Coronary Spasm as a Cause of Coronary Thrombosis and Myocardial Infarction

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1 Case Reports Coronary Spasm as a Cause of Coronary Thrombosis and Myocardial Infarction Masashi HORIMOTO, M.D., Takashi TAKENAKA, M.D., Keiichi IGARASHI, M.D. Masafumi FUJIWARA, M.D., and Sanjay BATRA, Ph.D. SUMMARY A 63-year-old man with an acute anterior myocardial infarction demonstrated an intracoronary nonocclusive thrombus distal to the organic stenosis of the left anterior descending coronary artery. One month after the infarction the thrombus was completely dissolved, and spontaneous and provoked spasm occurred overlying the organic stenosis of the coronary artery. Thus coronary spasm superimposed on the atherosclerotic stenosis was suggested as a cause of the thrombus formation that led to myocardial infarction. (Jpn Heart J 34: ,1993) Key Words: Coronary spasm Coronary thrombosis Coronary atherosclerosis Myocardial infarction T is generally known that coronary atherosclerosis, spasm and thrombosis are major factors contributing to myocardial infarction (MI). However, to the best of our knowledge, coexistence of those three factors has rarely been documented in MI. Coronary spasm and its association with coronary thrombosis and MI have previously been reported in the absence of angiographic coronary artery stenosis.1)-4) The present case demonstrated coronary thrombus during the acute phase of MI, and coronary spasm overlying an organic stenosis of the infarctrelated coronary artery during the chronic phase of MI. Thus this case verified the coexistence of coronary atherosclerosis, spasm and thrombosis, which worked in union to cause MI. CASE REPORT A 63-year-old man was referred to the hospital two and a half hours after the onset of an acute anterior MI. He experienced no chest pain before the MI. From the Division of Cardiology, Sapporo National Hospital, Sapporo, Japan. Address for Correspondence: Masashi Horimoto. M.D., Division of Cardiology, Sapporo National Hospital. Kikusui 4-2, Shiroishi-Ku, Sapporo 003, Japan. Received for publication February Accepted May 9,

2 628 HORIMOTO, ET AL. Jpn. Heart J. September 1993 Fig. 1. The ECG (A) on admission showed broad anterior myocardial infarction. One hour later elevation of ST-segments and T-waves disappeared (B). The ECG (C) one month after the infarction revealed anterior Q-wave infarction. Intracoronary acetylcholine caused slight ST-segment elevation in V2-5 (D). Physical examination revealed no abnormality except for an irregular pulse. His coronary risk factors were smoking and diabetes mellitus. On admission an electrocardiogram (ECG) (Fig. 1A) showed premature atrial contractions and large Q-waves in leads V1-3 with elevation of ST-segments and T-waves in leads V2-6. The ECG (Fig. 1B) one hour later showed disappearance of the ST-segment and T-wave elevation. Emergent coronary angiography showed the normal right coronary artery and left circumflex coronary artery (LCX). The left anterior descending coronary artery (LAD) revealed proximal subtotal occlusion (Fig. 2A) with a filling delay of contrast medium (Fig. 2B). With intracoronary administration of 2.5mg of isosorbide dinitrate (ISDN), the filling delay disappeared and an oval-shaped nonocclusive thrombus was visualized as a filling defect closely distal to the or-

3 Vol.34 CORONARY SPASM AND MYOCARDIAL INFARCTION 629 No.5 Fig. 2. On emergent coronary angiography, the image on a 3 -right anterior oblique view immediately after initiation of contrast injection into the left coronary artery revealed subtotal occlusion (black arrow in A) of the proximal LAD and a faint filling defect (white arrow in A). On full opacification of the left coronary artery (B), the subtotal occlusion of the LAD overlaps the first diagonal branch (D1), and filling delay of the LAD and the second diagonal branch (D2) is shown. Intracoronary nitrate resolved the filling delay (C) and the filling defect (arrow in C) due to thrombus was clearly visualized. A cranially tilted 45 -left anterior oblique view (D) also shows the nonocclusive thrombus (arrow in D) in the LAD. LAD=left anterior descending coronary artery; LCX=left circumflex coronary artery. ganic stenosis (Fig. 2C, D). Subsequent intracoronary urokinase (480,000 units) failed to dissolve the thrombus upon completion of catheterization. The peak value of creatine kinase was 5150 IU/1 at ten hours after the onset of infarction. The ECG recorded during the chronic phase (Fig. 1C) showed a QS pattern in V1-4 and negative T-waves in V3-6 and the inferior leads. Coronary angiography (Fig. 3A) one month after the onset of MI revealed 75% stenosis of the proximal LAD with disappearance of the thrombus noted in Fig. 2D, After repetitive opacification of the left coronary artery (LCA) with different angulation, spontaneous spasm of the proximal LAD achieving 90% stenosis (Fig. 3B) occurred with chest symptoms but without ECG changes. Intracoronary

