Cardiac structure and function in renovascular hypertension produced by unilateral and bilateral renal artery stenosis.
To evaluate cardiovascular status in human renovascular hypertension, quantitative echocardiographic findings were compared in 42 patients with arteriographically documented renovascular hypertension and 46 age- and sex-matched patients with essential hypertension. Left ventricular (LV) fractional shortening, a measure of systolic performance at rest, was subnormal (less than 26%) in 8 of 42 renovascular hypertensive patients (19%), 0 of 42 essential hypertensive patients (p less than 0.005) and 1 of 79 normal subjects (1%) (p less than 0.005). Fractional shortening was equally reduced in patients with arteriosclerotic and nonarteriosclerotic causes of renal artery stenosis (32 +/- 9% vs 32 +/- 6%, both p less than 0.025 compared with 36 +/- 5% in patients with essential hypertension). The depressed function in renovascular hypertension appeared to be a result of greater LV dilation (p less than 0.02) and septal but not LV free wall hypertrophy (p less than 0.01) that failed to offset the pressure load, allowing end-systolic stress, a measure of myocardial afterload, to increase to abnormal levels (101 +/- 47 X 10(3) dynes/cm2, p less than 0.001 vs 68 +/- 19 in essential hypertension). These data indicate that human renovascular hypertension is associated with more adverse cardiac involvement than essential hypertension of similar severity. In addition, the 14 patients with bilateral renovascular stenosis had a higher cardiac index (3.9 +/- 1.1 liters/min/m2) than the 28 with unilateral stenosis (3.2 +/- 1.1 liters/min/m2, p less than 0.05). This result supports the proposition that bilateral renovascular disease is analogous to 1-clip 1-kidney experimental renovascular hypertension, while unilateral renovascular disease resembles the 1-clip 2-kidney model.(ABSTRACT TRUNCATED AT 250 WORDS)
D001794:Blood Pressure; D002302:Cardiac Output; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006978:Hypertension, Renovascular / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction; D012078:Renal Artery Obstruction / Q000150:complications / Q000503:physiopathology*; D012083:Renin / Q000097:blood
D012083:Renin