Calcified nodules (CN) are recognized as high-risk morphological features; however, their prognostic impact on stable angina pectoris (SAP) in the contemporary era of intensive lipid-lowering therapy and advanced lesion preparation remains unclear. A total of 322 patients with SAP (450 procedures) who underwent elective intravascular ultrasound (IVUS)-guided percutaneous coronary intervention (PCI) were analyzed. CN was identified in 40 patients (12%) at the patient level and in 61 lesions (14%) at the lesion level. The primary endpoint was clinically driven target lesion revascularization (TLR) at the lesion level. All patients received statin therapy following the index PCI. The CN group had higher prevalences of hypertension and hemodialysis and lower estimated glomerular filtration rate than the non-CN group, whereas age, diabetes mellitus, chronic kidney disease, left ventricular ejection fraction, low-density lipoprotein cholesterol (LDL-C), estimated small dense LDL-C (Esd LDL-C), and statin use did not differ significantly between groups. Kaplan-Meier analysis demonstrated a significantly higher cumulative incidence of major adverse cardiocerebrovascular events (MACCE) (p = 0.007) and clinically driven TLR at both patient (p = 0.005) and lesion levels (p < 0.001) in the CN group than in the non-CN group. In multivariable Cox regression adjusting for baseline clinical and procedural variables, CN remained independently associated with TLR (hazard ratio [HR]: 3.63, 95% confidence interval [CI] 1.62-8.14, p = 0.002) and MACCE (HR: 2.59, 95% CI 1.14-5.87, p = 0.023), whereas neither LDL-C nor other lipid parameters independently predicted outcomes. The drug-eluting stent (DES) strategy was independently associated with a lower risk of TLR (HR: 0.25, p = 0.002). In patients with SAP undergoing elective IVUS-guided PCI, all of whom received statin therapy following the index PCI, CN was independently associated with adverse clinical outcomes irrespective of baseline LDL-C or other lipid parameters. These findings suggest that CN represents a distinct high-risk morphological phenotype associated with adverse outcomes after PCI. In the overall cohort, DES use was independently associated with lower TLR than DCB use, although the optimal device strategy for CN lesions warrants further investigation. IVUS-based plaque characterization is essential and may facilitate morphology-oriented risk stratification in contemporary PCI practice.

Experimental studies suggest that eosinophils promote myocardial repair after myocardial infarction; however, their clinical significance in post-infarction cardiac remodeling remains unclear. We investigated the association between admission peripheral eosinophil counts and left ventricular (LV) and left atrial (LA) remodeling after ST-segment elevation myocardial infarction (STEMI). This retrospective single-center study included 452 consecutive patients with first-time STEMI who underwent successful primary percutaneous coronary intervention between 2016 and 2024. Patients were divided into high and low eosinophil groups according to the median admission eosinophil count (70 cells/µL). Echocardiography was performed during the acute phase and at 6-12 months. Changes in LV end-diastolic diameter (ΔLVDd) and left atrial volume index (ΔLAVI) were evaluated. Multivariable linear regression analysis was performed to identify independent predictors of remodeling. Patients with higher eosinophil counts showed significantly smaller increases in LVDd (ΔLVDd: - 0.4 ± 6.3 vs. + 1.0 ± 4.8 mm, p = 0.03) and greater reductions in LAVI (ΔLAVI: - 2.2 ± 9.6 vs. + 1.1 ± 11.4 mL/m[2], p = 0.01) than those with lower eosinophil counts. Admission eosinophil count was independently associated with ΔLVDd (standardized β = - 0.154, p = 0.046), whereas no independent association was observed with ΔLAVI. In subgroup analysis, the favorable association between eosinophils and LA remodeling was observed primarily in patients with LAD infarction. No significant differences were observed in one-year mortality or heart failure readmission. Higher admission eosinophil counts were associated with favorable LV and LA remodeling after STEMI. Admission eosinophil count was independently associated with attenuation of LV remodeling, suggesting that it may serve as a practical biomarker for identifying patients at lower risk of adverse cardiac remodeling after STEMI.

We aimed to investigate association of three DanGer Shock trial criteria [systolic blood pressure [SBP] < 100 mmHg, lactate ≥ 2.5 mmol/L, and left ventricular ejection fraction (LVEF) < 45%] on clinical outcomes among patients with ST-elevation myocardial infarction (STEMI) in Japan and evaluate whether these criteria could serve as a simple prognostic model for risk stratification. This single-center, retrospective, observational study included 1,211 patients with STEMI who underwent percutaneous coronary intervention (PCI) between 2014 and October 2023. The primary outcome was all-cause mortality at 180 days after the index PCI. To estimate the predictor of all cause death, a multivariable logistic regression analysis was conducted, and a scoring system was developed based on the results of the analysis. Patients were stratified according to the derived scoring system, and the prognostic utility of this stratification was evaluated. Among them, 4.1% met all the 3 key inclusion criteria of the DanGer Shock trial. The overall 180-day mortality rate was 6.5%. In multivariable analysis, each of the 2 criteria (SBP < 100 mmHg and LVEF < 45%) was significantly associated with 180-day all-cause death. Based on a multivariable logistic regression model, a simple shock score was developed (SBP < 100 mmHg, 1 point; lactate ≥ 2.5 mmol/L, 1 point; and LVEF < 45%, 2 points). With higher total shock scores, 180-day mortality increased exponentially (score 0: 1.9%, score 1: 2.8%, score 2: 6.1%, score 3: 16.4%, score 4 points, 42.7%, log-rank P< 0.001). In real-world clinical practice, few patients with STEMI fulfilled the 3 key inclusion criteria of the DanGer Shock trial. The simple score based on modified DanGer Shock trial-derived criteria assessed at initial emergency room presentation effectively stratified 180-day mortality risk in patients with STEMI.

