Determinants of subclinical diabetic heart disease

Abstract

Aims/hypothesis: Subclinical left ventricular (LV) dysfunction has been shown by tissue Doppler and strain imaging in diabetic patients in the absence of coronary disease or LV hypertrophy, but the prevalence and aetiology of this finding remain unclear. This study sought to identify the prevalence and the determinants of subclinical diabetic heart disease. Methods: A group of 219 unselected patients with type 2 diabetes without known cardiac disease underwent resting and stress echocardiography. After exclusion of coronary artery disease or LV hypertrophy, the remaining 120 patients (age 57±10 years, 73 male) were studied with tissue Doppler imaging. Peak systolic strain of each wall and systolic (Sm) and diastolic (Em) velocity of each basal segment were measured from the three apical views and averaged for each patient. Significant subclinical LV dysfunction was identified according to Sm and Em normal ranges adjusted by age and sex. Strain and Em were correlated with clinical, therapeutic, echocardiographic and biochemical variables, and significant independent associations were sought using a multiple linear regression model. Results: Significant subclinical LV dysfunction was present in 27% diabetic patients. Myocardial systolic dysfunction by peak strain was independently associated with glycosylated haemoglobin level (p<0.001) and lack of angiotensin-converting enzyme inhibitor treatment (p=0.003). Myocardial diastolic function (Em) was independently predicted by age (p=0.013), hypertension (p=0.001), insulin (p=0.008) and metformin (p=0.01) treatment. Conclusions/interpretation: In patients with diabetes mellitus, subclinical LV dysfunction is common and associated with poor diabetic control, advancing age, hypertension and metformin treatment; ACE inhibitor and insulin therapies appear to be protective.

Impact of Improved Glycemic Control on Cardiac Function in Type 2 Diabetes Mellitus

“…Consistent with other published studies, 3,4,[13][14][15] our study demonstrated that patients with type 2 diabetes mellitus have impaired LV systolic and diastolic function despite a normal LV ejection fraction. Our study also showed that better glycemic control over a 12-month period resulted in improvements in LV systolic and diastolic function.…”

“…Some studies have shown that poor glycemic control was associated with abnormal LV relaxation, elevated LV filling pressures, and lower systolic strain. 13,19,20 Patients who had poorly controlled diabetes mellitus in the Strong Heart Study were found to have abnormal LV relaxation. 20 In 120 patients with type 2 diabetes mellitus after exclusion of ischemia and LV hypertrophy, peak systolic strain was independently associated with HbA1c levels, whereas septal e′ velocities were more related to age and hypertension but not related to glycemic control.…”

Cardiac Diastolic Function Is Impaired at Rest and Worsens With Exercise in Otherwise Healthy Individuals With Insulin Resistance

“…24) Briefly, an exercise induced increase in the E/e' ratio seems to be a good predictor of reduced ventricular compliance and decreased exercise capacity. 25) Due to direct metabolic effects on myocytes, 26) and disturbances in the microvascular function 27) and autonomic neuropathy; 28) myocardial dysfunction is a common involvement in T2DM. 29) Diastolic dysfunction is the earliest manifestation of diabetic cardiomyopathy and even a small amount is a predictor of a poor prognosis.…”

Pioglitazone Improves Cardiac Function and Alters Myocardial Substrate Metabolism Without Affecting Cardiac Triglyceride Accumulation and High-Energy Phosphate Metabolism in Patients With Well-Controlled Type 2 Diabetes Mellitus

“…12 However, although pioglitazone improved cardiac function in experimental diabetic cardiomyopathy, 13,14 its use in patients may result in heart failure due to fluid retention. 15 Inasmuch as the majority of patients in the PROactive study had CAD and longstanding diabetes, it is feasible that cardiac inability to accommodate metabolic changes may have contributed to the pioglitazone-related heart failures. Indeed, substrate manipulation in heart failure due to CAD decreased myocardial efficiency and cardiac function, 16 which reveals the close connection of metabolism and function in the compromised heart.…”