Background: Right ventricular (RV) dysfunction in chronic kidney disease (CKD) remains underrecognized. The tricuspid annular plane systolic excursion to systolic pulmonary artery pressure ratio (TAPSE/sPAP) reflects RV‐pulmonary arterial coupling, but its relationship with CKD severity is unknown. To evaluate the association between TAPSE/sPAP ratio and CKD stage severity and assess age‐related effect modification. Methods: This cross‐sectional study enrolled 120 participants: 40 patients with stage I–II CKD, 40 with stage III–IV CKD, and 40 healthy controls. All underwent echocardiography and nephrologist evaluation. Proportional odds regression models adjusted for cardiovascular risk factors evaluated the TAPSE/sPAP‐CKD association. ROC analysis assessed discriminatory performance. Age‐stratified analyses (<65 vs. ≥65 years) evaluated effect modification. Results: TAPSE/sPAP ratio declined progressively across CKD stages (controls: 0.67 ± 0.11, stage I–II: 0.61 ± 0.13, stage III–IV: 0.53 ± 0.13 mm/mmHg; p  < 0.01). Each 0.10‐unit decrease was independently associated with advanced CKD (adjusted OR 2.08, 95% CI 1.49–2.89, p < 0.001). TAPSE/sPAP ratio achieved the highest AUC (0.734, 95% CI 0.625–0.833), outperforming TAPSE alone (AUC 0.615; DeLong p  = 0.049), while statistically comparable to sPAP (AUC 0.715; DeLong p  = 0.400). Age‐stratified analysis revealed excellent performance in patients <65 years (AUC 0.819, sensitivity 78.6%, specificity 86.8%) but limited utility in those ≥65 years (AUC 0.579; p  = 0.015). Random forest analysis identified age (35.8%) and TAPSE/sPAP (22.0%) as dominant predictors. Conclusions: TAPSE/sPAP ratio is an independent marker of CKD severity enabling non‐invasive detection of RV‐PA uncoupling, with excellent discriminatory performance in younger but limited utility in older patients, suggesting that age‐specific interpretation and integration with renal biomarkers are recommended.

Background: Achieving target low-density lipoprotein cholesterol (LDL-C) levels in patients with atherosclerotic cardiovascular disease (ASCVD) frequently requires combination lipid-lowering therapy. Single-pill combination (SPC) regimens may improve adherence compared with free-dose combinations (FDC) in real-world clinical practice. Methods: This retrospective observational study included 450 ASCVD patients with baseline LDL-C levels of 70–189 mg/dL who were followed in cardiology outpatient clinics between January 2023 and December 2024. Patients received atorvastatin–ezetimibe either as a single-pill combination (SPC, n = 392) or as a free-dose combination (FDC, n = 58). Primary endpoints were LDL-C reduction and treatment adherence (≥ 80% of prescribed doses). Secondary endpoints included LDL-C target attainment and adverse events. Non-parametric tests and chi-square/Fisher’s exact tests were used for statistical analysis. Results: At 1 month, LDL-C levels were significantly lower in the SPC group compared with the FDC group (90.6 vs. 119 mg/dL; p = 0.005), and adherence was higher (89.8% vs. 70.7%; p < 0.001). At 4 months, LDL-C levels were comparable between groups, while continuous adherence remained significantly higher in the SPC group (86% vs. 69%; p = 0.001). A higher proportion of SPC-treated patients achieved LDL-C < 100 mg/dL at 1 month (81.9% vs. 67.2%; p = 0.009). Conclusions: In this real-world ASCVD cohort, SPC therapy with atorvastatin and ezetimibe was associated with superior adherence and comparable lipid-lowering efficacy despite lower statin doses. Fixed-dose combination strategies may represent an effective approach to optimize adherence and cardiovascular risk management.

