4. Burch GE, Giles TD. Cardiac causalgia. Arch Intern Med 1970;125:809-14. 5. Hutchins GM. Time course of infarct and healing. In: Wagner GS, Myocardial infarct size: measurement and intervention. Dordrecht, The Netherlands: Martinus-Nijhoff Publishers, 19823-20. 6. Karch SB, Billingham ME. Myocardial contraction bands revisited. Hum Path01 1986;17:9-13. 7. Hutchins GM. The pathology of heart transplantation. In: Baumeartner WA. Reitz BA. Achuff SC. eds. Heart and heart-lung transplantation. Philadelphia: WB Saunders Company, 1990. 8. Hutchins GM, Bulkley BH. Correlation of myocardial contraction band necrosis and vascular patency: a study of coronary artery bypass graft anastomoses at branch points. Lab Invest 1977;36:642-8. 9. Bulkley BH, Klacsmann PG, Hutchins GM. Angina pectoris, myocardial infarction and sudden cardiac death with normal coronary arteries: a clinicopathologic study of nine patients with progressive systemic sclerosis. AM HEART J 197&95:563-g. 10. Bauer TW, Moore GW, Hutchins GM. Morphologic evidence for coronary artery spasm in eclampsia. Circulation 1982; 65:255-59. 11. Ambrosio G, Becker LC, Hutchins GM, Weisman HF, Weisfeidt ML. Reduction in experimental infarct size by recombinant human superoxide dismutase: insights into the pathophysiology of reperfusion injury. Circulation 1986;74:1424-33. 12. Kalsner S. Cholinergic constriction in the general circulation and its role in coronary artery spasm. Circ Res 1989;65:237-57.
Delayed and spontaneous coronary artery rupture following nonpenetrating chest trauma A. Rubin, MD, and Bart G. Denys, MD Pittsburgh, Pa. Daniel
Cardiac complications of nonpenetrating chest trauma range from supraventricular arrhythmias to valvular and myocardial rupture. Coronary artery dissection following blunt chest trauma is rare. We detail a caseof delayed and spontaneouscoronary rupture following a physical assault. The victim, a 58-year-old man, presentedwith extensive lacerationsand fractures of the skull and face. Physical examination of the chest and lungs revealed no evidence of chest trauma. The electrocardiogram and routine laboratory findings were normal with the exception of a mild anemia,felt to be a consequenceof malnutrition. The chest x-ray examination was notable for upper lobe fibrosis and volume losscausedby chronic granulomatousdisease.The cardiac silhouette wasnormal. Lacerations of the skull and From the Division of Cardiology, University of Pittsburgh
School of Medicine and Presbyterian University Hospital. Reprint requests: Bart G. Denys, MD, Division of Cardiology, F-345 Presbyterian University Hospital. DeSoto at O’Hara Streets, Pittsburgh, PA 15213.
Brief Communications 1635 face were sutured and a tracheostomy was subsequently performed before repair of the facial fractures. The patient wasdischargedon day 10 only to return 2 days later complaining of suddenand severesubsternalchest pain, shortness of breath, and diaphoresis. Examination revealed bradycardia, hypotension, and presyncope; the patient respondedto fluids and atropine with a gradual decreasein his chest discomfort. No additional trauma preceding this presyncopal episodewas described. Serial electrocardiogramsover the following 48 hours demonstratedthe development of broad and diffuse precordial T wave inversions (Fig. 1, A and B) prompting urgent cardiac catheterization. There wasno recurrence of chest,pain and no neurologic changeswere present. Electrolytes and cardiac enzymes were unremarkable. The patient denied any previous cardiac history. Tobacco use was the only identifiable coronary risk factor. Medications included ranitidine, aspirin, and subcutaneousheparin. Physical examination revealed a thin male in no distress,with a blood pressureof 100/60 mm Hg and a regular heart rate of 60 beats/min. Head, ear, eyes,nose,and throat examination revealed a recent anterior skull suture line with compromiseof the extraocular musclesof the right eye from partial entrapment as a result of orbital fractures. The lungs were clear, with cardiac examination notable for a soft S4gallop. The abdomen,extremities, and pulses were unremarkable. Laboratory studies were remarkable for a hemoglobin of 9.3 gm/dl. Catheterization demonstratednormal right- and left-sided heart pressuresand hemodynamics. Left ventricular angiography revealed mild anterolateral hypokinesis and an ejection fraction of 61%. During left coronary arteriography, accumulation of contrast in at least three focal areas along the proximal portion of the left anterior descending artery was noted. These extravasations occurred at the terminal portions of very small septal perforator branches (Fig. 2, A). With time and with continued injection, distribution of dye was noted. This collection was visualized several minutes later during right coronary arteriography (Fig. 2, B). No extravasation wasnoted near the left main or adjacent left anterior descendingand circumflex arteries.There wasno significant atherosclerotic disease.Fluoroscopyat 24hours failed to showany remaining contrast. The patient’s recovery was uneventful. Spontaneous dissectionsof coronary arteries are most commonly a direct extensionof proximal aortic dissections. Isolated coronary dissectionis rare but is increasingly appreciated in diverse clinical settings including postpartum,l following coronary angiography,2and asa complication of vascular pathologiessuch ascystic medial necrosis3 andthe Marfan syndrome.4Nonpenetrating cardiactrauma is, asin the present case,often maskedby injuries to other areas and organs. The manifestations of cardiac trauma may alsoappeardays to weeksfollowing the inciting event. Parmley et a1.5demonstrated myocardial, pericardial, endocardial, coronary artery, and conduction systeminvolvement with blunt chest trauma. Contusions, perforations, ventricular aneurysms and lacerations, and tamponade have beendescribedfollowing myocardial trauma.5,6 Coronary injury hasincluded fistula formation7 thrombosis,s’ intimal tears,l” and lacerations.5 Reports of coronary
December 1992 Heart Journal
Fig. 1, A and 6. Standard E-lead electrocardiogramsupon presentation with complaints of chest pain (A) and 48 hours later (8). Marked T wave inversions are present precordially.
