The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026
Influence of donor-transmitted coronary artery disease on the progression of coronary vasculopathy after heart transplantation.
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Couto-Mallón David, Almenar-Bonet Luis, Barge-Caballero Eduardo, Hernández-Pérez Francisco José, Delgado-Jiménez Juan, Valero-Masa María Jesús, Castel-Lavilla María Ángeles, Mirabet-Pérez Sonia, Garrido-Bravo Iris Paula, Díez-López Carles, López-Granados Amador, Manrique-Antón Rebeca, Fernández-Pombo Carmen Neri, Muñiz Javier, Crespo-Leiro Maria Generosa
Аннотация
BACKGROUND: The prognostic significance of angiographically diagnosed donor-transmitted coronary artery disease (dtCAD) for post-heart transplant (HT) coronary artery disease (CAD) progression is poorly defined because of limited and heterogeneous evidence. We aimed to evaluate the role of angiographic dtCAD in the development and progression of CAD in HT recipients.
METHODS: Retrospective multicenter study including consecutive adult HT recipients (2008-2018) in Spain, with a coronary angiogram within 3 months post-HT. TCAD was classified as significant (s-dtCAD: ≥50% stenosis), non-significant (ns-dtCAD: <50%), or absent (no-dtCAD). CAD progression, defined as new (≥50% stenoses in previously unaffected territories) was evaluated using protocol-based (performed at 1 and 5 years post-transplant) and clinically indicated angiograms. Progression risk was assessed by means of competing risk analysis using the Fine-Gray method.
RESULTS: From a cohort of 1,918 recipients, 937 underwent baseline angiogram. dtCAD was identified in 172 patients (65 s-dtCAD). At follow-up, 791 patients had 1-year and 246 had 5-year angiograms. A total of 1,960 angiograms were evaluated. Cumulative incidence of CAD progression was 5.39% (95%CI 3.81-7.36) and 16.09% (95%CI 12.30-20.33) at 1 and 5 years, respectively. Progression rates were higher among patients with dtCAD compared with those with no-dtCAD: s-dtCAD: 9.65 per 100 person-years (95%CI 5.35- 17.43), ns-dtCAD: 9.24 (95%CI 5.82- 14.67), no-dtCAD: 2.72 (95%CI 2.00 - 3.69). Both s-dtCAD (adjusted SHR: 2.38; 95%CI: 1.26-4.52; p = 0.008) and ns-dtCAD (adjusted SHR: 2,92; 95%CI 1.67-5.08; p< 0.001) were independent predictors of CAD progression.
CONCLUSIONS: dtCAD was independently associated with a threefold increased risk of CAD progression after HT.
METHODS: Retrospective multicenter study including consecutive adult HT recipients (2008-2018) in Spain, with a coronary angiogram within 3 months post-HT. TCAD was classified as significant (s-dtCAD: ≥50% stenosis), non-significant (ns-dtCAD: <50%), or absent (no-dtCAD). CAD progression, defined as new (≥50% stenoses in previously unaffected territories) was evaluated using protocol-based (performed at 1 and 5 years post-transplant) and clinically indicated angiograms. Progression risk was assessed by means of competing risk analysis using the Fine-Gray method.
RESULTS: From a cohort of 1,918 recipients, 937 underwent baseline angiogram. dtCAD was identified in 172 patients (65 s-dtCAD). At follow-up, 791 patients had 1-year and 246 had 5-year angiograms. A total of 1,960 angiograms were evaluated. Cumulative incidence of CAD progression was 5.39% (95%CI 3.81-7.36) and 16.09% (95%CI 12.30-20.33) at 1 and 5 years, respectively. Progression rates were higher among patients with dtCAD compared with those with no-dtCAD: s-dtCAD: 9.65 per 100 person-years (95%CI 5.35- 17.43), ns-dtCAD: 9.24 (95%CI 5.82- 14.67), no-dtCAD: 2.72 (95%CI 2.00 - 3.69). Both s-dtCAD (adjusted SHR: 2.38; 95%CI: 1.26-4.52; p = 0.008) and ns-dtCAD (adjusted SHR: 2,92; 95%CI 1.67-5.08; p< 0.001) were independent predictors of CAD progression.
CONCLUSIONS: dtCAD was independently associated with a threefold increased risk of CAD progression after HT.