ABSTRACTS

LEFT VENTRICULAR PRESSURE-VOLUME CHANGES DURING SPONTANE- CORRELATIONS BETWEEN LATE VENTRICULAR DYSRHYTHMIAS OUS ANGINA PECTORIS AND INFARCT SIZE B.Sharma, M.D.; M. Hodges, M.D.,FACC; R.Asinger,M.D.; R. Johnson,M.D.; J.F.Goodwin,M.D.,FACC, Hennepin County Med- ical Center and the University of Minnesota, Minneapolis, MN and Hammersmith Hospital, London, England.

Ali A. Ehsani, MD; Mary K. Campbell, RN; Edward M. Geltman,

MD; Robert Roberts, MD, FACC; Burton E. Sobel, MD, FACC,

Washington University, St. Louis, Missouri

Most studies evaluating LV pressure and volume during angina have utilized atria1 pacing to produce ischemia. Although these studies have been criticized because they may not reflect the changes in volume that might occur during spontaneous angina pectoris (SAP), no study on LV volume during SAP has so far been reported. We measured LV pressure, volume and wall motion in 14 patients when they developed SAP during cardiac catheterization. In every patient control measurements had previously been made; further measurements were made after nitroglycerin (NTG) had relieved pain. Subsequently coronary angio- graphy showed significant 2 or 3 vessel disease in all 14 patients. The ST-segment was depressed in every patient during angina (ave. = -0.26~.13 mv; mean?SD); wall motion study revealed either a new area or further extension of an already existing area of asynergy in all patients. STATE LVEDP EDV ESV EF

(mm&) (ml/m*) (ml/m*) C./p) REST 18+8 80?20 36+14 56+12

Enzymatically estimated infarct size index (ISI) appears to be a

determinant of ventricular dysrhythmia and depressed left ven-

tricular ejection fraction within the first ten hours, and of mortality

within one month after acute myocardial infarction. To determine

whether ISI is also related to later events, we followed 63 patients

with enzymatically estimated infarct size, <&I years of age who

had sustained on initial infarction uncomplicated by an extension

during the initial admission and who survived for at least five days.

ISI in survivors was 22 i 2 (mean f SE) CK-g-eq/m2 BSA compared

to 71 f 7 in the five patients who succumbed (p < ,001). There

was na correlation between ISI cmd ejection fraction assessed more

than four months after infkction with99mTc-albumin in36 patients.

The frequency of premature ventricular complexes (PVCs) in 28

patients (none of whom had sustained additional infarctions)

assessed by automated analysis of 24-hour Halter tapes obtained

between 2 and 12 months after infarction averaged 241 f 117/24

hours in patients with small infarcts (ISI < 15) compared to

1292 i 840 in patients with large infarcts (ISI > 15) (p < .05).

These results indicate that among relatively young patients with

initial infarction, enzyinatically estimated infarct size presages

not only ventricular electrical instability and function during rhe

acute episode but also the severity of ventricular dysrhythmia as

long as one year after myocardial infarction.

PC.01 PC.001 p<.OOl 91r28 53?25 44+15

NTG > !;;:"' PC.03 PC.02 PC.01 83224 30+14 64+14

This study reveals that EDV significantly increases with the rise in LVEDP during SAP (associated with signif- icant ST depression and abnormal wall motion), indicating severe LV dysfunction. Nitroglycerin promptly reversed the depressed cardiac function induced by SAP. These pressure-volume changes are different from those of angina induced by atria1 pacing as reported in previous studies.

NONINVASIVE DlAG~osls OF IsCHEI~IC CARDIOMYOPATHY BY FLUOROSCOPIC DETECTION OF CORONARY ARTERIAL CALCIFICATION Allen Johnson, MD FACC; Stuart Laiken, MD; Ralph Shabetai, MD FACC, Univ of Calif and VA Hosp. San Diego, Calif.

