Case Reports Acta Cardiol Sin 2007;23:268-72

Acute of Double Major Associated with Amphetamine Abuse

Wei-Ren Lan, Hung-I Yeh, Charles Jia-Yin Hou and Yu-San Chou

Drug-induced acute is not a common phenomenon. The underlying mechanism in the majority of such patients has been related to coronary spasm, including in those with amphetamine abuse, in whom the coronary arteriogram was always found normal. We report a 30-year-old male amphetamine abuser with acute myocardial infarction owing to acute thrombosis of the left anterior descending coronary artery and left circumflex coronary artery. We postulate a relationship between the use of amphetamine and occurrence of acute thrombosis of multiple major coronary arteries.

Key Words: Amphetamine · Coronary · Thrombosis

INTRODUCTION after intruding into a private apartment when acute chest pain occurred. He was brought by policemen to our emer- Amphetamines have been gaining popularity as a gency unit 2 hours after the onset of acute chest pain, recreational drug worldwide over the past few decades. which radiated to the back and was accompanied by nausea Acute myocardial infarction (AMI) owing to amphe- and vomiting but no shortness of breath. The patient had no tamine abuse often occurs in young adults, in whom coro- history of , hyperlipidemia, diabetes mellitus, nary spasm is thought to be the underlying mechanism.1 atrial , or family history of coronary artery To our knowledge, there is no published registry of am- disease. He had smoked 2 packs of cigarettes daily for more phetamine-induced AMI with multiple coronary thrombo- than 10 years. Several hours before the onset of chest pain, sis. To highlight the occurrence of thrombosis in amphe- the patient had “snorted some amphetamine.” He also ad- tamine-induced AMI, we describe an amphetamine mitted frequent use of amphetamine for more than 2 years. abuser presenting with AMI owing to multivessel coro- On arrival, pressure was 96/69 mmHg, heart nary thrombosis. The patient failed to survive despite rate was 107 beats per minute, respirations were 20 brea- early percutaneous coronary intervention (PCI). ths per minute, and temperature was 36.1 °C, with an oxygen saturation of 100% on room air. His lungs were clear, and his abdominal examination revealed nothing CASE REPORT particular. An immediate electrocardiogram (ECG) (Fig- ure 1A) showed sinus rhythm with diffuse ST elevation A 30-year-old man was being arrested by policemen in the precordial leads (V2 through V6) and limb leads (I, II, III, and aVF) as well as the development of Q waves in leads V1~V5. Laboratory data showed total Received: November 8, 2006 Accepted: December 14, 2006 creatine kinase level of 2157 IU/L, creatine kinase-MB Division of , Department of Internal Medicine, Mackay Memorial Hospital, Taipei, Taiwan. level of 82 U/L, and troponin-I level of 11.70 ng/ml. No Address correspondence and reprint requests to: Dr. Leonard thrombocytosis (platelet count: 368,000/uL) was found. Wei-Ren Lan, M.D., Division of Cardiology, Department of Internal A urine drug screen was positive for amphetamines but Medicine, Mackay Memorial Hospital, No. 92, Chung Shan North Rd., Sec. 2, Taipei, Taiwan. Tel: 886-2-2543-3535 ext. 2456; Fax: negative for cocaine. Bedside cardiac ultrasonography 886-2-2543-3642; E-mail: [email protected] showed hypokinesia of the inferior, posterior and ante-

Acta Cardiol Sin 2007;23:268-72 268 Amphetamine Related Coronary Thrombosis

Figure 1. A, ECG on arrival shows diffuse ST-segment elevation in leads I, II, III, aVF, and V2-V6. B, partial resolution of ST-segment elevation after percutaneous coronary intervention. rior wall of the left ventricle. Under the impression of totally occluded at the distal-portion (Figure 2A, arrow). ST elevation AMI with cardiogenic shock, the patient Neither significant fixed stenotic lesion nor was given aspirin and subcutaneous low-molecular- were found in the right coronary artery (Figure 2B). The weight . Glycoprotein IIbIIIa antagonist was not LCx and LAD were considered to be the infarct-related administered then because we had failed to gain ap- arteries, due to their evident thrombi with sluggish flow. proval from the patient himself. A thrombectomy device (Thrombuster, Kaneka) was Although chest pain had recurred, unfortunately, pri- used sequentially through a 7-French guiding catheter, and mary PCI could only be performed 8 hours after the onset gained a TIMI grade 3 flow in both vessels. After large of initial chest pain after obtaining permission from the amount of thrombus was aspirated, a 2.75 ´ 32-mm and a prosecuting attorney. Coronary angiography revealed a 3.0 ´ 28-mm bare-metal were implanted to the dis- thrombus-like filling defect (Figure 2A, bold arrow) in tal-portion of the LCx and the proximal LAD, respectively. the mid-portion of the left anterior descending coronary A TIMI grade 3 antegrade flow and TIMI frame count of artery (LAD) as well as a 90% stenosis in the proximal 35 counts were achieved without residual stenosis in both LAD, with only TIMI grade II flow (Figure 2A, arrow- LCx (Figure 2C) and LAD (Figure 2D). The chest pain head). The left circumflex coronary artery (LCx) was also was attenuated and ECG showed resolution of ST eleva-

