Author + information
- Received April 16, 1985
- Revision received June 24, 1985
- Accepted July 12, 1985
- Published online December 1, 1985.
- Prediman K. Shah, MD, FACCa,
- Jamshid Maddahi, MD, FACC,
- Daniel S. Berman, MD, FACC,
- Max Pichler, MD and
- H.J.C. Swan, MD, PHD, FACC
- ↵aAddress for reprints: Prediman K. Shah, MD, Director, Inpatient Cardiology and Cardiac Care Unit, Room 5314, 8700 Beverly Boulevard, Los Angeles, California 90048.
To determine the clinical and hemodynamic correlates as well as therapeutic and prognostic implications of predominant right ventricular dysfunction complicating acute myocardial infarction, 43 consecutive patients with scintigraphic evidence of right ventricular dyssynergy and a depressed right ventricular ejection fraction (<0.39) in association with normal or near normal left ventricular ejection fraction (≥0.45) were prospectively evaluated. All 43 patients had acute inferior infarction, forming 40% of patients with acute inferior infarction, and only eight (24%) had elevated jugular venous pressure on admission. On hemodynamic monitoring, 74% of patients had a depressed cardiac index (≤2.5 liters/min per m2), averaging 2.0 ± 0.05 for the group. Of these, 30% did not demonstrate previously described hemodynamic criteria of predominant right ventricular infarction (right atrial pressure ≥ 10 mm Hg or right atrial to pulmonary capillary wedge pressure ratio 0.8, or both). The left ventricular end-diastolic volume was reduced to 49 ± 11 ml/m2 (n = 22) and correlated significantly with the stroke volume index (r = 0.82; p < 0.0001) and cardiac index (r = 0.57; p = 0.005).
The follow-up right ventricular ejection fraction, determined in 33 patients, showed an increase of 10% or greater in 26 (79%), increasing from a mean value of 0.30 ± 0.06 to 0.40 ± 0.09 (p < 0.0001) without a significant overall change in the mean left ventricular ejection fraction (0.56 ± 0.10 to 0.56 ± 0.11, p = NS). In-hospital complications occurred frequently and included bradycardia with hypotension in 25 (58%), low output syndrome or shock in 18 (41%), complete atrioventricular block in 6 (13%), early ventricular tachycardia or fibrillation in 7 (16%), ventricular septal rupture with mitral regurgitation in 1, ventricular septal and free wall rupture in 1 and severe mitral regurgitation in 1. The low output syndrome did not improve with volume loading alone (except in 1 patient) but required additional inotropic or vasodilator therapy, or both, in 13, intraaortic balloon pumping in 2 and atrial pacing in 1 patient. Two patients (4.6%), both with ventricular septal rupture, died.
It is concluded that scintigraphic evidence of predominant right ventricular dysfunction occurs frequently in acute inferior infarction and is associated with 1) frequent absence of clinically detectable elevation of jugular venous pressure or hemodynamic signs of predominant right ventricular dysfunction; 2) reduced left ventricular end-diastolic volume resulting in low cardiac output; 3) frequent spontaneous improvement in right ventricular function over time; 4) a high incidence of complications; and 5) good short-term survival in the absence of added mechanical complications. Furthermore, despite a reduced left ventricular end-diastolic volume and contrary to popular belief, the low output syndrome rarely improves with volume infusion alone and frequently requires additional inotropic or vasoactive drug therapy.
This study was supported in part by SCOR Grant 17651 from the National Institutes of Health, Bethesda, Maryland.
- Received April 16, 1985.
- Revision received June 24, 1985.
- Accepted July 12, 1985.
- American College of Cardiology Foundation