ABSTRACTS

REGIONAL FLOW ABNORMALITIES IN CORONARY DISEASE: REXA- TIONSHIP TO ANGINA AND ISCHEMIC ECG CHANGES John R. Wilson, MD, Jack L. Martin, MD, William J. Untereker, MD, FACC, Warren Lasked, MD, John W. Hirshfeld. MD, FACC, Hospital of the University of Pennsylvania, Philadelphia, PA.

To determine the relationship of regional flow abnor- malities in coronary disease to angina and ischemic ECG changes, we measured great cardiac vein flow (GCVF), draining the left anterior descending (LAD) territory, during atria1 pacing (P) in 21 patients. Ten patients had no LAD flow obstruction (Group I) and 11 had >75% stenosis of the left-main or LAD coronary artery (Group XI). Heart rate (HR) "as increased by 20 beats/minute increments to 150 or angina. In Group I, P increased the double product (DP) (systolic BP x HR) from 7804+1484 to 18383+3095 mmHg beats/min. Percent AGCVF/%ADP,an index of flow response, "as 1.10+.53 following the first 20 beat increment in HR and O-885.21 for the total pacing period. In Group II, P increased the DP from 7723+1456 to 16702+2821 mmHg beats/min. Percent AGCVF/%ADP follow- ing the first 20 beat increment in HR (0.41+.36) "as sig- nificantly lower than in Group I (p<.OO2) even though no clinical evidence of ischemia "as noted and the HR "as only 7756 beats/minute. At the peak pacing rate of 117t 19 beats/min, angina developed in all patients accompanied by >1 mm anterior ST changes in 9. Percent AGCvF/%ADP at the-time of angina c.37t.17) remained lower than in Group I (p<.OOl). These data-indicate that >75% coronary steno- ses impair myocardial perfusion during atria1 pacing at levels of myocardial oxygen demand substantially lower than those which produce angina and ischemic ECG changes. Therefore, clinically-silent myocardial ischemia may frequently develop during low level exertion in patients with severe coronary disease.

EXERCISE-INDUCED FALL IN FLOW THROUGH STENDTIC CORONARY ARTERIES Jeffrey S. Schwartz M.D., Bruce Tockman B.S., Jay N. Cohn M.D.. FACC. Robert J. Bathe M.D.. FACC. University of Minnesota, Minneapolis, Mu

In coronary stenosis (CS), it is believed that exer- cise (Exl-induced ischemia is due to an inadequate increase in flow. We studied Ex in 5 chronically instrumented dogs with severe CS. The dogs had a flow probe and a nmre distal wire snare occluder on the cir- cumflex (Cxl artery and catheters in the left atrium,_ left ventricle (LVl and aorta. Four dogs had Cx cathe- ters distal to the occluder. Measurements were done with the animals resting quietly and then during moderate Ex. With no stenosis, Cx flow increased with Ex. In 13 experiments with a severe Cx stenosis the changes from rest to Ex were: heart rate from 101+7 to 143+9 beats/min (p<O.OOll, mean aortic pressure fi;om 103T4 to 111+2 mm Hg (p<O.O51, distal Cx pessure from 716 to 40+2%m Hg (p<O.OOll, CS ressure gradient from 32T4 to 71T2 mm Hg (p<O.OOll, CS resistance from 2.3tO.7 to-11.3t3.4 units (p(O.01) and flow through the steiiotic artery-from 29+4 to 13+3 ml/min (p<O.OOll. LV filling Iressure rose Fom 8+1 To 14+2 mm Hg (p<O.O25). The fall in intraluninal Irexsure diztal to the CS and thus in the CS itself may have resulted in pssive narrowing of the stenotic segment which may have caused the fall in flow. Ex, therefore, may result in a fall in flow through a stenotic coronary artery.

ASSESSMENT OF INFERIOR REGIONAL LEFT VENTRICULAR BLOOD FLOW USING THEREP)DILUTION Robert L. Feldman, MD, FACC; Carl J. Pepine, MD, FACC; C. Richard Conti, MD, FACC, University of Florida, Gainsville, Fl.

Evaluation of inferior (INF) regional left ventricular (LV) blood flow (F) in patients (pts) with coronary (car) disease is difficult because car sinus F (CSF) alone may not always reflect INF regional changes. We tested the hypothesis that the difference between total LV (repre- sented by CSF) and anterior (ANT) region (represented by great cardiac vein flow (GCVF) flows assessed INF region F. We simultaneously measured GCVF and CSF before and during transient occlusion by spasm or balloon catheter of either left anterior descending (LAD) or right car artery (RCA) in 17 pts. A catheter was positioned in the CS with proximal thermistor between os and middle cardiac vein(s) and distal thermistor in GCV. For analysis the total LV was assumed to represent only 2 regions. Region F changes 25 ml/min were considered important.

During transient LAD occlusion in 11 pts ANT region F de- creased in each case as mean F declined (67+31 to 42+21 mllmin , ~~0.05) while INF region F was usuaily unchanged (61226 to 69528 ml/min, p=NS). By contrast, during RCA occlusion in 6 pts, ANT region F was unchanged in 5 cases and increased in 1 case (mean F 62+26 to 61+29 ml/min, p=NS) while INF region F decreased-in 5 ptsand was un- changed in 1 pt as mean F decreased mill, pc0.05).

These data suggest that subtraction total LVF provides an estimate of F the RCA.

(83+23 to 57238 ml/

of ANT region F from changes occurring in

INTRACORONARY THROMBOXANE RELEASE DURING ANGINA: RELATION TO ISCHEMIA AND EFFECT ON CORONARY RESISTANCE Jack L. Martin, MD; John R. Wilson, MD; William J. Untereker, MD, FACC; John Burch, MD; John W. Hirshfeld, MD, FACC, Hospital of the University of Pennsylvania, Philadelphia, PA.

It has been proposed that intracoronary release of thromboxane (TX) A2 during stress-induced angina exacer- bates myocardial ischemia. To examine this hypothesis, we measured arterial (Ao) and coronary sinus (CS) TxB2 and lactate concentrations, thermodilution CS flow, and Ao pressure during pacing-induced angina and immediately post-pacing in 35 patients with coronary disease. coro- nary resistance "as calculated as mean Ao pressure/CS flow. During pacing, intracoronary TX release (CS>Ao TX) "as not noted in any patient. However, myocardial lactate production occurred in 18 patients. Immediately post- pacing, intracoronary TX release developed in 8 patients: 7 of the 18 lactate-producers as opposed to only 1 of the 17 patients who did not produce lactate (p<.OS). This release resulted in CS TX levels of 510+370 pg/ml. De- spite these TX levels, termination of pacing was asso- ciated with an immediate return of coronary resistance to basal levels (Base: 1.2kO.5 vs post-pacing: 1.2~0.5 mmHg/ ml/min) and rapid relief of angina. Patients without TX release had a similar return of coronary resistance to basal levels (Base: 1.4kO.6 vs post-pacing: 1.3LO.7 mmHg/ ml/min) . We conclude that 1) intracoronary TX release frequently follows pacing-induced myocardial la+ste production but 2) this release does not alter coronary resistance or prolong angina, suggesting that it does not exacerbate ischemia.

948 March 1982 The American Journal of CARDIOLOGY Volume 49