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Acute Myocardial Infarction After Use of Pseudoephedrine for Sinus Congestion

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Acute Myocardial Infarction After Use of Pseudoephedrine for Sinus Congestion J Am Board Fam Pract: first published as 10.3122/jabfm.10.6.436 on 1 November 1997. Downloaded from BRIEl' RI~PORTS Acute Myocardial Infarction After Use of Pseudoephedrine for Sinus Congestion llector Derreza, MD, Michael D. Fine, M/), alld Ara Sadanimztz, MI) Coronary vasospasm has been recognized as an and walked 3 times per week for up to 1 hour with­ important factor for corollary atherogenesis and out chest pain. Since beginning the use of the sinus the development of symptoms associated with medication, he noted a mild chest pressure lasting coronary blood flow obstruction that can lead to from seconds to minutes that began 30 to 60 min­ ischemia and eventually myocardial infarction. 1 utes after ingestion of the sinus medication. He Association of drugs and coronary artery vaso­ had persistent sinus congestion before admission; spasm has been reported for such chemicals as in­ however, he was able to work and denied psy­ travenous ephedrine, cocaine, dipyridamole, tri­ chosocial stress. The day of admission he took his methaphan, and sumatriptan.2-fi Few cases have medication about 30 minutes before developing been reported in which pseudoephedrine is asso­ severe chest pressure similar in quality to previous ciated with myocardial infarction. Wiener et al fi episodes but greater in intensity. described a healthy 28-year-old man with no car­ On admission he was having severe chest pain. diac risk factors who had acute myocardial infarc­ His blood pressure was 180/115 mmHg, heart tion with ST segment elevation after taking 60 rate 66 beats per minute, and respiratory rate mg of pseudoephedrine. Subsequent coronary 26/min. He was diaphoretic, his jugular veins angiography showed normal coronary arteries in were not distended, his heart had a normal S 1 and this patient. We describe the association of angi­ S2, no Sl or S4, and no murmurs. Findings on an nal symptoms and eventual myocardial infarction abdominal examination were normal. His ex­ with ingestion of an over-the-counter remedy tremities had no edema, his pulses were palpable containing pseudoephedrine. bilaterally, and he had no cyanosis. Laboratory data on admission showed normal findings on a Case Report complete blood cell count and automated chem­ http://www.jabfm.org/ A 46-year-old man came to the hospital after an istry screening (sequential multiple analysis-7); acute onset of severe suhsternal chest pain associ­ his partial thromboplastin time was 25 sec, pro­ ated with mild shortness of breath and profuse di­ thrombin time 11.0 sec, international normalized aphoresis. His symptoms began 1 hour after taking ratio (INR) 0.9, magnesium 1.3 mEq, and creatine an over-the-counter medication containing 500 phosphokinase (CPK) 134 lUlL. Findings on his mg of acetaminophen and 15 mg of pseudo­ chest radiograph were normal. His electrocardio­ ephedrine hydrochloride, which he had been tak­ gram showed a normal sinus rhythm of 75 beats on 29 September 2021 by guest. Protected copyright. ing for 3 months for sinus congestion. He had per minute, a normal QRS axis, normal atrio­ been taking up to 1 tahlet every 6 hours. His car­ ventricular conduction, and 4-111l11 ST segll1ent el­ diac risk factors included male sex and heavy smok­ evations in the precordial leads V 1 through V, ing (30 pack-years), but his medical history was not (Figure 1). unusual. He had no family history of cardiac dis­ He received 4 sublingual nitroglycerin tablets ease and denied use of illegal drugs. He was taking and was given intravenous nitroglycerin. He sud­ no other medication. He worked as a truck driver denly developed transient monomorphic ventric­ ular tachycardia with a rate of 101 beats per minute, which resolved spontaneously. His elec­ Submitted, revised, 4.June I ()<)7. trocardiogram after this episode showed de­ From the Division of Cardiology, The Miriam j jospital, creased ST elevations and he became pain-free. It Brown University School of Ivledicine, Providence. Address reprint requests to Ara Sadaniantz, MD, Division of Cardiology, was thought that he spontaneously revascular­ The Miriam I Iospital, 164 Summit Ave, Providence, RI 02906. ized. He was admitted to the coronary care unit 436 JABFP Nov.