Severe coronary artery disease (CAD) may give rise to pro- gressive cardiomegaly and congestive heart failure (CHF) in the absence of a history of myocardial infarction. Coronary arteriography may be necessary to distinquish the resulting ischemic cardiomyopathy from nonischemic cardiomyopathy. To assess the value of fluoroscopic de- tection of coronary arterial calcification (CorCa++) in this differential diagnosis, all patients seen over a 3 year period with severe CHF and catdiomegaly who under- went catheterization had cardiac fluoroscopy prior to cor- onary arteriography. Those with a history of myocardial infarction or significant valvular disease were excluded. The 24 remaining patients all had evidence of marked hero- dynamic compromise (LVEDI>I10ml/M2, EFc.35). 10 of these patients had CorCa++ at fluoroscopy. All 10 had abnormal coronary arteriograms: 6 had 3 vessel disease, 3 had 2 vessel disease, and each had left anterior descending in- volvement. Each of the 14 patients without CorCa# had normal arteriograms. The group with CAD had a mean age of 52 (range 39-68). 50% had typical or atypical chest pain, 80% had at least one coronary risk factor, and 30% had ECG Q waves. The corresponding values for the nonischemic group were: age 44 (range 26-62), 21% with chest pain, 57% with at least 1 risk factor, and 43% w:th Q waves. Although chest pain and risk factors were more common in those with CAD, no clear separation could be made clini- cally between the 2 groups of pts. We conclude that fluoroscopic detection of CorCa++ provides a reliable non- invasive method for distinguishing patients with ischemic cardiomyopathy from those with nonischemlc cardiomyopathy, particularly when the diagnosis is not clinically apparent

ASYMPTOMATIC HEALTHY PERSONS WITH FREQUENT COMPLEX VENTRICULAR ECTOPY AND CORONARY ARTERY DISEASE. Harold L. Kennedy, MD, MPH, FACC; Janet E. Pescarmona; Richard J. Bouchard, MD;,and Derinis G. Caralis. MD, Department of Cardiovascular Services and Clmical Inve’stigations, U.S. Public Health Service Hospital, Baltimore, Maryland.

To determine if frequent complex ventricular ectopy detected by 24 hour ambulatory electrocardiography was an indicator of asymptomatic coronary artery disease (CAD) in apparently healthy subjects, forty-seven asymptomatic patients incidentally discovered to have frequent complex ventricular ectopy were clinically evaluated and found to be otherwise normal. Twenty subjects (17 men, 3 women, mean age 49 k12 yrs) granted informed consent to study by cardiac catheterization and coron- ary arteriography. Results disclosed patients with significant CAD (250% luminal narrowing); subclinical CAD (<50% luminal narrowing) and normal coronary arteries. Mean left ventricular end diastolic volumes (LVEDV) and systolic volumes (LVESV), ejection fractions (EF), and mean left ventriculal end diastolic pressures ILVEDP) were examined. Halter monitoring (24 Hr) measured mean frequency and types ot ventri- cular ectopic beats (VEB). Results showed:

Significant Subclinical Normals P

No. of Patients(%) LVEDVkc/M2) LVESV (cc/M2) EF(%) LVEDPlmm Hal

-CAD 6(3OJ

88 i8

x: z; 12 *g

CAD 305)

86 *7 24 *3 63 *2 14 *2

ll(55) 80 *5 31 k4 61 +3 7422

Value n.s. n.s. n.s. n.s. ns.

VEB(Beats/Hri. 442 i96 64;,;3my 34;&5; ns. Multiform VEB(%) n.s. VE8 Couplets(%) n.s. VEB Tachycardia(%) 2633)

In this study of asymptomatic apparently healthy persons with fk:’ quent complex ventricular ectopy: a) the majority of patients did not have significant CAD (70 Percent) b) mean frequency or complex types of ventricular ectopy could not pre-

dict the presence or absence of CAD c) left ventricular function measurements could not predict the presence

or severity of CAD or frequent complex ventricular arrhythmia.

424 February 1979 The American Journal of CARDIOLOGY Volume 41