Jellis, CL and Stanton, T and Leano, R and Martin, J and Marwick, TH, Usefulness of at rest and exercise hemodynamics to detect subclinical myocardial disease in type 2 diabetes mellitus, The American Journal of Cardiology, 107, (4) pp. 615-621. ISSN 0002-9149 (2011) [Refereed Article]
Copyright 2010 Elsevier
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.
In addition to hastening atherosclerosis, type 2 diabetes mellitus (T2DM) and the metabolic syndrome have been linked to myocardial disease in the absence of ischemic heart disease and hypertension. This is likely multifactorial, secondary to the accumulation of advanced glycated end products, myocardial fibrosis, microvascular disease, and autonomic neuropathy. Diabetic heart disease is initially asymptomatic; however, nonspecific symptoms of fatigue, dyspnea, or reduced exercise tolerance will gradually develop. Early detection might facilitate measures to prevent disease progression. Tissue velocity and deformation imaging can detect myocardial dysfunction when the conventional 2-dimensional echocardiographic parameters are normal. In early diabetic heart disease, myocardial function might be preserved at rest, with exercise unmasking a blunting of contraction and relaxation, indicative of an abnormal functional reserve. Longitudinal function is typically reduced initially, reflective of the early involvement of the subendocardial fibers. Impairment in the at rest and peak exercise systolic tissue velocity has been associated with common metabolic risk factors in asymptomatic patients. We sought to identify whether early diastolic tissue velocity (Em), deformation imaging, and tissue characterization could identify diabetic heart disease not apparent at rest and examined the correlates of myocardial dysfunction with exercise.
|Item Type:||Refereed Article|
|Research Division:||Medical and Health Sciences|
|Research Group:||Cardiorespiratory Medicine and Haematology|
|Research Field:||Cardiology (incl. Cardiovascular Diseases)|
|Objective Group:||Clinical Health (Organs, Diseases and Abnormal Conditions)|
|Objective Field:||Cardiovascular System and Diseases|
|UTAS Author:||Marwick, TH (Professor Tom Marwick)|
|Web of Science® Times Cited:||24|
|Deposited By:||Menzies Institute for Medical Research|
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