Enrique Rodilla1, José A Costa2, Joaquin Martín3, Carmen González4, Jose M Pascual5, Josep Redon6. 1. Unidad de Hipertensión y Riesgo Vascular, Servicio de Medicina Interna, Hospital de Sagunto, Agencia Valenciana de Salud, Sagunto, Valencia, Spain; Departamento de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad CEU-Cardenal Herrera, Castellón, Spain. Electronic address: rodilla_enr@gva.es. 2. Unidad de Hipertensión y Riesgo Vascular, Servicio de Medicina Interna, Hospital de Sagunto, Agencia Valenciana de Salud, Sagunto, Valencia, Spain. 3. Unidad de Cardiología, Servicio de Medicina Interna, Hospital de Sagunto, Agencia Valenciana de Salud, Sagunto, Valencia, Spain. 4. Servicio de Medicina Preventiva, Hospital de Sagunto, Agencia Valenciana de Salud, Sagunto, Valencia, Spain. 5. Unidad de Hipertensión y Riesgo Vascular, Servicio de Medicina Interna, Hospital de Sagunto, Agencia Valenciana de Salud, Sagunto, Valencia, Spain; Centro de Investigación Biomédica en Red de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain; Departamento de Medicina, Universidad de Valencia, Valencia, Spain. 6. Centro de Investigación Biomédica en Red de la Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III, Madrid, Spain; Departamento de Medicina, Universidad de Valencia, Valencia, Spain.
Abstract
BACKGROUND AND OBJECTIVES: The principal objective was to assess the prevalence of left ventricular hypertrophy (LVH) in hypertensive, never treated patients, depending on adjustment for body surface or height. Secondary objectives were to determine geometric alterations of the left ventricle and to analyze the interdependence of hypertension and obesity to induce LVH. PATIENTS AND METHODS: Cross-sectional study that included 750 patients (387 men) aged 47 (13, SD) years who underwent ambulatory blood pressure (ABPM) monitoring and echocardiography. RESULTS: The prevalence of LVH was 40.4% (303 patients), adjusted for body surface area (BSA, LVHBSA), and 61.7% (463 patients), adjusted for height(2.7) (LVHheight(2.7)). In a multivariate logistic analysis, systolic BP24h, gender and presence of elevated microalbuminuria were associated with both LVHBSA and LVHheight(2.7). Increased waist circumference was the strongest independent predictor of LVHheight(2.7), but was not associated with LVHBSA. We found a significant interaction between abdominal obesity and systolic BP24h in LVHheight(2.7). Concentric remodelling seems to be the most prevalent alteration of left ventricular geometry in early stages of hypertension (37.5%). CONCLUSIONS: The impact of obesity as predictor of LVH in never treated hypertensives is present only when left ventricular mass (LVM) is indexed to height(2.7). Obesity interacts with systolic BP24h in an additive but not merely synergistic manner. Systolic BP24h is the strongest determinant of LVH when indexed for BSA.
BACKGROUND AND OBJECTIVES: The principal objective was to assess the prevalence of left ventricular hypertrophy (LVH) in hypertensive, never treated patients, depending on adjustment for body surface or height. Secondary objectives were to determine geometric alterations of the left ventricle and to analyze the interdependence of hypertension and obesity to induce LVH. PATIENTS AND METHODS: Cross-sectional study that included 750 patients (387 men) aged 47 (13, SD) years who underwent ambulatory blood pressure (ABPM) monitoring and echocardiography. RESULTS: The prevalence of LVH was 40.4% (303 patients), adjusted for body surface area (BSA, LVHBSA), and 61.7% (463 patients), adjusted for height(2.7) (LVHheight(2.7)). In a multivariate logistic analysis, systolic BP24h, gender and presence of elevated microalbuminuria were associated with both LVHBSA and LVHheight(2.7). Increased waist circumference was the strongest independent predictor of LVHheight(2.7), but was not associated with LVHBSA. We found a significant interaction between abdominal obesity and systolic BP24h in LVHheight(2.7). Concentric remodelling seems to be the most prevalent alteration of left ventricular geometry in early stages of hypertension (37.5%). CONCLUSIONS: The impact of obesity as predictor of LVH in never treated hypertensives is present only when left ventricular mass (LVM) is indexed to height(2.7). Obesity interacts with systolic BP24h in an additive but not merely synergistic manner. Systolic BP24h is the strongest determinant of LVH when indexed for BSA.
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