Cardiomyopathy in type 1 diabetes – Does it exist? New article from the Oslo Study

We have shown significant reduced myocardial function in long term type 1 diabetes even without significant coronary heart disease. This may point to a subclinical diabetic cardiomyopathy and/or a microvascular defect as suggested by reduced myocardial Blood Flow reserve. The increased level of Glycation products may suggest that Glycation leads to “stiffer hearts”?

We all know that diabetes is a major risk factor for macrovascular coronary heart disease. Left ventricular dysfunction in the absence of hypertension, coronary artery and valvular heart disease has been defined as diabetic cardiomyopathy. However, there are still uncertainties about the diagnosis of diabetic cardiomyopathy and how it develops. Therefore we studied a cohort from the prospective Oslo Study in type 1 diabetes by modern echocardiography by two-dimensional strain and the ratio between pulsed Doppler transmitral early (E) velocity and tissue Doppler velocity (E′), to assess LV systolic and diastolic functions and in a control group. We also performed coronary angiography in the diabetes patients.

Strain was significantly reduced (−19.5% ± 1.9% vs −21.4% ± 3.5%, p < 0.05), and E/E′ increased in the diabetes patients compared to controls, 7.3 ± 2 versus 6.0 ± 1.5, p < 0.05. Significant lower Myocardial Blood Flow Reserve was present in the diabetes patients, 3.4 (2.1, 5.3) versus 5.9 (3.9, 9.6), p < 0.01. Both Advanced Glycation Endproducts (methylglyoxal derived hydroimidazolone and glyoxal hydroimidazolone) correlated significantly with E/E′. The impaired LV function with correlation to AGEs in concert with reduced MBFR in diabetics without coronary artery disease may indicate possible mechanisms for diabetic cardiomyopathy.

This study was a collaborative study between the Cardiology Department AHUS University Hospital, Department of Pathology and Biochemistry, CWRU University, Cleveland US, Oslo Diabetes Research Centre and Oslo University Hospital.

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