Korean Circulation Journal最新文献

Background and objectives: Rapid reduction of low-density lipoprotein cholesterol (LDL-C) in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI) is critical but challenging. This study evaluated the efficacy and safety of early triple lipid-lowering therapy with evolocumab, a moderate-intensity statin, and ezetimibe in statin-naïve ACS patients.

Methods: The C-STAR trial (Effect of Early Initiation of Evolocumab on Lipid Profile Changes in Patients with ACS Undergoing PCI) was a single-center, randomized, open-label trial conducted from December 2022 to January 2025. A total of 108 statin-naïve ACS patients undergoing PCI were randomized to evolocumab (140 mg) plus rosuvastatin 5 mg and ezetimibe 10 mg (n=54) or rosuvastatin 5 mg and ezetimibe 10 mg alone (n=54). The primary endpoint was LDL-C level at 2 weeks; cognitive safety was assessed using the Everyday Cognition (ECog) tool.

Results: Baseline LDL-C levels were similar between the 2 groups. At 2 weeks, LDL-C levels were lower in the evolocumab group compared to the non-evolocumab group (31±16 mg/dL vs. 63±17 mg/dL; p<0.001), with a greater percentage reduction (-77.5% vs. -53.3%, p<0.001). Target achievement rates were also higher in the evolocumab group (84.6% vs. 26.9%, p<0.001). Comparable cognitive functions were observed using ECog questionnaire (23.9±3.4 vs. 24.5±5.5; p=0.493).

Conclusions: Early initiation of evolocumab in combination therapy achieved greater LDL-C reduction and target achievement in ACS patients undergoing PCI.

Trial registration: ClinicalTrials.gov Identifier:NCT05661552.

Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis (CAVS), with plasma levels largely unaffected by lifestyle modification or conventional lipid-lowering therapy. Although international guidelines increasingly recognize Lp(a) as a risk-enhancing factor, in many Asian populations thresholds for high Lp(a) and treatment strategies remain undefined. This Korean position paper, developed by the Lp(a) Task Force of the Korean Society of Lipid and Atherosclerosis, presents an evidence-based summary of the pathophysiology, clinical relevance, and therapeutic landscape surrounding Lp(a), with a focus on Korean-specific data. It reviews the genetic architecture of Lp(a), ethnic variability in concentrations, and its mechanistic roles in inflammation, thrombosis, and calcification. Based on large Korean cohorts, a 3-tiered classification is proposed of normal (<30 mg/dL), borderline high (30-49 mg/dL), and high (≥50 mg/dL), harmonizing global thresholds with local data. The document also highlights the limitations of current Lp(a) assays in Korea, and calls for standardized, isoform-insensitive testing. Novel therapeutics, including antisense oligonucleotides, small interfering RNAs, and small molecular inhibitors, have shown promising Lp(a)-lowering effects, with multiple phase 3 trials currently ongoing, or in planning. Given the unmet clinical need, the paper recommends incorporating Lp(a) into cardiovascular risk assessment, and calls for Korean-specific longitudinal studies, national screening strategies, and participation in clinical trials. These efforts will help clarify Lp(a)-associated risk in Korean patients and guide the adoption of future targeted therapies.

Background and objectives: Distal radial access (DRA) has been recognized as an alternative to conventional radial access, with potential puncture sites at the anatomical snuffbox and on the dorsum of the hand. However, the optimal puncture site remains unknown. This study aims to evaluate the efficacy and safety of DRA at these two sites.

Methods: This analysis was performed using the KODRA (Korean Prospective Registry for Evaluating the Safety and Efficacy of Distal Radial Approach) registry. The primary efficacy endpoint was defined as successful puncture and completion of the coronary procedure without access-site crossover, while the primary safety endpoint was the DRA-related bleeding.

Results: A total of 4,977 and 4,644 patients were included in efficacy and safety analyses, respectively. DRA via the anatomical snuffbox improved the primary efficacy endpoint (odds ratio [OR], 2.358; 95% confidence interval [CI], 1.800-3.090; p<0.001), but did not differ from the dorsum of the hand approach in the primary safety endpoint (OR, 1.305; 95% CI, 0.792-2.150; p=0.296). The anatomical snuffbox approach was also associated with higher puncture success rates (OR, 2.244; 95% CI, 1.672-3.010; p<0.001), but with an increased rate of prolonged hemostasis >180 minutes (OR, 15.002; 95% CI, 7.708-29.197; p<0.001).

