Guidance Offered on Cocaine-Related Chest Pain


Patients who present with cocaine-associated chest pain or myocardial infarction should be treated similarly to patients with traditional acute coronary syndromes, with some exceptions, according to Dr. Jim McCord and his associates on the American Heart Association's acute cardiac care committee.

The committee reviewed the literature and issued a scientific statement in the March 17 online version of Circulation, with the aim of guiding diagnostic and therapeutic interventions for this subset of patients with acute chest pain.

Chest pain related to cocaine use is rarely caused by myocardial infarction, which develops in only 2%–6% of cases.

Therefore, risk stratification using well-established criteria, including electrocardiographic changes and a positive cardiac troponin test, “is feasible and safe.” But cocaine use can cause rhabdomyolysis and attendant abnormalities in creatine kinase and myoglobin levels, so those diagnostic tests may not be useful, said Dr. McCord of Henry Ford Hospital, Detroit, and his associates.

“In the absence of ischemic ECG changes or positive cardiac markers, intermediate- and low-risk patients can be safely managed in a chest pain observation unit for 9–12 hours, which can obviate the need for hospital admission in the majority of these patients,” they added.

Unlike patients with acute coronary syndrome unrelated to cocaine use, those with cocaine-associated chest pain should receive benzodiazepines immediately to relieve the pain, improve hemodynamics, and manage any neuropsychiatric manifestations that may accompany cocaine toxicity.

Also in contrast to ACS patients, those with cocaine-associated chest pain who do not have definite cardiac involvement may not need direct treatment of any hypertension and tachycardia they exhibit. Resolution of their anxiety with a benzodiazepine will often resolve the hypertension and tachycardia as well. If it doesn't, these can be managed with sodium nitroprusside, nitroglycerin, or intravenous phentolamine, the committee statement said.

For the few patients whose cocaine-associated chest pain is caused by ST-segment elevation myocardial infarction, percutaneous coronary intervention clearly is preferable to fibrinolysis.

There are few data regarding the use of drug-eluting stents in this patient population. Because most of these patients continue to use cocaine, they may have poor compliance with any long-term antiplatelet regimens. “Therefore, we recommend very careful consideration of the probability of long-term compliance before a drug-eluting stent is used in cocaine-associated MI,” the committee said.

β-Blockers should not be given in STEMI precipitated by cocaine use, because it may exacerbate coronary spasm. Whether calcium channel blockers are beneficial in this patient population is uncertain at best. Therefore, they should not be given as first-line treatment but can be considered for patients who don't respond to benzodiazepines and nitroglycerin, Dr. McCord and his associates said (doi: 10.1161/circulationaha.107.188950).

Antiplatelet and antithrombin therapies haven't been well studied for cocaine-related chest pain, but they may be beneficial, because cocaine injures the vascular epithelium, raises platelet aggregation, and impairs normal fibrinolysis. “We recommend aspirin be routinely administered and unfractionated heparin or low-molecular-weight heparin be given… unless there is a contraindication,” they said.

Finally, recidivism is common, with 60% of patients in one study admitting to continued cocaine use 1 year after being hospitalized for chest pain.

“Preliminary data suggest that a combination of intensive group and individual drug counseling has the greatest impact on recurrent cocaine use,” so these approaches should be recommended to these patients, the AHA committee said.

Chest pain associated with cocaine use is rarely caused by myocardial infarction. ©PhotoDisc

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