Echocardiographic detection of early diabetic myocardial disease

Cardiology Review® OnlineMay 2004
Volume 21
Issue 5

From the University of Queensland, Brisbane, Australia

Diabetes mellitus (DM) is associated with left ventricular dysfunction. Interstitial fibrosis has been shown in biopsy studies of diabetic hearts in the absence of hypertension or coronary artery disease (CAD),1,2 although left ventricular hypertrophy (LVH) is commonly present in this population and may itself be responsible for these changes. Previous noninvasive studies with calibrated integrated backscatter, a marker of myocardial reflectivity, have suggested a direct effect of diabetes on the myocardium; however, this modality is technically demanding and prone to artifact.3,4 We used sensitive new markers of systolic performance and myocardial reflectivity to determine early myocardial changes in diabetic patients with a normal ejection fraction, with and without LVH.

Patients and methods

We divided 186 individuals with normal ejection fraction and no evidence of CAD based on dobutamine stress echocardiography into four groups: 48 patients with diabetes only (DM group), 45 patients with LVH only (LVH group), 45 patients with both diabetes and LVH (DH group), and 48 normal control subjects. The peak strain and strain rate of each wall were measured in apical four-chamber, long-axis, and two-chamber views and were averaged for each patient. Calibrated integrated backscatter was assessed by comparing the septal or posterior wall with pericardial integrated backscatter intensity.


All patient groups (DM, DH, and LVH) showed significant decreases in peak strain (24% ± 3%, 22% ± 3%, and 24% ± 3%, respectively; P ≤ .001 for all) and strain rate (1.4 ± 0.3 s—1, P = .006; 1.3 ± 0.2 s–1, P < .001; and 1.4 ± 0.2 s–1,

P = .005, respectively) compared with peak strain (26% ± 4%) and strain rate (1.6 ± 0.3 s—1) in control subjects. Peak strain and strain rate were significantly lower in the DH group than in the DM group (P = .03 and P = .01, respectively) and in the LVH group (P = .02 and P = .01, respectively). With the exception of the posterior wall in the DM group, the three patient groups (DM, DH, and LVH) showed significant increases in calibrated integrated backscatter in the septum (–18.6 ± 7.9 dB, P = .045; –17.1 ± 7.0 dB, P = .001; and –7.2 ± 6.4 dB, P = .001, respectively) and in the posterior wall (–27.0 ± 7.0 dB; –23.8 ± 7.6 dB, P = .004; and –25.0 ± 7.7 dB, P = .046, respectively) compared with controls (–22.6 ± 6.6 dB in the septum and –29.0 ± 6.2 dB in the posterior wall). No significant differences in calibrated integrated backscatter, however, were found in the septal or posterior wall among the three patient groups (figure).


The existence of changes in both myocardial function and structure are supported by prominent histopathologic findings of myocellular hypertrophy and myocardial fibrosis in diabetic patients without CAD and hypertension.5 The noninvasive detection of these changes is dependent on the use of sensitive techniques, such as strain, strain rate, and calibrated integrated backscatter. The use of these methods has allowed identification of the role of diabetes alone in relation to myocardial dysfunction, after exclusion of patients with significant LVH and coronary disease.

Diabetes is independently associated with reduction of myocar-

dial contractility. Insulin deficiency causes chronic abnormalities in myocardial carbohydrate and lipid metabolism, including reduced aden-

osinetriphosphatase activity, decreased ability of the sarcoplasmic reticulum to take up calcium,6 and an intracellular accumulation of toxic fatty acid intermediates,7 resulting in adenosinetriphosphatase depletion, changes in calcium homeostasis, and increased myocardial oxygen consumption. These changes may produce a focal, progressive loss of myofibrils, transverse tubules, and sarcoplasmic reticulum, and separation of the fasciae adherens

at the intercalated disk within myocytes,8 leading to myocyte hypertrophy, loss and replacement of fibrosis, and eventually reduced myocardial contractility.

Some studies have shown normal contraction patterns at rest in diabetic patients without overt evidence of heart disease, although the contractile response during exercise was abnormal,9 indicating loss of contractile reserve at an early phase of diabetic heart disease. The reduced contractility at the early phase of diabetic heart disease may be too subtle to be identified with load-dependent indicators, such as ejection fraction, but it can be detected by peak strain and strain rate, as shown in this study. Moreover, diabetes and LVH appear to have synergistic effects on the myocardium, which is evidenced by the significant decrease in myocardial contractility measured by peak strain and strain rate in the DH group.

These findings are similar to previous studies showing that the combination of diabetes and hypertension has a deleterious effect on the myocardium.10 LVH in some diabetic hearts may be mainly secondary to diabetes rather than to hypertension, which was supported by seven patients in the DH group who did not have a history of hypertension.

Diabetes is independently related to increased myocardial reflectivity, implying increased myocardial fibrosis. Total fibrosis and heart weight have been shown to be positively associated in patients with diabetes alone and with both diabetes and LVH.10 Furthermore, col-lagen is the primary determinant

of echocardiographic scattering in myocardial tissue, and good correlation between collagen deposition and backscatter magnitude exists.11,12 This study showed that calibrated integrated backscatter was significantly increased in the three patient groups, which is similar to previous findings,10,13 and suggests that diabetes is as likely as LVH to be associated with myocardial fibrosis. This may play an important role in the early stage of diabetic heart disease. These results are also consistent with previous studies showing greater replacement of the myocardium by fibrosis in both diabetes and hypertension than in diabetes alone.14


Diabetic patients without overt heart disease and LVH showed evidence of systolic dysfunction (de-creased peak strain and strain rate) and changes in myocardial structure (increased calibrated integrated backscatter). These alterations may be progressive to the subsequent overt diabetic cardiomyopathy. Although these changes are similar to those caused by LVH, they are independent of and incremental to the effects of LVH.

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