269 Acta Cardiol Sin 2007;23:268-72 Wei-Ren Lan et al.

to congenital coronary anomaly, coagulopathy, prema- ture or coronary artery spasm or is drug- induced. AMI caused by thrombus-filled coronary ves- sels after the use of amphetamine is rare as compared with AMI caused by other illegal drugs (for example, co- caine).2 In our case, we clearly documented the existence of thrombus in multiple coronary arteries during emer- gency coronary angiography. AMI with multiple acute obstruction of major coronary vessels is a rare clinical and angiographic finding. To our knowledge, however, this is the first reported case of multivessel acute throm- bosis after amphetamine-induced myocardial infarction. There were few other cases reported in detail in the liter- ature; one was secondary to cocaine use;3 others usually occurred in patients with essential thrombocythemia.4,5 Several mechanisms have been proposed for am- phetamine-induced myocardial though induc- Figure 2. A, Left coronary angiogram in the right anterior oblique tion of coronary arterial spasm was the likely mechanism projection shows total occlusion of the left circumflex coronary artery at of amphetamine-related acute MI.2,6-8 Previous studies the distal portion (arrow) and a severe stenotic lesion at the proximal portion of the left anterior descending coronary artery (arrowhead) with have shown that cocaine can stimulate the release of ca- intraluminal thrombus at the middle portion (bold arrow). B, right techolamines from presynaptic nerve terminals, and block coronary angiogram in the left anterior oblique projection shows patent the reuptake of these catecholamines, resulting in a hy- right coronary artery. C, left coronary angiogram in right anterior peradrenergic state.2 Also, cocaine decreases concentra- oblique projection shows patent LCx after successful stenting. D,left coronary angiogram in right anterior oblique projection shows patent tions of protein C and antithrombin III, activate platelets, LAD after successful stenting. Arrows in C and D indicate the site of and potentiate thromboxane production, thereby facili- thrombosis before stenting. tating thrombotic coronary occlusion.1 However, the contribution to thrombus formation associated with am- tions (Figure 1B). During the course of PCI, reperfusion- phetamine has not been well documented. Speculation is induced such as VT or VF had never de- based on the effects of amphetamine being similar to veloped, but persistent hypotension with severe metabolic those of cocaine.2 Therefore, our observations suggest acidosis leading to frequent occurred and was the hypothesis that high catecholamine levels after expo- immediately restored after cardiac massages. sure to amphetamine may trigger AMI by enhancement Throughout PCI, the patient was actually handcuffed of platelet activation and thrombin generation,9 and to the table. He had been very uncooperative and was might be responsible for the thrombotic occlusion at the struggling hard at all times trying to free of the hand- site of multiple “vulnerable” plaques. A different expla- cuffs so that he could escape. As a result, intraaortic bal- nation is likely in our patient, i.e. acute occlusion of one loon pump and extracorporeal membrane oxygenation large culprit vessel may have triggered subsequent pump devices were not considered in this patient for safety rea- failure, thereby compromising flow in another coronary sons. Unfortunately, despite successful primary PCI and vessel where a severe stenosis was already present, and aggressive inotropic agents, the patient died of cardio- causing acute “secondary” thrombosis. The observations genic shock in the coronary care unit. in our patient with cardiogenic shock,9-11 although com- patible with the hypothesis of a “low-flow”-driven th- rombosis of a second vessel, cannot provide any definite DISCUSSION answer as to whether the shock was a cause for, or an ef- fect of, acute occlusion of multiple coronary vessels. AMI at a young age is unusual and is mainly owing The ECG change of extraordinary diffuse ST eleva-

