title: Computationally managed bradycardia improved cardiac energetics while restoring normal hemodynamics in heart failure.
abstract: In acute heart failure, systemic arterial pressure (AP), cardiac output (CO), and left atrial pressure (P (LA)) have to be controlled within acceptable ranges. Under this condition, cardiac energetic efficiency should also be improved. Theoretically, if heart rate (HR) is reduced while AP, CO, and P (LA) are maintained by preserving the functional slope of left ventricular (LV) Starling's curve (S (L)) with precisely increased LV end-systolic elastance (E (es)), it is possible to improve cardiac energetic efficiency and reduce LV oxygen consumption per minute (MVO (2)). We investigated whether this hemodynamics can be accomplished in acute heart failure using an automated hemodynamic regulator that we developed previously. In seven anesthetized dogs with acute heart failure (CO < 70 mL min(-1) kg(-1), P (LA) > 15 mmHg), the regulator simultaneously controlled S (L) with dobutamine, systemic vascular resistance with nitroprusside and stressed blood volume with dextran or furosemide, thereby controlling AP, CO, and P (LA). Normal hemodynamics were restored and maintained (CO; 88 +/- 3 mL min(-1) kg(-1), P (LA); 10.9 +/- 0.4 mmHg), even when zatebradine significantly reduced HR (-27 +/- 3%). Following HR reduction, E (es) increased (+34 +/- 14%), LV mechanical efficiency (stroke work/oxygen consumption) increased (+22 +/- 6%), and MVO (2) decreased (-17 +/- 4%) significantly. In conclusion, in a canine acute heart failure model, computationally managed bradycardia improved cardiac energetic efficiency while restoring normal hemodynamic conditions.
authors.affiliation: Department of Cardiovascular Dynamics, Advanced Medical Engineering Center, National Cardiovascular Center Research Institute, Fujishirodai, Suita, Japan. kuemura@ri.ncvc.go.jp
authors.forename: Kazunori
authors.initials: K
authors.lastname: Uemura
authors.forename: Kenji
authors.initials: K
authors.lastname: Sunagawa
authors.forename: Masaru
authors.initials: M
authors.lastname: Sugimachi
mesh_terms: D000208:Acute Disease; D000818:Animals; D001919:Bradycardia / Q000188:drug therapy* / Q000503:physiopathology; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D003198:Computer Simulation; D004285:Dogs; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006439:Hemodynamics; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology
chemical_list: D002316:Cardiotonic Agents