ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS REVERT ABNORMAL RIGHT-VENTRICULAR FILLING IN PATIENTS WITH RESTRICTIVE LEFT-VENTRICULAR DISEASE

Citation
My. Henein et al., ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS REVERT ABNORMAL RIGHT-VENTRICULAR FILLING IN PATIENTS WITH RESTRICTIVE LEFT-VENTRICULAR DISEASE, Journal of the American College of Cardiology, 32(5), 1998, pp. 1187-1193
Citations number
13
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
32
Issue
5
Year of publication
1998
Pages
1187 - 1193
Database
ISI
SICI code
0735-1097(1998)32:5<1187:AE(IRA>2.0.ZU;2-2
Abstract
Objectives. Our aim was to determine mechanisms underlying abnormaliti es of right ventricular (RV) diastolic function seen in heart failure. Background. It is not clear whether these right sided abnormalities a re due to primary RV disease or are secondary to restrictive physiolog y on the left side of the heart. The latter regresses with angiotensin -converting enzyme inhibition (ACE-I), Methods. Transthoracic echo Dop pler measurements of left- and right-ventricular function in 17 patien ts with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. Results. Before ACE-I, LV filling was restrictiv e, with isovolumic relaxation time short and transmitral E wave accele ration and deceleration rates increased (p < 0.001), Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the p ulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole, Right ventricular re laxation was very incoordinate and peak E wave velocity was reduced. P eak RV to right atrial (RA) pressure drop, estimated from tricuspid re gurgitation, was 45 +/- 6 mm Hg, and peak pulmonary stroke distance wa s 40% lower than normal (p < 0.001), With ACE-I, LV isovolumic relaxat ion time lengthened, E wave acceleration and deceleration rates decrea sed and RV to RA pressure drop fell to 30 +/- 5 mm Hg (p < 0.001) vers us pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates we re unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01), C onclusions. Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. Th is was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole. (C) 1998 by the American College of Cardiology.