Volume 131, Number 3 American Heart Journal Hussain, Heidenreich, and Benowitz 615 5. Pickering JG, Weir L, RosenfieldK, Stetz J, Jekanowski J, Isner JM. Smooth muscle cell outgrowth from human atherosclerotic plaque: im- plications for the assessment of lesion biology. J Am Coll Cardiol 1992;20:1430-9. 6. Nikol S, Isner JM, Picketing JG, Kearney M, Leclerc G, Weir L. Expressionoftransforming growth factor-beta 1 is increased in human vascular restenosis lesions. J Clin Invest 1992;90:1582-92. Recurrent non-Q-wave myocardial infarction associated with toluene abuse Tanveer F. Hussain, MD, Paul A. Heidenreich, MD, and Neal Benowitz, MD San Francisco, Calif. Toluene, a common substance of solvent abuse in the United States, is associated with significant cardiac mor- bidity and mortality after inhalation. Several reports have described cardiac complications of acute (arrhythmia, my- ocardial infarction 1) and chronic intoxication (dilated car- diomyopathy2). We report the case of a 55-year-old man with toluene-related recurrent non-Q-wave myocardial infarction. The patient is a 55-year-old Hawaiian man who first came to medical attention in March 1992 when he arrived with dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, peripheral edema, and vague chest discomfort. He gave a history of alcohol abuse but no tobacco or illicit drug use. On physical examination he was noted to have a blood pressure of 204/136, bibasilar rales, an elevated jugular venous pressure, and mild peripheral edema. An electrocardiogram demonstrated normal sinus rhythm and left ventricular hypertrophy with repolarization ab- normalities. Serial creatinine kinase determinations re- vealed a peak level of 94 IU/L with an elevated MB frac- tion. A chest x-ray examination showed cardiomegaly, and an echocardiogram demonstrated a left ventricular ejec- tion fraction of 45% with mild global hypokinesis and mild concentric left ventricular hypertrophy. A thallium exer- cise treadmill test demonstrated an inferior wall defect at exercise, but the patient did not return for a rest study. Cardiac catheterization revealed normal coronary arter- ies. Results of a complete blood count, electrolytes, and liver function tests were within normal limits, and a uri- nalysis was notable for mild proteinuria (30 mg/dl). The patient was successfully treated with a combination of ni- trates, diuretics, calcium channel blocker, and an angio- tensin-converting enzyme inhibitor. However, he was fre- quently noted to be noncompliant with his medications. From the Departments of Medicine at the University of California, San Francisco,and the San FranciscoGeneral Hospital, San Francisco,Califor- nia. Reprint requests: Paul A. Heidenreich, MD, Division of Cardiology,Box 0!24, University of California, San Francisco, 505 Parnassus, San Fran~ cisco, CA 94143. AMHEART J 1996;131:615-6. Copyright © 1996 by N[osby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4/4/68323 Since that initial visit the patient has had 11 admissions for non-Q-wave myocardial infarction over an 18-month period. His presentations to the emergency department were for acute episodes of severe substernal chest pain with radiation to the left arm; these episodes lasted more than 30 minutes, often occurred at rest and were associ- ated with nausea and diaphoresis. Admitting blood pres- sure varied from 135 to 200 mm Hg, and mild congestive heart failure was frequently noted on examination and chest radiography. Occasional transient electrocar- diographic changes showed pseudonormalization of the T-wave abnormalities or ST depression. Over time echocar- diographic studies showed decreased left ventricnlar ejec- tion fraction from 45% to 33%. He underwent two addi- tional cardiac catheterizations, again revealing normal coronary arteries. An ergonovine challenge test or myo- cardial biopsy was not performed. Throughout this time the results of his complete blood count, electrolytes, and liver function tests were within normal limits except for a trend toward hypokalemia and mild proteinuria. His tol- uene abuse was detected during his tenth admission for non-Q-wave myocardial infarction, when he was found saturating paper towels with industrial strength toluene in preparation for "sniffing" in the hospital. When con- fronted, the patient admitted to inhaling toluene in a sim- ilar manner one to two times per week since 1968, often immediately before chest pain developed. On the last recorded admission for non-Q-wave myocardial infarction, his electrolytes were notable for an anion gap acidosis with hypokalemia (Na 138, K 2.8, C1 106, CO2 13). A urinalysis showed worsening proteinuria (300 mg/dl) and numerous hyaline casts. The electrolyte abnormalities returned to normal at discharge. The cardiac toxicity of toluene most frequently described in the literature is arrhythmia, specifically ventricular tachycardia, ventricular fibrillation, and sinus bradycar- dia, often leading to sudden death. 3 Possible mechanisms of action include oversensitization of the heart to endoge- nous catecholamines and direct slowing of the sinoatrial node. 4 Coexisting electrolyte abnormalities caused by tol- uene's renal toxicity may also contribute to the develop- ment of these fatal arrhythmias. 5 Less commonly reported is the presence of dilated cardiomyopathy with toluene abuse. 2 Acute myocardial infarction has rarely been reported in the setting of solvent abuse. One case report describes a 16-year-old boy who had ventricular fibrillation and an anterior myocardial infarction shortly after prolonged in- 1 halation of an adhesive containing toluene. We believe our case to be the first linking toluene abuse to recurrent my- ocardial infarction. We postulate that acute exposure to toluene led to coronary vasospasm caused by increased sensitivity to catecholamines, 4 with the subsequent devel- opment of non-Q-wave myocardial infarction. The patient admitted to toluene use before the onset of the acute symptoms, linking the two processes temporally. Moreover the development of both an anion gap acidosis with hypokalemia and proteinuria is consistent with distal tu- bular acidosis, which is a well-known phenomenon in tol: uene abuse. 6