Korean Circulation Journal最新文献

Background and objectives: Patients with severe aortic stenosis (AS) often have mitral annular calcification (MAC) and aortic arch calcification (AAC). We investigated the clinical significance of a MAC and extensive AAC in patients with AS requiring aortic valve replacement (AVR).

Methods: We retrospectively analyzed 636 patients with severe AS who underwent AVR (surgical or transcatheter) at our institution. Preoperative echocardiography and computed tomography were used to identify MAC, and chest radiographs were reviewed for AAC.

Results: Of the 636 patients, 133 (20.9%) had MAC, while 156 (24.5%) had extensive AAC (≥180°). Patients with MAC were older and more often female, with higher Society of Thoracic Surgeons scores and greater comorbidities. Over a median follow-up of 5.2 years, 157 patients (24.7%) died. In univariate analysis, the presence of any MAC and extensive AAC was associated with significantly higher mortality. In multivariable analysis, however, neither was an independent predictor of mortality. Instead, age, male sex, diabetes mellitus, chronic kidney disease (eGFR <60 mL/min/1.73 m²), and dialysis emerged as independent risk factors.

Conclusions: MAC and extensive AAC identify a subset of patients with severe AS who are older and have more comorbid disease. Management of such patients should focus on optimizing overall risk factors, and the presence of MAC or AAC alone should not exclude patients from life-saving AVR therapies.

Background and objectives: Tricuspid regurgitation (TR) is common in advanced heart failure patients undergoing left ventricular assist device (LVAD) implantation, yet its independent prognostic value and post-LVAD trajectory remain uncertain.

Methods: This retrospective single-center study included 178 patients who underwent LVAD implantation without concomitant tricuspid valve intervention (TVI) between 2012 and 2024. Patients were stratified based on preoperative echocardiography into non-significant TR (n=141) and significant (≥ moderate) TR (n=37). Primary outcomes were early right ventricular (RV) failure, all-cause mortality and heart failure hospitalization.

Results: Significant baseline TR independently predicted early RV failure (odds ratio, 2.38; 95% confidence interval, 1.04 to 5.70; p=0.041), but was not associated with long-term outcomes, including all-cause mortality or heart failure hospitalization. During follow-up, TR severity improved in 60% of patients and most patients achieved hemodynamic optimization regardless of baseline TR severity. Functional recovery was observed in both groups, with a greater tendency of 6-minute walk improvement in patients with significant TR (p=0.057).

Conclusions: Baseline moderate-to-severe TR predicts early RV failure but not long-term adverse outcomes following LVAD implantation. Most patients experience spontaneous TR improvement and achieve similar hemodynamic optimization regardless of baseline TR severity. These findings suggest LVAD support alone promotes RV reverse remodeling without requiring routine concomitant TVI.

Background and objectives: Hypoxia/reoxygenation (H/R) injury is a major contributor to cardiac damage. The role of AT-rich interaction domain 1A (ARID1A) in cardiomyocyte H/R injury and its underlying mechanisms remain unclear.

Methods: An H/R injury model was established using H9c2 cardiomyoblasts. Key assessments included cell viability (cell counting kit-8), apoptosis (Terminal deoxynucleotidyl transferase dUTP Nick End Labeling), DNA fragmentation, inflammatory cytokine levels (interleukin [IL]-1β, IL-6, IL-18), cardiac injury markers (creatine kinase-MB [CK-MB], cardiac troponin-I [cTn-I]), oxidative stress markers (lactate dehydrogenase [LDH] release, reactive oxygen species [ROS], glutathione peroxidase [GSH-Px], superoxide dismutase [SOD] activity), pyroptosis marker expression (NLR family pyrin domain containing 3 [NLRP3], caspase-1, gasdermin D [GSDMD]; Western blot), and ARID1A-SOX9 interaction (co-immunoprecipitation).

