ABSTRACTS

FREQUENCY OF PROVOKED CORONARY ARTERIAL SPASM IN PATIENTS WITH RECENT TRANSMURAL MYOCARDIAL INFARCTION Michel E.Rertrand,MD,FACC;Jean M. Lablanche,MD;PierreY. Tilmant,MD;Marc G.Delforge,MD;Alain G.Carre,MD University hospital,Iiopital Cardiologique,Lille,France Provocative test with methergine(M) was performed in a group of 88 patients (pts) (82 men & 6 women)with recent (~6 weeks)transmural myocardial infarction(MI)vho underwent coronary arteriography for evaluation of vessel disease.The diagnosis of MI was established by typical chest pain ,appearanceof new Q waves and increase in serum creatine kinaselroa level above normal limits. 58 pts or 66% had anterior infarction,28 (32%)had inferior infarction and 2 lateral infarct.Coronary arteriography was performed 2629 (m_+SD) days after the onset of infarc- -tion(range6 to 45).37 or:42% had 1 vessel disease (VD), 25 (28%)had 2 VD,19 or 22% had 3 VD whilst 7 had minimal but insigni>?icant lesions.The provocative test was perfor med after the routine procedure of coronary arteriography using a protocol with a single bolus injection of 0.4 mg of methergine.Aortic pressure ,EKC and coronary arterio- grams of the 2 vessels (left and right coronary artery) were repeated 3 and 5 minutes later. Provoked coronary arterial spasm was observed in 18 or 20.5% of patients.9 patients or 10.25% had spasm superimposed on narrowings located on the vessel respons- ible of the infarction.In these cases spasm was not accompanied by pain or EKG changes.Nine other patients (10.25%)had provoked coronary arterial spasm located on a vessel which was not responsible of the infarction.In this group spasm<was acCompanied by pain and EKG changes. Conclusion:l-Provoked coronary arterial spasm can be induced in 20 % of pts with recent MI .2-The vessel with the narrowingrespons'iblefor the infarction remains sensitive to methergine in 10% of cases.3-In 10% of cases spasm can be induced in vessel unrelated to MI.

I MPORTANCE OF EARLY ADMINISTRATION OF INTRAVENOUS

NITROGLYCERIN TO PRESERVE ISCHEMIC MYOCARDIUM

John T. Flaherty,MD,FACC, Bernadine H. Bulkley,MD,FACC,

Myron L. Weisfeldt,MD,FACC, James L. Weiss,MD,FACC, Gary

Gerste&lith,MD,FACC, Clayton Kollman,ScM, Lewis C. Becker,

MD,FACC, Johre Hopkira Medical Institutionr, Baltimore, Md.

Intravenous nitroglycerin(IVTNG)improves hemodynomicr and

regional irchemia in patients (pts)with acute myocardiol infarction

(AMI). In a prospective randomized triol, 48 hr infusion of IV TNG

or Placebo(PlAC)was begun within 18 hr of onset of AMI in 104

pts to determine whether a prolonged infusion could preserve

ischemic myocordium. IV TNG was titrated to lower mean arterial

pressure 10%. Time between onset of pain and initiation of study

drug(tor>lOhr) defined early and late intervention. *OTThollium

perfusion scare and Tcgpm gated blood pool scans were performed

on days 1 and 10. Thallium defects were scored by computer and

were considered improved if a>*.5 unit reduction in scorewos ob-

tained (range -11 .O to +5.6). Resporae of ejection fraction (EF)was

considered good if EF remained~50% in pts with initial EF?50%(31

pts) and good if EF increosed25% in pts with initial EFL50%(20pk).

Defect Score TNG<lO hr TNG>lO hr PLAC< 10 hr PLAC>lO hr

Improved 12 2 3 2

Not Improved 12 15 11

w 17 ‘; 7 4

Bad 1 4 6 3

Only in TNG 410 hr subgroup was there significant improvement in

defect score (p.032). Likewise for EF only in the TNG<lO hr sulk

group was the beneficial effect significant (k.056). These results demonstmte that early administmtion of IV TNG is important for improving myocordial perfusion and preserving function following

AMI.

