Korean Circulation Journal最新文献

Background and objectives: Valvulitis is frequently found in Kawasaki disease (KD). However, the persistence and severity of mitral regurgitation (MR) in KD are not well-known. This study examined the correlation between MR and z-values of inflammatory serum biomarkers.

Methods: Patients with KD at Korea University Hospital over 15-year period were retrospectively investigated. Echocardiography and inflammatory serum biomarkers were examined in 371 patients with KD (241 with MR and 130 without) and 144 patients with febrile illness (control). Serum biomarkers (raw and z-values) were compared among the positive, negative, all, and no MR groups during each phase of KD.

Results: Neutrophil, z-neutrophil, lymphocyte, z-lymphocyte, neutrophil-lymphocyte ratio, hemoglobin, z-hemoglobin, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) all differed significantly between the positive and negative MR groups and between the all and no MR groups during the acute phase (p<0.05). A part of white blood cell (WBC), z-WBC, neutrophil, z-neutrophil, neutrophil to lymphocyte ratio, hemoglobin, z-hemoglobin, CRP, ESR, aspartate transaminase, and sodium were associated with severity of MR through correlation analysis and multivariate logistic regression (p<0.05). Optimal cut-off values of neutrophils, z-neutrophils, CRP, and ESR to predict persistent MR were 8,100 /μL, 2.2, 61 mg/dL, and 77 mm/h.

Conclusions: A comparison of hematological z-values in KD with MR and in KD without MR is useful for predicting more severe inflammation. Neutrophils, z-neutrophils, and ESR were significant and consistently associated with pathogenesis of MR and their levels during the early inflammation can predict the persistency and severity of MR.

Background and objectives: Atrial fibrillation (AF) is associated with an increased risk of cerebrovascular disease and cognitive impairment. However, evidence on the mediating role of brain structural changes in this association remains limited, especially in Asian populations. This study investigated the associations among AF, magnetic resonance imaging (MRI)-measured brain structures, and cognitive function, and evaluated the mediation effect of brain structural changes in the AF-cognition link.

Methods: Two thousand, six hundred sixty-two participants from the KoGES-CAVAS-C cohort were analyzed, who without a history of stroke or missing data. AF was identified with electrocardiograms and confirmed by cardiologists. Cognitive function was assessed using the Seoul Neuropsychological Screening Battery-Core. Brain volumes and white matter integrity were measured using standardized MRI protocols. Multivariable linear regression and mediation analyses were performed.

Results: Among 2,662 participants, 50 (1.9%) had AF. Participants with AF showed lower total brain volume, regardless of tissue type, and reduced volumes in multiple brain regions. Overall cognitive function and specific domains (memory and executive function) were poorer in the AF group than in the normal group. AF remained significantly associated with lower total brain volume (p=0.005) and cognitive scores (p=0.037) after adjustment. Total brain volume partially mediated the AF-cognition association (p=0.007), accounting for 11% of the effect.

Conclusions: AF is associated with brain atrophy and cognitive impairment, and brain structure partially mediates the association between AF and cognitive function. Our study findings suggest integrated cardiovascular and cognitive assessments in AF management.

Atrial cardiomyopathy is a progressive condition that promotes atrial fibrillation (AF) persistence and adverse outcomes. Although fibrosis has long been considered its hallmark, the histopathological basis in non-valvular AF remains incompletely defined due to limited tissue availability outside surgery or autopsy. To overcome this, we established an integrated approach combining intracardiac echocardiography-guided right atrial biopsy with high-density electroanatomic mapping in AF ablation patients. Our studies revealed that atrial voltage reduction reflects not only fibrosis but also intercellular space expansion, myofibrillar loss, reduced nuclear density, and compensatory cardiomyocyte hypertrophy. Notably, atrial biopsy detected atrial amyloidosis in ~7% of patients, often at an early stage, highlighting its potential for earlier diagnosis and intervention. Sex-based analysis revealed that women consistently had lower atrial voltage, attributable to smaller myocardial mass rather than more severe remodeling. These findings demonstrate that atrial biopsy enables patient-specific histopathological assessment, deepening mechanistic understanding of atrial cardiomyopathy and informing future strategies for AF management.

