Coronary Vasospasm While Treating Supraventricular Tachycardia: Is Adenosine Really to Blame?

Abstract

Coronary artery spasm has been reported during adenosine stress testing. Herein, we describe a transient ST-segment elevation following adenosine therapy for supraventricular tachycardia. A 38-year-old male presented to the emergency department with palpitations. Electrocardiogram showed supraventricular tachycardia with short RP interval. Vagal maneuvers were unsuccessful. Adenosine was then administered in two successive injections of 6 and 12 mg dosages, respectively. A subsequent 12-lead electrocardiogram revealed ST-segment elevation in inferior leads with reciprocal changes. Coronary angiography disclosed nonobstructive coronary disease. A postprocedure electrocardiogram exhibited normal sinus rhythm with nonspecific T wave abnormalities. Cardiac biomarkers were elevated with a peak troponin I of 0.32. Echocardiogram depicted bicuspid aortic valve and normal systolic function. Electrophysiological study revealed a concealed left accessory pathway and successful radiofrequency ablation was performed. Given the dynamic changes in the electrocardiogram, we hypothesize that this event was most likely a coronary vasospasm. The mechanism of coronary spasm following adenosine injection remains uncertain. Potential mediators include KATP channels and adenosine-2 receptors.

Torsades de pointes and myocardial infarction following reversal of supraventricular tachycardia with adenosine: a case report

“…( 19 ) There are two reports of vasospasm caused by adenosine during the treatment of supraventricular tachycardia. ( 20 , 21 )…”

“…(19) There are two reports of vasospasm caused by adenosine during the treatment of supraventricular tachycardia. (20,21) There are some possible explanations for adenosineinduced vasospasm. Four adenosine receptors have been identified: A1, A2A, A2B, and A3.…”

Incessant ventricular tachycardia

“…The inferior ST elevation revealed in the two QRS complexes after the shock, together with the significant rise in troponin and the vasospasm depicted on angiography favour myocardial ischaemia and not a post cardioversion status [ 2 ]. The incessant character of the VT, the persistence of ST elevation and coronary vasospasm for more than just a few minutes after adenosine infusion and reversion following administration of nitrate may suggest a coronary hypersensitivity prone to develop spasm [ 3 ], such as Prinzmetal angina. Sympathetic nervous system activation is able to induce ventricular arrhythmia and coronary spasm by catecholamine release secondary to the pain triggered by the withdrawing of the transseptal sheath from the groin.…”