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J Am Coll Cardiol, 2003; 41:611-617, doi:10.1016/S0735-1097(02)02869-3
© 2003 by the American College of Cardiology Foundation
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CLINICAL STUDY: CARDIOVASCULAR IMAGING

Echocardiographic detection of early diabetic myocardial disease

Zhi You Fang, BM, MHSc*, Satoshi Yuda, MD, PhD*, Vinah Anderson, BSN*, Leanne Short, BS*, Colin Case, MSc* and Thomas H. Marwick, MB.BS, PhD, FACC*,*

* University of Queensland, Brisbane, Australia

Manuscript received April 26, 2002; revised manuscript received August 26, 2002, accepted November 1, 2002.

* Reprint requests and correspondence: Prof. Thomas H. Marwick, University of Queensland Department of Medicine, Princess Alexandra Hospital, Ipswich Road, Brisbane, Qld 4012, Australia.
tmarwick{at}medicine.pa.uq.edu.au

OBJECTIVES: We sought to determine whether disturbances of myocardial contractility and reflectivity could be detected in diabetic patients without overt heart disease and whether these changes were independent and incremental to left ventricular hypertrophy (LVH).

BACKGROUND: Left ventricular (LV) dysfunction is associated with diabetes mellitus, but LVH is common in this population and the relationship between diabetic LV dysfunction and LVH is unclear.

METHODS: We studied 186 patients with normal ejection fraction and no evidence of CAD: 48 with diabetes mellitus only (DM group), 45 with LVH only (LVH group), 45 with both diabetes and LVH (DH group), and 48 normal controls. Peak strain and strain rate of six walls in apical four-chamber, long-axis, and two-chamber views were evaluated and averaged for each patient. Calibrated integrated backscatter (IB) was assessed by comparison of the septal or posterior wall with pericardial IB intensity.

RESULTS: All patient groups (DM, DH, LVH) showed reduced systolic function compared with controls, evidenced by lower peak strain (p < 0.001) and strain rate (p = 0.005). Calibrated IB, signifying myocardial reflectivity, was greater in each patient group than in controls (p < 0.05). Peak strain and strain rate were significantly lower in the DH group than in those in the DM alone (p < 0.03) or LVH alone (p = 0.01) groups.

CONCLUSIONS: Diabetic patients without overt heart disease demonstrate evidence of systolic dysfunction and increased myocardial reflectivity. Although these changes are similar to those caused by LVH, they are independent and incremental to the effects of LVH.

Abbreviations and Acronyms
  Am
  peak myocardial late diastolic velocity
  ANOVA
  analysis of variance
  CAD
  coronary artery disease
  DH group
  diabetic patients with left ventricular hypertrophy
  DM group
  diabetic patients without left ventricular hypertrophy
  Em
  peak myocardial early diastolic velocity
  HbA1c
  hemoglobin A1c
  IB
  integrated backscatter
  LV
  left ventricular
  LVH
  left ventricular hypertrophy
  LVH group
  nondiabetic patients with left ventricular hypertrophy




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