ABSTRACTS

LEFT VENTRICULAR ANFURYSM WITHOUm CORONARY ASTERY OBSTRUCTION OR OCCLUSIGN Pa010 Esente, MU; Goffredo C. Gensini, MD; Peter P. Huntington, MD; Ann E. Kelly, MS; Msgr.Tromey Cardiovas- cular Laboratory, St. Joseph!s Hospital, Syracuse, N.Y.

The most common cause of left ventricular aneurysm, (LVA) is severe obstruction or occlusion of a major coronary artery (CAO). In the last 1.%0 patients studied in our laboratory with selective tine coronary arteriopraphy (SCA) and left ventriculography (LV), we found 8 patier:ts (average &I yrs; 5M 3F), with unquestionable evidence of LVA and no or minimal CAO. Two hypotheses should be con- sidered: (1) That these LVA's were caused by reasons other than CAO, or (2) that CA0 occurred at one time but was no longer preaent at the moment of study. The first hypothesis could be ruled out in 7 of 8 patients, because of the absence of any history of trauma or of any signs consistent with other possible causative factors. The second hypothesis instead is supported by the history of previous MI end classical '?CG changes present in 7 of the 8 patients and by serial studies made in one. In this young man with a large apical LVA, a single CA0 of the anteri.or descending regressed after 10 yrs to(5G% lumen reduction. Apparently in some patients CA0 occurs at one point in time, leadinr to the develop- ment of LVA. Later, a complete or partial regression of CA0 ensues, leaving a normal or a minimally compromised vascular lumen. CA0 must be regarded as a dynamic phenomenon with an unpredictable future and an uncertain past. SCA defines the extent and severity of CA0 at the time of procedure. Predictions based on one SCA are valid from a statistical viewpoint on large patient populations but cannot be utilized to foretell the future of the atherosclerotic plaque or, for that matter, to construct the temporal sequence of past events in any one case.

NEW Q WAVES AFTER CORONARY ARTERY BYPASS FOR ANGINA PECTORIS Jaime Espinoza, MD, Janet Lipski, MD, Robert Litwek, MD, FACC, Ephraim Donoso, MD, FACC, Simon Dack, MD, FACC The Mount Sinai School of Medicine of the City University of New York, New York

Pre-op and post-op electrocardiograms (ECGS) of 44pa- tients (pts) with angina pectoris who underwent coronary artery bypass (CAB) were evaluated. 'Vitro groups were identified. Group A (GA) consisted of 37 pts with single or multiple CAB. Group B (GB) was composed of '7 pts with single or multiple CAB with valvular replacement in 4, erdventricular resection in 3.

In GA pre-op ECGs showed abnormal Q waves in 14/37 and in GB 3/T. Following CAB in GA new Q waves (NQW) ap- peared in 11/37 (29.7%) including l/9 (11.1%) with 1 ves- sel disease (VD), T/20 (35%) with 2VD and 3/S (37.5%) with 3VD. In GB none developed NQW but intraventricular conduction abnormalities (IVCA) appeared after CAB in 3/7 while in GA only k/37 had new IVCA. LVEDP in GA was nor- mal in 23/32; NQW appeared after CAB in 6123. LVEDP was elevated from 13 to 33 mmHg in 9132; N&W were disclosed in 3/9. In GB LVEDP was normal in 216 and from 13 to 23 mmHg in 4/6. None developed NQW. In GA 9137 had lCAB, 219 developed NQW (22.2%); 21/37 had PCAB, 5/21 disclosed NQW (23.8%); 6/37 had 3CAB, 4/6 showed NQW (66.6%); l/37 had kCAB with no NQW following surgery. In GB 3/7 had lCAB, 2/7 2CAB and 2/7 3CAB, none developed N&W.

There was no correlation between NQW and LVEDP. The incidence of NQW was higher in patients who had 2 or 3W as well as in those who had 3CAB. The nature and origin of the Q waves are unknown and requires further investi- gation.

