Why the study?
Do men with volume-dependent hypertension (PA and LREH) have greater left ventricular remodeling compared to those with normal-renin essential hypertension?
Do men with volume-dependent hypertension (PA and LREH) have greater left ventricular remodeling compared to those with normal-renin essential hypertension?
Plasma volume overload in salt-sensitive hypertension (PA and LREH) is associated with greater left ventricular cavity dimensions and eccentric hypertrophy compared to normal-renin essential hypertension.
Answers are grounded in this paper and cite their sources.
LV dilation linked to volume-dependent hypertension; hypothesis-generating for eccentric remodeling differences versus NREH.
We evaluated the influence of increased intravascular volume on the heart anatomy in salt-sensitive types of hypertension, represented by primary aldosteronism (PA) and low-renin essential hypertension (LREH). Echocardiography was performed in 128 males with moderate to severe or resistant hypertension: 44 patients had PA, 40 patients had LREH and 44 patients had normal-renin essential hypertension (NREH). Groups were comparable in demographic characteristics, blood pressure, duration of hypertension and previous antihypertensive treatment. Patients with PA and LREH, in comparison with NREH patients, showed both greater end-systolic (37.6±5.4 and 35.6±4.5 vs 32.6±4.4 mm, p<0.001 and p<0.05) and end-diastolic (56.1±4.5 and 54.0±4.8 vs 50.4±5.1 mm; p<0.001 and p<0.01) left ventricle (LV) diameter. There were no significant differences either in LV wall thicknesses or LV mass, although a higher percentage of patients with PA and LREH met the criteria of eccentric hypertrophy (p<0.001 and p<0.05 respectively). Aldosterone concentration was positively related to LV cavity dimensions, whether wall thicknesses were rather associated with blood pressure levels. In conclusion, plasma volume overload was identified as an important factor influencing LV remodeling in PA and LREH, whether due to excessive aldosterone levels in PA or other pathophysiological mechanisms.
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Indra et al. (2012) studied this question.
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