Korean Circulation Journal最新文献

Background and objective: Hypothyroidism has been linked to increased atrial fibrillation (AF) susceptibility. We aimed to identify factors associated with AF recurrence after catheter ablation and to compare arrhythmogenic substrates and recurrence rates between euthyroid and hypothyroid patients.

Materials and methods: We retrospectively reviewed patients who underwent AF ablation from 2015 to 2019. Baseline clinical, echocardiographic, and electrophysiologic parameters were compared between hypothyroid and euthyroid groups. Pulmonary vein (PV) and non-PV (NPV) triggers, as well as AF drivers, were analyzed. Multivariate Cox regression identified predictors of AF recurrence.

Results: Among 591 patients (mean age 57.2±11.1 years; 450 male), 65 (10.9%) had hypothyroidism. These patients had more hypertension (49.2% vs. 34.0%, p=0.016), larger left atrial diameter (LAD, 41.1±6.3 mm vs. 39.1 ± 6.3 mm, p=0.015), more NPV triggers (41.5% vs. 26.4%, p=0.01), and more AF drivers (26.2% vs. 12.5%, p=0.003). AF recurrence was higher in the hypothyroid group (44.6% vs. 18.1%, p<0.001). Independent predictors of recurrence included AF drivers, NPV triggers, LAD, Peak E velocity, and E/e' ratio. Hypothyroidism was not an independent predictor, but mediation analysis showed that its effect on recurrence was predominantly indirect. Kaplan-Meier analysis showed higher recurrence in hypothyroid patients (log-rank p<0.0001).

Conclusions: Hypothyroidism was associated with a higher burden of atrial triggers, drivers, and AF recurrence. Its impact on recurrence was likely an indirect effect of structural and arrhythmogenic remodeling. Comprehensive driver mapping may improve ablation outcomes in this population, warranting further prospective validation.

Background and objectives: CR6-interacting factor 1 (CRIF1) is essential for the synthesis and insertion of mitochondrial oxidative phosphorylation (OXPHOS) complexes. Although Crif1 deficiency has been linked to mitochondrial dysfunction in various tissues, its role in cardiac function remains unclear. Therefore, this study aimed to investigate the role of Crif1 in regulating mitochondrial function in the heart.

Methods: To determine the role of Crif1 and examine mitochondrial dysfunction in the heart, we generated cardiac-specific Crif1 knock-down mice using a Myh6-Cre system. Mitochondrial function was assessed by measuring oxygen consumption rates. Histological and echocardiographic examinations were performed at baseline and 2 weeks after isoproterenol infusion.

Results: Crif1 knock-down in the heart led to structural mitochondrial abnormalities and decreased maximal oxygen consumption rates in cardiomyocytes. Although cardiac-specific Crif1 knock-down resulted in mitochondrial dysfunction, the cardiac phenotype remained normal showing preserved ejection fraction (EF) and fractional shortening (FS). However, cardiac dysfunction was aggravated under isoproterenol-induced stress, resulting in a decreased EF and FS. Cardiac hypertrophy, a typical adaptive response to isoproterenol stimulation, was attenuated.

Conclusions: These findings suggest that Crif1 is critical for maintaining the structure and function of mitochondria in cardiomyocytes. Additionally, mitochondrial abnormalities in the heart impair stress adaptation, leading to aggravated cardiac dysfunction under stress.

Background and objectives: The atrial metabolic profile and underlying pathophysiology of young-onset atrial fibrillation (AF) may differ from those of old-onset AF, but age-related alterations in atrial metabolism remain poorly understood. We explored potential age-related atrial metabolic differences using ¹⁸F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging.

Methods: We prospectively performed FDG PET with myocardial suppression in 40 young-onset and 40 old-onset AF patients. FDG uptake of the right and left atrium (RA and LA) was assessed visually (grade 0-3) and quantitatively using target-to-background ratio (TBR).

Results: The mean age was 59.3±13.5 (young-onset, 47.0±5.2; old-onset, 71.6±5.5) years, with a median AF duration of 3.6 (0.8-6.8) years. Among 80 patients (41 paroxysmal, 39 persistent AF), the distribution of AF type was similar between age groups (p=0.121). A total of 51 patients (63.7%) showed atrial FDG uptake ≥mild (grade≥1). No significant age-related differences were observed in visual FDG uptake or TBR in either atrial wall or appendage. Current drinking and persistent AF type were independently associated with increased atrial FDG uptake, primarily in the RA. Persistent AF was consistently associated with elevated RA uptake across age groups (adjusted odds ratio, 10.2, 95% confidence interval, 1.9-55.3; p=0.007). Quantitative analysis revealed significantly higher RA-to-LA metabolic ratios in persistent AF, consistent across age groups.

Conclusions: Atrial FDG uptake patterns did not differ by age in patients with AF. Increased RA FDG uptake in persistent AF was consistently observed, suggesting a shared metabolic alteration underlying AF progression transcending age-related pathological differences.

