Sudden cardiac death in acute coronary occlusion: potential roles of sino-atrial nodal artery and conus artery

Abstract An estimated 80% of sudden cardiac death (SCD) is due to coronary artery disease1. Ventricular arrhythmia (VA) is most commonly associated with LAD infarctions, likely due to the larger extent of affected myocardium, but non-LAD territory infarctions also present with VA. We propose two potential contributors, the sinoatrial nodal artery (SANa) and conus artery (CA). We retrospectively analyzed 2 cohorts of patients presenting with STEMI complicated by SCD due to VA, and whether these arteries were compromised in non-LAD territory STEMI, compared with uncomplicated STEMI. In the first, cohort A, we compared 127 consecutive STEMI patients presenting with cardiac arrest, with 100 uncomplicated STEMI. SANa and CA involvement was assessed in patients presenting with non-LAD territory STEMI. In the second, cohort B, we looked at patients presenting with inferior STEMI involving the RCA only, 20 complicated by aborted SCD due to VA compared with 24 uncomplicated patients. Cohort A (see table) showed a preponderance of single vessel and proximal LAD culprits in the arrest group and a significant number of non-LAD culprits. The extent and complexity of coronary disease and amount of myocardium at risk, reflected in SYNTAX and modified Jeopardy scores, were not significantly different between arrest and non-arrest groups. In those with RCA or Circumflex culprits, 77% in the Arrest group had the SANa arising from the culprit vessel, with only 33% of patients in the Control group, p<0.005. In cohort B, 70% of arrest and 21% of non-arrest patients had SANa involvement, p<0.005. In this cohort, we also observed that 74% of the arrest patients had CA involvement, compared with only 21% of Control patients, p<0.005. There were no significant differences in heart rate nor incidence of complete heart block and atrial arrhythmia in either cohort. There was significantly more ST elevation in standard leads V1-V2, suggesting RVOT ischemia, in those with aborted SCD and RCA culprit in both cohorts (cohort B: Arrests 85% vs non-arrest 21%, p<0.005. The SANa arises from the proximal RCA in 60% of people, and 40% from the left system. Transient ischemia leading to sinus bradycardia may not result in as marked QT prolongation compared with AV block at comparable heart rates, but in the ischemic environment, with hypotension provoking sympathetic upregulation, may lead to enough repolarization heterogeneity to induce VA. The CA arises from the RCA in 50% or more, and otherwise from the right coronary sinus, supplying the RVOT, a region prone to arrhythmogenesis, even in structurally normal hearts, more so if ischemic. Recognizing the potential role of these arterial branches in the VA mechanism would alert operators into preserving their patency. Transient disturbances may not translate into long term adverse outcomes, but whereas permanent damage to the SAN is more readily remedied, further study is needed to assess any long-term sequelae of RVOT infarction.