Right ventricular infarction complicates 50% of acute inferior STEMI cases and causes severe hemodynamic compromise, though reperfusion facilitates recovery due to the RV's resistance to infarction.
Right ventricular infarction requires specific management strategies due to its unique pathophysiology, including reperfusion and potentially mechanical circulatory support for persistent hemodynamic compromise.
Right ventricular infarction (RVI) complicates 50% of cases of acute inferior ST-segment elevation myocardial infarction, and is associated with high in-hospital morbidity and mortality. Ischemic right ventricular (RV) systolic dysfunction decreases left ventricular preload delivery, resulting in low-output hypotension with clear lungs, and disproportionate right heart failure. RV systolic performance is generated by left ventricular contractile contributions mediated by the septum. Augmented right atrial contraction optimizes RV performance, whereas very proximal occlusions induce right atrial ischemia exacerbating hemodynamic compromise. RVI is associated with vagal mediated bradyarrhythmias, both during acute occlusion and abruptly with reperfusion. The ischemic dilated RV is also prone to malignant ventricular arrhythmias. Nevertheless, RV is remarkably resistant to infarction. Reperfusion facilitates RV recovery, even after prolonged occlusion and in patients with severe shock. However, in some cases hemodynamic compromise persists, necessitating pharmacological and mechanical circulatory support with dedicated RV assist devices as a "bridge to recovery."
Goldstein et al. (Mon,) conducted a review in Right ventricular infarction complicating acute inferior ST-segment elevation myocardial infarction. Right ventricular infarction complicates 50% of acute inferior STEMI cases and causes severe hemodynamic compromise, though reperfusion facilitates recovery due to the RV's resistance to infarction.