ABSTRACTS

LACK OF ACUTE EFFECTS OF NITRATES ON EXERCISE CAPACITY IN CONGESTIVE HEART FAILURE J. A. Franciosa, MD, FACC; J. N. Cohn, MD, FACC, Univer- sity of Minnesota and Veterans Administration Hospitals, Minneapolis, Minnesota

Vasodilators acutely improve resting hemodynamics in congestive heart failure (CHF) but their immediate effects on the response to exercise (E), also a vasodila- tor stimulus, in CHF are not known. We performed bicycle E to symptomatic maximum in 8 patients with class II-III CHF before and 1.5 hrs after 40 mg of oral isosorbide di- nitrate (IS). Expired air was collected for oxygen con- sumption (VO)and cardiac index (Cl by CO2 rebreathing), and pulmonary wedge pressure (PWP) was monitored by Swan- Gans catheter. Resting hemodynamics were unchanged after IS except for a fall in PWP to 15.4 2 2.7 (SEM) from 23.6 + 3.3 mm Hg (p<O.OOl). Exercise duration was unchanged by IS (9.5 ?r 1.8 vs 9.6 r 1.8 min). VO at maximum E was unchanged by IS (15.5 t 2.2 ml/kg/min before and 15.3 ? 1.7 ml/kg/min after) as well as maximal CI (4.21 ? 0.49 L/min/m2 vs 4.24 + 0.47 Lfminfm2). Heart rate and mean arterial pressure at peak E were unchanged by IS while systemic vascular resistance averaged 14.7 t 2.3 units before and 14.3 + 2.7 units after IS. PWP at peak E was reduced insignificantly from 40.4 ? 2.4 mm Hg to 36.0 + 2.9 mm Hg after IS. In conclusion, nitrates which may chronically increase E tolerance in CHF do not acutely improve E capacity or alter E hemodynamics in CHF, perhaps because they do not acutely augment the vaso- dilation induced by E itself.

EXERCISE TESTING IN MITRAL VALVE PROLAPSE Peter J. Engel, MD; Barry L. Alpert, MD; John H. Triebwasser, MD; Malcolm C. Lancaster, MD, FACC USAF School of Aerospace Medicine, Brooks Air Force Base, Texas

Abnormal repolarization responses to treadmill exercise testing (TM) have been noted in patients (pts) with mitral valve prolapse (MVP); yet the true frequency of this association is unknown. During aeromedical evalu- ation since 1972, 23 aircrew members (all male, mean age 37 + 7 years) were found to have MVP (without evidence of other cardiovascular disease), as defined by the presence of typical findings in at least two of the following categories: auscultation-phonocardiography (AP - 20 .pts), echocardiography (22 pts), and left ventricular cineangiography (8 pts). Twenty of the patients were asymptomatic, including the 3 patients without AP. At least one maximal TM (modified Balke protocol, monitoring orthogonal leads X, Y, and 2 and a modified lead V5) was available for review in each patient. An abnormal repolarisation response'was defined as at least 1 mm of horizontal or downsloping ST segment depression. Of the 23 patients, 7 had at least one abnormal TM (30%). Six of these 7 patients were asympto- matic, and 3 were without AP. Six underwent diagnostic catheterization including coronary arteriography, and all were free of coronary artery disease (CAD). No specific pattern of lead positivity was noted.

In conclusion, MVP appears to be frequently associated with abnormal TM in the absence of CAD. In addition, MVP should be considered in the differential diagnosis of an abnormal TM even in the absence of symptoms and typical auscultatory abnormalities of MVP.

EXERCISE-INDUCED HYPOTENSION IN THE YEAR FOLLOWING lfYO- CARDIAL INFARCTION. Dennis Davidson MD, Robert DeBusk MD, FACC, Stanford Univ. School of Medicine, Stanford, CA.

To evaluate the prevalence and mechanisms of exercise- induced hypotension (EHP) following myocardial infarction (MI), 150 men, mean age 54,had treadmill testing(T 3, 7,11,26 and 52 weeks post-MI. EHP, always an endpoint in exercise testing, was defined as a fall of ~10 mm Hg in indirectly measured systolic blood pressure (SBP) from the peak exercise value.,'There was no significant difference between anterior MI (AMI) and inferior MI (IMI) patients (pts) in the incidence of pre-HI angina, extent of infarc- tion, in-hospital hypotension or post-MI TM maximum SBP, work load and ST depression.

EHP occurred in ll-19% of pts at each testing period. Forty-seven of 150 (31%) pts had 1 or more EHP episodes: 21 of 41 (51%) with AMI, 20 of 95 (20%) with IMI and 6 of 14 (43%) with non-transmural MI. None developed heart failure. The incidence of EHP remained constant through- out the year. There was no correlation of MI site with TM maximum work load, SBP or EHP occurrence at any of the 5 testing periods. At 3 and 7 weeks, IMI pts had EHP at significantly lower heart rates (HR) (118, 120) than AM1 pts (132,150). Max. work load and the incidence of TM is- chemia were equal for EHP and non-EHP pts. These data suggest a different mechanism of EHP for AM1 and IMI pts, particularly early post-MI. During a mean followup of 2 yrs, 4 of 41 AM1 pts and 5

of 95 IMI pts had another MI. Of the 95 IMI pts, 2 of 20 EHP and 3 of 75 non-EHP pts had another MI; 1 of 20 EHP and 3 of 75 non-EHP pts had sudden death. No AM1 pt had

sudden death. CONCLUSION: Compared to AM1 pts, IMI pts developed EHP

less frequently, but at lower heart rates during 3 and 7 week post-MI TM. EHP was not correlated with ischemia or with prognosis.

EFFECT OF EXERCISE ON LEFT VENTRICULAR EJECTION FRACTION IN PATIENTS WITH CORONARY DISEASE John K. Frischknecht, MD; Peter P. Steele, MD; Dennis L. Kirch, MSEE; Robert A. Vogel, MD, Denver Veterans Administration Hospital, Denver, Colorado.

Left ventricular (LV), ejection fraction (EF) was meas- ured at rest and during graded supine bicycle exercise in 31 men with arteriographically defined coronary disease (CAD) and in 15 normal men. LVEF was calculated from a LV time vs activity curve (collimated dual crystal scintillation probe; first transit; ggmTechnetium) as the fractional fall in LV count-rate divided by the back- ground-corrected LV end-diastolic count-rate. In normal men LVEF at rest averaged .59 f .06 (* SD) and during exercise averaged .72 ?: .08. The dual crystal probe measurement of LVEF correlated (r=0.89) with LVEF computed from single plane (RAO) contrast LV cineangio- gram (N=25). Average LVEF failed to increase with exercise in men with CAD (.55 ?r .03 to .57 ? .03; AVE f SEM; NS). In 17 men with CAD who had ST depression (> 1 mn) during exercise, LVEF either failed to increase (9 .05) or decreased in all (.55 * .04 to .49 ? .03; NS); whereas in 14 without ST depression, LVEF increased in 10 (71%) and failed to increase in 4 (29%) (.54 ? .04 to .66 f .04; PcO.05). Of 10 men with CAD, normal restin LVEF (> .46) and without exercise ST depression, 4 (40% 3 had an abnormal exercise LVEF and 6 (60%) had an increase of LVEF with exercise. Results suggest that LVEF normally increases during exercise and that men with CAD and exercise ST depression have an abnormal LVEF response to exercise. An abnormal exercise LVEF was frequently observed in men with CAD who did not have ST depression, suggesting that measurement of exercise LVEF may increase the sensitivity of exercise testing.

430 February 1978 The American Journal of CARDIOLOGY Volume 41