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Ephedrine-Induced Coronary Artery Vasospasm in a Patient with Prior Cocaine Use

1997; Lippincott Williams & Wilkins; Volume: 84; Issue: 4 Linguagem: Inglês

10.1213/00000539-199704000-00045

1526-7598

Stewart J. Lustik, Ashwani K. Chhibber, Miller van Vliet, Richard M. Pomerantz,

Cardiac pacing and defibrillation studies

It is well known that acute cocaine use is associated with myocardial ischemia and infarction [1-6]. However, there have been no reports of intraoperative cardiac ischemia secondary to prior cocaine use. This report describes a patient with cocaine use four days prior to surgery who developed evidence of probable coronary artery vasospasm after receiving ephedrine. Case Report A 42-yr-old male with peripheral vascular disease presented for a right femoral-popliteal bypass procedure. Despite lower extremity claudication, the patient worked 10-13 h daily at an automotive plant, assembling heavy machinery and pulling carts weighing up to 120 pounds. He denied chest pain, palpitations, or syncope. Although his arterial blood pressure during preoperative evaluation 5 days prior to surgery was 173/55 mm Hg, he had no history of hypertension and multiple subsequent blood pressures were normotensive with a normal pulse pressure. He had a history of untreated glucose intolerance; a nonfasting preoperative blood glucose level was 132 mg/dL. He had smoked three-fourths of a pack of cigarettes per day for 15 yr. He used cocaine almost daily many years ago, but claimed only monthly use over the last 10 yr and that he last used cocaine at a party 4 days prior to surgery. He was taking no medications. Electrocardiogram (ECG) revealed sinus bradycardia at 55 bpm. The patient desired spinal anesthesia. In the preanesthesia room, he received 4 mg of midazolam intravenously (IV). After infusing 700 mL IV of lactated Ringer's solution, 15 mg of bupivacaine and 0.2 mg of preservative-free morphine were injected intrathecally at the L3-4 interspace. The patient was placed in the right lateral decubitus position for 5 min, and then placed supine with a sensory block to the T-6 dermatome. Arterial blood pressure decreased from 115/60 mm Hg to 88/40 mm Hg with an increase in heart rate from 65 to 70 bpm, and the patient complained of nausea. Ephedrine 10 mg was given IV. Approximately 30 s later, the patient developed a wide complex, regular rhythm at 145 bpm consistent with ventricular tachycardia, and he complained of chest pain. While the cardiac defibrillator was readied, the patient was given oxygen, 100 mg of IV lidocaine, and 2 mg of IV midazolam. Just prior to electrical discharge, he converted to sinus rhythm at 70 bpm with an arterial blood pressure of 120/75 mm Hg. The patient continued to complain of chest pain and had new 3.9-mm ST segment elevation in lead II. After he was given two nitroglycerin 0.4-mg tablets sublingually, the chest pain resolved, but the ECG changes persisted. Surgery was canceled, and the patient was immediately taken to the postanesthesia care unit for emergent cardiology consultation. ECG revealed 4-mm ST segment elevation in leads II, III, and aVF consistent with an acute inferior myocardial infarction. The patient was given an aspirin to chew and 5000 U of IV heparin. He emergently underwent cardiac catheterization and angiography revealed a 10%-20% lesion of the mid-right coronary artery (Figure 1), luminal irregularities without obstruction in the left anterior descending artery, and a normal left circumflex artery. There was akinesis of the inferoapex and an ejection fraction of 43% (Figure 2). Spasm was not visualized. The patient was taken to the medical intensive care unit for a stable course including no further chest pain or arrhythmias, with resolution of his ST segment elevation several hours later, and negative creatine phophokinase-MB isoenzyme fractions. Results of a urine screen for cocaine as well as nicotine, caffeine, opiates, and ethanol were negative. The patient was discharged home 2 days later with a prescription for diltiazem and a strong admonition to refrain from further cocaine use. Six weeks later, a transthoracic echocardiogram revealed no wall motion abnormalities and an ejection fraction of 60%. When the patient returned for surgery 9 wk after discharge, he denied cocaine use since prior to the previous hospital admission and underwent uneventful general anesthesia for femoral-popliteal bypass.Figure 1: Right coronary artery. The 30 degrees left anterior occipital view (A) demonstrates a large right coronary artery which supplied the inferior and apical walls. The 30 degrees left anterior oblique and the 30 degrees right anterior oblique views (B) illustrate a minimal 20% mid-lesion (white arrows).Figure 2: Ventriculography obtained in the 30 degrees RAO view after injection of 44 mL of contrast. Akinesis of the inferoapex is noted in the systolic frame (B) by a white arrow in comparison with the end-diastolic frame (A).Discussion The effects of acute cocaine ingestion are well described, as is the accumulation of catecholamines at postsynaptic receptors which causes tachycardia and hypertension that may lead to cardiac ischemia [7-10]. Cocaine