Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
Hypertension. 2010 May;55(5):1137-42. doi: 10.1161/HYPERTENSIONAHA.109.141531. Epub 2010 Mar 29.
We have shown previously that patients with resistant hypertension and hyperaldosteronism have increased brain natriuretic peptide suggestive of increased intravascular volume. In the present study, we tested the hypothesis that hyperaldosteronism contributes to cardiac volume overload. Thirty-seven resistant hypertensive patients with hyperaldosteronism (urinary aldosterone > or = 12 microg/24 hours and plasma renin activity < or = 1.0 ng/mL per hour) and 71 patients with normal aldosterone status were studied. Both groups had similar blood pressure and left ventricular mass, whereas left and right ventricular end-diastolic volumes measured by cardiac MRI were greater in high versus normal aldosterone subjects (P<0.05). Spironolactone treatment (19 patients in the high aldosterone group and 15 patients from the normal aldosterone group participated in the follow-up) resulted in a significant decrease in clinic systolic blood pressure, right and left ventricular end diastolic volumes, left atrial volume, left ventricular mass, and brain natriuretic peptide at 3 and 6 months of follow-up in patients with high aldosterone, whereas in those with normal aldosterone status, spironolactone decreased blood pressure and left ventricular mass without changes in ventricular or atrial volumes or plasma brain natriuretic peptide. Hyperaldosteronism causes intracardiac volume overload in patients with resistant hypertension in spite of conventional thiazide diuretic use. Mineralocorticoid receptor blockade induces rapid regression of left ventricular hypertrophy irrespective of aldosterone status. In subjects with high aldosterone, mineralocorticoid receptor blockade induces a prominent diuretic effect compared with a greater vasodilatory effect in subjects with normal aldosterone status.
我们之前已经表明，患有耐药性高血压和醛固酮增多症的患者脑利钠肽增加，提示血管内容量增加。在本研究中，我们检验了醛固酮增多症导致心脏容量超负荷的假设。我们研究了 37 例患有耐药性高血压伴醛固酮增多症的患者（尿醛固酮 > 或 = 12 微克/24 小时，血浆肾素活性 < 或 = 1.0 纳克/毫升/小时）和 71 例醛固酮正常的患者。两组的血压和左心室质量相似，而心脏 MRI 测量的左、右心室舒张末期容积在高醛固酮组中高于正常醛固酮组（P<0.05）。螺内酯治疗（高醛固酮组 19 例，正常醛固酮组 15 例参与随访）在 3 个月和 6 个月的随访中，高醛固酮组患者的临床收缩压、右和左心室舒张末期容积、左心房容积、左心室质量和脑利钠肽显著下降，而在正常醛固酮组患者中，螺内酯降低了血压和左心室质量，而心室或心房容积或血浆脑利钠肽没有变化。尽管常规使用噻嗪类利尿剂，醛固酮增多症仍会导致耐药性高血压患者的心脏内容量超负荷。盐皮质激素受体阻断剂可迅速逆转左心室肥厚，而与醛固酮状态无关。在高醛固酮组中，与正常醛固酮组相比，盐皮质激素受体阻断剂引起明显的利尿作用，而不是更大的血管扩张作用。
