[Experimental study of systemic ventriculo-arterial coupling. Effects of modifications of thoracic aortic mechanical properties and myocardial ischemia on left ventricular performance].
We quantified systemic ventriculo-arterial coupling in the pressure-volume (PV) plane, using a model of elastic chambers of the cardio-vascular system. In such a model, the ratio between left ventricular (LV) end-systolic elastance, and effective arterial elastance measures the coupling between the heart and the systemic vasculature, and the effects of cardiac diseases and of vasoactive agents on the coupling relationship can be independently evaluated in vivo. Furthermore, the analysis in the PV plane gives insights into LV mechanical efficiency, defined by the ratio between stroke work and pressure-volume area. Our results demonstrating that an augmentation of aortic compliance decreases the energetic cost of LV ejection should be considered when replacing the thoracic aorta by an artificial prosthesis. The homeometric autoregulation, suggesting a mechanism by which the heart can maintain a constant stroke volume, in the face of increased afterload, without using the Starling mechanism and independently of baroreflex integrity, is of paramount importance in heart transplant patients. Indeed, such patients, although lacking cardiac innervation, can adapt their cardiac output, stroke volume, end-systolic and end-diastolic pressures, without simultaneous changes in heart rate. Finally, our data demonstrate that the acutely ischemic LV must face an hostile hemodynamic environment, characterised by early vasoconstriction, later combined with decreased vascular compliance. These results are important when choosing vasoactive agents in the setting of acute myocardial infarction.
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D001013:Aorta, Thoracic / Q000502:physiology*; D017704:Baroreflex / Q000502:physiology; D001696:Biomechanical Phenomena; D002302:Cardiac Output / Q000502:physiology; D004734:Energy Metabolism; D006439:Hemodynamics; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000503:physiopathology*; D013318:Stroke Volume; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*