[Neurohumoral factors in hypertensive patients with and without left ventricular hypertrophy].
Increased pressure load and neurohumoral activation are main factors involved in pathomechanism of left ventricular hypertrophy (LVH) in hypertension (HT). To gain insight into the involvement of neurohumoral factors responsible for cardiac hypertrophy, plasma level of aldosterone (Aldo), plasma renin activity (PRA), insulin-like growth factor-1 (IGF-1), pro-endothelin-1 (pro-ET) and atrial natriuretic peptide (ANP) were measured in HT patients (pts) and compared between pts with and without LVH. Also relationships between neurohormones and LV mass index (LVMI), mean blood pressure (MBP) were assessed separately in HT pts with and without LVH. 121 HT patients (pts) of age 17-79 (mean 48 +/- 15.3) were divided into three groups: 1-53 pts with mild HT, 2-44 pts with moderate HT and 3-24 pts with severe HT. Each of the group was divided into pts with and without LVH further all HT pts were divided into two groups; with and without LVH. Control group consisted of 39 healthy normotensives. LV mass was assessed echocardiographically and plasma levels of IGF-1, PRA, Aldo, pro-ET, and ANP were measured by radioimmunoassay in each pts and controls. LVH was found in 35.8% pts with mild HT, in 68.18% pts with moderate HT and in 100% pts with severe HT. The level of all measured neurohormones were significantly higher in pts with LVH compared to pts without LVH (p < 0.001). In pts with LVH there was significant correlation between LVMI and IGF-1, PRA, Aldo, pro-ET-1 and ANP, contrary to pts without LVH in which such correlations was not found. In pts with LVH there was also significant correlation between MBP and IGF-1, PRA, ANP and pro-ET-1. Increased plasma level of PRA, Aldo, IGF-1, pro-ET-1 and ANP in HT pts with LVH and significant correlation between measured neurohormones and LVMI suggests their contribution to LVH in HT pts. Significant correlation between LVMI, MBP and IGF-1 level, PRA and ANP indicate interplay between hemodynamic and neuroendocrine factors in pathomechanism of LVH.
Katedra i Klinika Kardiologii AM we Wrocławiu.
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Karasek
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Witkowska
D000293:Adolescent; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D009320:Atrial Natriuretic Factor / Q000097:blood; D019332:Endothelin-1; D016232:Endothelins / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications*; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000150:complications*; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D008875:Middle Aged; D018377:Neurotransmitter Agents / Q000097:blood*; D011498:Protein Precursors / Q000097:blood; D012083:Renin / Q000097:blood
D019332:Endothelin-1; D016232:Endothelins; D018377:Neurotransmitter Agents; D011498:Protein Precursors; C093240:proendothelin 1; D000450:Aldosterone; D007334:Insulin-Like Growth Factor I; D009320:Atrial Natriuretic Factor; D012083:Renin