LETTERS

COMMENT: I

We have a great deal to learn about coronary spasm. At this time, the prevalence of spasm in patients with chest pain with or without anatomic coronary lesions is unknown. Aside from scattered case reports, the lethality of spasm as well as its role in converting coronary disease with stable angina pectoris into acute myocardial infarction is also unknown. That provocative testing for spasm carries risk is certain. The question of whether the risk is worthwhile will ultimately be answered in a general way by the collection of more information about the natural history of coronary spasm. In an individual case, a decision to attempt to provoke a potentially life-threatening entity will (and should) always be a difficult one, made with the patient’s full understanding and agreement and carried out with appropriate caution.

Catherine Nelson, MD Stanley A. Forwand, MD, FACC Harvard Medical School Mount Auburn Hospital Cambridge, Massachusetts

COMMENT: II

Dr. Bauman reports on a man with probable Prinzmetal’s angina and relatively normal coronary arteries who experi- enced severe unrelenting chest pain and arrhythmias due to near-occlusive right coronary arterial spasm in response to provocative administration of ergonovine maleate. This case emphasizes the need for a careful and systematic approach to such induction of coronary spasm in patients with suspected Prinzmetal’s angina. The points to be learned from this case are as follows:

1. Reproduction of the coronary spasm and clinical syn- drome of Prinzmetal’s angina by ergonovine maleate is certain to be accompanied occasionally by arrhythmias because of their large incidence during spontaneous episodes.‘J

2. The route of administration of ergonovine maleate may be important. Reported series have utilized only intravenous administration, allowing substantial dilution before coronary arterial perfusion. 3-5 The intraaortic or intracoronary route should be reserved for investigational purposes.

3. Methodic sequential administration of increasing doses of ergonovine maleate may be important. Reports of series have generally utilized doses of 0.1 to 0.4 mg. Because patients with Prinzmetal’s angina appear to be sensitive to a certain dose of ergonovine maleate, we urge a sequential increase in dosage based on reported experience, that is, 0.1 mg initially, 0.15 mg at 3 and 0.2 mg at 3 to 5 minute intervals with serial angiograms to document effect. If the patient has had docu- mented spontaneous episodes of S-T elevation 0.05 mg should be given as the initial dose.

4. Repeat coronary arteriography, at least of the suspect coronary artery, should be performed after each injection because coronary spasm may well occur without complete occlusion or reproduction of symptoms. Nonocclusive spasm of the right coronary artery may well have occurred after the second or third dose of 0.05 mg of ergonovine maleate without reproduction of symptoms in the case report by Bauman. Repeat coronary angiography at that time might have averted the final larger dose of 0.2 mg that precipitated the unrelenting right coronary spasm.

5. The primary goal of therapy, after reproduction of Prinzmetal’s angina and coronary spasm and its documen- tation, should be reversal of the coronary spasm because it is the presumed cause of the arrhythmias. We suggest admin-

istration of l/100 grain of nitroglycerin sublingually, repeated once or twice over 5 minutes for unrelenting spasm. Intrave- nous nitroglycerin or nitroprusside can also be given if the spasm fails to resolve after 5 to 10 minutes.

6. Finally, we believe that reproduction of the clinical syndrome of Prinzmetal’s angina during coronary angiography is worth the small risk because of the implications for long- term therapy with vasodilators. This is particularly true in view of the reported marked efficacy of calcium-antagonist drugs for this syndrome.6-*

John Speer Schroeder, MD, FACC Coronary Care Unit Cardiology Division Stanford University School of Medicine Stanford, California

References

1. Prlnzmetal M, Kennamer R, K&as R, et al: Angina pectoris. I. A variant form of angina pectoris. Preliminary report. Am J Med 27:375-37,8, 1959

2. Hiaalnr C. Wexler L. Silverman J. et al: Clinical and arterioaraphic features of P&teta~s variant angina: docu&ntation of etiolcgic factors. &n J Cardiol 37: 831-839. 1976

3. Nelson C, Nowak B, Chllds H, et al: Provocative testing for coronary arterial spasm: rationale, risk and clinical illustrations. Am J Cardiol 40:624-629, 1977

4. Curry RC Jr. Peplne CJ, Sabom MB, et al: Effects of ergonovine an patients with and without coronary artery disease. Circulation 56:803-809. 1977

5. Heuplsr F. Proudflt W, Siegel W, et al: The ergonovine maleate test for the diagnosis of coronary artery spasm. Circulation 51, 52:Suppl ll:ll-11. 1975

6. Bosserf F, Valor W: Dihydropyridine. eine neue Gruppe start wirksamer Coronarth- eraoeutika. Naturwissen 58:578. 1971

7. H&da S, Klmura E: In. proceedings, First International Nifedipine (Ad&t) Symposium, Tokyo 1973 (Hashimato K, Kimura E. Kobayashi T. ed). Tokyo, University of Tokyo Press, 1974, p 175

8. Muller JE, Gunther BJ: Nifedipine therapy for Prinzmetal’s angina. Circulation 57: 137-139. 1978

“NORMAL” CHOLESTEROL AND ATHEROSCLEROSIS

There is reason to question the basis of the definition of nor- mal lipids used by Lie et al.’ The issue is more than one of semantics, and potentially leads to an underestimate of the role of nutrition in the prevention of atherosclerosis. Choles- terol values for the group designated as “normolipemic” ranged from 214 to 291 mg/dl, whereas “hyperlipemic” pat- ients had cholesterol values greater than 308 mg/dl. Using “normal” in a biologic sense,2 not as an average or a statistical term, an international perspective would suggest that a cho- lesterol level much above 180 mg/dl is “abnormal” and leads to atherosclerosis on a wide scale.3$4 It is worth noting that the lowest cholesterol value in a patient who came to surgery in this series was 214 mg/dl. Obviously the risk increases as cholesterol increases, but it would appear that a threshold can be defined. Lie et al. conclude that “the observation that mi- croscopic changes of atherosclerosis may occur in saphenous vein grafts in some patients without hyperlipemia also em- phasizes the importance of effective control not only of blood lipids but also of the other recognized risk factors for athero- sclerosis.” Although control of other risk factors is crucial in the hyperlipemic population in the United States, perhaps 214 to 291 mg/dl is not yet an optimal level of serum cholesterol, and should not be accepted as normal.

Richard Cooper, MD Department of Community Health ‘Northwestern University Chicago, Illinois

References

1. Lie JT. Lawrle GM, Morris GC: Aortocoronary bypass saphenous vein graft athero- sclerosis: anatomic study of 99 vein grafts from ncfmal and hyperlipoproteinemic patients up to 75 months postoperatively. Am J Cardiol 40: 906-914, 1977

2. Wynder EL, Hill P: Blood lipids: how normal is normal? Prev Med 1:161-166. 1972

October 1978 The American Journal of CARDIOLOGY Volume 42 895