Case Presentation: A 56 year old man presented to the emergency department with sudden onset of severe chest pain that radiated to his back. He had an initial HR of 72 and BP of 208/114. CT angiogram of the chest and abdomen revealed a large type B aortic dissection (AD). The patient was treated with continuous infusions of esmolol and nitroprusside (NTP). His pain and hypertension resolved, and he was admitted for further medical management.

Over the next few days, labetalol was added and aggressively uptitrated in order to wean esmolol and NTP. Shortly after NTP was discontinued, the patient complained of dizziness. On exam, his HR was in the 40s, his BP was undetectable by the non-invasive monitor, and he appeared somnolent. Telemetry captured the rhythm in Figure 1a. Given concern for symptomatic bradycardia, the patient was treated with atropine, and within minutes, his HR, BP, and EKG normalized.

A few minutes later, the patient once again became somnolent and bradycardic to the 40s. His EKG is shown in Figure 1b. This time, coronary artery vasospasm (CAV) was suspected, and the patient was treated with an infusion of nitroglycerin. His symptoms resolved, and he was subsequently transitioned to an oral BP regimen, which included a long-acting nitrate. He had no additional recurrences of CAV.

Discussion: Hemodynamic instability in a patient with type B AD should prompt a search for complications, such as rupture and retrograde extension. In this case, EKGs showed atrioventricular dissociation and tall inferior ST elevations, which were initially misidentified as a wide complex bradycardia. These findings could be caused by retrograde involvement of the aortic valve and coronary ostia, rare but disastrous sequelae of AD. However, in this case, their transient nature is best explained by vasospasm of the right coronary artery.

CAV in AD has been previously reported. The pathogenesis is not understood, but possible mechanisms include vasoactive effects of the breakdown products of blood within the false lumen and imbalance of α1 and β2 adrenergic stimulation of vascular smooth muscle caused by non-selective β blockers. Given the striking juxtaposition of events in this case, we theorize that rebound vasoconstriction due to NTP withdrawal was another contributing factor. Treating the patient with a more prolonged course of nitrodilator therapy prevented further episodes of CAV.

Conclusions: Most serious complications of AD require prompt surgical management; however, clinicians should also consider CAV in patients with new chest pain, symptoms of hypoperfusion, or ischemic EKG changes. In addition, the common practice of simultaneously uptitrating β blockers while tapering NTP may increase the risk of CAV, and this area may benefit from further study.