Tricuspid regurgitation (TR) is related to a poor prognosis in atrial fibrillation (AF). Although right atrial (RA) structural remodeling contributes to TR progression, the impact of RA functional remodeling on the progression of TR remains unclear. We investigated whether RA function influences TR progression in AF. Among 664 AF patients with baseline and follow-up echocardiography, 484 (mean 68 ± 12 years, 38% female) with insignificant (mild or less) TR at baseline were included. Patients with prior cardiac surgery, cardiac implantable electronic devices, significant (at least moderate) valvular diseases, LVEF < 50%, suboptimal images for strain analysis, or follow-up echocardiography < 6 months were excluded. A cut-off value for RA reservoir strain was 12.6%, as determined by ROC analysis. Over a mean 3.6 ± 2.7 years, 46 (9.5%) patients developed significant TR. Patients with RA reservoir strain < 12.6% were older, had more persistent AF, higher E/e' and pulmonary artery systolic pressure (PASP), larger left atrium (LA) and RA, and lower LA strain. On multivariable regression, RA reservoir strain < 12.6% was independently associated with TR progression after adjustment for age, sex, and RA volume (p = 0.027), and remained significant after further adjustment for E/e' or PASP. Impaired RA reservoir strain was independently associated with TR progression in AF patients with initially insignificant TR, suggesting that RA functional assessment may provide additional information complementary to RA structural remodeling and help identify patients at higher risk of TR progression.

We evaluated the prognostic value of a four-group classification combining estimated plasma volume status (ePVS) and serum creatinine (Cre) in patients hospitalized for acute decompensated heart failure (ADHF). We analyzed 914 patients from the SAKURA HF Registry-2 enrolled between September 2018 and December 2023. At discharge, patients were stratified into four groups using ePVS (cutoff, 5.5 mL/g) and Cre (cutoff, 1.1 mg/dL): low-ePVS/low-Cre (n = 285), high-ePVS/low-Cre (n = 136), low-ePVS/high-Cre (n = 263), and high-ePVS/high-Cre (n = 230). The primary endpoint was a composite of all-cause mortality or heart failure rehospitalization. Multivariable Cox models were adjusted for clinical, laboratory, echocardiographic, and discharge-medication covariates. Median age was 74 years and 68% were men. Over a median follow-up of 368 days (interquartile range [IQR], 89-548), 349 patients (38.2%) experienced the primary endpoint, with significant differences among groups (log-rank p < 0.001). In multivariable models, compared with low-ePVS/low-Cre, risk was higher in high-ePVS/low-Cre (hazard ratio [HR] 2.38, 95% confidence interval [CI] 1.31-4.30; p = 0.004) and high-ePVS/high-Cre (HR 1.98, 95% CI 1.12-3.48; p = 0.018), but not in low-ePVS/high-Cre (HR 1.62, 95% CI 0.94-2.79; p = 0.08). A discharge-based ePVS-Cre classification provided clinically relevant risk stratification after ADHF. Elevated ePVS despite non-elevated serum creatinine independently predicted adverse outcomes. When ePVS was low, the excess risk associated with elevated creatinine was attenuated after adjustment, whereas concomitant elevation of ePVS and creatinine remained a high-risk category. This simple bedside framework may support discharge risk assessment.

Cardiac sarcoidosis (CS) is an inflammatory/granulomatous disease that affects the heart and is responsible for mortality due to fatal arrhythmias or systolic heart failure. The efficacy and outcomes of cardiac resynchronization therapy (CRT) for CS remain uncertain. We retrospectively analyzed a cohort of 108 patients diagnosed with CS at Nippon Medical School Hospital and extracted 19 patients who underwent CRT implantation between 2007 and 2024 (68% female, mean age 70 ± 8 years). The mean follow-up period was 6.7 ± 4.3 years. Of 19 patients with CRT devices (2 CRT-Ps and 17 CRT-Ds), 5 patients were upgraded from pacemakers and 5 from ICDs. At 6 months after device implantation, QRS duration shortened (172 ± 34 vs. 128 ± 27ms, p < 0.001), NYHA (2.6 ± 0.8 vs. 2.1 ± 1.0, p = 0.037) improved, and BiV pacing percentage was 98 ± 2%. However, LVESV (147 ± 74 vs. 155 ± 70 ml, p = 0.878) and LVEF (28 ± 9 vs. 28 ± 11%, p = 0.452) did not improve. During the follow-up period, 8 hospitalizations due to heart failure, 2 appropriate ICD shocks, and 6 deaths due to progressive heart failure were observed. Device-related complications developed in 4 patients. In this small retrospective cohort of patients with advanced cardiac sarcoidosis undergoing CRT implantation, echocardiographic reverse remodeling was limited despite improvements in QRS duration and NYHA functional class. Clinical outcomes remained poor, likely reflecting the advanced and heterogeneous nature of the underlying disease. Further comparative studies are warranted.