title: Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the "nonstressed" ventricle.
abstract: Left ventricular hypertrophy in left ventricular pressure overload occurs in response to excessive work load imposed on the left ventricle by increased impedance to ejection. Right ventricular hypertrophy may occur in patients with these findings, but has been considered to be secondary to pulmonary hypertension. To determine the frequency of right ventricular hypertrophy and its relation to increased left ventricular wall thickness in patients with left ventricular pressure overload, right ventricular wall thickness was measured using M-mode echocardiography with two-dimensional echocardiographic guidance in 65 patients with left ventricular pressure overload; 49 patients had essential hypertension and 16 had aortic valve stenosis. These measurements were compared with data from 13 patients with "thin-walled" dilated cardiomyopathy and 20 normal subjects. Average right ventricular wall thickness in hypertensive patients (7 +/- 2 mm) and patients with aortic stenosis (6 +/- 2 mm) was significantly greater than that in normal subjects (4 +/- 1 mm) and patients with dilated cardiomyopathy (4 +/- 1 mm) who had normal left ventricular wall thickness, even though left ventricular mass was increased in all patient groups. Increased right ventricular wall thickness was present in 40 (80%) of 49 patients with hypertension and 10 (63%) of 16 patients with aortic stenosis. The magnitude of increase in right ventricular wall thickness was linearly correlated (r = 0.76, p less than 0.005) with left ventricular wall thickness, but was not associated with pulmonary hypertension. It is concluded that increased right ventricular wall thickness is common in patients with left ventricular pressure overload, is directly related to increases in left ventricular wall thickness, and is independent of right ventricular hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.forename: J S
authors.initials: JS
authors.lastname: Gottdiener
authors.forename: J A
authors.initials: JA
authors.lastname: Gay
authors.forename: B J
authors.initials: BJ
authors.lastname: Maron
authors.forename: R D
authors.initials: RD
authors.lastname: Fletcher
mesh_terms: D000328:Adult; D000368:Aged; D001024:Aortic Valve Stenosis / Q000503:physiopathology*; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology*; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D011312:Pressure; D013312:Stress, Physiological / Q000503:physiopathology