title: Right ventricular failure resulting from pressure overload: role of intra-aortic balloon counterpulsation and vasopressor therapy.
abstract: BACKGROUND
  Augmentation of coronary perfusion may improve right ventricular (RV) failure following acute increases of RV afterload. We investigated whether intra-aortic balloon counterpulsation (IABP) can improve cardiac function by enhancing myocardial perfusion and reversing compromised biventricular interactions using a model of acute pressure overload.
  
  
  METHODS
  In 10 anesthetized pigs, RV failure was induced by pulmonary artery constriction and systemic hypertension strategies with IABP, phenylephrine (PE), or the combination of both were tested. Systemic and ventricular hemodynamics [cardiac index(CI), ventricular pressures, coronary driving pressures (CDP)] were measured and echocardiography was used to assess tricuspid valve regurgitation, septal positioning (eccentricity index (ECI)), and changes in ventricular and septal dimensions and function [myocardial performance index (MPI), peak longitudinal strain].
  
  
  RESULTS
  Pulmonary artery constriction resulted in doubling of RV systolic pressure (54 ± 4mm Hg), RV distension, severe TR (4+) with decreased RV function (strain: -33%; MPI: +56%), septal flattening (Wt%: -35%) and leftward septal shift (ECI:1.36), resulting in global hemodynamic deterioration (CI: -51%; SvO(2): -26%), and impaired CDP (-30%; P<0.05). IABP support alone failed to improve RV function despite higher CDP (+33%; P<0.05). Systemic hypertension by PE improved CDP (+70%), RV function (strain: +22%; MPI: -21%), septal positioning (ECI:1.12) and minimized TR, but LV dysfunction (strain: -25%; MPI: +31%) occurred after LV afterloading (P<0.05). With IABP, less PE (-41%) was needed to maintain hypertension and CDP was further augmented (+25%). IABP resulted in LV unloading and restored LV function, and increased CI (+46%) and SvO(2) (+29%; P<0.05).
  
  
  CONCLUSIONS
  IABP with minimal vasopressors augments myocardial perfusion pressure and optimizes RV function after pressure-induced failure.
authors.affiliation: Department of Surgery, Division of Cardiothoracic Surgery, David Geffen School of Medicine at University of California Los Angeles, California, USA. oliver.liakopouos@uk-koeln.de
authors.forename: Oliver J
authors.initials: OJ
authors.lastname: Liakopoulos
authors.forename: Jonathan K
authors.initials: JK
authors.lastname: Ho
authors.forename: Aaron B
authors.initials: AB
authors.lastname: Yezbick
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Sanchez
authors.forename: Vivek
authors.initials: V
authors.lastname: Singh
authors.forename: Aman
authors.initials: A
authors.lastname: Mahajan
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003131:Combined Modality Therapy; D003326:Coronary Circulation / Q000187:drug effects; D004195:Disease Models, Animal; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000188:drug therapy*; D006973:Hypertension / Q000139:chemically induced*; D007423:Intra-Aortic Balloon Pumping; D010656:Phenylephrine / Q000494:pharmacology*; D011651:Pulmonary Artery / Q000503:physiopathology; D034421:Sus scrofa; D014463:Ultrasonography; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D016277:Ventricular Function, Left / Q000187:drug effects; D017725:Ventricular Pressure / Q000187:drug effects / Q000502:physiology
chemical_list: D014662:Vasoconstrictor Agents; D010656:Phenylephrine