{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,12]],"date-time":"2025-10-12T06:04:50Z","timestamp":1760249090642},"reference-count":41,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,1,12]],"date-time":"2004-01-12T00:00:00Z","timestamp":1073865600000},"content-version":"vor","delay-in-days":11,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Echocardiography"],"published-print":{"date-parts":[[2004,1]]},"abstract":"<jats:p> <jats:italic>The effects of chronic volume or pressure overload on the velocity of right ventricular ejection have not been previously well defined. We hypothesized that, as formerly shown for the left ventricle, there would be a direct relationship between the velocity of ejection and an estimate of systolic wall stress. Methods: Echocardiograms of asymptomatic patients, not on cardiac medications, with either an isolated secundum atrial septal defect \u2265 5 mm in diameter or isolated pulmonic stenosis with a peak instantaneous pressure gradient \u2265 20 mmHg, were reviewed. Forty\u2010one patients with an atrial septal defect and 34 with pulmonary stenosis met criteria, and were compared to age\u2010matched normal controls. Total subjects were 127 with ages ranging from 1 day to 54 years. Right ventricular monoplane ejection fraction, ejection time corrected for heart rate (ET<jats:sub>c<\/jats:sub>), mean normalized systolic ejection rate (MNSER<jats:sub>c<\/jats:sub>) and meridianal peak\u2010systolic wall stress (WS<jats:sub>ps<\/jats:sub>) were measured. Results: Compared to controls, ejection fractions were not significantly different, but WS<jats:sub>ps<\/jats:sub> averaged 81% and 110% higher, ET<jats:sub>c<\/jats:sub> 8% and 9% longer, and MNSER<jats:sub>c<\/jats:sub> 5% and 9% slower in the atrial septal defect and pulmonary stenosis groups, respectively. Among all subjects WS<jats:sub>ps<\/jats:sub> had a significant linear correlation with ET<jats:sub>c<\/jats:sub> (r = 0.61, P &lt; 0.01), MNSER<jats:sub>c<\/jats:sub> (r =\u22120.46, P &lt; 0.01), and ejection fraction (r =\u22120.19, P &lt; 0.05). Conclusions: Increases in WS<jats:sub>ps<\/jats:sub> cause an incremental slowing of MNSER<jats:sub>c<\/jats:sub> in the right ventricle, with a relationship that is linear over a wide range of normal and abnormal loading conditions. 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