4 630 HORIMOTO, ET AL. Jpn. Heart J. September 1993 Fig. 3. Coronary angiography one month after the infarction showed 75% stenosis (arrow in A) of the proximal LAD with disappearance of thrombus on a cranially tilted 45 -left anterior oblique view. Spontaneous spasm of the proximal LAD achieving 90% stenosis (arrow in B) was observed. Intracoronary nitrate resolved the spasm and the proximal LAD returned to 75% stenosis (C). Subsequent intracoronary acetylcholine provoked intense spasm of the proximal LAD (arrow in D) with filling delay (D). ISDN (2.5mg) resolved the spasm and the proximal LAD returned to 75% stenosis (Fig. 3C). To verify the association of coronary spasm with the MI, a provocative test for spasm was subsequently performed with intracoronary injection of acetylcholine (ACh). The injection of 50ƒÊg ACh into the LCA provoked intense spasm achieving subtotal occlusion of the proximal LAD with a filling delay and diffuse constriction of the LCX (Fig. 3D). The spasm was accompanied by chest pain and ST-segment elevation in V2-5 (Fig. 1D) and was resolved with intracoronary ISDN. DISCUSSION Coronary atherosclerosis, coronary spasm and thrombosis have been considered as major causes of MI. However, coexistence of these three factors has

5 Vol.34 No.5 CORONARY SPASM AND MYOCARDIAL INFARCTION 631 rarely been documented in MI. Coronary spasm associated with coronary thrombosis that caused MI has previously been described.1)-5) Two reports1),5) directly demonstrated that coronary spasm caused thrombus formation and MI. Three other reports2)-4) documented intracoronary thrombus in acute MI and provoked spasm of the infarct-related coronary artery during the chronic phase of MI. These reports1)-4) demonstrated coronary spasm and thrombosis in angiographically normal or near normal coronary arteries and thus failed to document the coexistence of the three major pathogeneses described above. Marchena et al6) recently reported the coexistence of angiographic coronary atherosclerosis, coronary spasm and thrombosis in an infarct-related coronary artery. However, the association of the thrombosis with MI is unclear, since the thrombosis was not documented during the acute phase of MI. The present case demonstrated an intracoronary thrombus during the acute phase of MI; the thrombus was located distal to the site of subtotal occlusion of the LAD. One month after the MI the thrombus was dissolved, and spontaneous and provoked coronary spasm overlying an organic stenosis of the LAD was noted. Although chest pain before the MI was absent and the possibility that the intracoronary thrombus elicited coronary spasm was not completely eliminated, the occurrence of spontaneous spasm of the infarct-related coronary artery strongly supports the concept that coronary spasm induced thrombus formation and led to MI. In conclusion, this case verified the coexistence of coronary atherosclerotic stenosis, coronary spasm and thrombosis in MI, and strongly suggested that coronary spasm overlying the stenosis caused MI through thrombus formation. REFERENCES 1. Vincent GM, Anderson JL, Marshall HW: Coronary spasm producing coronary thrombosis and myocardial infarction. N Engl J Med 309: 220, Benacerraf A, Scholl JM, Achard F, Tonnelier M, Lavergne G: Coronary spasm and thrombosis associated with myocardial infarction a patient with nearly normal coronary arteries. Circulation 67: 1147, Naito H, Yorozu T, Matsuda Y, Yamaguchi M, Tanabe Y, Nakashima H, Kusuwada R: Coronary spasm producing coronary thrombosis in a patient with acute myocardial infarction. Clin Cardiol 10: 275, Takashiba K, Matsuda Y, Hamada Y Ohno H. Hyakuna E, Fujii M, Ebihara H: Recurrence of myocardial infarction related to different vessels in a patient with diffuse coronary artery spasm without underlying severe organic stenosis. Clin Cardiol 11: 265, Klevan T, Deckelbaum LI, Wohlgelernter DW, Cleman MW: Coronary vasospasm culminating thrombosis and infarction following successful coronary angioplasty. Am Heart J 113: 1220, Marchena EJ, Trohman RG, Palomo AR, Myerburg RJ, Kessler KM: Angiographic demonstration of atherosclerotic stenosis, arterial spasm, and thrombus formation in an infarct-related coronary artery. Cathet Cardiovasc Diag 15: 169, 1988