Hiren Patel has completed his MD at the age 25 from Avalon University School of Medicine and is currently a PGY-2 Internal Medicine resident at Baton Rouge General, an affiliate of Tulane University School of Medicine, in Baton Rouge, Louisiana. He has an interest to pursue a cardiology fellowship post-residency.
Cocaine abuse has been associated with multiple cardiovascular events including myocardial ischemia and infarction commonly due to coronary vasospasms, thrombo-occlusion and systemic hypertension. Spontaneous non-traumatic coronary artery dissections are rare but well documented occurrence in cocaine-abusers, and only a few cases have been reported in the literature. We present a case of cocaine-induced coronary artery aneurysm (CAA) and spontaneous coronary artery dissection (SCAD) in a post-menopausal woman with a non-ST elevation myocardial infarction. A 62-year-old African-American female with previous history of coronary artery disease, hypertension, and tobacco-abuse presented with an acute onset of sharp chest pain radiating to the left arm with palpitations. She admitted using “crack” cocaine within hours prior to symptom onset. Electrocardiogram revealed lateral lead T-wave inversions. Troponin was 20.8 ng/mL. Immediate coronary angiography under optical coherence tomography (OCT) guidance revealed 99% mid-segment dissection of the first obtuse marginal branch by presence of a double-lumen with superimposed thrombi. After balloon angioplasty and stent placement, the OCT confirmed disappearance of the double-lumen. The proximal right coronary artery had an aneurysm with intraluminal filling defect with normal distal blood flow and no significant obstructive disease, therefor no interventions were undertaken. The use of cocaine preceding the SCAD leads to a likely association between the two events. Prior studies have found increased prevalence of CAA, and association of SCAD as a potential rare complication of cocaine abuse. The proposed mechanism of injury appears to be multi-factorial predominantly related to cocaine’s adrenergic properties. Cocaine-associated acute coronary syndromes should not be overlooked as transient vasospasms and that immediate coronary angiography may be needed instead of medical management to evaluate for life-threatening complications such as CAA and SCAD. This case illustrates the successful management of cocaine-induced SCAD with immediate PCI under OCT guidance.
Martin Binesh has completed his MD from American University of Caribbean and is currently a PGY-1 Internal Medicine resident at Baton Rouge General, an affiliate of Tulane University School of Medicine, in Baton Rouge, Louisiana. Has a future goal to pursue a cardiology fellowship.
Troponin elevation with non-obstructive coronary arteries in setting of demand myocardial ischemia is defined as Type 2 non-ST elevation myocardial infarction (NSTEMI). Degree of troponin elevation in such setting is not often studied. We present a case where an unusually high troponin elevation was observed in a patient with a Type 2 NSTEMI. 73-year-old male with a previous history of tobacco abuse, HTN, and coronary artery disease with stent placement 7 months prior admitted with atypical chest pain. Admission vitals included a blood pressure of 211/142 and a heart rate of 120. Physical exam was unremarkable. Electrocardiogram showed sinus tachycardia with no ST changes. Initial troponin was 0.46ng/ml and peaked at 197.7ng/ml within 12 hours. Transthoracic echocardiogram showed severe left ventricular hypertrophy, normal systolic and diastolic function with no wall motion abnormalities. Subsequent coronary angiography revealed non-obstructive epicardial arteries and a patent prior stent. With optimal blood pressure and heart rate control, the patient became asymptomatic and the troponins continued to trend down. Given the above patient’s presentation, non-obstructive epicardial arteries, and normal echocardiographic findings, we concluded that hypertensive emergency likely caused a Type 2 NSTEMI. Often with demand myocardial ischemia, such high troponins as noted in this case are not typically observed. Previous studies report with a troponin >100ng/ml suggest a large myocardial infarction with poor prognosis, which is not the case in this patient. We hypothesize that this patient’s large left ventricular myocardial mass from hypertrophy could have lead to a more than usual troponin leak in setting of a Type 2 NSTEMI. Thorough literature search on PubMed did not yield any similar cases. This case promotes the need for more studies to evaluate the relation of left ventricular mass to the degree of troponin elevation in setting of acute coronary syndromes.