Isolated resting perfusion defect in a pediatric patient with acute cocaine ingestion (QF_TH_064)

A 3-year-old previously-healthy boy was referred to our cardiac ICU due to V-fib arrest of unclear etiology. He had been complaining of chest pain after being picked up from a friend’s house and subsequently experienced loss of consciousness and apnea. He received CPR from his mother and by EMS, who  cardioverted for V-fib, and ROSC was achieved. High sensitivity troponin I was elevated to 4757 ng/l and pro-BNP elevated to 1757 pg/ml Electrocardiogram demonstrated non-specific ST changes. Echocardiogram demonstrated normal left ventricular ejection fraction of 65% and no obvious wall motion abnormality. Urine toxicology was positive for cocaine metabolites,  which was presumed to be the cause of his arrest. Cardiac MRI was obtained to rule out other underlying pathologies. He subsequently recovered with no subsequent arrhythmia and was discharged to the care of a family member. He has not yet undergone follow-up cardiac MRI.

Diagnostic Techniques and Their Most Important Findings: Cardiac MRI was performed on a 1.5-T scanner about 36-48 hours after the ingestion event. The patient was sedated and intubated with positive-pressure ventilation. Standard cine steady-state free procession (SSFP) sequences were obtained in the ventricular short axis and horizontal and vertical long axes for assessment of ventricular volume and function. Native T1 and T2 maps were obtained in three short-axis slices with a motion correction technique. Resting first-pass perfusion images were obtained after injection of ~0.2 mmol/kg of gadolinium contrast. Short-axis LGE images were obtained 10-20 minutes after contrast injection using a single-shot SSFP technique. Additionally, gray-blood LGE images were obtained by adjusting inversion time to null the blood pool rather than viable myocardium.  Findings included a first-pass perfusion defect in the mid-ventricular anterior, anteroseptal, and anterolateral left ventricular subendocardial myocardium, including the anterolateral papillary muscle, corresponding to left anterior descending coronary distribution (Fig. 1). There was no corresponding change in native T1 or T2 time in the affected area and no evidence of fibrosis on standard or gray-blood LGE imaging (Figs, 2, 3). Left ventricular ejection fraction was mildly decreased at 52% with no apparent regional wall-motion abnormality.

Learning Points from this Case: Cardiovascular effects of acute and chronic cocaine use have been well-described in adults and include coronary vasospasm, myocarditis, catecholamine-induced acute cardiomyopathy, and chronic cardiomyopathy with abnormal myocardial strain and LGE. Our patient demonstrated a resting perfusion defect corresponding to a coronary territory, suspicious for cocaine-induced vasospasm, with no evidence of myocarditis or myocardial tissue abnormalities. This perfusion defect was present over 36 hours following the time of ingestion, consistent with reports in adult patients of cocaine-related myocardial infarction occurring days following ingestion due to the presence of circulating cocaine metabolites.