Quantitative assessment of left ventricular and left atrial functions by strain rate imaging in diabetic patients with and without hypertension.

Abstract

Impaired left ventricular (LV) function is shown by strain rate (SR) imaging in patients with diabetes mellitus (DM). Left atrium (LA) function in patients with DM, however, has not been assessed by this method and the effect of hypertension (HT) on LV and LA functions in diabetic patients has not been fully studied. The aim of this study was to quantitatively assess LA function in diabetic patients with and without HT in combination with LV function.
Conventional echocardiographic and SR imaging studies were performed in 55 subjects with normal systolic LV function (LV ejection fraction of 55% or more) and no evidence of coronary artery disease: 17 with DM (DM group), 22 who have both DM and HT (DM+HT group), and 16 age-matched controls. SR imaging was performed from three apical views, and peak SR was measured at 12 LV segments and 5 LA segments. Mean peak systolic SR (LVs and LAs, respectively), early diastolic SR (LVe and LAe, respectively) and late diastolic SR (LVa and LAa, respectively) were calculated by averaging data in each LV and LA segment.
Despite no significant differences in age, LV ejection fraction and E/A ratio among the three groups, systolic blood pressure, LA dimension and LV mass index in the DM+HT group were significantly larger than those in the controls. The DM group had reduced systolic and diastolic LV functions and impaired LA reservoir and conduit functions compared with those in the controls, as shown by lower LVs (P < 0.05), LVe (P < 0.01), LAs (P < 0.01), and LAe (P < 0.05). The DM+HT group had reduced LVs (P < 0.01), LVe (P < 0.01), LAs (P < 0.01) and LAe (P < 0.01) compared with those in the controls. The DM+HT group had significantly lower LVe (P < 0.05) and LAe (P < 0.05) than did the DM group.
SR imaging can detect impairment of LA reservoir and conduit functions as well as LV systolic and diastolic dysfunctions in patients with DM, even in the absence of LV hypertrophy and LA dilatation. Coexisting HT augments the impairment of LV diastolic and LA conduit functions in diabetic patients.