Background and Objectives: Heart failure (HF) imposes a significant global burden, yet awareness and implementation of guideline-directed management remain suboptimal. This study evaluated HF awareness, diagnostic patterns, and therapeutic strategies among physicians in Korea. Methods: A nationwide online survey was conducted from July to August 2019, targeting primary care physicians (PCPs; n=8,000) and hospital-based cardiology specialists (n=1,339) across Korea. The questionnaire comprised 23 items covering baseline characteristics, perceptions of HF prognosis, diagnostic approaches, and treatment practices. Results: A total of 543 physicians responded (209 PCPs and 334 cardiology specialists). While the majority correctly defined HF, a substantial proportion underestimated the lifetime risk and poor prognosis. Cardiology specialists were more likely than PCPs to use objective diagnostic tools, including echocardiography (97% vs. 61%, p<0.001) and natriuretic peptide testing (90% vs. 57%, p<0.001). Among PCPs, 29% reported diagnosing HF based on symptoms and physical findings without objective testing, and 27% reported referring patients to general hospitals for diagnostic evaluation. Prescription rates for guideline-directed medical therapies, including renin-angiotensin system blockers and beta-blockers, were consistently higher among cardiology specialists.PCPs more frequently cited advanced age as a barrier to prescribing evidence-based medications. Conclusions Physicians’ awareness and clinical practices regarding HF in Korea remain suboptimal. Given the growing burden, high mortality, and substantial costs of HF, early detection, appropriate diagnostic evaluation, and timely referral are essential. Targeted education and system-level strategies to improve guideline implementation, particularly in primary care settings, are warranted.

Inclisiran and bempedoic acid (BA) are non-statin lipid-lowering agents that have been approved for use in the US and Europe. Inclisiran, a subcutaneously administered small interfering RNA targeting proprotein convertase subtilisin/kexin type 9 messenger RNA, is effectively delivered to the liver via lipid nanoparticles and conjugation. In several phase 3 trials, it has successfully reduced low-density lipoprotein cholesterol (LDL-C) by 50% and has an acceptable safety profile. Currently, the results of clinical outcome studies are awaited. While it is indicated for both primary and secondary cardiovascular prevention, it is selectively recommended after statin-based regimens. BA, an oral inhibitor of adenosine triphosphate-citrate lyase, decreases cholesterol production and enhances LDL uptake by hepatocytes. This enzyme is absent in muscle cells, and BA has fewer muscle-related adverse events. In clinical trials, it lowered LDL-C by 17%–21% compared to placebo and showed a clinical outcome benefit in patients with statin intolerance. This agent modestly increases the incidence of gout and cholelithiasis. For primary and secondary prevention, it may be recommended as a non-first-line agent, either alone or in combination therapy.

Inclisiran and bempedoic acid (BA) are non-statin lipid-lowering agents that have been approved for use in the US and Europe. Inclisiran, a subcutaneously administered small interfering RNA targeting proprotein convertase subtilisin/kexin type 9 messenger RNA, is effectively delivered to the liver via lipid nanoparticles and conjugation. In several phase 3 trials, it has successfully reduced low-density lipoprotein cholesterol (LDL-C) by 50% and has an acceptable safety profile. Currently, the results of clinical outcome studies are awaited. While it is indicated for both primary and secondary cardiovascular prevention, it is selectively recommended after statin-based regimens. BA, an oral inhibitor of adenosine triphosphate-citrate lyase, decreases cholesterol production and enhances LDL uptake by hepatocytes. This enzyme is absent in muscle cells, and BA has fewer muscle-related adverse events. In clinical trials, it lowered LDL-C by 17%–21% compared to placebo and showed a clinical outcome benefit in patients with statin intolerance. This agent modestly increases the incidence of gout and cholelithiasis. For primary and secondary prevention, it may be recommended as a non-first-line agent, either alone or in combination therapy.

Inclisiran and bempedoic acid (BA) are non-statin lipid-lowering agents that have been approved for use in the US and Europe. Inclisiran, a subcutaneously administered small interfering RNA targeting proprotein convertase subtilisin/kexin type 9 messenger RNA, is effectively delivered to the liver via lipid nanoparticles and conjugation. In several phase 3 trials, it has successfully reduced low-density lipoprotein cholesterol (LDL-C) by 50% and has an acceptable safety profile. Currently, the results of clinical outcome studies are awaited. While it is indicated for both primary and secondary cardiovascular prevention, it is selectively recommended after statin-based regimens. BA, an oral inhibitor of adenosine triphosphate-citrate lyase, decreases cholesterol production and enhances LDL uptake by hepatocytes. This enzyme is absent in muscle cells, and BA has fewer muscle-related adverse events. In clinical trials, it lowered LDL-C by 17%–21% compared to placebo and showed a clinical outcome benefit in patients with statin intolerance. This agent modestly increases the incidence of gout and cholelithiasis. For primary and secondary prevention, it may be recommended as a non-first-line agent, either alone or in combination therapy.