RELATION OF ALCOHOLIC CARDIAC CONDUCTION ABNORNALITIES TO DURATION OF ALCOHOLISM Philip 0. Ettinger, MD, FACC, Timothy J. Regan, NU, Mohammad I. Khan, MD, Michael Lyons, NU, College of Medi- cine and Dentistry of New Jersey, Newark, New Jersey.

Although the pathogenesis of alcoholic heart disease has been obscured when associated with malnutrition, myocar- dial function has been shown to be impaired even in the well-nourished, chronic alcoholic animal. To sssess the effect of duration of alcoholism upon cardiac conduction, well-nourished male mongrel dogs with normal plasma vitamins, proteins and hematocrits were fed 36% of calo- ries as ethanol for 7-33 months. His and left bundle branch electrograms and high speed, high frequency EKG's were recorded in ten dogs, sequentially in some. Prolon- gation of H-Q time was observed in five animals maintain- ed for more than one year (35+3 meet, normals 26+1 msec, P<O.OOl) with QRS widening (80+5 msec, normals 6?+2 msec, PcO.01) in this group and occurred without significant ventricular hypertrophy. These changes were less in five animals after shorter ingestion periods or incomplete consumption. No abnormalities of atria1 conduction were evident. The morphologic correlates included significant accumulation of mucopolysaccharide-like material in the interstitium evident on light microscopy (Alcian blue stain) and dilatation of sarcoplasmic reticulum on elec- tron microscopy. These abnormalities are suggestively related to the altered conduction. Several chronic animals died suddenly and unexpectedly, suggesting a possible relationship to conduction abnormalities and arrhythmias. Thus, prolonged intake of ethanol was pro- gressively toxic to the cardiac conduction system, resulting in histopathologic alterations and ventricular conduction abnormalities despite normal nutritional state.

LEFT VENTRICULAR FUNCTION CURVES AND EJECTION FRACTION IN POST-MYOCARDIAL INFARCTION PATIENTS Bolling J. Feild, MD; Richard 0. Russell, Jr., MD, FACC; McKamy Smith, MD, PhD; Charles E. Rackley, MD, FACC; University of Alabama, Birmingham, Alabama.

Left ventricular (LV) function has classically been des- cribed in terms of "ventricular function curves" (VFC). Recently the ejection fraction (EF) has been proposed and used as an index of LV function. In the present study the relation of these two expressions of LV function was investigated. The subjects were 15 consecutively studied post-myocardial infarction patients (pts) having cardiac catheterization with both quantitative biplane angiocar- diography (6 or 12 frames/set) and dextran infusion (DI). Thirty to 45 minutes after ventriculography, 200-600 cc of dextran was rapidly infused into the central venous cir- culation. Cardiac output (by green dye method) and LV fil- ling pressure (P) (LV end-diastolic pressure - 13 pts; pulmonary artery end-diastolic pressure - 2 pts) were mea- sured inunediatel prior to DI and after 200 ml increments. Stroke index (SI 3 and P were related to construct VCF. In general, any pt with high P following angiography did not have DI. However, 2 pts had baseline P > 18 mnHg with EF of 0.44 and 0.39; VFC were flat. The remaining 13 pts had baseline P of 5 16 mmHg. EF was > 0.50 for 3 pts; VFC were steep with > 40% maximum increase in SI. EF was < 0.30 for 3 pts; VFC were flat with < 10% increase in SI. EF was between 0.30-0.49 in 7 pts; one had a flat curve, 6 had moderately depressed curves with SI increasing be- tween 18 and 36% (mean 31). Each VFC (for pts with base- line P 5 16 mmHg) was described as a parabola in order to make objective comparisons. VFC described as a parabola correlated with EF with r = 0.74. Thus, in post-myocar- dial infarction pts having baseline P of <- 16 mnHg, the VFC reflected the level of ventricular performance as described by the EF.

130 January1973 The AmericanJournalofCARDlOLOGY Volume31