Medalists With Extreme Duration of Type 1 Diabetes Exhibit Only Mild Diastolic Dysfunction and Myocardial Fibrosis

Medalists are a unique subset of patients with more than 50 years of type 1 diabetes. One would expect these patients to have significant microvascular and macrovascular complications. However, the Joslin observational study showed that of their medalists, a substantial proportion remained free of proliferative diabetic retinopathy (42.6%), nephropathy (86.9%), and neuropathy (39.4%) (1). Whether this protection extends to the heart is unknown.

We therefore comprehensively investigated cardiac structure and function in 14 medalists and 9 control subjects. They underwent rest and stress (vasodilator) perfusion MRI to exclude significant coronary artery disease and echocardiography to quantify cardiac structure and left ventricular systolic function, including strain, strain rate, torsion, and diastolic dimensions. Pulsed-wave Doppler sequences of the mitral valve assessing passive early (E) and active atrial (A) diastolic filling as well as tissue Doppler imaging of mitral annular movement allowed an assessment of diastolic dysfunction. Myocardial fibrosis was assessed using calibrated integrated backscatter.

Comparing medalists to control subjects (Table 1), BMI, blood pressure, serum cholesterol, and triglycerides were comparable. HbA_1c (P < 0.0001) and HDL (P < 0.05) were higher, and LDL (P < 0.05) was significantly lower. Medalists and control subjects had similar left ventricular end-diastolic and end-systolic diameters, ejection fraction, longitudinal strain, and torsion. However, medalists had a higher E/E’ ratio, lower E/A ratio, and higher integrated backscatter (P < 0.05) compared with control subjects.

Medalists had poor glycemic control but a favorable lipid profile with a lower LDL and higher HDL, possibly explaining the lack of coronary artery disease observed on MRI and the low prevalence of cardiovascular events in this population (1). Furthermore, the medalist group was slightly older, which emphasizes the cardiac protection they have exhibited, as age independently predicts an abnormal echocardiogram in patients with type 1 diabetes (2).

Furthermore, to our surprise there was no difference in longitudinal and circumferential strain, strain rate, peak apical/basal rotation, peak apical back rotation rate, and peak LV twist/untwist between medalists and control subjects. This is in contrast with previous studies showing abnormal strain, rotation, and twist in patients with type 1 diabetes (3) and systolic dysfunction in type 1 diabetic adolescents during short exercise, implying a loss of systolic reserve (4). Medalists did exhibit diastolic dysfunction, evidenced by lower E/A ratios and higher E/E’ ratios, but this was mild and has been demonstrated in patients with a much shorter duration of diabetes (5). Furthermore, there was also evidence of only mild myocardial fibrosis, despite poor glycemic control and such an extreme duration of diabetes.

The sample size of this study was small; however, we believe this is a unique cardiac phenotyping study in a unique group of patients with type 1 diabetes.

In summary, we demonstrate protection from systolic dysfunction and abnormalities in cardiac structure with only mild diastolic dysfunction and myocardial fibrosis in medalists. This makes the medalists a unique cohort of patients with type 1 diabetes who merit further detailed study to identify the mechanistic basis of this protection from cardiovascular disease.