Cocaineinduced Ekg Changesthink Beyond Cardiac Cath

1Case Western Reserve UniversitySt. Vincent Charity Medical Center, Cleveland, OH
2Cleveland Clinic, Cleveland, OH

Meeting: Hospital Medicine 2012, April 1-4, San Diego, Calif.

Abstract number: 97908

Case Presentation:

A 67–year–old male presented to our emergency department complaining of typical chest pain few minutes after smoking cocaine. Pain was retrosternal and radiating to left shoulder associated with diaphoresis and nausea but no vomiting. On arrival, he continues to be in pain with stable vital signs. He was diaphoretic and distressed with normal cardiovascular exam. The remainder of exam was unremarkable. Initial EKG in the emergency department showed sinus tachycardia with no ischemic changes and cardiac markers were normal. Patient received benzodiazepine, sublingual nitroglycerine, aspirin, calcium channel blocker, and oxygen. Despite of all actions taken, chest pain persisted. Repeated EKG revealed new LBBB. En route to left heart catheterization (LHC), patient reported resolution of chest pain. EKG was repeated and showed resolution of LBBB. LHC was cancelled and patient was admitted to hospital. Elective cardiac catheterization was done later and it showed normal coronaries.

Discussion:

The potential of cocaine to induce coronary spasm has been demonstrated both in vitro and in vivo. In addition, thrombosis, platelets activation and hyper–aggregability after cocaine use have been suggested as another mechanism for heart ischemia. 90% cardiovascular events occur within the first 12 hours after cocaine ingestion. Both calcium channel blockers (CCB) and benzodiazepines should be included in the treatment for patients presented with cocaine induced–chest pain. CCB inhibits or reverse cocaine–induced vasoconstriction. On the other hand, benzodiazepines control psychomotor agitation, tachycardia, hypertension, hyperthermia and limit myocardial oxygen demands. The current ACC/AHA guidelines recommend immediate cardiac angiography for patients who present with chest pain and ST elevation or new LBBB irrespective of cocaine use. However, almost half of the patients have normal coronary angiograms without evidence of atherosclerotic disease. Furthermore, LHC in the sitting of cocaine abuse may lead to further worsening of coronary spasm in some cases and worsening of myocardial ischemia. We are reporting a case of a patient who presented with chest pain in the context of cocaine abuse with transient new LBBB that resolved with conservative treatments. Similar to our case, most patients with cocaine induced chest pain do well with a low incidence of cardiovascular complications.

Conclusions:

For hospitalists taking care of patients with cocaine–induced cardiac ischemia, this case emphasizes on the importance of frequent evaluation to avoid unnecessary and potentially harmful procedures. It also highlights the importance of essential medical treatment which should be applied in these cases.

Figure 1EKG illustrating the transient left bundle branch block due to cocaine–induced ischemia.

Figure 2Diagram shows the mechanism of cocaine–induced ischemia.

To cite this abstract:

Ibrahim A, Pradhan G, Shaheen K, Alraies M, Amro O. Cocaineinduced Ekg Changesthink Beyond Cardiac Cath. Abstract published at Hospital Medicine 2012, April 1-4, San Diego, Calif. Abstract 97908. Journal of Hospital Medicine. 2012; 7 (suppl 2). https://www.shmabstracts.com/abstract/cocaineinduced-ekg-changesthink-beyond-cardiac-cath/. Accessed November 15, 2019.

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