Acta Cardiol Sin 2007;23:268-72 270 Amphetamine Related Coronary Thrombosis tion in our patient suggests an extensive myocardial in- 4. Michaels AD. Whisenant B. MacGregor JS. Multivessel coronary farction, in which acute multivessel obstruction should thrombosis treated with abciximab (ReoPro) in a patient with es- be considered. However, a large infarction usually kills sential thrombocythemia. Clin Cardiol. 1998;21(2):134-8. 5. Hamada Y. Matsuda Y. Fujii B, et al. Multiple coronary thrombo- the patient before he can come to medical attention9,12,13 sis in a patient with thrombocytosis. Clin Cardiol. 1989;12(12): or is associated with severe circulatory impairment, as 723-4. presented in our patient who failed to survive soon after 6. Waksman J, Taylor RN Jr, Bodor GS, et al. Acute myocardial in- AMI. farction associated with amphetamine use. Mayo Clin Pro 2001; Medical treatment for amphetamine-induced myo- 76:323-6. cardial infarction deviates from the standard treatment in 7. Turnipseed SD, Richards JR, Kirk JD, et al. Frequency of acute certain aspects. In amphetamine abusers presenting with coronary syndrome in patients presenting to the emergency de- partment with chest pain after methamphetamine use. JEmerg chest pain, oxygen, aspirin, coronary vasodilators and Med 2003;24:369-73. 14 b benzodiazepines can be given initially. -blockers were 8. Ragland AS, Ismail Y, Arsura EL. Myocardial infarction after avoided because of the concern of unopposed a activa- amphetamine use. Am Heart J. 1993;125:247-9. tion, which could result in severe hypertension.15 9. Pérez-Castellano N, Garcia E, Serrano JA, et al. Efficacy of inva- In conclusion, our case report demonstrates that sive strategy for the management of acute myocardial infarction acute occlusion of multiple coronary vessels by throm- complicated by cardiogenic shock. Am J Cardiol 1999;83:989-93 bosis can occur in amphetamine abusers. Further study 10. Falk E. Plaque rupture with severe pre-existing stenosis precipi- tating coronary thrombosis: characteristics of coronary athero- of the effects of amphetamine on vascular biology is re- sclerotic plaques underlying fatal occlusive thrombi. Br Heart J quired to clarify the mechanisms underlying the acute 1983;50:127-34. coronary thrombosis by amphetamine. 11. Davies MJ, Thomas A. Thrombosis and acute coronary artery le- sions in sudden cardiac ischemic death. N Engl J Med 1984; 310:1137-40. REFERENCES 12. Garcia-Cantu E, Corcos T, Favereau X, et al. Multiple stenting in acute myocardial infarction with double-vessel occlusion, 1. Menyar Ayman A El. Drug-induced myocardial infarction se- complicated with cardiogenic shock. J Invasive Cardiol 1995; condary to coronary adults coronary artery spasm in teenagers 7:283-7 and young adults. J Postgrad Med 2006;52:51-6. 13. Antoniucci D, Valenti R, Buonamici P, et al. Direct angioplasty 2. Bashour T. Acute myocardial infarction resulting from amphe- and stenting of the infarct-related artery in acute myocardial in- tamine abuse: a spasmthrombus interplay? Am Heart J 1994; farction. Am J Cardiol 1996;78:568-71. 128:1237-9. 14. Ghuran A, Nolan J. Recreational drug misuse: issues for the 3. Meltser H, Bhakta D, Kalaria V. Multivessel coronary thrombosis cardiologist. Heart 2000;83:627-33 secondary to cocaine use successfully treated with multivessel 15. Qasim A, Towsnend J, Davies MK. Ecstasy-induced acute myo- primary angioplasty. Int J Cardiovasc Intervent. 2004;6(1):39-42 cardial infarction. Heart 2001;85:e10.

271 Acta Cardiol Sin 2007;23:268-72 Case Reports Acta Cardiol Sin 2007;23:268−72

在一個安非他命濫用者發生雙冠狀動脈急性血栓 的病例報告

藍偉仁 葉宏一 侯嘉殷 周友三 台北市 馬偕紀念醫院 心臟內科

藥物引起的急性心肌梗塞並不是一個常見的現象。而且大部分病例中，其發生的機轉與冠 狀動脈痙攣有關，包括安非他命濫用者，其冠狀動脈攝影通常都是正常。我們報告一個 30 歲男性安非他命濫用者發生左前降枝及左迴旋枝的急性冠狀動脈血栓造成急性心肌梗塞。 我們推論安非他命的使用和發生多重冠狀動脈急性血栓的形成存在著因果關係。

關鍵詞：安非它命、冠狀動脈、血栓。

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