aneurysm formation are rare.“, l2 Delayed spontaneous rupture of a coronary artery has not been reported. The history and findings at catheterization in the present casesuggestthat this patient developedaneurysmsof small terminal coronary vesselsafter the initial assault.Delayed and spontaneousrupture likely produced the described chest discomfort with bradyarrhythmia and hypotension. The presence of chest pain and electrocardiographic changesbefore catheterization and the absenceof left main involvement argue against a procedural artifact. Given the above findings and the fact that congenital coronary fistulasmorecommonly arisefrom the right coronary artery and are rarely associatedwith chest pain, a congenital fistula manifesting itself similarly ishighly unlikely. The observed anterolateral hypokinesesis likely a direct result of myocardial contusion rather than aneurysmal rupture of the small coronary branches.This report is the first to document spontaneousand delayed rupture of a coronary artery
following blunt chest trauma. The high index of suspicion required in evaluating victims of trauma, even in the absenceof visible chest involvement, is underscored. REFERENCES
1. Jewett JF. Two dissecting coronary artery aneurysms postpartum. N Engl J Med 19’78;298:1255-6. 2. Guss SB, Zir LM, Garrison HB, Daggett WM, Block PC, Dinsmore RE. Coronary occlusion during angiography. Circulation 1975;52:1063-8. 3. Kaufman G, Engelbrecht WJ. Hemorrhagic intramedial dissection of coronary artery with cystic medial necrosis. Am J Cardiol 1969;24:409-13. McKeown F. Dissecting aneurysm of the coronary artery in arachnodactyly. Br Heart J 1960;22:434-6. Parmley LF, Manion WC, Mattingly TW. Nonpenetrating traumatic injury of the heart. Circulation 1958;18:371-96. Rothstein RJ. Myocardial contusion. JAMA 1983;250:218991. DeSa’Neto A, Padnick MB, Desser KB, Steinhoff NG. Right
Fig. 2. A, Initial coronary injection demonstrating three focal areasof extravasation (arrows) from the terminal portions of small septal perforators (30-degreeright anterior oblique projection). B, Extravasat,ionsvisualized severalminutes later (arrows) during right coronary angiography (30-degreeright anterior oblique projection).
8. 9. 10. 11. 12.
sinus of Valsalve-right atrial fistula secondary to nonpenetrating chest. trauma. Circulation 1979;60:205-9. Wainwright RJ, Edwards AC, Maisey MN, Sowton E. Early occlusion and late stricture of normal coronary arteries following blunt chest trauma. Chest 1980;78:796-8. Vlay SC, Blumenthal DS, Shoback D, Fehir K, Bulkley BH. Delayed acute myocardial infarction after blunt chest trauma in ayoungwoman. AM HEART3 1980;100:907-16. Pringle SD, Davidson KG. Myocardial infarction caused by coronary artery damage from blunt chest injury. Br Heart J 1987;57:375-6. Baker P, Keyhani-Rofagha S, Graham R, Sharma H. Dissecting hematoma (aneurysm) of coronary arteries. Am J Med 1986;80:317-9. Bjorn-Hansen LS, Thomassen AR, Nielsen TT. Aneurysm of the left anterior descending coronary artery after chest trauma. Eur Heart J 1989:10:177-9.
Asymptomatic pseudoaneurysm of the left ventricle and coronary artery fistula after closed-chest ablation of an accessory pathway Philippe Mabo, MD, Herve Le Breton, MD, Christian De Place, MD, and Claude Daubert, MD Rennes, France
The efficacy of a high-energy direct current (DC) shockhas beendemonstrated for ablating the atrioventricular accesFrom
Reprint requests: Philippe Dieu/CHRU, 35033 Rennes 414141406
University MD, Service France.
sory pathway (AP) in the Wolff-Parkinson-White syndrome.lm5 Despite the reliability and safety of this method, sideeffects suchascoronary sinusrupture, coronary artery spasm,pericardial effusion, or atrioventricular block’, 2,5,6 have been previously reported. One caseof suddendeath after hospital dischargewasalsoreported.4 The site of ablation on the atrioventricular anulus is often very closeto the coronary vessels,especiallyto the right and circumflex coronary arteries, and to the ostium of the coronary sinus. Thus there is a potential risk of coronary vessel lesions during the procedure. We report a caseof asymptomatic pseudoaneurysmof the posterior wall of the left ventricle (LV) and coronary fistula between a lateral branch of the circumflex artery and the LV, revealed by systematically performed LV cineangiogramand coronary arteriography 2 months after successfulDC shock ablation of a left free wall AP. The patient wasa 49-year-old man with permanent preexcitation on surface electrocardiograms(ECGs). He suffered from episodesof recurrent atrioventricular reentrant tachycardia and of poorly tolerated paroxysmal atria1 fibrillation requiring cardioversion. Treatments with propafenone, flecainide, and amiodarone were ineffective to prevent atria1 fibrillation attacks. According to Gallagher’s classification, the location of the AP wasthe left free wall. Electrophysiologic study documented a short anterograde effective refractory period of 230 msecat rest and of 180 msecduring exercise.The minimal R-R interval between two preexcited QRS complexes in atria1 fibrillation was very short, 170 msec during exercise. The earliest retrograde atria1 activation during induced orthodromic reentrant tachycardia wasrecordedin the distal coronary sinus. After the patient gave his consent, DC shock ablation was attempted. A retrograde transaortic approach, as previously described by Haissaguerre and Warin was per-