Results: H/R significantly upregulated ARID1A and SOX9 expression in H9c2 cells. ARID1A knockdown effectively attenuated H/R-induced damage, including improved cell viability, reduced apoptosis and DNA fragmentation, suppressed pro-inflammatory cytokine release (IL-1β, IL-6, IL-18), lowered CK-MB and cTn-I levels, decreased LDH release and ROS generation, enhanced antioxidant enzyme activity (GSH-Px, SOD), and reduced expression of pyroptosis markers (NLRP3, caspase-1, GSDMD). Mechanistically, ARID1A physically bound to SOX9 and promoted its expression. Crucially, the protective effects of si-ARID1A against H/R injury (apoptosis, inflammation, oxidative stress, pyroptosis) were consistently reversed by SOX9 overexpression.

Conclusions: ARID1A is upregulated during H/R injury and exacerbates cardiomyocyte damage by promoting apoptosis, inflammation, oxidative stress, and pyroptosis. ARID1A exerts its effects by binding to and positively regulating the expression of SOX9. Targeting the ARID1A/SOX9 axis represents a potential therapeutic strategy for mitigating H/R-induced cardiac injury.

Background and objectives: Comprehensive data on the changing landscape of cardiovascular disease (CVD) burden in cancer patients remains limited. We aimed to analyze the temporal trend in the burden of CVD among cancer patients.

Methods: Using a nationwide administrative claims database in Korea, we analyzed 1,322,502 adults (aged ≥18) newly diagnosed with cancer (2005-2022). The primary outcomes were: 1) temporal trends in CVD incidence, including ischemic heart disease (IHD), heart failure (HF), and stroke; and 2) cause-specific mortality trends, focusing on cancer and CVD-related deaths. Both crude and age-standardized rates were calculated for CVD incidence and mortality.

Results: The 1-year age-standardized cancer mortality rate showed a substantial decline from 134.0 to 76.3 per 1,000 person-years. While the age-standardized 1-year CVD incidence initially decreased from 91.7 to 50.6 per 1,000 person-years (2005-2014), this improvement plateaued and showed an upward trend thereafter. Analysis of CVD subtypes revealed divergent patterns: age-standardized IHD incidence declined, while HF incidence rose by 136%, 52%, and 37% at 1-, 3-, and 5-year follow-ups. Despite improvements in cancer mortality, the proportion of deaths attributed to CVD increased from 1.0% to 1.5% at 1-year, corresponding to a 50% relative rise and showed a similar upward trend at 5-year follow-up, with HF emerging as an increasingly cause of cardiovascular death (increasing from 10.8% to 26.3% of CVD mortality).

Conclusions: While cancer-specific mortality has improved significantly, cardiovascular mortality remains a growing concern, due to the increasing burden of HF in cancer patients. Ongoing CVD pattern surveillance in cancer patients is crucial for targeted interventions and prevention.

Background and objectives: We aimed to evaluate the efficacy and safety of coronavirus disease 2019 (COVID-19) vaccination in patients with heart failure (HF) using national databases.

Methods: We retrospectively analyzed the data from the Korean nationwide COVID-19 cohort, including patients with HF from February 2021 to June 2022. The study population was divided into the vaccinated (≥2 doses) and unvaccinated (≤1 dose) groups. Clinical outcomes assessed included hospitalization for HF, COVID-19-related events, and cardiovascular complications. Patients were matched by age, sex, and comorbidities, and were followed up for up to 15 months to assess vaccination-associated risks.

Results: We included 651,127 patients with HF (mean age 69.5 years; 50.2% male), of whom 112,693 (17.3%) were unvaccinated, and 538,434 (82.7%) were vaccinated. After propensity score matching, 73,559 patients in each group were compared. Over a median follow-up of 6 months, vaccination was associated with a significantly reduced risk of COVID-19 (hazard ratio [HR], 0.27; 95% confidence interval [CI], 0.22-0.33) and critical COVID-19 infection (HR, 0.47; 95% CI, 0.31-0.71). The vaccinated group also had a significantly lower risk of hospitalization for HF (HR, 0.53; 95% CI, 0.52-0.55) and all-cause mortality (HR, 0.18; 95% CI, 0.17-0.18) compared with the unvaccinated group. Additionally, vaccination was associated with a significantly lower risk of stroke, myocardial infarction, myocarditis/pericarditis, and venous thromboembolism compared with the unvaccinated patients (all, p<0.0001).

Conclusions: COVID-19 vaccination in patients with HF was associated with a reduced risk of hospitalization for HF, all-cause mortality, and other cardiovascular events.