Su-A Kim1, Seong-Mi Park2, Mi-Na Kim3, Wan Joo Shim3. 1. Division of Cardiology, Department of Internal Medicine, Cheil General Hospital, DanKook University College of Medicine, Seoul, Republic of Korea. 2. Division of Cardiology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Republic of Korea. Electronic address: smparkmd@korea.ac.kr. 3. Division of Cardiology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Republic of Korea.
Abstract
BACKGROUND: Systemic arterial hypertension causes functional and structural remodelling of the left ventricle, which is related to subclinical left ventricular (LV) dysfunction and heart failure. This study assessed LV functional change using layer-specific strain and its relationship to structural remodelling in patients with hypertension. METHODS: A total of 145 patients (61 ± 12 years) with primary hypertension and preserved LV ejection fraction and 31 normotensive controls (63 ± 9 years) were prospectively included. Longitudinal strains of the endocardium, myocardium, and epicardium (LSendo, LSmyo, and LSepi) were obtained by averaging peak systolic strain of the left ventricle, with 18 segments in each layer. RESULTS: Layer-specific strains showed a decreasing gradient from the endocardium to the epicardium in both controls and patients with hypertension (P < 0.001 in both) and were significantly different between controls and patients with hypertension in all 3 layers (LSendo, -20.4% ± 2.4% vs -19.2% ± 2.2%; P = 0.007; LSmyo, -15.8% ± 2.0% vs -14.8% ± 1.9%; P = 0.005; LSepi, -11.8% ± 2.0% vs -11.0% ± 1.8%,; P = 0.04). Both LSendo and LSmyo were lower even in patients with hypertension and no LV hypertrophy than in controls (both P < 0.05), although global LS was not different. New patients with hypertension showed more decreased LSendo and LSmyo than controls even with their younger age. LSs of all 3 layers were related to LV mass index and mitral annular velocity parameters. CONCLUSIONS: Layer-specific evaluation of the left ventricle provides an understanding of the layer-specific properties of the LV wall and the process of LV impairment, and it may be helpful in managing patients with hypertension, thus preventing further damage.
RCT Entities:
BACKGROUND: Systemic arterial hypertension causes functional and structural remodelling of the left ventricle, which is related to subclinical left ventricular (LV) dysfunction and heart failure. This study assessed LV functional change using layer-specific strain and its relationship to structural remodelling in patients with hypertension. METHODS: A total of 145 patients (61 ± 12 years) with primary hypertension and preserved LV ejection fraction and 31 normotensive controls (63 ± 9 years) were prospectively included. Longitudinal strains of the endocardium, myocardium, and epicardium (LSendo, LSmyo, and LSepi) were obtained by averaging peak systolic strain of the left ventricle, with 18 segments in each layer. RESULTS: Layer-specific strains showed a decreasing gradient from the endocardium to the epicardium in both controls and patients with hypertension (P < 0.001 in both) and were significantly different between controls and patients with hypertension in all 3 layers (LSendo, -20.4% ± 2.4% vs -19.2% ± 2.2%; P = 0.007; LSmyo, -15.8% ± 2.0% vs -14.8% ± 1.9%; P = 0.005; LSepi, -11.8% ± 2.0% vs -11.0% ± 1.8%,; P = 0.04). Both LSendo and LSmyo were lower even in patients with hypertension and no LV hypertrophy than in controls (both P < 0.05), although global LS was not different. New patients with hypertension showed more decreased LSendo and LSmyo than controls even with their younger age. LSs of all 3 layers were related to LV mass index and mitral annular velocity parameters. CONCLUSIONS: Layer-specific evaluation of the left ventricle provides an understanding of the layer-specific properties of the LV wall and the process of LV impairment, and it may be helpful in managing patients with hypertension, thus preventing further damage.
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