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Usefulness of At Rest and Exercise Hemodynamics to Detect Subclinical Myocardial Disease in Type 2 Diabetes Mellitus

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Patients with type 2 diabetes mellitus (T2DM) might have subclinical myocardial dysfunction identified at rest or unmasked during exercise. We examined the correlates of the myocardial exercise response in patients with T2DM. Myocardial dysfunction was sought during at rest and exercise echocardiography in 167 healthy patients with T2DM (97 men, 55 ± 10 years). Myocardial ischemia was excluded using stress echocardiography. Standard echocardiography and color tissue Doppler imaging measures (early diastolic tissue velocity [Em], strain, and strain rate) were acquired at baseline and peak stress. The calibrated integrated backscatter was calculated from the at rest parasternal long-axis view. The longitudinal diastolic functional reserve index after exercise was defined as ΔEm [1 − (1/Embase)]. The clinical, anthropometric, and metabolic data were collected at rest and stress. Subclinical myocardial dysfunction at baseline (n = 24) was independently associated with weight (odds ratio [OR] 1.02, p = 0.04) and hemoglobin A1c (OR 1.36, p = 0.03). This group displayed an impaired exercise response that was independently associated with a reduced exercise capacity (OR 0.84, p = 0.034) and longitudinal diastolic functional reserve index (OR 0.69, p = 0.001). Inducible myocardial dysfunction (stress Em <−9.9 cm/s) was identified after exercise in 70 of the remaining 143 subjects. This finding was associated with calibrated integrated backscatter (OR 1.08, p = 0.04) and lower peak heart rate (OR 0.97, p = 0.002) but not metabolic control. The intensity of the metabolic derangement in patients with T2DM was associated with subclinical at rest myocardial dysfunction, but not with the myocardial exercise response. In conclusion, the association of an abnormal stress response with nonmetabolic factors, including backscatter and blunted peak heart rate, suggests potential roles for myocardial fibrosis and cardiac autonomic neuropathy in patients with nonischemic diabetic heart disease.

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Methods

A total of 167 apparently healthy subjects with T2DM (97 men, 55 ± 10 years) and no macro- or microvascular complications of T2DM or history of hypertension or valvular, congenital, or ischemic heart disease were recruited from the hospital clinics of the Princess Alexandra Hospital and its local community. Sinus rhythm and normal renal function were required for inclusion. Antihypertensive medications were withheld for ≥12 hours before testing. The human research ethics committees of Princess

Results

All 167 subjects had an ejection fraction at rest of >50% and no evidence of inducible ischemia on the exercise stress echocardiogram. Sinus rhythm was maintained throughout testing in all participants. At baseline, 24 subjects had subclinical dysfunction as shown by a reduced at rest Em (septal Em <2 SD of normal for age). Differences were noted between the metabolic parameters of those with abnormal findings and the 143 subjects with normal at rest myocardial function (Table 1). The subjects

Discussion

The intensity of metabolic disturbances in those with T2DM has been associated with subclinical myocardial dysfunction for both diastolic and systolic parameters at rest but was unrelated to the stress response. Instead, abnormal stress responses appear to be associated with myocardial properties consistent with structural change. Diabetic heart disease is characterized by myocardial collagen deposition and myofibrillar hypertrophy in the absence of valvular, congenital, hypertensive, or

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This study was supported in part by a Centres for Clinical Research Excellence award (455832) from the National Health and Medical Research Council, Canberra, Australia. Dr. Jellis was supported by a Research Entry Scholarship from the Vincent Fairfax Family Foundation, Sydney, Australia; and the Royal Australasian College of Physicians, Sydney, Australia.

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