How significant is the cardiomyopathy associated with cocaine use?

The link between cocaine and the development of cardiomyopathy has been supported by animal studies that show the drug’s depressant effect on cardiac function. Acute as well as chronic left ventricular dilatation and dysfunction may lead to significantly depressed cardiac function. Other causes of cardiomyopathy should be ruled out, (e.g., ischemia, cardiomyopathy associated with acquired immunodeficiency syndrome [AIDS]). Patients may present with significant cardiomyopathy and heart failure, in a large study at the University of Colorado, 13% of a young population (mean age: 36 years) of cocaine users had left ventricular dysfunction or ejection fraction 50%.

With symptoms of shortness of breath and fatigue, the diagnosis may be missed. All cocaine users with symptoms suggestive of congestive heart failure should be elevated by echocardiogram for cocaine-induced cardiomyopathy. In a significant number of patients (7%, according to one study) asymptomatic cardiomyopathy may promote arrhythmias.

What electrophysiologic abnormalities are seen in cocaine users?

Cocaine blocks the fast sodium channels in the myocardium, thus producing a depression of depolarization and a slowing of conduction velocity. The refractoriness of the atrial and ventricular muscle is also prolonged. Cocaine is similar in its electrophysiologic properties to class 1 antiarrhythmic agents, and QT prolongation and ventricular arrhythmias, including torsade de pointes, occur. Transient heart block of the second and third degrees also has been reported. Heart block as well as arrhythmias may respond to correction of acidosis, hypokalemia, and hypomagnesemia.

What ECG changes are seen in cocaine users?

A study of cocaine users presenting to the emergency department (ED) found significant ECG abnormalities in 50% of patients. The major abnormalities included prolonged PR, QRS, and QT intervals (with an increase in atrial and ventricular refractoriness), tachycardias or bradycardias, increased QRS voltage, poor R wave progression, nonspecific ST-T wave changes, early repolarization, and ST elevation (with possible ischemia), and ventricular and atrial arrhythmias. Another study of asymptomatic cocaine users found abnormal ECGs in up to 29%. During the first weeks of withdrawal cocaine abusers frequently develop silent myocardial ischemia, manifested as ST elevation, during ambulatory ECG monitoring. These changes were believed to be associated with coronary vasospasm.

How should patients with cocaine-induced chest pain be evaluated? Should they be admitted to the hospital?

The etiology of chest pain after cocaine use is most likely multifactoral, myocardial ischemia, infarction, and aortic dissection must not be overlooked. Chest radiographs should be considered to rule out cocaine-induced pneumomediastinum, pneumothorax, and widened mediastinum. Prompt EKG is important to evaluate patients with ischemia because of the common occurrence of early repolarization. The creatinine kinase level may be elevated as a result of rhabdomyolysis; although the pattern is different from that in acute MI, the distinction is not helpful in the ED. In one study, angina was ruled out in 101 consecutive cocaine users presenting to the ED with suggestive chest pain, but there was no work-up for cardiac risk. Another study looked at risk stratification in cocaine users (mean age: 37 years) presenting with chest pain and found a significant amount of coronary artery disease (40% with 70% stenosis and 21% with 70% stenosis). Young cocaine users, therefore, seem to be predisposed to myocardial ischemia, coronary artery disease, or infarction. As a result, many authors recommend admission of cocaine users who present with typical or atypical chest pain to a coronary care unit or monitored bed if infarction is suspected. Even hours after cocaine use, coronary spasm and arrhythmias may occur.

Is endocarditis frequently seen in cocaine users?

Yes. Intravenous cocaine abuse has strong association with endocarditis; Staphylococcus aureus is the most commonly isolated organism. Unfortunately, because the staphylococci may be resistant, drug sensitivity must be established. Moreover, rare organisms may be the culprit. In intravenous users, the tricuspid valve is more commonly involved in the endocarditis, patients are prone to develop paravalvular abscess, which may require transesophageal echocardiography.

Which arrhythmias are most commonly seen with cocaine abuse?

The most common arrhythmias are tachycardia and premature ventricular beats, which are usually transient and do not require treatment. Cocaine-induced supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation are also seen; management depends on etiology and hemodynamic status of the patient. The underlying problems may be myocardial infarction or ischemia, QT interval prolongation, reperfusion after coronary spasm, or electrolyte imbalance. Bradycardia also has been reported in the absence of infarction, but it is transient.

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