Catena Cristiana, Verheyen Nicolas D, Url-Michitsch Marion, Kraigher-Krainer Elisabeth, Colussi GianLuca, Pilz Stefan, Tomaschitz Andreas, Pieske Burkert, Sechi Leonardo A
Division of Cardiology, Department of Medicine, Medical University of Graz, Graz, Austria; Internal Medicine, Department of Experimental and Clinical Medical Sciences, University of Udine, Udine, Italy;
Division of Cardiology, Department of Medicine, Medical University of Graz, Graz, Austria;
Am J Hypertens. 2016 Mar;29(3):303-10. doi: 10.1093/ajh/hpv104. Epub 2015 Jul 10.
Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular morbidity in hypertension. Current evidence suggests a contribution to LVH of plasma aldosterone levels that are inappropriately elevated for the salt status. The aim of this study was to investigate whether inappropriate modulation of aldosterone production by a saline load is associated with left ventricular (LV) mass in hypertensive patients.
In 90 hypertensive patients free of clinically relevant cardiovascular complications in whom secondary forms of hypertension were ruled out, we performed a standard intravenous saline load (0.9% NaCl, 2 l in 4 hours) with measurement of plasma aldosterone and active renin at baseline and end of infusion. Bi-dimensional echocardiography was performed for the assessment of cardiac morphology and function.
LVH was present in 19% of patients who had significantly worse renal function and higher body mass, blood pressure, and plasma aldosterone levels measured both at baseline and after the saline load than patients without LVH. LV mass was directly related to age, body mass, systolic blood pressure, duration of hypertension, baseline, and post-saline load plasma aldosterone levels and inversely to glomerular filtration. Multivariate regression analysis showed independent correlation of LV mass with body mass, systolic blood pressure, and plasma aldosterone levels measured after intravenous saline load, but not at baseline.
In patients with hypertension, aldosterone levels measured after intravenous saline load are related to LV mass independent of age, body mass, and blood pressure, suggesting that limited ability of salt to modulate aldosterone production could contribute to LVH.
左心室肥厚(LVH)是高血压患者心血管发病的独立危险因素。当前证据表明,对于盐状态而言,血浆醛固酮水平不适当升高会导致LVH。本研究的目的是调查盐负荷对醛固酮分泌的不适当调节是否与高血压患者的左心室(LV)质量相关。
在90例排除了继发性高血压且无临床相关心血管并发症的高血压患者中,我们进行了标准静脉盐水负荷试验(0.9%氯化钠,4小时内输注2升),并在基线和输注结束时测量血浆醛固酮和活性肾素。采用二维超声心动图评估心脏形态和功能。
19%的患者存在LVH,与无LVH的患者相比,这些患者的肾功能明显更差,且在基线和盐水负荷后测量的体重、血压和血浆醛固酮水平更高。LV质量与年龄、体重、收缩压、高血压病程、基线及盐水负荷后血浆醛固酮水平直接相关,与肾小球滤过呈负相关。多变量回归分析显示,LV质量与体重、收缩压及静脉盐水负荷后测量的血浆醛固酮水平独立相关,但与基线时无关。
在高血压患者中,静脉盐水负荷后测量的醛固酮水平与LV质量相关,且独立于年龄、体重和血压,这表明盐调节醛固酮分泌的能力有限可能导致LVH。