Background and Objectives: Lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor associated with atherosclerosis, vascular inflammation, and endothelial dysfunction. However, data regarding its relationship with hypertension-mediated organ damage and circadian blood pressure abnormalities remain limited. We aimed to investigate the association of elevated Lp(a) levels with carotid atherosclerosis and nocturnal blood pressure dipping patterns in patients with hypertension. Materials and Methods: This retrospective cross-sectional study included 80 nondiabetic patients with essential hypertension. Patients were categorized according to serum Lp(a) levels into elevated Lp(a) (≥50 mg/dL, n = 20) and lower Lp(a) (<50 mg/dL, n = 60) groups. All participants underwent carotid ultrasonography, transthoracic echocardiography, ambulatory blood pressure monitoring, and ophthalmologic evaluation. Multivariable logistic and linear regression analyses were performed to determine independent associations between Lp(a), carotid plaque presence, and nocturnal dipping percentage. Results: Patients with elevated Lp(a) levels had a significantly higher prevalence of carotid plaque (55.0% vs. 23.3%, p = 0.008) and non-dipper hypertension (75.0% vs. 46.7%, p = 0.028) compared with patients with lower Lp(a) levels. Serum Lp(a) concentrations were inversely correlated with nocturnal dipping percentage (r = −0.362, p = 0.001). In multivariable logistic regression analysis adjusted for age, sex, LDL cholesterol, and active smoking, elevated Lp(a) remained independently associated with carotid plaque presence (OR 3.24, 95% CI 1.06–9.80, p = 0.039). In multiple linear regression analysis adjusted for age, sex, LDL cholesterol, and office systolic blood pressure, higher Lp(a) levels remained independently associated with lower nocturnal dipping percentage (β = −0.294, p = 0.008). No significant associations were observed between Lp(a) and carotid intima–media thickness, left ventricular hypertrophy, hypertensive retinopathy, or renal functional parameters. Conclusions: Elevated Lp(a) levels were independently associated with carotid plaque presence and impaired nocturnal blood pressure decline in hypertensive patients. These findings suggest that Lp(a) may be more closely linked to focal macrovascular atherosclerosis and abnormal circadian blood pressure regulation rather than diffuse hypertensive structural remodeling.

Objective: Early-onset paroxysmal atrial fibrillation (PAF) in individuals without conventional cardiovascular risk factors has traditionally been labeled as “lone AF.” Recent evidence suggests that subtle structural, electrical, and functional abnormalities may still exist. This study evaluated atrial conduction, diastolic function, endothelial function, and systemic inflammation in early-onset PAF patients without structural heart disease or overt comorbidities. Methods: In this cross-sectional study, 40 patients aged 18–65 years with documented early-onset PAF were compared with 40 age and sex matched healthy individuals in sinus rhythm. All subjects underwent measurement of P wave dispersion and signal-averaged P wave duration, echocardiographic assessment of diastolic parameters, evaluation of endothelial function using flow-mediated dilation (FMD), and analysis of systemic inflammation via high-sensitivity C-reactive protein (hsCRP). Results: Patients with PAF demonstrated significantly increased P wave dispersion (51.63 ± 11.17 ms vs. 35.13 ± 6.15 ms; p < 0.001) and prolonged signal-averaged P wave duration (146.75 ± 19.68 ms vs. 124.40 ± 9.05 ms; p < 0.001). Diastolic dysfunction was evident, characterized by a reduced E/A ratio and elevated septal E/E′. Left atrial volume index was significantly higher in the PAF group (29.79 ± 3.94 mL/m² vs. 28.23 ± 1.74 mL/m²; p = 0.025). Endothelial function was impaired, as reflected by lower FMD values (5.27 ± 1.94% vs. 6.65 ± 1.78%; p = 0.001), while hsCRP levels were significantly higher in the PAF group (0.40 [0.30–0.55] vs. 0.24 [0.20–0.30] mg/dL; p < 0.001). Multivariate analysis identified signal-averaged P wave duration, P wave dispersion, mitral E wave velocity, septal E/E′, and left atrial volume index as independent predictors of PAF. Conclusion: Even in the absence of overt cardiovascular disease, early-onset PAF is associated with meaningful disturbances in atrial conduction, diastolic performance, endothelial function, and systemic inflammation. These findings support the presence of early atrial cardiomyopathy and underscore the need for comprehensive cardiovascular evaluation in younger PAF patients.