may also cause myocardial infarctions by inducing coronary artery vasospasm [3] and increasing platelet aggregation [11]. Cocaine induces vasospasm by stimulating alpha receptors on large epicardial arteries as well as by a direct constrictor effect on vascular smooth muscle [12,13]. Our patient's symptoms were not caused by acute cocaine ingestion, as he denied recent use and had no cocaine metabolites in his urine (cocaine metabolites are detectable in the urine for 24 to 60 hours after cocaine use [14]. However, there are data to support the contention that prior cocaine use may have contributed to his coronary vasospasm. In a study of 21 chronic cocaine users admitted to a substance abuse treatment program, 24-hour Holter monitoring revealed episodes of ST segment elevation in 45% of patients within one week of admission [15]. Episodes of ST segment elevation were present up to four weeks after admission, despite verification of no recent cocaine use. The authors postulated that chronic cocaine use caused dopamine depletion, resulting in coronary artery sensitivity to alpha-adrenergic stimulation and thus, coronary artery vasospasm. There is also a report of a patient suffering a myocardial infarction with exercise three days after using cocaine. The authors theorized that chronic cocaine use causes up-regulation of alpha receptors which results in an exaggerated response to catecholamines [16]. Up-regulation of alpha-adrenergic receptors could result from total catecholamine depletion at the nerve terminals, despite excess catecholamines in the junction [17]. This was further demonstrated by Jones and Tackett [18], who found that the coronary arteries in dogs treated chronically with cocaine had increased sensitivity to vasoconstrictor drugs. As hypothesized above, our patient's chronic cocaine use may have caused up-regulation of alpha receptors on his epicardial arteries. After receiving ephedrine (a mostly indirect alpha and beta agonist) to treat hypotension, our patient most likely had vasospasm of the right coronary artery which caused myocardial ischemia. This was evident by chest pain, ST segment elevation in the inferior leads, and reversible akinesis of the inferoapex. Ventricular tachycardia was probably due to myocardial ischemia or IV ephedrine administration and converted to sinus rhythm with administration of lidocaine. Other less likely etiologies of this patient's myocardial ischemia include spinal-induced hypotension or acute thrombus formation with spontaneous lysis. Hypotension-induced ischemia is unlikely for the following reasons: The patient had excellent exercise tolerance with no angina and no significant coronary artery disease on catheterization, thus mild hypotension was unlikely to cause myocardial ischemia. The short period of hypotension (less than three minutes) should not result in the prolonged myocardial stunning seen on ventriculography in the absence of significant coronary artery disease. Also, if hypotension were the etiology of this patient's ischemia, one would expect to see ST segment depression, as is commonly seen with subendocardial ischemia during exercise stress tests. The ST segment elevation on this patient's ECG and subsequent myocardial stunning were consistent with complete occlusion of an epicardial coronary artery due to either vasospasm or thrombosis. Given the lack of residual thrombus on angiography and the patient's prior history, vasospasm is most likely in this instance. Perioperative management should be altered in patients with prior cocaine use. alpha-Adrenergic agonists should be used cautiously. If ST segment elevation occurs, this represents threatening myocardial infarction, which should be treated with oxygen, sedation, aspirin, and nitroglycerin [10,19]. However, treatment differs from patients with acute coronary artery thrombosis. beta-Adrenergic blockade decreases infarct size and mortality in patients with acute thrombosis [20,21], but beta2-adrenergic blockade may result in worsening vasospasm and should be avoided in patients with cocaine-induced coronary spasm [22]. In patients presenting with an acute thrombotic myocardial infarction, calcium channel blockade worsens outcome and should be avoided [23]. However, calcium channel blockers [7,9] and alpha-adrenergic blockers [3] are potentially beneficial in cocaine-induced vasospasm. If ST segment elevation persists despite treatment with coronary vasodilators, vasospasm-induced thrombosis should be suspected, and catheterization with possible angioplasty or intracoronary vasodilators may be indicated [24,25]. Systemic thrombolytic therapy is an alternative to angioplasty [1,24-26]; however, thrombolytics are relatively contraindicated in patients who have undergone recent surgery due to the risk of severe bleeding complications. In conclusion, alpha-adrenergic agonists may precipitate coronary artery vasospasm in patients with prior cocaine use. If there is evidence of coronary artery spasm, initial treatment includes coronary artery dilators, such as nitroglycerin, calcium channel blockers, or alpha blockers. If evidence of myocardial injury or chest pain persists, emergent coronary artery angiography should be considered.