We thank Dr. Humpert et al. (1) for their interest in our study (2). The authors present data that support the presence of left ventricular (LV) asynchrony in patients with type 2 diabetes in association with cardiovascular autonomic dysfunction (CAN) and LV function.
The authors divided their type 2 diabetic cohort into three groups based on tertiles of expiration-to-inspiration ratio of heart rate variability. Interestingly, although they found a decrease in LV ejection fraction with decreasing autonomic function, there were no differences in diastolic function among the three groups. This result appears to contradict our recent findings in type 1 diabetic patients (2). We and others found a further impairment in diastolic function in patients with type 1 diabetes and CAN compared with diabetic patients without CAN and normal control subjects (2–4). A possible explanation for this disagreement is the pathophysiological differences between the two types of diabetes. Moreover, there are some methodological differences between the two studies. We excluded patients with hypertension, whereas it is unknown whether Humpert et al. did the same. Furthermore, their screening for coronary artery disease (CAD) was based only on history and symptoms, whereas we also performed thallium scintigraphy to ensure the absence of significant CAD. Additionally, our type 1 diabetic cohort had longer duration of disease (more than 20 years) than the authors’ type 2 diabetic cohort (14 years for the lowest tertile of expiration-to-inspiration ratio).
Humpert et al.'s finding that the diabetic patients with diastolic dysfunction, as determined by tissue Doppler imaging, showed higher LV asynchrony than patients without diastolic impairment is interesting but raises some concerns. First, there is a discrepancy between this finding and what the same authors support in a similar recent study where patients with type 2 diabetes and significant diastolic dysfunction showed an extent of asynchrony similar to that in diabetic patients with normal diastolic function (5). Moreover, what is the pathophysiological explanation of the higher LV asynchrony in patients with type 2 diabetes and diastolic dysfunction? Can this be explained by myocardial fibrosis or CAN? We believe that this concept should be further investigated by larger studies in solely type 1 or type 2 diabetic cohorts. In conclusion, although S. Rubler suggested the existence of diabetic cardiomyopathy more than 35 years ago, there still seems to be controversy regarding the specific effects of diabetes on the human myocardium.
