Abstract

A 43 year-old male was referred for pharmacological stress testing in 2010 in the setting of increasing dyspnea on exertion and atypical chest pain. He had been diagnosed with hypertrophic cardiomyopathy following a ventricular fibrillation arrest in 2004. At that time, he underwent a negative evaluation for coronary atherosclerosis and intracardiac defibrillator implantation, and had done well since. Upon regadenoson injection (0.4 mg over 10 s) he became tachycardic, diaphoretic, and complained of severe chest tightness. His ECG showed exaggeration of baseline abnormalities, non-specific for ischemia (Figs. 1, 2). He was given aminophylline (150 mg intravenous) with resolution of his symptoms. Myocardial imaging revealed a moderate to large-sized reversible defect involving the anteroseptal, anterior, and inferolateral walls, as well as stress-associated left ventricular dilation (Fig. 3). Subsequent coronary angiography was negative for significant coronary artery disease or anatomical coronary anomalies (Fig. 4). Adenosine and its analogs provoke coronary vasodilation via activation of A2A type adenosine receptors, and are useful as pharmacological stress agents by exploiting flow-reserve differences between normal and atherosclerotic coronary artery segments [1]. However, coronary vasospasm is a well-known occurrence of adenosine administration, and milder side effects are frequently encountered, likely related to the activation of non-A2A type receptors [2].

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