The detection of early myocardial changes in asymptomatic diabetic individuals by 99mTc - Myoview gated-SPET and heart rate variability measurement.

Abstract

Incidence of early myocardial changes in asymptomatic diabetic individuals is not clearly documented. In the present study, we examined diabetic patients without a history of cardiovascular disease with negative treadmill test and no signs of systolic dysfunction for presence of cardiac autonomic neuropathy established by measurement of heart rate variability (HRV) and (99m)Tc - Myoview gated-SPET. 47 type I and type II diabetic patients were subjected to prospective study including echocardiography and HRV measurement using the combination of Ewing´s testing and spectral analysis. Subsequently, patients underwent treadmill test and stress myocardial perfusion scintigraphy. Additionally, vascular and metabolic parameters were collected. Treadmill test was negative in all patients. Diastolic dysfunction was found in 10 % of T1DM and 11 % of T2DM patients by echocardiography, whereas none of the patients had systolic dysfunction. SPET confirmed hypoperfusion in 35 % T1DM (p=0.01) and in 60 % T2DM (p=0.001). Diagnosis of cardiac autonomic neuropathy based on Ewing´s testing and HRV examination was established in 60 % of T1DM patients (p=0.001) and 77 % of T2DM patients (p=0.001). In T1DM group, significant association was found between cardiac autonomic neuropathy (CAN) and frequency of hypoglycaemia (p=0.04). No such correlations were found in patients with T2DM. The results of the present study show high incidence of myocardial hypoperfusion and cardiac autonomic neuropathy among asymptomatic diabetic patients, whereas the standard diagnostic approaches including treadmill test and echocardiography failed to show any changes. Therefore, we conclude that diabetic heart disease remains underdiagnosed by standard approaches, but could be detected in asymptomatic patients by more sensitive methods, such as HRV measurement and myocardial scintigraphy (Tab. 2, Fig. 2, Ref. 26).