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Calcium Channel Blockers Cannot Prevent Pure Vasospastic Myocardial Infarction

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Calcium Channel Blockers Cannot Prevent Pure Vasospastic Myocardial Infarction Postgrad Med J: first published as 10.1136/pgmj.63.735.41 on 1 January 1987. Downloaded from Postgraduate Medical Journal (1987) 63, 41-44 Calcium channel blockers cannot prevent pure vasospastic myocardial infarction P. Depelchin and S. Degre Department ofMedical Cardiology, H6pital Academique Erasme, Universite Libre de Bruxelles, 808 route de Lennik, 1070 Bruxelles, Belgium. Summary: Coronary artery spasm is a recognized cause of myocardial infarction. This report describes a case of myocardial infarction attributed to pure coronary spasm which was halted by a double perfusion with streptokinase and nitroglycerin. Further coronary artery spasm leading to a myocardial infarction could not be avoided several weeks later, although the patient was left on calcium channel blocker therapy. The two attacks were not preceded by warning angina pectoris, contrary to accepted belief. The best objective ofend-point drug therapy and its assessment in vasospastic angina are discussed. Introduction Coronary artery spasm alone or superimposed on an atheromatous lesion is now recognized as a cause of myocardial infarction.' Our therapeutic approach has therefore been directed not only towards treating by copyright. factors which increase myocardial oxygen demand but also to modulating smooth-muscle contraction res- ponsible for the coronary artery spasm. Calcium channel blockers and nitroglycerin compounds are potent smooth-muscle relaxing drugs and are effective in suppressing spasm-induced angina. However, nitroglycerin, even intracoronary administered after induced coronary spasms, has sometimes been unable to reverse the spasm.2 We present a patient free from http://pmj.bmj.com/ arteriosclerotic coronary artery disease who de- veloped pure vasospastic myocardial infarction in spite of calcium channel blocking therapy. Figure 1 Electrocardiogram at entry The tracing shows marked ST elevation in leads . aVF and V5 segment III, on September 25, 2021 by guest. Protected A 63 year old woman was admitted to the coronary V6. care unit (CCU) with constrictive precordial pain. Serial electrocardiograms (ECG) demonstrated hall- marks of an evolving inferior myocardial infarction: programme routinely used in our hospital for impend ST segment elevation with upward convexity and ing inferior wall myocardial infarction:A concomitant inverted T wave in lead II, III, and aVF, reciprocal ST gradually increased intravenous nitroglycerin drip was segment depression in anterior leads. Those modifica- also begun because a coronary vasospasm could not tions were refractory to sublingual dinitrate isosorbide defimitely be excluded. Precordial pain was only administration (Figure 1). The patient was therefore relieved 6 hours after the beginning of thrombolysis put on a peripheral streptokinase thrombolysis and 8 hours after the beginning of the pain. At this moment a nonsustained ventricular tachycardia, Correspondence: P. Depelchin, M.D., rue Vilain XIIII, # 32 probably due to reperfusion justified institution of an 1050 Bruxelles, Belgium. antiarrhythmic treatment; anticoagulation therapy Accepted: 4 August 1986 with heparin was also instituted Serial cardiac enzyme d The Fellowship of Postgraduate Medicine 1987 Postgrad Med J: first published as 10.1136/pgmj.63.735.41 on 1 January 1987. Downloaded from 42 CLINICAL REPORTS levels showed only mild elevation (twice the normal balance and regulation of coronary artery tone by range). Coronary arteriography and contrast ven- various vasoactive substances are clearly demon- triculography carried out 2 days later revealed a strated.3 Whatever the real mechanism(s) of spasms, coronary artery tree free from atherosclerotic lesions the final common pathway involves an increase in and an almost normally contracting left ventricle. intracellular calcium. Calcium antagonists block the Right coronary artery spasm was suspected, but an Ca2+ -channels and suppress the entry ofCa2" into the ergonovine test was not carried out because of its cell. They diminish the membrane permeability of hazards. The patient was put on nifedipine 10mg three coronary artery smooth-muscle cells involved in the times/day. The one week hospital course was unevent- spasm and have progressively gained wide-spread ful: no relapsing precordial discomfort nor abnor- acceptance in the treatment ofcoronary heart disease. mality on a 3-day ECG monitoring survey in the CCU Spasm may be sufficiently severe to resist sublingual or were described. A 24-hour dynamic electrocardiogram even intravenous nitroglycerin administration, and be recording (Holter) also failed to show signs of a only reversed by intracoronary nitroglycerin