-Dec.1997 Vol. 10 No.6 J Am Board Fam Pract: first published as 10.3122/jabfm.10.6.436 on 1 November 1997. Downloaded from Figure 1. The electrocardiogram showing 4-mm ST segment elevations in the precordial leads VI through V5 con­ sistent with an acute anterior myocardial infarction. on intravenous heparin and intravenous nitro­ spasm because of its sympathomimetic action.9 glycerin. He received 325 mg of chewable aspirin Age, sex, hypertension, diabetes, and serum levels and 25 mg of metoprolol orally. His first CPK of cholesterol and uric acid have no notable pre­ was 1701 lUlL with MB fraction of 155 ng/mL dictive value for coronary vasospasm. IO Dipyri­ and MB index of 9.1 percent (normal value for damole, trimethaphan, cocaine, ephedrine, and our laboratory is MB index less than 4 percent). A sumatriptan have also been associated with coro­ toxicology screening test of the urine was nega­ nary vasospasm.2-5 tive for cocaine. On his lipid profile he had a total We report a case in which the use of pseu­ cholesterol of 199 mg/dL, high-density lipopro­ doephedrine was associated with symptoms sug­ tein 66 mg/dL, low-density lipoprotein 121 gestive of angina pectoris. Eventually the patient mg/dL, and triglyceride level 58 mg/dL. came to the emergency department with an acute He underwent cardiac catheterization on hospi­ myocardial infarction a fter taking pseudo­ http://www.jabfm.org/ tal day 2. The ventriculogram showed anterolat­ ephedrine and was found to have angiographically eral and apical hypokinesis with an ejection frac­ minimal coronary artery disease. Because of the tion of 50 percent. On coronary angiography the predictable association of developing symptoms mid-right coronary artery had 10 percent plaque, and the left anterior descending artery had mild plaques of 30 percent proximally and 20 percent at on 29 September 2021 by guest. Protected copyright. its mid portion (Figure 2). Nitroglycerin caused unbearable headaches and was discontinued. He was prescribed amlodipine 10 mg/d and was dis­ charged to home on hospital day 6 in good condi­ tion. He was advised to avoid the use of any sym­ pathomimetic agent. Nine months after discharge he remains free of anginal symptoms. Discussion Coronary artery spasm plays an important role in acute ischemic events, including acute myocardial infarction and exertional angina. I,7,s Smoking is Figure 2. Coronary angiography of the left coronary the most important risk factor for coronary artery system with mild plaques. Myocardial Infarction and Pseudoephedrine 437 J Am Board Fam Pract: first published as 10.3122/jabfm.10.6.436 on 1 November 1997. Downloaded from and the ingestion of the medication, it is highly of coronary artery spasm in acute myocardial infarc­ likely that there was a cause-and-effect relation. tion. Circulation 1977;56:366-74. He did not have symptoms of angina either be­ 2. Amin M, Gabelman G, Karpel], Buttrick P. Acute myocardial infarction and chest pain syndromes af­ fore starting or after stopping the medication. It ter cocaine use. Am J Cardiol 1990;66: 1434-7. is possible, but not likely, that the timing was co­ 3. Weinmann P, Le Guludec D, Moretti JL. Coronary incident and that he had an episode of variant spasm induced by dipyridamole during a myocardial angina independent of the pseudoephedrine. scintigraphy. lilt] CardioI1994;43:75-8. One other case of myocardial infarction, with 4. Higa K, Mori M, Shono S, Dan K. Trimethaphan ST segment elevations, associated with the use of may cause coronary artery spasm. Eur] Anaesthesiol 6 1995;12:529-32. pseudoephedrine has been reported. Pseudo­ 5. Lippolis A, Castini 0, Cirino D, Ornaghi M. Coro­ ephedrine is a congener of ephedrine, which has nary vasospasm secondary to subcutaneous admin­ both a direct and an indirect effect on sympa­ istration of sumatriptan. G Ital Cardiol 1994;24: thetic nerve endings. Side effects include hyper­ 883-6. tension, cardiac arrhythmias, and insomnia. 6. Wiener I, Tilkian AG, Palazzolo M. Coronary artery spasm and myocardial infarction in a patient Although not many cases of pseudoephedrine­ with normal coronary arteries: temporal relationship induced myocardial infarction have been previ­ to pseudoephedrine ingestion. Cathet Cardiovasc ously reported, this case provides evidence of a Diagn 1990;20:51-3. causal relation between pseudoephedrine use and 7. Chahine RA. [Role ofthe spasm in coronary pathol­ acute myocardial infarction in one susceptible pa­ ogy.] Ann Cardiol Angeiol (Paris) 1982;31:563-70. tient. We question the safety of this medication in 8. Maseri A, Chierchia S, L'Abbate A, Biagini A, Dis­ tante A, Parodi 0, et al. [The role of spasm in angina over-the-counter preparations in susceptible pa­ pectoris, myocardial infarction and sudden death. tients and suggest awareness of this uncommon Indications for future research and treatment.] Arch but potentially fatal side effect. Further research Mal CoeurVaiss 1982;75:701-16. might be directed to recognition of persons sus­ 9. Ball K, Turner R. Smoking and the heart: the basis for action. Lancet 1974;2:822-6. ceptible to myocardial ischemia with this type of 10. Nobuyoshi M, Abe M, Nosaka H, Kimura T, Yokoi medication. H, Hamasaki N, et al. Statistical analysis of clinical risk factors for coronary artery spasm: identification References of the most important determinant. Am Heart ] 1. Oliva PB, Breckinridge]C. Arteriographic evidence 1992;124:32-8. http://www.jabfm.org/ on 29 September 2021 by guest. Protected copyright. 438 JABFP Nov.-Dec. 1997 Vo1.10No.6 .
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