Recurrent myocardial infarction and sudden death after sport

January

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angioplasty situation,6jI and all patients progressedinto full-blown infarction. To our knowledge,our patient is the first with typical variant angina in whom thrombosis, most probably secondary to spasm,wasdocumented. The reversal of the processpossibly prevented the evolution of myocardial infarction. This shouldlend further support to the hypothesis that spasm, as such, may serve as a precursor to thrombosis and/or consequent infarction. Studies in the basic 1aboratoryShave previously demonstrated that transient localized constriction of a coronary or carotid artery could result in endothelial cellular damage and formation of microthrombi. However, there has been no clinical demonstration of reversible coronary thrombus formation secondary to spasmin humans.This casestudy appearsto provide the best such documentation to date. While many instances of spontaneous or provoked attacks of Prinzmetal’s variant angina have been documented by coronary angiography without necessarily showingevidence of thrombus formation, one would wonder what may be different in this case.The most important parameter to consider is time. The attack in this patient might have been more prolonged than the usual transient attacks, thus creating an environment favorable for formation of the thrombus. If there was no intervention with vasodilator and anticoagulant therapy, it is very likely that the patient could have progressed into full clinical infarction. Many casesof well-documented myocardial infarctions that are studied weeksor months after the attack and are found to have angiographically normal or near normal coronary arteries may represent similar instances.The opportunity to document the spasmand/or the thrombus in suchcasesmay have been missedbecause the patients were not studied in the acute phase.This case therefore presents an exciting observation that should serve as a stimulus to look for more documentation of a possibly important relationship between vasospasticphenomena and the thrombotic process. REFERENCES

1. Chahine RA. Coronary artery spasm.Mount Kisco, NY: Futura Publishing Co, 1983. 2. Hellstrom HT. Coronary artery vasospasm: the likely immediate cause of acute myocardial infarction. Br Heart J 1979; 41:426-32. 3. Ganz W. Coronary spasm in myocardial infarction: fact or fiction? Circulation 1981;63:487-8. 4. Zelinger AB, Abramowitz BM, Schick EC, Ryan TJ. Variant angina culminating in coronary thrombosis and myocardial infarction. Cheat 1982:82:188-90. 5. Vincent GM, Anderson -JL, Marshall HW. Coronary spasm producing coronary thrombosis and myocardial infarction. N Engl J Med 1983;309:220-3. 6. Zimmerman FH, Gust&on GM, Kemp HG. Recurrent myocardial infarction associated with cocaine abuse in a young man with normal coronary arteries: evidence for coronary artery spasm culminating in thrombosis. J Am Co11 Cardiol 1987;9:964-8. I. Klevan T, Deckelbaum LI, Wohlgelernter DW, Cleman MW. Coronary vaeospaem culminating in thrombosis and infarction following “successful” coronary angioplasty. AM HEART J 1987;113:1220-2.

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8. Gertz SD, Uretsky G, Wajnberg RS, Navot N, Gotsman MS. Endothelial cell damage and thrombus formation after partial arterial construction: relevance to the role of coronary artery spasm in the pathogenesis of myocardial infarction. Circulation 1981;63:476-86.

Recurrent myocardial infarction sudden death after sport

and

Renzo Ciampricotti, MD, and Mamdouh El Gamal, MD, FRCP (Edin). Eindhoven,

The Netherlands

The occurrence of acute myocardial infarction (AMI) and suddendeath (SD) after sport in previously asymptomatic individuals is well known but the pathogenesisof this phenomenon is still hypothetical. We report the unique caseof a patient who experienced two episodesof AM1 and one of SD after sporting activities. The acute coronary angiographic findings in this case can be helpful in understanding the mechanism(s)of AM1 and SD after sport. A 34-year-old man was seenat the emergencyroom on July 15, 1981, becauseof breathlessnessand chest pain that occurred 30 minutes after a football match. Being a member of a veterans club, he played football three times a week and exercised regularly on a racing bicycle. He smoked 30 cigarettes a day, but there were no other risk factors. On admission, physical examination, routine blood investigation, and chest x-ray films were normal. The electrocardiogram (ECG) showed2 mm ST-T elevation in leadsV, to V,. He developed a non-Q wave anterior myocardial infarction with a peak serum creatine kinase (CK) of 700 U/L (normal up to 120 U/L). Coronary angiography (CAG) 20 days later (Fig. 1, A) showed no evident obstructive diseasein the left and right coronary arteries. After discharge, a maximal exercise stress test was normal. The patient resumedhis sporting activities and stopped smoking. On August 7, 1984, at 2 PM, about 30 minutes after playing football, he suddenly fainted. Onlookers immediately started cardiopulmonary resuscitation. Ambulance personnel at 2.10 PM monitored ventricular fibrillation, and he waspromptly defibrillated. On admission,physical examination revealed a comatose slightly cyanotic man with inadequate spontaneousrespiration. The pulse was regular at SO/min, and the blood pressurewas 120/80mm Hg. Mechanical ventilation was initiated. The ECG showed2 mm ST-T elevation in leadsII, III, aVF and in V, to V,. The chest x-ray film wasnormal. In view of AMI,

From the Department Reprint Catharina

requests:

of Cardiology,

hkndouh

El Gamal,

Catharina

Hospital.

