorbidities, frailty, and patient preference. While both options offer significant benefits to patients in terms of clinical outcomes and quality of life, there is growing interest in expanding the indications for TAVI due to its minimally invasive approach. However, it is worth noting that there are several discrepancies in TAVI outcomes in regards to various endpoints, including death, stroke, and major cardiovascular events. It is unclear why these discrepancies exist, but potential explanations include the diversity of etiologies for aortic stenosis, complex patient comorbidities, and ongoing advancements in both medical therapies and devices. Of these possibilities, we propose that phenotypic variation of aortic stenosis has the most significant impact on post-TAVI clinical outcomes. Such variability in phenotypes is often due to a complex interplay between underlying comorbidities and environmental and inherent patient risk factors. However, there is growing evidence to suggest that patient genetics may also play a role in aortic stenosis pathology. As such, we propose that the selection and management of TAVI patients should emphasize a precision medicine approach.