Subramanian Senthilkumaran1, Suresh S David2, Narendra Nath Jena3, Ritesh G Menezes4, Ponniah Thirumalaikolundusubramanian5. 1. Department of Emergency and Critical Care Medicine, Sri Gokulam Hospitals and Research Institute, Salem, Tamil Nadu, India. 2. Department of Emergency Medicine, Christian Medical College and Hospital, Vellore, Tamil Nadu, India. 3. Department of Emergency Medicine, Meenakshi Mission Hospital and Research Centre, Madurai, Tamil Nadu, India. 4. Department of Forensic Medicine and Toxicology, Employees State Insurance Corporation Medical College and Post Graduates Institute of Medical Science and Research, Bangalore, Karnataka, India. 5. Department of Internal medicine, Chennai Medical College and Research Center, Irungalur, Trichy, Tamil Nadu, India.
Sir,The article by Sarkar et al.,[1] is indeed interesting and timely as practitioners and emergency physicians have started seeing cases of cocaine intoxication in India. However, a few aspects of this paper require contemplation. The authors have administered thrombolytic agent initially for cocaine associated myocardial infraction (CAMI) which is not congruent with current evidence.[2] Current literature questions the routine use of thrombolytic therapy for patients with CAMI and there are reports of severe complications associated with thrombolytics in cocaine users.[3] The frequent presence of contraindications to thrombolysis, including severe hypertension, seizures, intracerebral hemorrhage, and aortic dissection in cocaine abusers precludes the liberal use of thrombolytic agents. Moreover, the standard electrocardiographic criteria (ST elevation) for thrombolytic therapy is hampered by the high rate of abnormal or nondiagnostic electrocardiogram (ECG)'s in patients presenting with cocaine associated chest pain. The guidelines issued by American College of Cardiology and American Heart Association[4] advocate the use of thrombolytic therapy in CAMI only if ST segments remain elevated despite nitroglycerin and calcium antagonists and coronary angiography is not possible.Secondly, the recent cocaine use can alter the specificity of cardiac biomarkers and making them difficult to interpret in CAMI, especially the serum creatinine kinase level is not a reliable indicator of myocardial injury and is increased in almost half of cocaine users irrespective of concurrent MI possibly because of cocaine-induced hyperthermia, increased skeletal muscle activity, and rhabdomyolysis.[5] The awareness of reliability of cardiac biomarkers in cocaine associated chest pain is warranted for effective management. The American Heart Association recommends nitroglycerin and benzodiazepines as first-line agents for cocaine associated chest pain. Benzodiazepines are administrated especially in cocaine-addictedpatients with associated hypertension, tachycardia, or anxiety after the cocaine use. Intuitively, dexmedetomidine, a central sympatholytic agent is highly effective in reversing the cocaine's sympathomimetic actions.[6] Substance abuse remains one of the major public health issues across the globe, despite health education on prevention; the incidence of illicit substances is escalating. Since many patients with cocaine toxicity will present with chest pain to the emergency department, it is essential that these patients be recognized early and managed appropriately to prevent complications.
Authors: James McCord; Hani Jneid; Judd E Hollander; James A de Lemos; Bojan Cercek; Priscilla Hsue; W Brian Gibler; E Magnus Ohman; Barbara Drew; George Philippides; L Kristin Newby Journal: Circulation Date: 2008-03-17 Impact factor: 29.690