Sürdürülebilir Kalkınma Amaçları

• 2

Yazarlar

• Akbuga, Kursat(1)
• Akcay, Murat(1)
• Akdogan, Murat(1)
• Boyaci, Faruk(1)
• Caglioglu, Hakan(1)
• Civici, Huseyin(1)
• Kaya, Enes(1)
• Kokcu, Halil Ibrahim(1)
• Koçu, Gokturk Kaan(1)
• Ozturk, Berkant(1)
• Sahin, Mustafa Kursat(1)
• Sahin, Yusuf Bozkurt(1)
• Seker, Onur Osman(1)
• Sezgin, Ali(1)
• Seçkin, Ozden(1)
• Tanik, Veysel Ozan(1)
• Tunca, Cagatay(1)
• Ucar, Melisa(1)
• Yanik, Ahmet(1)
• Yenercag, Mustafa(1)
• Yilmaz, Mustafa(1)
• Özkan, Mehmet Taha(1)
• Özlek, Bulent(1)
• Öztürk, Enes Furkan(1)

• MakaleAçık Erişim2026/r/gumushane/16439
  The COPD-augmented R2CHA2DS2-VA score: development and internal assessment for predicting one-year outcomes after transcatheter aortic valve implantation

  Boyaci, Faruk; Sahin, Mustafa Kursat; Akcay, Murat; Yanik, Ahmet; Yenercag, Mustafa; Seker, Onur Osman; Ucar, Melisa; Kokcu, Halil Ibrahim; Ozturk, Berkant; Kaya, Enes

  Background Existing CHA(2)DS(2)-VASc-based scores incompletely capture the prognostic impact of chronic obstructive pulmonary disease (COPD) and of graded renal dysfunction in patients undergoing transcatheter aortic valve implantation (TAVI). We acknowledge that the score's development in a high-risk, high-comorbidity cohort may produce optimistic performance estimates that require attenuation through external validation. We aimed to develop a novel COPD-augmented R(2)CHA(2)DS(2)-VA (COPD-R(2)CHA(2)DS(2)-VA) score that systematically integrates quantitative renal function and COPD, and to internally assess its discriminative performance for one-year all-cause mortality and major adverse cardiovascular events (MACE). Methods In this single-center, retrospective cohort study, 622 consecutive patients undergoing TAVI for severe aortic stenosis (2018-2024) were analyzed. The COPD-R(2)CHA(2)DS(2)-VA score was constructed as a prespecified clinical tool by augmenting the R(2)CHA(2)DS(2)-VA framework with COPD (1 point) and refining renal dysfunction into two graded estimated glomerular filtration rate strata (eGFR 30-59 mL/min/1.73 m & sup2;: 1 point; eGFR < 30: 2 points). Discriminative performance was evaluated using receiver operating characteristic curve analysis with bootstrap internal validation (2,000 resamples) and compared with established CHA(2)DS(2)-VASc-based scores. Multivariable logistic regression assessed the independent prognostic value of the score treated as a continuous variable. Results The COPD-R(2)CHA(2)DS(2)-VA score demonstrated encouraging discriminative ability for one-year all-cause mortality (apparent area under the curve [AUC] 0.946, 95% CI 0.926-0.971). As a prespecified tool with fixed component weights, bootstrap internal validation confirmed negligible optimism (mean optimism - 0.00014), with bias-corrected AUC identical to the apparent value. The addition of COPD significantly improved mortality discrimination over the R(2)CHA(2)DS(2)-VA score (Delta AUC + 0.033, p = 0.0001). For one-year MACE, the apparent AUC was 0.806 (95% CI 0.765-0.852); the addition of COPD did not significantly enhance MACE discrimination (Delta AUC + 0.001, p = 0.853). In multivariable analysis, each one-point increase in the COPD-R(2)CHA(2)DS(2)-VA score was independently associated with 3.52-fold higher odds of one-year mortality (95% CI 2.45-5.06, p < 0.001) and 2.02-fold higher odds of MACE (95% CI 1.67-2.46, p < 0.001). The bias-corrected AUC of the full multivariable model was 0.973 (95% CI 0.962-0.984) for mortality and 0.795 (95% CI 0.752-0.841) for MACE. Conclusions The COPD-R(2)CHA(2)DS(2)-VA score demonstrated encouraging discriminative ability for one-year all-cause mortality after TAVI in this single-center development cohort (apparent AUC 0.946). However, this high discriminative performance is likely influenced by the elevated comorbidity burden in our cohort and the single-center design, and should be interpreted as an upper-bound estimate. The addition of COPD provides a statistically significant but clinically modest incremental improvement for mortality (Delta AUC + 0.033, p = 0.0001), with no significant enhancement for MACE (Delta AUC + 0.001, p = 0.853). These findings are preliminary and hypothesis-generating; urgent external validation in diverse, prospective cohorts is essential before any clinical application can be considered. At present, this score should be regarded as a development-phase, hypothesis-generating tool that complements rather than replaces guideline-recommended instruments such as STS-PROM and EuroSCORE II. The score's clinical utility remains unproven.

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• MakaleYalnız künye2025/r/gumushane/16421
  Pan-immune-inflammation value predicts sustained ventricular arrhythmias in NSTEMI: a novel inflammatory risk marker

  Sahin, Yusuf Bozkurt; Tanik, Veysel Ozan; Koçu, Gokturk Kaan; Özkan, Mehmet Taha; Akdogan, Murat; Seçkin, Ozden; Tunca, Cagatay; Sezgin, Ali; Akbuga, Kursat; Özlek, Bulent

  BackgroundSystemic inflammation contributes to arrhythmogenesis in acute coronary syndromes, but its role in NSTEMI-related ventricular arrhythmias remains poorly defined. The pan-immune-inflammation value (PIV) is a novel composite biomarker reflecting immune and thrombotic activity derived from routine blood counts. This study aimed to assess the association between PIV and the risk of sustained VT/VF in NSTEMI.MethodsIn this retrospective cohort study, 1,788 NSTEMI patients who underwent percutaneous coronary intervention were analyzed. The primary endpoint was the occurrence of sustained VT or VF during hospitalization. PIV was calculated as (neutrophil x platelet x monocyte)/lymphocyte. Logistic regression, ROC analysis, Kaplan - Meier curves, reclassification indices (NRI, IDI), and restricted cubic spline modeling were used.ResultsVT/VF occurred in 34 patients (1.9%). Those with VT/VF had significantly higher PIV values (median 1132 vs. 329, p < 0.001). In multivariable analysis, PIV remained an independent predictor (OR: 1.356 per 1000 unit increase; 95% CI: 1.028-1.787; p = 0.031). The risk of VT/VF rose progressively across PIV quartiles (Q4 vs. Q1 OR: 4.0, p for trend < 0.001). Adding PIV to conventional predictors improved risk classification (NRI: +0.089; IDI: 0.007). Kaplan - Meier analysis showed significantly reduced arrhythmia-free survival in high-PIV tertiles (log-rank p < 0.001), and cubic spline modeling revealed a non-linear association with increased arrhythmic risk at higher PIV levels.ConclusionsElevated PIV is independently associated with malignant ventricular arrhythmias in NSTEMI. As an accessible biomarker, PIV may aid early arrhythmic risk stratification and guide clinical surveillance strategies.

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