Conclusions: Compared to the dorsum of the hand approach, DRA via the anatomical snuffbox demonstrated higher procedural efficacy, but was associated with prolonged hemostasis, without an increase in DRA-related bleeding. Further research is needed to determine the optimal site for DRA.

Background and objectives: Aortic stenosis (AS) is a prevalent valvular heart disease that is increasing due to aging population and longer life expectancy. While most individuals have a tricuspid aortic valve (TAV), some are congenitally born with a bicuspid aortic valve (BAV). The mechanisms underlying AS pathogenesis remain unclear, limiting advancements in clinical treatment and biomedical research. This study aimed to identify differentially expressed protein (DEPs) in aortic valve interstitial cells (VICs) from AS patients with TAV and BAV using quantitative proteomic analysis.

Methods: VICs were isolated from AS patients with TAV (n=10) and BAV (n=10), as well as from normal aortic valves of heart transplant patients (TAV, n=11). Spectral library generation was performed using a data-dependent acquisition approach, followed by data-independent acquisition analysis. Immunohistochemical staining validated key DEPs.

Results: A total of 39 DEPs were identified, including 13 upregulated and 26 downregulated proteins. These were categorized into 4 groups: cellular structural protein (keratin family, SYNPO, PFDN1, COL5A1); kinase and transferase (OXSR1, DNMT1), mitochondrial-related proteins (SOD2, SQOR), and calcification-related proteins (SPARC, MXRA7, PTMA). Comparative analysis revealed 5 common DEPs in TAV- and BAV-AS, including SQOR, 20 TAV-AS-specific proteins (e.g., keratin family, oxidoreductase-related proteins), and 3 BAV-AS-specific proteins (e.g., SPARC, PTMA).

Conclusions: This proteomic analysis identified potential molecular targets associated with AS pathogenesis, providing a foundation for further research on disease mechanism and therapeutic development.

Background and objectives: Substantial efforts have been made to categorize the diverse and broad population of individuals with primary hypertension into more defined, homogeneous subgroups according to their hormonal responses to biological stimuli, such as low-renin hypertension. This study aimed to explore the phenotype and prognosis of patients with untreated primary hypertension with high renin and aldosterone levels.

Methods: In this study, we explored hypertensive phenotypes related to renin and aldosterone levels in untreated patients with primary hypertension (n=747). Patients were stratified into 4 groups on the basis of plasma renin activity (≥1.0 ng/mL/hr or <1.0 ng/mL/hr) and the plasma aldosterone concentration (≥15 ng/dL or <15 ng/dL).: high renin and aldosterone (n=172), low renin and high aldosterone (n=70), high renin and low aldosterone (n=308), and low renin and aldosterone (n=196).

Results: Multinomial logistic regression analysis revealed that younger age (p<0.001), higher pulse rates (p=0.002), and greater nighttime systolic blood pressure (p=0.046) were independent predictors of high renin and aldosterone levels. Microalbuminuria (25.5%, p<0.001) and elevated uric acid levels (5.5±1.4 mg/dL, p=0.006) were also more prevalent in this group.

Conclusions: These findings highlight the importance of stratifying hypertensive phenotypes to enable personalized treatment for primary hypertensives with elevated renin and aldosterone levels.

Background and objectives: The 2022 revised pulmonary hypertension guidelines emphasize risk stratification to enhance outcomes, necessitating investigation into adherence. This study aimed to examine the treatment patterns of patients in the Pulmonary Arterial Hypertension (PAH) Platform for deep Phenotyping in Korean Subjects (PHOENIKS) study cohort.

Methods: A total of 321 patients from the PHOENIKS cohort were included, consisting of 101 patients in phase 1 (2018-2020) and 220 in phase 2 (2021-2023). A total of 275 patients with either idiopathic PAH or associated PAH were included in the final analysis. Risk assessment was conducted utilizing an online calculator that integrates multiple validated risk stratification models. Adherence to the revised guidelines was evaluated, and survival outcomes were analyzed over the study period.

Results: The cohort consisted primarily of middle-aged and female patients (mean age 51.96±15 years, 71% female). A total of 53% had idiopathic PAH and 47% had associated PAH. Intermediate-risk patients comprised 62% of the cohort during the initial diagnosis. The proportion of low-risk patients increased from 34% to 64% throughout the follow-up period. Adherence to the revised guidelines slightly improved during the study period, though only 26% of patients demonstrated compliance. The one-year survival rate was 96%, whereas the 3-year survival rate was 87%.

Conclusions: The current Korean PAH treatment strategy must be improved to align with the revised guidelines and optimize patient outcomes. Further efforts are needed to change health insurance coverage criteria to enhance guideline adherence.