MD,

Department

of Cardiology,

Hospital, Michelangelolaan 2,6623 EJ Eindhoven, The Nether-

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Fig. 1. A, Left coronary angiogram20 days after a non-Q wave anterior myocardial infarction without evident abnormalities. 0, Three years later, 60 minutes after resuscitation from sudden death, showing proximal occlusion of the circumflex artery. C, Fifteen minutes after intracoronary infusion of streptokinase, reperfusion has been achieved, there is a subtotal concentric stenosis.D, After angioplasty of the segment,a steerable guide wire is still seenin the circumflex artery.

CAG was performed at 3.10 PM. This disclosedproximal occlusion of the circumflex (Cx) artery (Fig. 1, B). No changeoccurred after lintracoronary administration of 200 H of nitroglycerin. Streptokinase was infused by the intracoronary route at a rate of 5000U/min. Reperfusion resulted after 15 minutes (Fig. 1, C). Transluminal balloon angioplasty was then sluccessfullyperformed (Fig. 1, D). The patient developed an inferoposterolateral infarction (peak CK 1366U/L). The ECG showedsmall Q waves in leads II, III, and aVF. There was complete resolution of his neurologic impairment 2 days after admission.There were no cardiac complications. He recovered and was dischargedon oral anticoagulant therapy with a coumarin derivative and pindolol(10 mg a day). Repeat CAG (Fig. 2, A) 3 months later showedno evident obstructive lesion at the site of the previous occlusion.During follow-up, repeat bicycle exercise tests were normal.

On July 22, 1986, he was readmitted because,of chest pain that started about 20 minutes after a bicycle race. The ECG on admissionshowedacute anterior transmural ischemia. CAG was performed 70 minutes after onset of pain and disclosed a subtotal obstruction in the left anterior descendingartery (LAD) Wig. 2, B). There wasno change after the administration of mtracoronary nitroglycerin. Urokinase wasthen infused via the intracoronary route at a rate of 10,000U/min. After 20 minutes there wes a decreasein flow acrossthe obstruction and poor distal coronary filling. Balloon angioplasty wasthen immediately performed (Fig. 2, C). After the procedure, the ECG normalized. There was a maxims1CK rise of 180 U/L. He wasmobilized and dischargedon therapy with aspirin, 80 mg a day. In October 1987, control CAG showed no evident obstructive diseasein the Cx and LAD (Fig. 2, D). The left ventriculogram showedlocalized apical hypokine-

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Fig. 2. A, Left coronary angiogram3 months after angioplasty, showingslight lumen irregularities at the

site of previous occlusion. 6, Two years later, 70 minutes after onset of pain, showing a subtotal obstruction half way down the courseof the left anterior descendingartery (arrow). C, After angioplasty of the obstructed segment. D, Four months after angioplasty, showing no evident obstructive coronary disease. sia. The ejection fraction was 70%. During 22 months of follow-up, repeat exercise stresstests were normal. Although numerous studies have reported the occurrence of AMI and SD precipitated by sport, acute coronary angiographic findings are lacking under these circumstances.The pathophysiology of AMI and SD related to sport is still unsettled.’ Necropsy studies have documented that coronary diseaseis the most usual finding in SD associatedwith sport.’ In one case,2coronary thrombosis was suggestedas the cause of AMI after an exercise stresstest. Coronary spasmhas alsobeen suggestedto be the trigger responsible for SD after sport. However, although coronary spasmhasbeen documented3during or shortly after exercise, a delayed onset has never been described.In recent necrospy studies; it has beendemonstrated that fissuring or rupture of atheromathous plaques,which can lead to intimal hemorrhageand coro-

nary thrombosis and/or spasm,can representthe anatomic substrate of unstable angina, AMI, and SD. In a previous angiographic study6 we proposed that plaque rupture could be the etiologic factor of AMI and SD after sport. In the present case,coronary angiography was not performed acutely on admission at the time of the patient’s first AMI. The episodeof SD was shown to be related to coronary occlusionof the Cx. Reperfusion after streptokinase indicated the presenceof coronary thrombosis.The secondAM1 wasdue to subtotal obstruction of the LAD. During infusion of urokinase, coronary flow worsened, indicating progression of the obstruction. Hypothetically this may be due to an increasein thrombus formation despite a thrombolytic agent. On the other hand, it is unlikely that primary thrombosiscould occur in a patient on chronic anticoagulant therapy. A more likely explanation could be provided by a ruptured plaque with

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intimal hemorrhage leading to subtotal coronary obstruction.‘s6 The presence of coronary spasm could not be proved in this patient. This report presents several unique features. First, the recurrence of AM1 and the episode of SD after sport in the same patient has never been previously reported. This case demonstrates a relation between sport and coronary events that cannot further be referred to as “merely coincidental.” Additionally, although reperfusion arrhythmias have been implicated in the occurrence of SD after sport,l this construction seems improbable when, as in our case, SD is delayed. Finally, coronary thrombosis alone cannot satisfactorily explain the angiographic findings in our patient. According to recent observations,’ either coronary thromb’osis and/or spasm with or without occlusion can be the possible manifestations of the same anatomic pathologic substrate represented by plaque rupture. Although definitive proof can only be obtained at necropsy,4* E we suggest that exercise-precipitated plaque rupture with intimal hemorrhage with or without coronary thrombosis and/or subtotal coronary occlusion can explain both the angiographic findings of the recurrent AM1 and SD in our patient. REFERENCES

1.

