{"id":"b77fc97db822","type":"article","url":"https://hartvaat.nl/2026/05/05/apicale-myocardfibrose-bij-lvad-implantatie-voorspelt-cardiale-mortaliteit-singl/","title":"Apicale myocardfibrose bij LVAD-implantatie voorspelt cardiale mortaliteit (single-center, n=47)","title_en":"","category":"hartfalen","category_label":"Hartfalen","professions":["cardioloog"],"tags":[],"journal":"ESC heart failure","doi":"10.1093/eschf/xvag135","source_url":"https://doi.org/10.1093/eschf/xvag135","authors":["İbrahim Demir","Bilge Ecemiş","Ayşe Zorba","Işık İkbal Barış","Berhan Keskin","Emir Cantürk","Yahya Yıldız","İbrahim Oğuz Karaca","Korhan Erkanlı"],"significance":5,"published":"2026-06-30","source_date":"2026-05-05","image":"","kennis":["https://hartvaat.nl/kennis/hartfalen/cardiale-remodellering/","https://hartvaat.nl/kennis/diagnostiek/cardiale-mri/"],"congress":"","summary_en":"Single-centre retrospective cohort of 47 consecutive patients undergoing durable LVAD implantation (2019-2025; median age 63 years, 14.9% female). At implantation, tissue from the apical LV core was analysed by structured histopathology (THS-10 score) and digital morphometry (QuPath). Median follow-up 1,513 days; 27 deaths (16 cardiovascular, 11 non-cardiac). A threshold of 33.7% collagen-positive area gave the best discrimination for overall mortality (AUC 0.739). On univariable Cox analysis, fibrosis burden (HR 39.4) and THS-10 score (HR 1.51) were strongly associated with mortality. After adjustment for clinical severity (including INTERMACS profile), the all-cause-mortality association attenuated, but fibrosis burden independently predicted cardiac mortality (sHR ≈ 4.1; p=0.02). The cohort-derived threshold for cardiac death was 39.6% (AUC 0.752). The results support myocardial-substrate assessment in LVAD selection; external validation in larger cohorts is needed.","created":"2026-07-03T10:33:08Z","updated":"2026-07-03T13:32:02Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Single-center retrospectieve cohortstudie bij 47 opeenvolgende patiënten met duurzame LVAD-implantatie (2019-2025; mediane leeftijd 63 jaar, 14,9% vrouw). Op het tijdstip van implantatie werd weefsel uit de apicale LV-core histopathologisch (THS-10-score) en met digitale morfometrie (QuPath) geanalyseerd. Mediane follow-up 1.513 dagen; 27 sterftes (16 cardiovasculair, 11 niet-cardiaal). Een drempel van 33,7% collageen-positief oppervlak gaf de beste discriminatie voor totale sterfte (AUC 0,739). In univariabele Cox-analyse waren fibroselast (HR 39,4) en THS-10-score (HR 1,51) sterk geassocieerd met sterfte. Na correctie voor klinische ernst (incl. INTERMACS-profiel) verdween de associatie met totale sterfte, maar fibroselast voorspelde wel onafhankelijk cardiale sterfte (sHR ≈ 4,1; p=0,02). Cohort-afgeleide drempel voor cardiale sterfte was 39,6% (AUC 0,752). De resultaten ondersteunen myocardiale substraat-evaluatie bij LVAD-selectie; externe validatie in grotere cohorten is nodig.","abstract_original":"INTRODUCTION: Advanced heart failure is characterized by progressive myocardial remodelling, with fibrosis representing a final common pathway of chronic injury. We investigated whether quantitatively assessed apical myocardial fibrosis burden at the time of left ventricular assist device (LVAD) implantation is associated with overall and cause-specific mortality. METHODS: This single-centre retrospective cohort study included 47 consecutive patients undergoing durable LVAD implantation between 2019 and 2025. Median age was 63 years and 14.9% were female. Myocardial tissue obtained from the left ventricular apical core at implantation was analysed using structured histopathologic scoring (THS-10) and quantitative digital morphometry (QuPath). Fibrosis burden was quantified as collagen-positive area relative to total myocardial area. Overall survival was assessed using Kaplan-Meier analysis and Cox regression. Cardiac mortality was evaluated using Fine-Gray competing-risk models, with non-cardiac death treated as a competing event. RESULTS: Median follow-up was 1513 days. During follow-up, 27 deaths occurred (57.4%), including 16 cardiovascular and 11 non-cardiac deaths. Quantitative fibrosis burden showed a strong unadjusted association with overall survival (log-rank P = .00042). Receiver operating characteristic (ROC) analysis identified a cohort-derived fibrosis threshold of 33.7% for overall mortality risk stratification (area under the curve [AUC] 0.739, 95% confidence interval [CI] 0.566-0.912). In univariable Cox analysis, fibrosis burden and THS-10 score were associated with mortality (hazard ratio [HR] 39.39, 95% CI 2.61-594.56, P = .008; and HR 1.51, 95% CI 1.14-2.01, P = .005, respectively). After multivariable adjustment for clinical severity, including INTERMACS profile and key laboratory parameters, the association with all-cause mortality was attenuated. In competing-risk analysis, high fibrosis burden independently predicted cardiac mortality (subdistribution HR approximately 4.1, P = .02). Additional exploratory ROC analysis for cardiovascular death showed an AUC of 0.752, with a cohort-derived threshold of 39.6%. CONCLUSION: Quantitatively assessed apical myocardial fibrosis burden identifies a biologically high-risk myocardial phenotype in LVAD recipients. While the association with all-cause mortality is attenuated after adjustment, fibrosis burden shows a specific relationship with cardiac mortality when competing non-cardiac risk is taken into account. These findings support the prognostic relevance of myocardial substrate and warrant external validation in larger prospective cohorts."}