Key result
Hypertensive LVH linked to ~14% lower midwall circumferential shortening despite preserved LVEF.
Why the study?
In hypertensive left ventricular hypertrophy, whole-heart studies show normal systolic function by ejection fraction-systolic stress relations, whereas isolated muscle data show depressed contractility, a discrepancy potentially related to geometric factors.
Cross-Sectional (n=93)
Absolute Event Rate: 18% vs 21%
p-value: p=<0.01
In hypertensive left ventricular hypertrophy, high relative wall thickness allows preserved ejection fraction and normal endocardial circumferential shortening despite depressed midwall and long-axis myocardial shortening.
Supports geometry-specific systolic assessment in hypertensive LVH; leaves open outcome prediction and practice change pending prospective data.
OBJECTIVES: This study of hypertensive left ventricular hypertrophy 1) assessed myocardial shortening in both the circumferential and long-axis planes, and 2) investigated the relation between geometry and systolic function. BACKGROUND: In hypertensive left ventricular hypertrophy, whole-heart studies have suggested normal systolic function on the basis of ejection fraction-systolic stress relations. By contrast, isolated muscle data show that contractility is depressed. It occurred to use that this discrepancy could be related to geometric factors (relative wall thickness). METHODS: We studied 43 patients with hypertensive left ventricular hypertrophy and normal ejection fraction (mean +/- SD 69 +/- 13%) and 50 clinically normal subjects. By echocardiography, percent myocardial shortening was measured in two orthogonal planes; circumferential shortening was measured at the endocardium and at the midwall, and long-axis shortening was derived from mitral annular motion (apical four-chamber view). Circumferential shortening was related to end-systolic circumferential stress and long-axis shortening to meridional stress. RESULTS: Endocardial circumferential shortening was higher than normal (42 +/- 10% vs. 37 +/- 5%, p < 0.01) and midwall circumferential shortening lower than normal in the left ventricular hypertrophy group (18 +/- 3% vs. 21 +/- 3%, p < 0.01). Differences between endocardial and midwall circumferential shortening are directly related to differences in relative wall thickness. Long-axis shortening was also depressed in the left ventricular hypertrophy group (18 +/- 6% in the left ventricular hypertrophy group, 21 +/- 5% in control subjects, p < 0.05). Midwall circumferential shortening and end-systolic circumferential stress relations in the normal group showed the expected inverse relation; those for approximately 33% of the left ventricular hypertrophy group were > 2 SD of normal relations, indicating depressed myocardial function. There was no significant relation between long-axis shortening and meridional stress, indicating that factors other than afterload influence shortening in this plane. CONCLUSIONS: High relative wall thickness allows preserved ejection fraction and normal circumferential shortening at the endocardium despite depressed myocardial shortening in two orthogonal planes.
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Aurigemma et al. (1995) conducted a cross-sectional in Hypertensive left ventricular hypertrophy (n=93). Hypertensive left ventricular hypertrophy vs. Clinically normal subjects was evaluated on Midwall circumferential shortening (p=<0.01). Hypertensive left ventricular hypertrophy was associated with depressed midwall circumferential shortening (18% vs 21%, p<0.01) despite preserved ejection fraction and normal endocardial shortening.
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