Background and objectives: The objective of this study was to investigate whether genetic, structural, and clinical factors were associated with atrial fibrillation (AF) in patients with hypertrophic cardiomyopathy (HCM).

Methods: Of the 212 prospectively enrolled patients in the HCM genetic registry, 33 had initial AF, and the remaining 179 (126 males, 58±13 years) were followed up for the development of new-onset AF.

Results: Patients with initial AF had older age, lower estimated glomerular filtration rate (eGFR), lower left ventricular (LV) global longitudinal strain, higher left atrial volume index (LAVI), and higher LV extracellular volume fraction. During a median follow-up period of 916 (400-1,327) days, AF occurred in 12 (6.7%) patients. In Cox regression analysis, lower eGFR (hazard ratio per 1 mL/min/1.73 m² increase, 0.93; p=0.007), LV ejection fraction (hazard ratio, 0.82; p=0.009), and higher LAVI (hazard ratio, 1.07; p=0.010) were associated with increased risk of future AF. The addition of eGFR to LAVI significantly increased the global χ² value (8.508 to 15.017; p=0.006). Among patients younger than 65 years (n=128), those with any sarcomere variants (pathogenic and variants of uncertain significance [VUS], n=77) had a higher prevalence of overall AF (initial and new-onset, 82.4% vs. 56.8%; p=0.045).

Conclusions: In patients with HCM, decreased renal function provides an additive predictive value on LAVI for future AF. In patients younger than 65, the presence of sarcomere variants, including VUS, is related to a higher prevalence of AF.

Statin-associated muscle symptoms (SAMS) are a common clinical challenge that often lead to poor adherence or discontinuation of statin therapy, thereby undermining its well-established cardiovascular benefits. This review explores the current understanding of the epidemiology, pathophysiology, clinical presentation, and diagnostic considerations of SAMS, with a particular focus on distinguishing true statin intolerance from nonspecific muscle complaints. We discuss evidence-based management strategies, including statin dose adjustment, rechallenge protocols, and the application of alternative lipid-lowering therapies such as ezetimibe, PCSK9 inhibitors, and bempedoic acid. Recent clinical trials support the efficacy and tolerability of combination therapy with moderate-intensity statins and ezetimibe, particularly in high-risk patients. A pragmatic, patient-centered approach is crucial for maintaining lipid-lowering therapy, minimizing adverse effects, and effectively reducing cardiovascular risk.

Background and objectives: The prognosis of unrevascularized non-culprit lesions (NCLs) and the benefits of non-culprit percutaneous coronary intervention (PCI) may depend on their functional significance and location in patients with acute myocardial infarction (AMI) and multivessel coronary disease (MVD). We investigated the differential outcomes of fractional flow reserve (FFR) versus angiography-guided PCI for NCL between the left anterior descending artery (LAD) and non-LAD arteries.

Methods: This was a prespecified post hoc analysis of the FRAME-AMI trial. The primary endpoint, a composite of time to death, myocardial infarction, or repeat revascularization, was matched between the two strategies according to the NCL location.

Results: Among 562 patients, the proportions of NCL in the LAD and non-LAD groups were 55.0% and 45.0%, respectively. PCI rates (82.2% vs. 78.3%; p=0.242) and the primary outcome (9.4% vs. 11.5%; p=0.421) were comparable between the two groups. In the non-culprit LAD group, FFR-guided PCI was associated with a lower rate of the primary outcome compared to angiography-guided PCI (5.7% vs. 14.3%, p=0.010). In the non-culprit non-LAD group, the outcome rate did not significantly differ between FFR- and angiography-guided PCI (7.4% vs. 14.5%, p=0.081). Nevertheless, the interaction between the non-culprit location and FFR- or angiography-guided PCI did not affect the primary outcome (p=0.667).

Conclusions: The NCL location did not affect the favorable outcomes of FFR-guided PCI over angiography-guided PCI in patients with AMI and MVD.