Effects of direct mechanical ventricular assistance on regional myocardial function in an animal model of acute heart failure.
Direct mechanical ventricular assistance (DMVA) improves hemodynamics in failing hearts without complications associated with a blood/device interface. Epicardial Doppler displacement transducers provide exact measurements of tissue displacement and regional myocardial function (RMF). An in vivo porcine model of acute heart failure was used to examine the effects of DMVA on RMF, which have not been reported before. In 8 anesthetized pigs cardiac output (CO), left ventricular pressure (LVP), aortic blood pressure (BP), systolic contractility (dp/dt max), and systolic wall thickening fraction (WT%) were measured. A multichamber pump system (IMPS) surrounding the left ventricle was implanted and the measurements were repeated. Then acute heart failure was induced by beta-blockade, resulting in a decline of all measured parameters to more than 30% compared to baseline values. In the further course of the experiment, repeated measurements were taken at several intervals with and without DMVA by the implanted device. The IMPS implantation caused no significant hemodynamic changes. Under conditions of acute heart failure DMVA improved LVP (46 +/- 7 to 81 +/- 9 mm Hg), dp/dt max (532 +/- 207 to 744 +/- 361 mm Hg/s), CO (1.5 +/- 0.1 to 1.9 +/- 0.5 L/min) and WT% (19 +/- 7% to 32 +/- 8%). Left ventricular myocardium not directly assisted by external pressure application showed improved regional myocardial function during DMVA. We conclude that DMVA is capable of improving hemodynamics due to extrinsic compression. It also enhances the remaining myocardial function of the failing heart, which might lead to myocardial recovery. These synergistic effects are considered responsible for the high efficiency shown by the IMPS in previous investigations.
Kaczmarek
Ingo
I
Department of Thoracic and Cardiovascular Surgery, University Hospital, Heinrich-Heine University, Dusseldorf, Germany. dr4maus1@aol.com
Feindt
Peter
P
Boeken
Udo
U
Guerler
Semih
S
Gams
Emmeran
E
D000208:Acute Disease; D000818:Animals; D002302:Cardiac Output / Q000502:physiology; D002303:Cardiac Output, Low / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D004195:Disease Models, Animal; D015150:Echocardiography, Doppler; D004562:Electrocardiography; D004867:Equipment Design; D006321:Heart / Q000503:physiopathology*; D006353:Heart-Assist Devices; D006439:Hemodynamics / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology; D013552:Swine; D014160:Transducers, Pressure; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*