title: Left ventricular systolic dysfunction is associated with adverse outcomes in acute right ventricular infarction.
abstract: BACKGROUND
  In patients with acute right ventricular infarction (RVI), global right ventricular (RV) performance is dependent on compensatory left ventricular (LV)-septal contractile contributions. This study was designed to assess the influence of depressed left ventricular ejection fraction (LVEF) on hemodynamics and clinical outcomes in patients with RVI.
  
  
  RESULTS
  We retrospectively identified 338 patients with acute inferior ST elevation myocardial infarction (STEMI) undergoing a primary percutaneous coronary intervention. RVI was determined echocardiographically by right ventricular free wall motion abnormalities and depressed global RV performance (fractional area change); LV function was similarly calculated. RVI was documented in 185 (55%) cases. Compared with those with inferior myocardial infarction alone, patients with RVI suffered more hemodynamic compromise (need for inotropes or vasopressors 39 vs. 15%, P<0.0001, and intra-aortic balloon pump 32 vs. 13%, P<0.0001) and higher in-hospital mortality (14 vs. 3%, P=0.0006). In cases without RVI, the status of LV function did not influence in-hospital mortality (ejection fraction≤40%=7.3% vs. ejection fraction>40%=1.8, P=0.12). In contrast, in patients with RVI, LVEF was an important determinant of outcome: those with LVEF ≤ 40% suffered more hemodynamic compromise (need for inotropes or vasopressors 63 vs. 30%, P<0.0001, and intra-aortic balloon pump 59 vs. 22%, P<0.0001) and had markedly higher in-hospital mortality (33 vs. 7%, P<0.0001).
  
  
  CONCLUSIONS
  In patients with acute inferior myocardial infarction complicated by RVI, depressed LVEF is associated with greater hemodynamic compromise and higher in-hospital mortality. These findings may have clinical implications for supportive efforts in such cases.
authors.affiliation: aDepartment of Cardiovascular Medicine, Beaumont Health System, Royal Oak bHurley Medical System, Flint, Michigan, USA.
authors.forename: James A
authors.initials: JA
authors.lastname: Goldstein
authors.forename: Naga
authors.initials: N
authors.lastname: Kommuri
authors.forename: Simon R
authors.initials: SR
authors.lastname: Dixon
mesh_terms: D000368:Aged; D002316:Cardiotonic Agents / Q000627:therapeutic use; D016208:Databases, Factual; D004452:Echocardiography; D005260:Female; D017052:Hospital Mortality; D006801:Humans; D056989:Inferior Wall Myocardial Infarction / Q000000981:diagnostic imaging / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D007423:Intra-Aortic Balloon Pumping; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D000072657:ST Elevation Myocardial Infarction / Q000000981:diagnostic imaging / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D013318:Stroke Volume; D013599:Systole; D016896:Treatment Outcome; D014662:Vasoconstrictor Agents / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D016277:Ventricular Function, Left / Q000187:drug effects; D016278:Ventricular Function, Right / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D014662:Vasoconstrictor Agents