Background and objectives: Daily activity has a distinct hierarchy of movement behaviors. The association between 24-hour movement behaviors and cardiac conduction disease (CCD) remains unclear. We aimed to investigate the association between accelerometer-measured 24-hour movement behaviors and CCD risk.

Methods: A total of 92,436 UK Biobank participants who wore wrist accelerometers for 7 consecutive days were included, with a median follow-up of 6.1 years. Multivariable Cox proportional hazards models were used to investigate the associations between 24-hour movement behaviors (sleep, sedentary behavior, light-intensity physical activity [LIPA], and moderate-to-vigorous intensity physical activity [MVPA]) and the risk of CCD. Compositional data analysis was performed to estimate the effects of reallocating time among 24-hour movement behaviors.

Results: Among the 92,436 participants (median age 58 years; interquartile range, 50-63; 54% female), 1,442 developed incident CCD (2.58 per 1,000 person-years) during the follow-up. Greater sedentary behavior was associated with an increased risk of CCD (hazard ration [HR], 1.05; 95% confidence interval [CI], 1.02-1.08), whereas higher MVPA was associated with a lower risk (HR, 0.83; 95% CI, 0.75-0.92). Sleep duration and LIPA were not significantly associated with CCD risk. Reallocating 30 min/day to MVPA from other movement behaviors was associated with a 4% lower risk of CCD (HR, 0.96; 95% CI, 0.93-0.98). Conversely, reallocating 30 minutes/day to sedentary behavior was associated with a 3% increased risk (HR, 1.03; 95% CI, 1.01-1.05). Similar patterns were observed for specific CCD outcomes, including second- or third-degree atrioventricular block and pacemaker implantation.

Conclusions: Higher volumes of MVPA were associated with a lower risk of CCD, whereas increased sedentary behavior was associated with higher risk, highlighting the importance of preventive activity patterns.

Heart failure (HF) registries were established to bridge the gap between explanatory randomized clinical trials and daily clinical practice. Early hospital-based initiatives, such as ADHERE (2001) and the EuroHeart Failure Survey I (2000-2001), were followed by nationwide quality registries (e.g. SwedeHF, GWTG-HF) and global programmes (INTER-CHF, G-CHF), all together enrolling millions of patients across the acute-to-chronic HF spectrum. Registry-based analyses have provided insights into HF epidemiology, phenotypes, risk factors, prognosis, real-world therapy implementation, and have been hypotheses-generating for repurposing already existing treatments. Registries address questions that are unlikely to be answered in randomized trials, such as therapy effectiveness in underrepresented subgroups and settings that would be ethically challenging to study in a randomized setting (e.g., therapy withdrawal). Registry-based randomized controlled trials utilize the registry infrastructure for trial conduct and offer the opportunity to pragmatically test interventions at substantially lower costs than conventional randomized trials. Registries are a crucial part of a learning healthcare system, and will likely become increasingly relevant as methodological advances, including electronic record linkage, harmonized data standards, and modern causal inference techniques, enhance their validity. In this review, we provide a global overview of HF registries' evolution, scientific yield, and future potential.

Antiplatelet therapy is crucial for patients after percutaneous coronary intervention (PCI), but there is limited high-quality evidence guiding the best strategy for those with bifurcation lesions. The antiplatelet strategy for bifurcation PCI requires balancing the patient's overall thrombotic and bleeding risks. Bifurcation lesions present a complex, high-thrombotic-risk milieu because the procedure often causes plaque disruption and forms an inevitable gap in the sealing of the stent, compounded by turbulent blood flow that promotes thrombosis. Factors like stent malapposition, underexpansion, and low/oscillatory shear stress also contribute to increased local thrombotic risk, making the optimal antiplatelet therapy for bifurcation PCI difficult to define. Previous observational registry data broadly suggested a prolonged duration of dual antiplatelet therapy (DAPT) may be safer than a shorter duration of DAPT in reducing major adverse clinical outcomes. However, the reliability of these findings is limited by the inherent flaws of registry data, including the retrospective study design, lack of clinical event adjudication, and lack of specific protocol of PCI or DAPT strategy. Moreover, specific lesions factors such as complex PCI and left main bifurcation lesions or patient factors such as the presence of high bleeding risk or clopidogrel resistance necessitate special consideration, which leads to a individualized DAPT strategy beyond registry generalizations. The future of care points toward precision medicine, necessitating dedicated, prospective randomized controlled trials with standardized procedures to establish clear, evidence-based recommendations.

Myocardial stiffness is a key determinant of cardiac function. So far, its assessment required invasive methods such as pressure-volume loop measurements or mechanical testing of tissue biopsies, which are both not suited for daily clinical use. However, recent advances in echocardiography offer promising non-invasive alternatives. Initial clinical studies in different pathologies are encouraging and indicate a huge potential of these new ultrasound-based techniques for evaluating myocardial stiffness. In this review, we explain the concept of myocardial stiffness, explore the most promising ultrasound techniques currently available for its evaluation, and discuss key insights from recent clinical research in the field.