Introduction & Purpose:
Maintenance of left ventricular systolic and diastolic function after heart transplantation (HTx) is crucial for clinical outcomes and survival. While post-transplant systolic dysfunction has been extensively studied, risk factors and pathomechanisms leading to diastolic dysfunction remain poorly understood. Inflammatory processes and metabolic comorbidities such as diabetes may play an important role in the development of post-transplant diastolic dysfunction. Here, we aim to evaluate the association between diabetes, myocardial inflammation and diastolic function after heart transplantation.
Methods:
158 HTx recipients with or without type 2 diabetes mellitus (T2DM) were enrolled in an ongoing single-center, prospective, observational trial between 2016 and 2025. Within the first three years after HTx, we annually performed echocardiography to assess the ratio of early to late diastolic transmitral flow velocity (E/A), and cardiac magnetic resonance imaging to assess left ventricular global longitudinal and circumferential strain (GLS, GCS), left ventricular early and late diastolic longitudinal (GLSRe and GLSRa) and circumferential strain rate (GCSRe and GCSRa), time-to-peak GLSRe (TTPGLSRe), left atrial volume index (LAVI), and T2 relaxation time (T2).
Results:
Two years after HTx (n=158 with 31.0% T2DM), GCSRe (1.05±0.19/s vs. 1.24±1.05/s, p=0.015) was lower, whereas GLS (-14.3±2.0% vs. -16.4±1.9%, p=0.002), GCS (-16.0±4.2% vs. -18.8±2.6%, p=0.02), GCSRa (0.43±0.20/s vs. 0.29±0.10/s, p= 0.029) and LAVI (54.2±19.6ml/m² vs. 38.3±12.6ml/m², p=0.008) were higher in the T2DM group.
Three years after HTx (n=128 with 31.3% T2DM), E/A (1.82±0.014 vs. 2.31±0.84, p=0.01) was lower, and GLSRa (0.48±0.19/s vs. 0.37±0.15/s, p=0.039), GCSRa (0.38±0.15 vs. 0.29±0.11, p=0.04), and TTPGLSRe (141.7±23.7ms vs. 122.1±31.8ms, p=0.02) were higher in the T2DM group.
HbA1c was associated with worse GLS (r=0.22, p=0.007), GLSRe (r=-0.20, p=0.013), GCSRe (r=-0.17, p=0.038) and tended to be associated with lower E/A (r=-0.16, p=0.053) and higher GCS (r=0.16, p=0.058). Within the patients with T2DM, T2 correlated significantly with GLS (r=0.53, p=0.008), GCS (r=0.51, p=0.011) and nearly significantly with LAVI (r=0.35, p= 0.065).
Conclusion(s):
Heart transplant recipients with T2DM exhibit impaired diastolic function in the first three years after HTx, which is aggravated in those with worse glycemic control. The hyperglyemic state (HbA1c) and myocardial inflammation represented by T2 times were associated with reduced diastolic function, possibly hinting towards pathomechanisms linked to post-transplant diastolic dysfunction.