Inclisiran and bempedoic acid (BA) are non-statin lipid-lowering agents that have been approved for use in the US and Europe. Inclisiran, a subcutaneously administered small interfering RNA targeting proprotein convertase subtilisin/kexin type 9 messenger RNA, is effectively delivered to the liver via lipid nanoparticles and conjugation. In several phase 3 trials, it has successfully reduced low-density lipoprotein cholesterol (LDL-C) by 50% and has an acceptable safety profile. Currently, the results of clinical outcome studies are awaited. While it is indicated for both primary and secondary cardiovascular prevention, it is selectively recommended after statin-based regimens. BA, an oral inhibitor of adenosine triphosphate-citrate lyase, decreases cholesterol production and enhances LDL uptake by hepatocytes. This enzyme is absent in muscle cells, and BA has fewer muscle-related adverse events. In clinical trials, it lowered LDL-C by 17%–21% compared to placebo and showed a clinical outcome benefit in patients with statin intolerance. This agent modestly increases the incidence of gout and cholelithiasis. For primary and secondary prevention, it may be recommended as a non-first-line agent, either alone or in combination therapy.

Hypertension is a significant risk factor for a variety of cardiovascular diseases, including stroke, coronary artery disease, heart failure, and peripheral arterial disease. Achieving and maintaining a specific target blood pressure (BP) is crucial for effectively reducing the risk associated with these conditions. This involves customizing treatments to meet the individual needs of patients with hypertension, ensuring that each person receives the most appropriate care for their particular circumstances. Previously, based on the findings from the ACCORD (Action to Control Cardiovascular Risk in Diabetes) study conducted over the past decade, the target BP for patients with hypertension was set at <140/90 mmHg, regardless of the patient's risk profile. However, new insights from reanalyzed data of studies such as the SPRINT (Systolic Blood Pressure Intervention Trial), the STEP (Strategy of Blood Pressure Intervention in the Elderly Hypertensive Patients) study, and ACCORD subgroup reanalysis have led to a change in this approach. These studies support a more aggressive target BP of <130/80 mmHg, especially for high-risk patients. The purpose of this article is to offer a thorough review of these updated recommendations and to explain the reasoning behind the revised target BP guidelines for individuals with hypertension.

Coronary artery disease (CAD) remains the leading cause of mortality worldwide, driven primarily by atherogenesis. Recent efforts to understand sex differences in CAD have revealed distinct patterns in disease burden, risk factors, and clinical presentations. This review examines these sex differences in CAD, underscoring the importance of customized diagnostic and management strategies. Although men typically have higher rates of CAD prevalence and incidence, women face unique challenges, such as delayed diagnosis, atypical symptoms, and lower rates of medication prescription. Hormonal, genetic, and lifestyle factors all play a role in these disparities, with estrogen notably reducing CAD risk in women. Nontraditional risk factors, including chronic inflammation, psychological stress, socioeconomic status, and reproductive history, also contribute to CAD development and are often neglected in clinical settings. Addressing these differences requires increased awareness, more accurate diagnosis, and equitable healthcare access for both sexes. Furthermore, greater inclusion of women in CAD research is essential to better understand sex-specific mechanisms and optimize treatment outcomes. Personalizing CAD management based on sex-specific knowledge has the potential to improve prognosis and decrease disease incidence for both men and women.

Background/Aims: Sex differences in the prognosis of heart failure (HF) have yielded inconsistent results, and data from Asian populations are even rare. This study aimed to investigate sex differences in clinical characteristics and long-term prognosis among Korean patients with HF. Methods: A total of 5,625 Korean patients hospitalized for acute HF were analyzed using a prospective multi-center registry database. Baseline clinical characteristics and long-term outcomes including HF readmission and death were compared between sexes. Results: Women were older than men and had worse symptoms with higher N-terminal pro B-type natriuretic peptide levels. Women had a significantly higher proportion of HF with preserved ejection fraction (HFpEF). There were no significant differences in in-hospital mortality and rate of guideline-directed medical therapies in men and women. During median follow- up of 3.4 years, cardiovascular death (adjusted hazard ratio [HR], 1.38; 95% confidence interval [CI], 1.07–1.78; p = 0.014), and composite outcomes of death and HF readmission (adjusted HR, 1.13; 95% CI, 1.01–1.27; p = 0.030) were significantly higher in men than women. When evaluating heart failure with reduced ejection fraction (HFrEF) and HFpEF separately, men were an independent risk factor of cardiovascular death in patients with HFrEF. Clinical outcome was not different between sexes in HFpEF. Conclusions In the Korean multi-center registry, despite having better clinical characteristics, men exhibited a higher risk of all-cause mortality and readmission for HF. The main cause of these disparities was the higher cardiovascular mortality rate observed in men compared to women with HFrEF.

Heart failure with preserved ejection fraction (HFpEF) is prevalent and associated with a poor prognosis, imposing a significant burden on society. Arterial stiffness is increasingly recognized as a crucial factor in the pathophysiology of HFpEF, affecting diagnosis, management, and prognosis. As a hallmark of vascular aging, arterial stiffness contributes to increased afterload on the left ventricle (LV), leading to diastolic dysfunction, a key feature of HFpEF. Elevated arterial stiffness is linked with common cardiovascular risk factors in HFpEF, such as hypertension, diabetes and obesity, exacerbating the progression of disease. Studies have demonstrated that patients with HFpEF exhibit significantly higher levels of arterial stiffness compared to those without HFpEF, highlighting the value of arterial stiffness measurements as both diagnostic and prognostic tools. Moreover, interventions aimed at reducing arterial stiffness, whether through pharmacological therapies or lifestyle modifications, have shown potential in improving LV diastolic function and patient outcomes. Despite these advancements, the precise mechanisms by which arterial stiffness contributes to HFpEF are still not fully understood, necessitating the need for further research.