Man With Chest Pain After Cocaine Use
A 53-year-old man presents to the emergency department (ED) with chest pain that started the previous night. The pain began about 30 minutes after he had smoked marijuana and inhaled cocaine. He describes the pain as tightness in the left side of the chest that radiates into the neck; he also has a tingling sensation in both the left side of the neck and the left arm.
Initially, the pain was accompanied by mild dyspnea and light-headedness but was not associated with palpitations, nausea, or vomiting. After the patient rested, the pain subsided somewhat and he was able to fall asleep for several hours; however, when he awakened, it was still present. Two sublingual nitroglycerin tablets administered on his arrival at the ED relieved his chest discomfort.
HISTORY
The patient denies a history of similar episodes. He had formerly used cocaine on the weekends, but he insists that he has not done so for 18 months as a condition of his employment.
He has a 10-year history of hypertension and takes nifedipine (sustained-release), 60 mg/d. There is a strong family history of coronary disease: his mother died in her 50s of an acute myocardial infarction (MI), and his sister sustained an acute MI at about the same age. He uses alcohol on weekends but has never smoked cigarettes.
PHYSICAL EXAMINATION
The patient is anxious, has a headache, and is still having episodes of chest pressure, although they are much less intense. Heart rate is 58 beats per minute; respiration rate, 18 breaths per minute; and blood pressure, 149/82 mm Hg. Oxygen saturation is 97% on room air. Heart examination reveals regular heart rate and rhythm without murmurs or gallops. There are no carotid bruits, and the chest is clear. Peripheral pulses are good; no edema.
LABORATORY AND IMAGING RESULTS
Electrolyte levels, biochemistry panels, and a hemogram are normal. Myoglobin level is 101 ng/mL, and cardiac troponin I level is normal at 0.1 ng/mL. Creatine kinase is 681 U/L (normal is less than 200 U/L), but MB fraction is 1% (normal). An ECG shows a PR interval of 0.28 seconds, complete right bundle branch block (RBBB), and Q waves in the initial deflections of leads II, III, and aVF. T waves are upright in II, III, and aVF and inverted in the precordial leads.
Which of the following is the most appropriate management strategy for this patient?
A. Reassure the patient that the chest pain is cocaine-related and will improve in the next several hours and discharge him with a supply of nitroglycerin.
B. Retain the patient in the hospital’s 23-hour chest pain observation unit to rule out MI; use nitroglycerin and verapamil as needed.
C. Retain the patient in the hospital’s 23-hour chest pain observation unit to rule out MI; use nitroglycerin and propranolol as needed.
D. Retain the patient in the hospital’s 23-hour chest pain observation unit to rule out MI, use nitroglycerin and verapamil as needed, and evaluate for underlying coronary artery disease (CAD).
What's Your Diagnosis?
CORRECT ANSWER: D
Cocaine-related myocardial ischemia and infarction have been reported frequently in the literature. The relative risk of acute MI during the hour after cocaine use exceeds 20, even in persons who are otherwise at low risk. This risk is independent of the amount of cocaine ingested, the route of administration, and frequency of use.1
Typically, in patients with cocaine-related myocardial ischemia, infarction cannot be ruled out by traditional clinical findings, such as pain quality, duration of pain, and risk factors. However, this patient’s age and highly abnormal ECG findings may set him apart.
ST-segment elevation is usually associated with cocaine- related ischemia. This ECG change occurs in up to 43% of patients who have chest pain following cocaine use—whether or not they sustain an acute MI.2 This patient’s ECG pattern of first-degree heart block and complete RBBB is less typical of cocaine-related myocardial ischemia; these ECG findings—particularly complete RBBB—were recently shown to be important markers of significant underlying heart disease.3
Thus, most authorities would agree that a patient such as this man is at heightened risk for a subsequent ischemic event; in addition to ruling out acute MI and treating the cocaine-induced ischemia symptomatically, an evaluation for CAD is recommended (choice D).
Choice A does not represent an adequate strategy for 2 reasons. First, at least 6% of patients who present with cocaine-induced ischemia exhibit enzymatic evidence of acute MI2; however, at least half of the patients with acute MI do not have coronary atherosclerosis. Second, the time interval during which complications (eg, ventricular arrhythmias, congestive heart failure, or death) are likely to occur is about 12 hours from initial presentation. Thus, the patient should be under medical observation for at least that long.
Cocaine causes marked vasoconstriction of coronary arteries, primarily by stimulation of α-adrenergic receptors. 4 β-Adrenergic antagonists, such as propranolol, have been shown to potentiate this vasoconstriction; thus, these drugs are contraindicated in cocaine-related chest pain.5 The use of β-blockers in a patient with the ECG abnormalities seen here (ie, bifascicular block—complete RBBB and first-degree atrioventricular block) is also problematic. Thus, choice C is incorrect.
Choice B, which includes observation of the patient for an adequate period to exclude acute MI and the use of 2 agents (nitroglycerin and verapamil) that are well-known to reverse cocaine-induced vasoconstriction of coronary arteries and hypertension, is a sound diagnostic and therapeutic strategy for many patients with cocaine-related chest pain. However, this patient’s ECG and, to a lesser extent, his age suggest a substantial risk of underlying CAD. Thus, in this case it is necessary to be more aggressive diagnostically. This patient would be a good candidate for further study regardless of his ischemic symptoms.
Outcome of this case. Acute MI was excluded by standard criteria. A stress thallium study revealed a fixed defect inferiorly and a reversible defect laterally. The patient was referred for cardiac catheterization for definitive diagnosis and therapy.