ABSTRACTS

THE PREDICTIVE VALUE OF THE MAXIMAZ TREADMILL EXERCISE ELECTROCARDIOGRAM

Clifford C. Hallam, MD; Paul L. McHenry, MD, FACC;

John W. Jordan, MD, Krannert Institute of Cardiology, Department of Medicine, Indiana University School of

Medicine, Indianapolis, Indiana.

To assess the predictive value of the maximal treadmill exercise ECG (MTME) in respect to the future development of new coronary events (angina, myocardial infarction or

sudden death ) 727 normal male members of the Indiana State Police Force were tested between 1968-1970 and then followed clinically. Their ST segment responses

were quantitated by a previously described computer pro- gram. The subjects were divided into two age groups, 40 yrs. and under (Group A) and over 40 yrs. (Group B). There were 539 subjects in group A and 4 had a positive

ST response (cl%). There were 190 subjects in group B and 21 and a positive ST response (11%). During a mean follow-up period of 6 yrs., 4 subjects in group A and 13

in group B manifested a new coronary event. Two of the 4

in group A and 6 of the 13 in group B demonstrated a positive ST response at the onset of the study (sensitiv-

ity 8/17 or 47%). Of the 25 subjects with an abnormal

ST response at the onset of the study, 8 manifested a new coronary event in 6 years (specificity 32%). Only

one subject died suddenly during the study period. Thus

with MTME and computer quantitation of the exercise ECG we were able to identify 45% of the subjects who went on to develop a new coronary event during a 6 year follow-up

period. The risk ratio for those subjects with an abnormal ST response proved to be 25:l.

REPRODUCIBILITY AND CAUSES OF VARIABILITY IN PRECORD-

IAL ST-MAPS FOLLOWING ACUiE MYOCARDIAL INFARCTION

Thordur Hardarson, MD, PhD; Hortmut Henning, MD; Robert A.

O’Rourke, MD, FACC; John Ross, Jr., MD, FACC, University of

California, San Diego, California

In 36 patients (pts) with acute first antbrior myocardial infarcts,

uncomplicated by hypotension, infarct extension and conduction

disturbances, the time evolution and reproducibility of ST-seg-

ment elevation was examined during the first 48 hours (h) after on-

set of acute’symptoms. Thirty-five lead precordial ECG’s were

recorded and the sums of ST-elevations (XT) in 173 maps were an-

alysed. In IO patients studied early, the>ST declined by 24%

from 6 to I2 h (4.9*0.9 (SEM) to 3.7*0.6 cm ~~0.05). There

was a correlation (r = 0.58) between the first>ST recorded and the

heart rate (HR) systolic blood pressure (SBP) product. An increase

in>ST from 5.1*0.9 to 6.3*0.9 cm occurred with the appearance

of a pericardial rub in 6 pts (p<O.OOl). Beta-blocking and after-

load reducing agents produced an abrupt decrease i&ST in II of I2

pts. We assessed short-term reproducibility ofZST in 22 pts studied

at 12-48 h when the meanZST fell unsignificantly (5%) and while the pts were clinically stable. The mean absolute difference be-

tween 24 paired readings l-2 h apart was 0.4lkO.5 cm (SD); and between 32 readings 2-4 h apart0.84*0.49 cm, the difference and SD being small during both periods. However, the mean ab-

solute difference between 74 paired readings 4-8 h apart was I. I

cm with a wide SD of 1.2 cm. We conclude that there is a size-

able foil inZST at 6-12 h but little change occurs at 12-48 h; re-

producibility ofIZST is good over l-4 h, although cardiovascular

drugs, HR, SBP and pericarditis importantly affect5ST.

VALUE AND LIMITATIONS OF EXERCISE TESTING IN DETECTING CORONARY DISEASE IN THE PRESENCE OF ST-T ABNORMALITIES ON STANDARD 12-LEAD ELECTROCARDIOGRAM Fred J. Harris, MD; Dean T. Mason, MD, FACC; Garrett Lee, MD; Ezra A. Amsterdam, MD, FACC; Anthony N. DeMaria, MD, FACC, University of California, Davis, California

Little data are available regarding the sensitivity and specificity of exercise electrocardiogram (ECG) in detect- ing coronary disease (CAD) with abnormal STsegment& Twave (ST-T) on standard 12-lead resting ECG. Therefore, this study evaluated exercise ECG in 44 patients (pts) with ST- T abnormalities at rest who underwent maximal graded trea& mill exercise tests (MTE). CAD was determined by coronary arteriography in all pts; no pt was taking digitalis, had Q waves >.03 seconds on resting ECG, or had valvular heart disease. All pts attained 70% of their maximal heart rate on exercise in the absence of chest pain or fall in blood pressure. Of 31 pts in whom MTE induced additional 1 mm ST+ for at least .08 seconds, 25 pts had CAD; while CAD was present in a smilar number (7 of 13) of pts without this ECG change during FITE (p>.O5). Further, no difference existed between the number of pts with CAD (25 of 32) and those without CAD (6 of 12) who manifested 1 mm ST+ (p>. 05). In contrast, of 18 pts exhibiting 2 mm additional ST+ during MTE, 17 had CAD: significantly more (pc.05) than the 15 of 26 pts without this additional ST+. Moreover, although only 17 of 32 (53%) CAD pts manifested 2 mm addi- tional ST+ this occurred in only 1 of 12 (9%) subjects without CAD (pc.05). Thus the additional criteria of myo- cardial ischemia of 1 mm ST+ cannot be applied in the presence of an abnormal resting ECG. However, 2 mm addi- tional ST+ during MTE occurs in the majority of CAD pts and identifies such pts with a high degree of specificity.

POST-INFARCT FIBRINOLYTIC ACTIVITY: INHIBITION BY

TRASYLOL.

Joseph Hartmann, MD; Jawed Fareed; Harry Messmore, MD; John Robinson, MD; Rolf Gunnar, MD, Loyola University Medical School, Maywood, Ill.

Trasylol is a non-specific inhibitor of proteolysis which has been shown to decrease infarct size. Its exact mech- anism in reducing infarct size has not been elucidated. We have studied the coagulation profile in the coronary sinus of the dog model in control and Trasylol treated

dogs. Modification of infarct size was measured in 10

control dogs and 8 dogs treated with Trasylol (50,000 units I.V. q 6 hrs) l/2 hr post-infarct. Comparing ST segment elevation 15 min post-infarct with myocardial CPK 24 hrs later gave a. line indicating severity of ischemic injury. For control dogs, CPK=52-5.4 ST (r=.78). For

Trasylol dogs, CPK=52-2.1 ST (r=.65, pc.01). Throughout

the 6 hr study period there was no change in coronary sinus prothrombin time, partial thromboplastin time, or thrombin time. Coronary sinus plasminogen and fibrinogen

fell significantly in control dogs over the 1st two hrs, returning to normal by the 3rd hr. There was a correspond ing rise in coronary sinus active plasmin. In vitro

addition of Trasylol in concentrations expected in the dogs produced no change in plasminogen or plasmin content. In Trasylol treated dogs the drop in plasminogen and fibrinogen was significantly less, returning to normal at 2 hrs. Sequential plasminogen levels were inversely cor- related with chemotactic signals in the coronary sinus.

Conclusion: Trasylol decreases ischemic injury, inhibits plasminogen activation, and suppresses chemotactic re- sponse to acute infarction. This may be the mechanism for its limitation of ischemic injury. Activated plasmin may be responsible for the initial chemotactic response seen after infarction.

January 1976 The American Journal of CARDIOLOGY Volume 37 141