690 BRIEF REPORTS

The fulminant course of this patient’s heart disease emphasizes the importance of considering coronary arteritis in patients with acute myocardial infarction in the setting of rheumatoid disease. Rheumatoid-as- sociated coronary arteritis causing clinically evident myocardial infarction is rare; only 3 case reports with complete pathologic description are available for com- parison of features which may define patients at risk of this complication of rheumatoid disease.2-4 The pres- ence of rheumatoid nodules, overt vasculitis [skin le- sions, neuropathy or scleritis), high titers of rheuma- toid factor and progressive rheumatoid involvement at the time of myocardial infarction may be characteristic of patients with rheumatoid-associated coronary arter- itis Although the number of reported cases is limited, the distinction between coronary atherosclerosis and coronary vasculitis may have potential therapeutic im- plications, because a variety of other vasculitic syn- dromes are responsive to specific immunosuppressive and cytotoxic therapies5

All 4 reported patients with myocardial infarction due to rheumatoid-associated coronary arteritis were receiving prednisone at the time of infarction. Al-

though the administration of corticosteroids may actu- ally precipitate diffuse necrotizing arteritis in certain patients with rheumatoid arthritis, it is more likely that vasculitis is a feature of more severe rheumatoid ar- thritis which, in turn, is more likely to be treated with corticosteroids.6 Thus, current recommendations for initial therapy ,of rheumatoid-associated coronary ar- teritis include corticosteroids in addition to conven- tional antianginal medications. The role of cytotoxic therapy is uncertain; it should probably be reserved for patients whose vasculitis is unresponsive to cor- ticosteroids.5

References 1. Sokoloff L. Cardiac involvement in rheumatoid arthritis and allied disor- ders: current concepts. Mod Concepts Cardiovasc Dis 1964;33:847-850. 2. Swezey RL. Myocardial infarction due to rheumatoid arthritis. JAMA 1967;199%55-857. 3. Karten I. Arteritis, myocardial infarction, and rheumatoid arthritis. JAMA 1969;210:1717-1720. 4. Voyles WF, Searles RP, Bankhurst AD. Myocardial infarction caused by rheumatoid vasculitis. Arthritis Rheum 1980;23:860-863, 5. Parrillo JE, Fauci AS. Coronary vasculitis. In: Ansell BM, Simkin PA, eds. The heart and rheumatic disease. London: Batterworth and Co., 1984:213-233. 6. Schmid FR, Cooper NS, Ziff M, McEwen C. Arteritis in rheumatoid arthri- tis. Am J Med 1961;30:56-83.

Acute Myocardial Infarction in Buerger’s Disease

HIROSHI OHNO, MD YASUO MATSUDA, MD

KIYOSHI TAKASHIBA, MD YOSHIO HAMADA, MD

HIRONORI EBIHARA, MD EIJI HYAKUNA, MD

W hether Buerger’s disease involves parts of the vas- cular system other than the peripheral vessels of the extremeties has been questioned. Acute myocardial infarction (AMI) is more frequent in patients with Buerger’s disease than in those of similar age and sex without this condition? The relation of AM1 to Buerger’s disease, however, is not clearly defined.

Y.A., a 32-year-old man, had had the third toe of the right foot amputated at age 26 years and the right leg at age 31 years. The diagnosis was Buerger’s dis- ease. The patient smoked 41 to 60 cigarettes daily for 12 years. No cardiac disease was pointed out previous- ly. The serum total cholesterol level was 174 mg/dl. None of the family members had heart disease before age 50 years. The patient had no history or chemical

From the Department of Cardiology, Saiseikai Shimonoseki General Hospital 3 Kifune, Shimonoseki, Yamaguchi 751, and Yamaguchi University School of Medicine, Ube, Yamaguchi 755, Japan. Manuscript received May 20, 1985; revised manu- script received July 18,1985, accepted July Z&1985.

A B C

II

VS

FIGURE 1. Electrocardiograms before admission (A) and before (i3) and after (C) cardiac catheterization in the course of acute myocar- dial infarction.

March 1, 1986 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 57 69‘s

evidence of diabetes meilitus. The patient was re- ferred for severe chest pain at rest, which started 3 hours before admission. He had no history of chest pain. The electrocardiogram (ECG) recorded just be- fore admission showed ST elevation in leads II, III and aVF and the precordial leads (Fig. 3). On admis- sion, the ECG showed further ST elevation in the pre- cordial leads. Coronary angiograms revealed 70% di- ameter narrowing in the distal right coronary artery and the proximal left anterior descending coronary artery (Fig. 2). The angiographic appearance of these lesions was suggestive of thrombus. Urokinase was in- jected into the right (240,000 units) and the left (240,000 units) coronary arteries. The stenosis in the Ieft anteri- or descending coronary artery regressed to 30%. The stenosis in the right coronary artery remained un- changed. A left ventriculogram revealed akinesia in the anteroapical wall and hypokinesia in the inferior wall. An ECG showed abnormal Q waves in II, III and aVF and poor R-wave progression in the precordial leads (Fig. I). The peak serum creatine kinase level rose to 3,060 units/liter, with an MB fraction of 8%. No more chest pain was noted and the patient recovered from the AMI uneventfully. Coronary angiography was repeated 4 weeks after onset of the AMI. The thrombi of the right and left coronary arteries were resolved and the coronary artery appeared normal. Ergonovine test results were negative. The left ven- triculogram remained unchanged from that recorded during the acute phase. The patient was sent home with vasodilator and anticoagulant therapy and was advised to stop smoking.

It has been contended that the peripheral vascular disease termed Buerger’s disease is a result of either atherosclerosis, systemic arterial embolism, intravas- cular thrombosis, or a combination of these. Histo- pathologic section of a coronary artery from a patient with Buerger’s disease have been reported to show changes compatible with Buerger’s disease.2 Other reports documented that most of the patients with Buerger’s disease had the changes of coronary athero- sclerosis.3 It has been documented that smoking is the well recognized precipitating factor for Buerger’s dis- ease,4 and is one of the most important risk factors in younger patients with myocardial infarction.5 Our case demonstrated the complete resolution of multiple

FIGURE 2. Left coronary artery in the left anterior hemiaxial projec- tion (A and C) and right coronary artery in the left anterior oblique projection (6 and 0) in the acute and chronic phases of myocardial infarction. Filling defects in the right and left anterior descending coronary arteries (arrows) in the acute phase (B and A) are com- pletely thrombolyzed in the chronic phase (D and C).

thromboses in the right and left coronary arteries in a patient with Buerger’s disease.

References 1. Goodman RM, Elian B, Mazes M, Deutsch B. Buerger’s disease in Israel. Am J Med 1965;39:601-615. 2. Hausner E, Allen EV. Vascular clinics VIII. Generalized arterial involve- ment in thromboangiitis obliterans of a pulmonary artery. Proc Staff Meet Mayo Clin 1940;15:7-13. 3. McPherson JR, Juergens JL, Gifford RW. Thromboangiitis obliterans and arteriosclerosis obliterans. Clinical and prognostic differences. Ann Intern Med 1963;59:288-296. 4. Eisen ME. Coexistence of thromboangiitis obliterans and arteriosclerosis: relationship to smoking. J Am Geriatr Society 1966;14:846-856. 5. Glover MU, Kuber MT, Warren SE, Vieweg WVR. Myocardial infarction before age 36: risk factor and orteriographic analysis. Am J Cardiol 1982; 49:1600-1603.