“Spasms in Silence”: A case of coronary vasospasm‐induced ventricular fibrillation

A 56-year-old man presented following an aborted cardiac arrest. His initial ECGs showed episodes of transient repolarization abnormalities. Coronary vasospasm can be a precipitant for ventricular arrhythmia in these patients, underpinning the importance of continuous ECG for accurate diagnosis and management. A 56-year-old man presented after an aborted out-of-hospital cardiac arrest. The patient was well before the event, with no reported symptoms of chest pain, palpitations, presyncope, or syncope. His presenting ECG showed episodes of transient repolarization abnormalities (Figure 1). ECGs (Figure 2) and continuous telemetry monitoring (Figure 3), during in-hospital, revealed a Shark fin sign ST-segment elevation commonly associated with multivessel coronary vasospasm,1 with an initiating premature ventricular complex at 600 ms and runs of nonsustained polymorphic ventricular tachycardia. The patient had no significant background history or family history of sudden cardiac death. Workup including a toxicology screen, trans-thoracic echocardiogram, cardiac MR, and procainamide challenge were all normal. A coronary angiography, which was performed demonstrated the absence of flow-limiting coronary artery disease, however on several coronary injections, showed slow distal flow and raised the possibility of vasospasm. We did not perform provocation testing to confirm the diagnosis, given the lack of intracoronary ergonovine or acetylcholine and the associated complications of repeated ventricular fibrillation in our patient who had full neurological recovery.2 The presumptive diagnosis was coronary vasospasm resulting in ventricular fibrillation. Treatment was commenced with a nitro-glycerine patch and oral calcium channel blockers (CCB). Given his presentation, we elected to implant a subcutaneous defibrillation for secondary prevention. 9-months postdischarge, he has remained free of recurrent ventricular arrhythmia with a similar ECG as the initial presentation (Figure 4). Additionally, given the possibility of early repolarization syndrome, he underwent a broad sudden death genetic panel, which did not reveal any pathologic genetic abnormalities. Coronary vasospasm has been reported as the precipitant for ventricular arrhythmia in 7% of patients who suffered an aborted out-of-hospital cardiac arrest.3 The exact mechanism of coronary artery vasospasm is not fully understood; however, several theories have been elucidated. Vascular smooth muscle hyper-reactivity secondary to Ca2+-mediated myosin light-chain phosphorylation, nitric oxide deficiency because of endothelial dysfunction, oxidative stress, and lifestyle factors, such as smoking, have been implicated. The risk of recurrent arrhythmia in this population is unclear. A prior paper has quoted an annual incidence of sudden death of 6% in patients with coronary vasospasm associated with VF,3 and experts have suggested that an ICD implantation may be reasonable.4 To date, there have been no randomized controlled trials comparing ICD and medical therapy with medical therapy alone in survivors of sudden death presumed to be because of coronary vasospasm. Though rare, coronary vasospasm can result in fatal ventricular arrhythmias, and patients should be assessed for recurrence and risk of sudden death. In a recent study of 34 patients with inferolateral J point elevation, 38% of patients were asymptomatic preceding a VF event and were deemed to have a silent coronary artery vasospasm,5 and this might be the case in our patient. Our case highlights that vasospasm may occur in the absence of symptoms and demonstrates the utility of continuous ECG monitoring to assist in the diagnosis of this phenomenon. Although CCB can reduce the risk of recurrence of episodes, it does not eliminate the risk of ventricular arrhythmia, as such in high-risk patients, an implantable defibrillator may be appropriate. Authors declare no conflict of interests for this article.