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See Videos 1 and 3
Cocaine-Induced Coronary Artery Vasospasm.
A 58-year-old woman presented to the emergency department with intermittent, nonexertional chest pain of 2 days’ duration, with each episode lasting 15 minutes. The pain was relieved by sublingual nitroglycerin and acetaminophen with hydrocodone. Her medical history was notable for tobacco and alcohol use, hypertension, and hyperlipidemia. She had been admitted for similar symptoms 2 months earlier, at which time a coronary angiogram revealed normal coronary anatomy (Video 1). She was discharged home with a diagnosis of pericarditis, and treatment with colchicine and ibuprofen was started. Electrocardiography performed during her more recent visit revealed anterior T-wave inversions (Panel A), which had also been observed during her previous visit. Her initial troponin I level was 0.04 ng per milliliter (reference range, 0 to 0.03 ng per milliliter); it rose to 5.7 ng per milliliter at 6 hours and peaked at 6.4 ng per milliliter before falling to 0.71 ng per milliliter. A transthoracic echocardiogram (Video 2) revealed a pericardial effusion that was small to moderate in size, normal ventricular function, and no abnormalities in wall motion. She was admitted to the hospital with a diagnosis of myopericarditis and was treated with oral glucocorticoids; her symptoms resolved.
On hospital day 3, she had a cardiopulmonary arrest (ventricular fibrillation). After she received advanced cardiopulmonary life support for 5 minutes, spontaneous circulation returned. An electrocardiogram obtained after her circulation returned revealed ST-segment elevation of 2 mm in the anteroseptal lead and ST-segment depression of 1 to 2 mm in the lateral and inferior leads (Panel B). Emergency coronary angiography (Video 3) revealed severe coronary spasm involving the left main, left anterior descending, and circumflex arteries (Thrombolysis in Myocardial Infarction [TIMI] flow of 1). The spasm was reversed on administration of intracoronary nitroglycerin (TIMI flow of 3) (Video 4). A urine toxicology test was performed, and the results were positive for cocaine. It appears that this patient used cocaine during hospitalization, which led to active coronary spasm. The patient died from complications of myocardial infarction.
Nureddin Almaddah, M.D.
Tokunbo O. Ajayi, M.D.
North Shore Medical Center, Salem, MA
nalmaddah@partners.org
http://www.nejm.org/doi/full/10.1056/NEJMicm1503339?query=featured_cardiology
Cocaine-Induced Coronary Artery Vasospasm.
A 58-year-old woman presented to the emergency department with intermittent, nonexertional chest pain of 2 days’ duration, with each episode lasting 15 minutes. The pain was relieved by sublingual nitroglycerin and acetaminophen with hydrocodone. Her medical history was notable for tobacco and alcohol use, hypertension, and hyperlipidemia. She had been admitted for similar symptoms 2 months earlier, at which time a coronary angiogram revealed normal coronary anatomy (Video 1). She was discharged home with a diagnosis of pericarditis, and treatment with colchicine and ibuprofen was started. Electrocardiography performed during her more recent visit revealed anterior T-wave inversions (Panel A), which had also been observed during her previous visit. Her initial troponin I level was 0.04 ng per milliliter (reference range, 0 to 0.03 ng per milliliter); it rose to 5.7 ng per milliliter at 6 hours and peaked at 6.4 ng per milliliter before falling to 0.71 ng per milliliter. A transthoracic echocardiogram (Video 2) revealed a pericardial effusion that was small to moderate in size, normal ventricular function, and no abnormalities in wall motion. She was admitted to the hospital with a diagnosis of myopericarditis and was treated with oral glucocorticoids; her symptoms resolved.
On hospital day 3, she had a cardiopulmonary arrest (ventricular fibrillation). After she received advanced cardiopulmonary life support for 5 minutes, spontaneous circulation returned. An electrocardiogram obtained after her circulation returned revealed ST-segment elevation of 2 mm in the anteroseptal lead and ST-segment depression of 1 to 2 mm in the lateral and inferior leads (Panel B). Emergency coronary angiography (Video 3) revealed severe coronary spasm involving the left main, left anterior descending, and circumflex arteries (Thrombolysis in Myocardial Infarction [TIMI] flow of 1). The spasm was reversed on administration of intracoronary nitroglycerin (TIMI flow of 3) (Video 4). A urine toxicology test was performed, and the results were positive for cocaine. It appears that this patient used cocaine during hospitalization, which led to active coronary spasm. The patient died from complications of myocardial infarction.
Nureddin Almaddah, M.D.
Tokunbo O. Ajayi, M.D.
North Shore Medical Center, Salem, MA
nalmaddah@partners.org
http://www.nejm.org/doi/full/10.1056/NEJMicm1503339?query=featured_cardiology
