ABSTRACTS

of medical therapy and the need for mechanical cardiac assistance, and to identify those MI patients in whom acute myocardial revascularization offers the only chance for survival.

Electrophysiological Correlates of Aberrancy in Diseased Hearts

DONALD H. SINGER, MD, FACC*; ROBERT E. TEN EICK; RA- MALINGAIER PARAMESWARAN, Chicago, Illinois

Conduction disturbances, including aberrancy (Ab), seems to be more common in diseased than in normal hearts. The causes of increased aberrancy are un- certain. Electrophysiologic study of diseased human heart muscle provides clues in this regard. Transmem- brane potentials were recorded from specimens of hu- man papillary muscle with attached Purkinje fibers, and left ventricular free wall. Records were obtained during stimulation at cycle lengths of 200 to 2,000 msec and during spontaneous beating. Diastolic po- tential was reduced (-45 to -75 mv) due to low resting potential or diastolic depolarization of .automatic cells. Amplitude and maximal rate of rise (Vmax) of action potentials (AP) initiated in such cells were low. Vmax of AP from left ventricular muscle was less than pre- dicted, suggesting reduced responsiveness. Occurrence of similar changes in appropriate portions of the bundle-branch system (BBS) would predispose to in- creased Ab in diseased hearts, as would prolongation of the terminal phases of repolarization, which was com- monly seen. Finally, findings that very early non- propagated premature responses sometimes resulted in a striking decrease in the Vmax of the postextrasystolic beat suggest that concealed reentry within the BBS could be an additional factor underlying increased Ab.

Experimental Left Ventricular Akinesis

SIDNEY C. SMITH, Jr., LCDR, MC, USNR, MD*; WILL LLOYD- JONES, MD, FRCS; JUAN SERUR, MD; CHARLES W. URSCHEL, MD; EDMUND H. SONNENBLICK, MD, FACC; F. HENRY ELLIS, Jr., MD, Boston, Massachusetts

Experimental myocardial infarction resulting in chronic left ventricular akinesis was created using a 2-stage ligation and agar injection of branches of the left coronary artery in 8 mongrel dogs. The effects of atria1 pacing, increased afterload and beta blockade on left ventricular (LV) hemodynamics were studied 8 weeks after infarction. Atria1 pacing from 120 to 180 beats/min caused a striking decrease in LV end-dia- stolic pressure (EDP) from 40 f 3 to 14 & 3 mm Hg. In the paced state LV end-diastolic volume measured cineangiographically decreased, whereas cardiac out- put and mean aortic pressure were unchanged. Beta blockade at a fixed paced rate increased LV failure with a rise in LVEDP of 6 mm Hg and a 20% decrease in cardiac output. Angiotensin induced increases in after- load at fixed paced rates resulted in similar deteriora- tion in LV function with a 12 mm Hg increase in LVEDP over resting levels. These studies suggest that (1) the postinfarction chronically akinetic LV is de- pendent upon catecholamine support, and (2) pacing at

high rates in the presence of chronic LV akinesis strikingly improves LV function.

Changes in Left Ventricular Wall Movement Following Exercise, Atrial Pacing and Acute Myocardial Infarction Measured by Reflected Ultrasound

CHARLES SMITHEN, MD*; CHRISTOPHER WHARTON, BM, MRCP; EDGAR SOWTON, MD, FRCP, FACC, New York, New York and London, England

Movement of the posterior wall of the left ventricle was assessed using an ultrasound technique in a variety of clinical circumstances. Maximal posterior wall velocity (PWV) was measured as the maximal slope of the wall movement from the end-diastolic position to the end- systolic position, and posterior wall excursion (PWE) was measured as the maximal amplitude of movement anteriorly. In 11 normal subjects maximal PWV in- creased from a mean of 37 mm/see at rest to 96 mm/ set after maximal erect exercise (P <O.OOl), and PWE increased from 4.0 mm at rest to 6.8 mm after exercise (P <O.OOl). The effect of heart rate (HR) alone on posterior wall movement was evaluated in 6 patients using the technique of atria1 pacing. Increasing the HR resulted in a reduction in both maximal PWV and PWE. At identical HR in 5 patients there was a sig- nificant increase in both PWV and PWE during ex- ercise compared to atria1 pacing. In 8 patients with documented acute anterior myocardial infarction maxi- mal PWV decreased by 26% and PWE decreased by 46% during the first 36 hours after infarction. In the 2 patients in whom it was measured an increase in pulmonary arterial pressure was associated with a re- duction in both PWV and PWE and as the pulmonary arterial pressure returned toward normal, the posterior wall motion also improved. It is suggested that this method provides a noninvasive bedside assessment of left ventricular function following acute myocardial infarction independent of HR.

Left Ventricular Function and Coronary Anatomy Before and After Myocardial Infarction

DOUGLAS K. STEWART, MD*; GLEN W. HAMILTON, MD; JOHN A. MURRAY, MD, FACC; J. W. KENNEDY, MD, Seattle, Washington

Complete clinical, hemodynamic and angiographic studies were performed in 5 patients before and from 2 to 22 months after myocardial infarction. Four had anteroseptal infarctions and 1 an inferior infarction. In all cases there was significant progression of coro- nary artery disease which correlated with the electro- cardiographic area of infarction and the site of left ventricular contraction abnormality. Deterioration in contraction pattern, end-diastolic and end-systolic ven- tricular volumes (EDV, ESV), stroke work (SW) and systolic ejection fraction (SEF) were pronounced in 4 of 5 patients (Table I). The study provided a unique opportunity to compare left ventricular function before and after infarction by quantitative angiographic methods. The data confirm our previous impression that angiographic methods are sensitive to changes in left ventricular function associated with coronary ar-

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