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Updated: Aug 5, 2026

Cardiac Loading using Passive Left Atrial Pressurization and Passive Afterload for Graft Assessment
Published on: August 2, 2024
Post-transplant diabetes is associated with late systolic left ventricular dysfunction after heart transplantation
Anna Werther Evaldsson1, Ashkan Labaf1, Grunde Gjesdal1
1Department of Clinical Sciences, Lund, Cardiology, and the Section for Heart Failure and Valvular Disease, Skåne University Hospital, Lund University, Lund, Sweden.
Background:
Post-transplant diabetes mellitus (PTDM) is common after orthotopic heart transplantation (OHT), but its long-term impact on myocardial function is unclear. We aimed to evaluate the effects of PTDM on left ventricular (LV) systolic function.
Methods:
We prospectively studied 102 OHT recipients with echocardiographic follow-up at 1-, 3-, and 5-year post-transplant. Patients were classified according to PTDM status at 1 year. LV systolic function was assessed using ejection fraction (EF) and global longitudinal strain (GLS). Linear mixed-effects models were used to evaluate longitudinal associations, adjusting for age, sex, systolic blood pressure, and cardiac allograft vasculopathy (CAV).
Results:
PTDM was present in 36% of patients. At 1-year, EF and GLS were similar between groups. At 3 years, patients with PTDM exhibited significantly lower systolic function as assessed by GLS (-14.9±2.8 vs. -16.0±3.0%, p=0.022), and at 5 years, EF was also significantly lower (52±4 vs. 57±7%, p=0.002). In longitudinal analyses, PTDM was associated with persistently impaired GLS without a significant interaction with time (p=0.192). In contrast, EF demonstrated a significant PTDM×time interaction (p=0.039), reflecting a greater decline over time in patients with PTDM. These associations remained significant after adjustment for CAV, which was not independently associated with GLS or EF.
Conclusion:
PTDM after OHT is associated with early and persistent impairment in myocardial deformation, followed by a progressive decline in systolic function. These findings suggest a metabolically mediated myocardial effect independent of chronic graft failure and highlight the importance of early detection and management of PTDM in heart transplant recipients.
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