Amaç: Pan-immün-inflamasyon değeri (PIV), kardiyovasküler hastalıklarda araştırılan bileşik bir inflamatuvar biyobelirteçtir. Bu çalışmada, karotis arter stentleme (KAS) uygulanan hastalarda PIV ile vasküler komorbidite yükü arasındaki ilişkinin araştırılması amaçlandı. Gereç ve Yöntemler: Retrospektif çalışmaya 2010–2025 yılları arasında KAS uygulanan 221 hasta dahil edildi. PIV periferik kan hücrelerinden hesaplandı. Vasküler yük skoru; hipertansiyon, diabetes mellitus, hiperlipidemi, sigara, koroner arter hastalığı ve geçirilmiş serebrovasküler olaydan oluşan altı bileşenle belirlendi. Hastalar düşük (0–2) ve yüksek (3–5) yük gruplarına ayrıldı. İlişkiler korelasyon ve regresyon analizleriyle, ayırt edici performans ROC analiziyle değerlendirildi. Bulgular: PIV, yüksek vasküler yük grubunda daha yüksekti (428,9 [287,1–701,9] vs. 287,1 [202,1–452,5], p=0,001). PIV ile vasküler yük arasında pozitif korelasyon vardı (rho=0,317, p<0,001). Her 100 birimlik PIV artışı, yüksek vasküler yük ile bağımsız ilişkiliydi (OR=1,152; %95 GA: 1,058–1,255; p=0,001). Düzeltilmiş ordinal regresyonda PIV, daha yüksek vasküler yük ile ilişkiliydi (OR=1,116; %95 GA: 1,062–1,174; p<0,001). ROC analizinde AUC 0,651 (%95 GA: 0,577–0,725) bulundu. Sonuç: Yüksek PIV, KAS hastalarında daha yüksek vasküler komorbidite yükü ile bağımsız ilişkilidir. Ancak sınırlı ayırt edici performansı nedeniyle PIV tek başına risk sınıflandırma aracı olarak kullanılmamalıdır.

Background: Benidipine is a long-acting calcium channel blocker used for the treatment of hypertension and chronic coronary syndrome. Although it effectively lowers blood pressure (BP), the relationship between BP reduction and improvement in angina-related health status during benidipine therapy remains uncertain. This study evaluated changes in BP and patient-reported angina-related health status in a large real-world cohort. Methods: This prospective, multicenter, observational cohort study included 1659 patients with hypertension and/or chronic coronary syndrome who underwent baseline clinical assessment before initiation of benidipine therapy and were reassessed after 3 months. Changes in systolic and diastolic BP and Seattle Angina Questionnaire-7 (SAQ-7) scores were evaluated. Multivariable linear regression analyses were performed to identify predictors of BP reduction and symptomatic improvement. A propensity score-matched analysis according to coronary artery disease (CAD) status was conducted to further explore differences in treatment response. Results: The mean age was 62.2 ± 12.2 years, and 54.0% of participants were women. Systolic BP decreased by 13.8 mmHg and diastolic BP by 6.7 mmHg (both p < 0.001). Mean SAQ-7 score increased by 8.1 points (p < 0.001), exceeding the established threshold for clinically meaningful improvement. Baseline SAQ-7 score showed the strongest association with change in SAQ-7, whereas baseline systolic BP was the strongest predictor of BP reduction. The correlation between changes in systolic BP and SAQ-7 was weak (r = 0.058, p = 0.023). In the propensity score-matched cohort (n = 732), BP reduction was similar regardless of CAD status, whereas improvement in SAQ-7 was greater in patients without obstructive CAD. Conclusions: In this multicenter real-world cohort, benidipine therapy was associated with significant BP reduction and clinically meaningful improvement in angina-related health status over 3 months. Symptomatic improvement showed only a weak association with BP reduction. These findings should be interpreted within the limitations of an observational study and warrant confirmation in controlled comparative studies.