Díez J, Laviades C
Department of Medicine, University of Zaragoza, Spain.
J Hypertens Suppl. 1994 Jul;12(4):S31-6.
Preliminary studies have shown that patients with essential hypertension and left ventricular hypertrophy have an excess of circulating insulin-like growth factor-1 (IGF-1). In addition, an association has been found between the decrease in IGF-1 after antihypertensive treatment and regression of left ventricular hypertrophy.
To determine whether the effect of angiotensin converting enzyme (ACE) inhibitors on left ventricular hypertrophy in patients with essential hypertension is related to ACE inhibitor effects on IGF-1 levels.
The relationship between echocardiographically determined left ventricular hypertrophy and plasma IGF-1 levels was investigated in 87 patients with essential hypertension before and after 6 months of randomly allocated treatment with captopril (n = 30), lisinopril (n = 37) or quinapril (n = 20). The control group consisted of 30 age- and sex-matched normotensive subjects without left ventricular hypertrophy.
Baseline IGF-1 levels were higher in hypertensive patients than in normotensive controls (280 +/- 21 versus 240 +/- 15 ng/ml, means +/- SEM, P < 0.02). IGF-1 levels were higher in hypertensive patients with left ventricular hypertrophy (n = 25, 316 +/- 41 ng/ml) than in those without left ventricular hypertrophy (n = 62, 242 +/- 16 ng/ml, P < 0.05). There was a direct correlation between baseline IGF-1 and left ventricular mass in the hypertensive patients (r = 0.365, P < 0.001). All three ACE inhibitors caused similar reductions in IGF-1 levels, the left ventricular mass index and blood pressure after the treatment period. The effect of ACE inhibition on mean blood pressure was similar in patients with (-13%) and without (-12%) a regression of left ventricular hypertrophy. The mean change in IGF-1 levels with treatment was more pronounced in those patients in whom left ventricular hypertrophy regressed (-25 versus -12%).
These results indicate that circulating IGF-1 levels are increased in essential hypertension. Furthermore, there is an association between high IGF-1 levels and left ventricular hypertrophy in hypertensive patients. Our findings suggest that the ability of ACE inhibitors to induce regression of hypertensive cardiac hypertrophy may be related to their ability to normalize IGF-1 and also supports the view that ACE inhibition affects left ventricular mass through pathways other than blood pressure reduction.
初步研究表明,原发性高血压合并左心室肥厚患者循环中的胰岛素样生长因子-1(IGF-1)水平过高。此外,还发现降压治疗后IGF-1水平降低与左心室肥厚消退之间存在关联。
确定血管紧张素转换酶(ACE)抑制剂对原发性高血压患者左心室肥厚的作用是否与其对IGF-1水平的影响有关。
对87例原发性高血压患者进行研究,在随机分配接受卡托普利(n = 30)、赖诺普利(n = 37)或喹那普利(n = 20)治疗6个月前后,通过超声心动图测定左心室肥厚情况,并检测血浆IGF-1水平。对照组由30名年龄和性别匹配、无左心室肥厚的血压正常受试者组成。
高血压患者的基线IGF-1水平高于血压正常对照组(280±21对240±15 ng/ml,均值±标准误,P<0.02)。有左心室肥厚的高血压患者(n = 25,316±41 ng/ml)的IGF-1水平高于无左心室肥厚的患者(n = 62,242±16 ng/ml,P<0.05)。高血压患者的基线IGF-1与左心室质量之间存在直接相关性(r = 0.365,P<0. .001)。治疗期结束后,所有三种ACE抑制剂均使IGF-1水平、左心室质量指数和血压出现相似程度的降低。ACE抑制对平均血压的作用在左心室肥厚消退的患者(-13%)和未消退的患者(-12%)中相似。治疗后IGF-1水平的平均变化在左心室肥厚消退的患者中更为明显(-25对-12%)。
这些结果表明,原发性高血压患者循环中的IGF-1水平升高。此外,高血压患者中IGF-1水平升高与左心室肥厚之间存在关联。我们的研究结果表明,ACE抑制剂诱导高血压性心脏肥厚消退的能力可能与其使IGF-1水平正常化的能力有关,也支持了ACE抑制通过降低血压以外的途径影响左心室质量的观点。