2. 3. 4. 5.

6.

Northcote RJ, Ballantine D. Cardiovascular implications of strenuous exerc:ise. Int J Cardiol 1985;8:3. Barold SS. Hannss RJ. Falkoff MD. Senrmnta A. Exercise-induced myocardial infarction due to coronary thrombosis. AM HEART J 19,55;109:590. Maseri A, Chierchia S. Coronary artery spasm: demonstration, definition, diagnosis and consequences. Prog Cardiovasc Dis 1982;25:169. Davies MJ, Thomas AC. Plaque fissuring; the cause of acute myocardial infarction, sudden ischemic death and crescendo angina. Br Heart J 1985;53:363. Ciamnricotti R. El Gamal M. Salah S. Gelder B van. Bonnier JJ. Miocardial infarction ani sudden’death after spbrt: acute coronary angiograpbic findings. Circulation 1987;76(Suppl IV):361. Mattfeldt T, Sclhwarz F, Schuler G, Hofmann M, Kubler W. Necropsy evaluation in seven patients with evolving acute myocardial infarction treated with thrombolytic therapy. Am J Cardiol 1984;54:530.

Postpartum myocardial infarction in a patient with intermittent ventricular preexcitation Mark D. Wittry, MD; Thomas J. Zimmerman, MD, Denise L. Janosik, MD,c and George A. Williams, MD.c St. Louis, MO., and Peoria, Ill, From ‘St. Louis University Hospital, St. Louis; W. Francis Medical Canter, Peoria; and ‘Div:ision of Cardiology, Veterans Administration, John Co&ran Division, St. Louis.

Reprint requests: Denise L. Jan&k, MD, Division of Cardiology, Veterans Administration, John Cc&ran Division, 915 N. Grand, St. Louis, MO 63106.

Brief Communications 191 Postpartum myocardial infarction is an unusual but welldocumentedphenomenon.I-3This event may be maskedor mimicked by ventricular preexcitation and the diagnosis may be misinterpreted or missed entirely. This report describesan occurrence of postpartum myocardial infarction in which the clinical diagnosiswas delayed due to intermittent ventricular preexcitation that occurred during the acute infarction. A 34-year-old white multigravida developed substernal chest pressure 12 hours after a spontaneous vaginal delivery. Her past medical history was unremarkable except for a 15 pack-year history of smoking. Clinical evaluation revealed a hypotensive patient with a rapid, irregular pulse and no other remarkable physican findings. Cardiac telemetry showed atrial fibrillation with rates up to 150 beata/min, narrow QRS complexes, and frequent ventricular ectopic beats.Coagulation and hematologic studies were normal. A chest radiograph showed pulmonary vascular congestion. Arterial blood gaseson oxygen at 10 L/min showed a compensated metabolic acidosis with the following values: PO, = 133 mm Hg; Pcol = 30 mm Hg; HCO, = 17 mEq/L, pH = 7.35. The patient clinically stabilized and an electrocardiogram (ECG) was obtained (Fig. 1). The ECG was initially interpreted as showing sinus tachycardia, complete right bundle branch block, and possible diffuse subepicardial injury; the house staff felt (erroneously) that the ECG findings were consistent with acute car pulmononale. However, pulmonary angiography was normal. A repeat ECG showed sinus rhythm with resolution of the ECG abnormalities. The patient’s chest pain recurred 24 hours later and a repeat ECG (Fig. 2) demonstrated an acute anterolateral myocardiai infarction. The patient underwent emergency cardiac catheterization becausesof persistent chest pain unresponsive to intravenous nitroglycerin or hydromorphone hydrochloride. The left ventriculogram revealed moderate hypokinesis of the anterior wall of the left ventricle and coronary arteriography demonstrated a long stenosiswith near occlusionof the left anterior descending artery (Fig. 3). Emergency coronary artery bypasssurgery was performed with placement of a saphenousvein graft to the left anterior descendingartery becauseof continued chest pain. Examination of the left anterior descending artery at surgery revealed a hard plaque consistent with atherosclerosisat the site of the angiographic abnormality. Creatine phosphokinasepeakedat 3191IU and 5 % MB fraction (normal range 0 to 125 IU, <4% MB). An ECG performed postoperatively (Fig. 4) revealed a slightly faster sinus rate with ventricular preexcitation masking the recent anterior myocardial infarction.4 Detailed analysisof the initial ECG (Fig. 1) alsodemonstrated ventricular preexcitation. The initial positive deflection of the delta wave in the right precordial leads minimized the acute myocardial injury pattern and appearssimilar to a right bundle branch block. The diagnosisof ventricular preexcitation was further obscured by the presenceof a