ABSTRACTS

pass, no change occurred. These findings indicate that in patients with left ventricular asynergy not due to infarct, appropriate aortocoronary bypass can improve segmental contraction patterns.

Comparison of the Beta Adrenergic Blocking Properties and Negative lnotropic Effects of Oxprenolol and Propranolol in Patients

YVES CHOQUET. MD’; ROBERT J. CAPONE, MD; DEAN T. MASON, MD, FACC; EZRA A. AMSTERDAM, MD, FACC; ROBERT ZELIS, MD, FACC, Davis, California

The effectiveness of beta receptor antagonists as potent antiarrhythmic agents has prompted considerable ef- fort in developing newer compounds with attenuated negative inotropic properties so that their usefulness can be extended to patients with reduced myocardial reserve. Thus, the inotropic and beta blocking proper- ties of oxprenolol (Ox) were evaluated in 8 patients at diagnostic left heart catheterization and compared with propranolol (Prop) in 6 additional subjects. Fifteen minutes after intravenous administration of Ox (5 mg), heart rate (HR) slowed significantly from 74.7 to 65 beats/min (P <O.Ol). However, left ventricular end- diastolic pressure (LVEDP) (11.3-11.1 mm Hg) and stroke volume index (SI) (41-39.4 ml/mz) were un- changed (NS). In contrast, Prop (5 mg intravenously) significantly reduced HR (78.2-65.2, P <O.Ol) and in- creased LVEDP (9.7-14.8, P <O.Ol), without changing SI (38.4-38.8, NS), thus suggesting a reduction in myo- cardial contractility. The first derivative (dp/dt) of high fidelity left ventricular pressure (LVP) at 50 mm Hg (dp/dt [SO]) was unchanged after Ox (1,277-1,185 mm Hg/sec) but was reduced by Prop (1,545-1,330, P <0.02). Contractile element velocity (VCE = dp/dt/ 32sdeveloped LVP) plotted against instantaneous de- veloped LVP and extrapolated to 0 LVP (Vmax) was unchanged after Ox (1.02-1.02 muscle lengths/set, NS) but was significantly reduced after Prop (1.38-1.28, P <0.02). At this dose, both drugs are equipotent beta blockers ; Ox attenuated the isoproterenol-induced (1 pg intravenously) increase in HR ‘780/c, dp/dt [50] 93% and Vmax 930/c, similar to Prop (78, 98, and loo%, respectively). Therefore, in equivalent mg and beta blocking doses, Ox appears to possess consider- ably less negative inotropic effect than Prop.

The Clinical Triad of Traumatic Ventricular Septal Defect, Occlusion of Left Anterior Descending Coronary Artery and Ventricular Aneurysm

LAWRENCE S. COHEN, MD, FACC*; DEAN T. MASON, MD, FACC; EZRA A. AMSTERDAM, MD, FACC; WILLIAM C. ROBERTS, MD, FACC; J. EDWARD ROSENTHAL, MD; ROBERT F. ZELIS, MD, FACC, Bethesda, Maryland, New Haven, Connecticut, and Davis, California

Although it is appreciated that acquired ventricular septal defect (VSD) can result from acute myocardial infarction, particularly with occlusion of the left an- terior descending coronary artery (LAD), it is not well recognized that VSD can occur with both penetrat- ing and blunt chest trauma. VSD may develop acutely or several days after the trauma. Five consecutive pa- tients with traumatic VSD (1 blunt, 4 penetrating) were catheterized including left ventricular and coro- nary angiography. The average pulmonic to systemic flow ratio was 2 : 1, with shunting clearly documented at

the ventricular level. Three patients also had a left ventricular aneurysm, and 2 had localized occlusion of the LAD. It appears that closed or penetrating injury to the anterior precordium which produces a VSD, may interrupt the LAD. The ventricular aneurysm results from the LAD occlusion or from the associated myo- cardial trauma itself. Thus when traumatic VSD oc- curs because of blunt or penetrating injury, the re- maining components of the clinical triad (LAD occlu- sion and ventricular aneurysm) should be anticipated, diligently sought, and considered in the management of this defect.

Ultrasound Determination of Mean Fiber-Shortening Rate in Man

RONALD COOPER, BS; JOEL S. KARLINER, MD’; ROBERT A. O’ROURKE MD; KIRK L. PETERSON, MD; GEORGE LEOPOLD, MD, La Jolla, California

Recently it has been shown that cineangiocardiographic measurement of the mean rate of circumferential fiber shortening (MRFS) at the minor left ventricular equa- tor is a reliable method for evaluating the mechanics of cardiac performance. However, an accurate noninvasive method for assessing left ventricular myocardial me- chanics would be desirable. Accordingly, in 16 patients the MRFS in the plane perpendicular to the interven- tricular septum and left ventricular posterior wall was measured by reflected ultrasound, and compared with the MRFS derived from a eineangiocardiogram per- formed within 24 hours of the ultrasound determina- tion. The MRFS by ultrasound averaged 1.0 circumfer- ences/sec (range 0.54 to 1.44) and correlated well with the MRFS measured by angiography (r = 0.90, P <O.Ol).

The ultrasound technique detected abnormal myocar- dial function in 93% of patients. One additional pa- tient with marked anterior wall dyskinesis and a re- duced MRFS by angiography had a normal MRFS by ultrasound. The ejection fraction (EF) derived from ultrasound measurements averaged 0.55 (range 0.33 to 0.77) and correlated significantly with the EF calcu- lated by cineangiography (T = 0.85, P <O.Ol). By ul- trasound, EF correlated well with MRFS (T = 0.96, P <O.Ol), and by cineangiography the correlation was also significant (r = 0.90, P <O.Ol). The average maxi- mal velocity of posterior wall motion was 4.2 cm/set (range 1.9 to 6.4) and did not consistently distinguish normal from impaired cardiac function. It is concluded that in the absence of marked anterior wall dyskinesis, ultrasound measurement of MRFS is a reliable nonin- vasive technique for the evaluation of left ventricular performance.

Production of a Myocardial Depressant Factor in Shock Following Acute Myocardial Infarction: Preliminary Evaluation of Treatment With Methylprednisolone

RICHARD S. CRAMPTON, MD, FACC*; S. L. WANGENSTEEN, MD; W. L. LOVETT, MD; J. N. MORRIS, Jr., BA; R. H. HARRIS, MD; R. WEITZMANN, MD; .T. M. GLENN, PhD; A. M. LEFER, PhD, Char- lottesville, Virginia

In 13 of 15 patients with cardiogenic shock (CS) after acute myocardial infarction (AMI), plasma concentra- tions of a myocardial depressant factor (MDF, normal 15-25 units) and cathepsin D or B-glucuronidase were

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