Discussion
We diagnosed our patient with coronary vasospasm given the visible
resolution of stenosis after intracoronary nitroglycerin. Our workup did
not reveal any evidence of coronary artery disease or structural heart
disease (Figure 4). A thromboembolic phenomenon would also be unlikely
since the patient was receiving therapeutic anticoagulation throughout
his hospitalization. Treatment modalities for coronary vasospasm after
diagnosis include nitrates or calcium blockers. However, our patient was
not a candidate for treatment due to his hemodynamic instability.
Coronary vasospasm is defined as a transient abnormal contraction of the
muscle layer of an epicardial coronary artery resulting in myocardial
ischemia [1]. Previous cases of ST-segment elevation have shown
normal coronary arteries on angiography [2]. In these cases,
transient coronary vasospasm should be considered as a cause of the
ST-elevation changes seen in COVID-19 patients. It is likely that
coronary vasospasm is more prevalent than currently reported in
COVID-19. However, most patients do not have the vasospasm captured on
cardiac catheterization. Although the pathogenesis is unclear, we
postulate that the severe inflammatory response due to COVID-19 may
contribute to endothelial dysfunction and provoking a pulseless
electrical activity arrest secondary to coronary vasospasm. Our theory
is supported by prior studies reporting that the release of inflammatory
mediators during hypersensitivity and anaphylactic reactions have been
implicated in inducing coronary vasospasm [3]. Hyperventilation is
also another cause of coronary vasospasm, and should be considered in
COVID-19 patients due to both respiratory distress and anxiety [4].