Background-Obesity is associated with heart failure, but an effect of weight, independent of comorbidities, on cardiac structure and function is not well established. We sought whether body mass index (BMI) and insulin levels were associated with subclinical myocardial disturbances. Methods and Results-Transthoracic echocardiography, myocardial Doppler-derived systolic (sm) and early diastolic velocity (em), strain and strain rate imaging and tissue characterization with cyclic variation (CVIB), and calibrated integrated backscatter (cIB) were obtained in 109 overweight or obese subjects and 33 referents (BMI Ͻ25 kg/m 2 ). BMI correlated with left ventricular (LV) mass and wall thickness (PϽ0.001). Severely obese subjects (BMI Ͼ35) had reduced LV systolic and diastolic function and increased myocardial reflectivity compared with referents, evidenced by lower average long-axis strain, sm, cIB, lower CVIB, and reduced em, whereas LV ejection fraction remained normal. Differences in regional or global strain, sm, and em were identified between the severely obese (BMI Ͼ35) and the referent patients (PϽ0.001). Similar but lesser degrees of reduced function by sm, em, and basal septal strain and increased reflectivity by cIB were present in overweight (BMI, 25 to 29.9) and mildly obese (BMI, 30 to 35) groups (PϽ0.05). Although tissue Doppler measures were not associated with duration of obesity, they did correlate with fasting insulin levels and reduced exercise capacity. BMI was independently related to average LV strain (␤ϭ0.40, Pϭ0.02), sm (␤ϭϪ0.36, Pϭ0.002), and em (␤ϭϪ0.41, PϽ0.001). Conclusions-Overweight subjects without overt heart disease have subclinical changes of LV structure and function even after adjustment for mean arterial pressure, age, gender, and LV mass.

The interpretation of wall motion is an important component of echocardiography but remains a source of variation between observers. It has been believed that automated quantification of left ventricular (LV) systolic function by measurement of LV systolic strain from speckle-tracking echocardiography might be helpful. This multicenter study of nearly 250 volunteers without evidence of cardiovascular disease showed an average LV peak systolic strain of -18.6 +/- 0.1%. Although strain was influenced by weight, blood pressure, and heart rate, these features accounted for only 16% of variance. However, there was significant segmental variation of regional strain to necessitate the use of site-specific normal ranges.

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Background-Although

The combined assessment of long-axis and short-axis function using 2D strain may be used to identify TME.

Subclinical left ventricular (LV) dysfunction may be identified by reduced longitudinal contraction. We sought to define the effects of subclinical LV dysfunction on radial contractility in 53 patients with diabetes mellitus with no LV hypertrophy, normal ejection fraction and no ischaemia as assessed by dobutamine echocardiography, in comparison with age-matched controls. Radial peak myocardial systolic velocity (Sm) and early diastolic velocity (Em), strain and strain rate were measured in the mid-posterior and mid-anteroseptal walls in parasternal views and each variable was averaged for individual patients (radial contractility). These variables were also measured in the mid-posterior and mid-anteroseptal walls in the apical long-axis view and each variable was averaged for individual patients (longitudinal contractility). Mean radial Sm, strain and strain rate were significantly increased in diabetic patients (2.9 +/- 0.6 cm/s, 28 +/- 5% and 1.8 +/- 0.4 s(-1) respectively) compared with controls (2.4 +/- 0.7 cm/s, 23 +/- 4% and 1.6 +/- 0.3 s(-1) respectively; all P<0.001), but there was no difference in Em (3.3 +/- 1.2 compared with 3.1 +/- 1.1 cm/s, P=not significant). In contrast, longitudinal Sm, Em, strain and strain rate were significantly lower in diabetic patients (3.6 +/- 1.1 cm/s, 4.3 +/- 1.6 cm/s, 21 +/- 4% and 1.6 +/- 0.3 s(-1) respectively) than in controls (4.3 +/- 1.0 cm/s, 5.7 +/- 2.3 cm/s, 26 +/- 4% and 1.9 +/- 0.3 s(-1) respectively; all P< or =0.001). Thus radial contractility appears to compensate for reduced longitudinal contractility in subclinical LV dysfunction occurring in the absence of ischaemia or LV hypertrophy.

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Increasing BMI is associated with increasing severity of RV dysfunction in overweight and obese subjects without overt heart disease, independent of sleep apnea.