NIFEDIPINE THERAPY FOR RECURRENT ISCHBMIC PAIN FOLLOWING ACUTE MYOCARDIAL INFARCTION Peter H. Stone, M.D. and James E. Muller, M.D., Harvard Medical School, Brigham 6 Women's Hospital, Boston, MA.

Following acute myocardial infarction (MI) patients often experience recurrent episodes of ischemic pain at rest which may be due to coronary vasospasm. In order to determine the efficacy of nifedipine, a potent coronary vasodilator, in relieving rest ischemia, we administered nifedipine to 9 patients (pts) with recurrent rest pain a mean of 9.2 days post MI (range 2-42 days). Prior to MI, all of the pts had a history of exertional angina only, yet following the MI episodes of recurrent ischemia occurred at rest (mean # daily episodes 2.4, range 2-6) in spite of maximal medical management with 8-blockers and/or nitrate preparations. Six of the 9 pts had a subendocardial MI, 3 had a transmural MI. Ischemic episodes were associated with ST-segment (ST) deviations in the same leads that displayed the acute MI pattern: 5 pts had ST elevation, 4 pts had ST depression or T inversion. Coronary angiography in 6 pts demonstrated multivessel coronary disease. In all pts the episodes of rest ischemia ceased following the initiation of nifedi- pine (mean daily dose 60 mg, range 40-120 mg). Two pts continued to have myocardial ischemia with minimal exer- tion and underwent coronary bypass surgery for pain relief. The other 7 pts have been managed medically for a mean of 5.4 months (range 1-12 months) and have remained pain free on combined regimens of nifedipine, B-blockers, and/or nitrate preparations. We conclude that nifedipine may be efficacious for the relief of recurrent myocardial ischemia at rest following acute infarction. In some pts nifedipine may eliminate the need for coronary artery bypass surgery and in others it may provide clinical stability prior to operation.

REDUCTION IN INFARCT SIZE AN0 NORBIOITY BY EARLY INTRA-

VENOUS BETAELOCKAOE

Salim Yusuf, MB &I David Ramsdale. NRCP; Richard Peto,

si. MO; Lynnette Furze.SRN: David

Bennett, NRCP; Colin Bray, FRCP; Peter Sleight, FRCP.

Oepartment of Cardiovascular Medicine, John Radcliffe

Hospital, Headington, Oxford

400 patients were studied in a randomised trial to

determine whether administration of intravenous Atenolol

(AT1 (a cardioselective betablocker) within 12 hours of chest pain reduces eventual infarct size, morbidity and

mortality. Infarct size and morbidity data (first 214 ~- patients). 135 patients already had ECG evidence of

infarction at entry: 72 received AT which significantly

decreased subsequent cumulative MB-CPK release from

4-hourly measurements [intravenous AT and Control means = 121 I.U., SE * 10 and 176 I.U., SE f 171 2p<O.O051

and enhanced R-wave preservation [mean R-wave score in

AT and Control = 46% l 3 and 36% t 3; 2p<O.O21. 79

patients had no evidence of infarction at entryi 44 did

not receive AT and 27 of these subsequently developed

infarction, whereas only 11 of the 35 treated patients

infarcted during their hospital stay [2pk 0.011. In

hospital fewer AT patients had non-fatal cardiac arrest

(2 versus 61 or required therapy for heart failure in

hospital (36 versus 47, 2~4 0.101 or at discharge (19

versus 31, 2p< 0.051. Mortality (400 patients): 14 AT -.- patients and 24 Control patients have died since the

start of the study (2p<O.101. Conclusion: Intravenous

Atenolol within 12 hours of pain prevents infarction in

patients with initial threatened infarcts, and reduces

infarct size and morbidity in Acute Myocardial Infarction.

490 February 1961 The American Journal of CARDIOLOGY Volume 47