adminis- persistent vasospasm. The patient was therefore all- tration.' Experimental studies and some clinical owed to return home with the same calcium blocking observations suggest that the coronary vasospasm can agent regimen (nifedipine 10mg three times/day). induce endothelial cell damage and thrombus forma- One month later following discharge the patient was tion which together lead to myocardial infarction.4 readmitted because ofa sudden constrictive precordial The right coronary spasm of our patient was severe pain arising at rest and which, this time, led to an enough to require 6 hours peripheral thrombolysis and inferior wall infarction. No warning anginal pain was intravenous nitroglycerin therapy. Only a limited described and the patient regularly took her tablets. A myocardial infarction could be demonstrated by elec- subsequent ergonovine test taken under cineangiogra- trocardiogram (diminished R wave without a true Q phic control demonstrated right coronary artery necrosis wave), plasma enzyme screening and contrast spasm and an inferior akinesia (Figure 2). At the time ventriculography. The patient subsequently developed of discharge the patient was free of congestive heart myocardial infarction in the assumed spastic coronary disease and residual angina pectoris. area in spite of a prophylactic dose of nifedipine. by copyright. Because the coronary arteries were free from ath- erosclerotic lesions and right coronary spasm was Discussion demonstrated on a post-infarction angiogram, we suggest that a vasospastic process produced the infarc- In recent years many investigations have indicated tion. Although the case report represents an anecdotal that coronary spasms play a role in variant, resting incident and modest doses ofnifedipine were used, we and exertional angina, and acute myocardial infarc- believe it calls for some more general considerations. tion. The pathophysiology of coronary artery spasm Despite continuous intravenous nitroglycerin in- which is a transient constriction of an epicardial fusion at a rate of 300 fg/min accompanying a strep- coronary artery has not been clearly elucidated, tokinase infusion, reperfusion was only achieved 6 http://pmj.bmj.com/ although circadian variations of the tone of the hours later. Late onset reperfusion after intravenous coronary arteries, autonomous nervous system im- thrombolysis is quite uncommon in our experience on September 25, 2021 by guest. Protected Figure 2 Coronary arteriography carried out after occurrence ofthe myocardial infarct shows patent left and right coronary arteries. After ergonovine test the right coronary artery (A) discloses diffuse vasospasm (B). Postgrad Med J: first published as 10.1136/pgmj.63.735.41 on 1 January 1987. Downloaded from CLINICAL REPORTS 43 and in the literature.5 This author showed that the satisfactory technical quality ofangiograms and use of average time from the beginning of the infusion of multi-incidental views leaves no doubt about the streptokinase to reperfusion is about 54 minutes. This accuracy of the method for assessing right coronary observation adds afortiori support to the statement of artery patency.'2 Buxton et al.2 that vasospasms may be sometimes What is an optimal drug schedule? What is good for sufficiently potent to resist intravenous infusion and most is not necessarily the best for everyone and in the require intracoronary nitroglycerin administration to setting of vasospasm it must be remembered that even disappear. the most effective vasodilators will do no good if they Although the 3-day ECG monitoring survey in the are not present in effective concentrations at times CCU was uneventful and the patient was asymp- when the patient is susceptible to attacks. Muller & tomatic on nifedipine 10mg 3 times/day, the Gunther"3 have demonstrated the ineffectiveness of occurrence of a subsequent myocardial infarction was low doses of Ca2+-blockers approximately 4 hours not avoided. Therefore, suppression ofattacks ofpain after administration. A 3- or 4-times-a-day supportive obviously could not be the objective end-point ofdrug schedule ordinarily used with calcium channel block- therapy. Vasospastic angina includes symptomatic ers may not be appropriate for every patient. The attacks as well as attacks without symptoms, which in omission of this pharmacological feature may explain some patients may be more numerous than those with nifedipine therapy failure in our patient since vasocon- symptoms.4 Many patients with vasospastic angina stricting adverse environmental influences favouring will have spontaneous remission, and circadian varia- spasm (smoking, aspirin and other cyclo-oxygenase tion of the tone of coronary arteries has been demon- inhibitors, sudden withdrawal from organic nitrates, strated; both facts make evaluation of drug therapy ergot alkaloids, beta-adrenergic antagonists, difficult.
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