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Published on: April 8, 2013
Improvement in midwall myocardial shortening with regression of left ventricular hypertrophy
1Department of Cardiology, St. Mary's Hospital Praed Street, London W2 1NY, UK. j.mayet@ic.ac.uk
Insights
Hypertensive patients with left ventricular hypertrophy (LVH) show reduced midwall systolic shortening. Antihypertensive therapy improved this midwall function, normalizing it after LVH regression.
Area of Science:
- Cardiology
- Hypertension Research
- Echocardiography
Background:
- Hypertension often leads to left ventricular hypertrophy (LVH).
- LVH in hypertensive patients may present with impaired midwall systolic shortening despite normal overall left ventricular (LV) function.
- The impact of antihypertensive therapy on midwall systolic function in LVH requires further investigation.
Purpose of the Study:
- To confirm depressed midwall systolic shortening in hypertensive patients with LVH compared to normotensives.
- To evaluate the effect of antihypertensive treatment causing LVH regression on LV systolic function, specifically midwall and endocardial shortening.
Main Methods:
- Echocardiography was used to compare 38 hypertensive patients with LVH against 38 normotensive controls.
- Midwall and endocardial fractional shortening were assessed.
- 32 hypertensive patients with LVH received antihypertensive therapy (ramipril, felodipine, bendrofluazide) to achieve blood pressure <140/90 mm Hg.
- Echocardiography was performed at baseline, after blood pressure control, and after 6 months of sustained control.
Main Results:
- Hypertensive patients with LVH had significantly lower midwall shortening (17.9%) than controls (21.6%), while endocardial shortening and ejection fraction were similar.
- Antihypertensive therapy successfully reduced blood pressure and LV mass index.
- Midwall shortening significantly improved after LVH regression, reaching levels comparable to normotensive controls.
Conclusions:
- Hypertensive patients with LVH exhibit reduced midwall systolic shortening, indicating subclinical myocardial dysfunction.
- Effective blood pressure control and subsequent regression of LVH can normalize midwall systolic function.
- Midwall shortening is a sensitive marker for assessing LV systolic function in hypertensive heart disease.
Abstract:
Despite normal indices of left ventricular (LV) chamber function, patients with LV hypertrophy (LVH) due to hypertension are thought to have depressed midwall systolic shortening compared with normotensives. The aims of the present study were (1) to confirm this observation and (2) to assess the effects of antihypertensive therapy that cause regression of LVH on LV systolic function assessed at both the midwall and endocardium. Thirty-eight previously untreated hypertensive subjects with LVH underwent echocardiography and were compared with 38 normotensive control subjects. Comparisons between the group with LVH and the control group revealed no significant differences in cardiac output (4. 32+/-0.23 versus 4.55+/-0.21 L/min), ejection fraction (62.5+/-2% versus 66.4+/-1.07%), or endocardial fractional shortening (34.5+/-1.45% versus 37.0+/-0.82%), but shortening assessed at the midwall was significantly less in the group with LVH (17.9+/-1.11% versus 21.6+/-0.63%, P<0.01). Subsequently, 32 patients with uncontrolled hypertension (24 previously untreated and 8 on existing antihypertensive therapy) underwent treatment with ramipril, with the addition of felodipine and bendrofluazide if required, to reduce blood pressure to <140/90 mm Hg. These 32 patients underwent echocardiography at baseline, after blood pressure control, and after an additional 6 months of tight blood pressure control. Good blood pressure control was achieved after 6 months compared with baseline (143/86+/-2.8/1.4 versus 174/103+/-4.1/1.9 mm Hg; P<0.01) with significant regression of LV mass index (124+/-3.4 versus 145+/-3.8 g/m(2), P<0.01). LV fractional shortening assessed at the midwall improved with regression of LVH (21.9+/-0.84 and 18.7+/-1. 19%, P<0.05), with posttreatment midwall shortening being similar to that of the normal control subjects evaluated in the first study. Hypertensive patients with LVH have depressed midwall systolic shortening despite normal indices of LV chamber function. Regression of LVH after good blood pressure control improved midwall shortening to normal levels.
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