TY - JOUR
T1 - Effect of reduced aortic compliance on cardiac efficiency and contractile function of in situ canine left ventricle
AU - Kelly, Raymond P.
AU - Tunin, Richard
AU - Kass, David A.
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1992/9
Y1 - 1992/9
N2 - This study tests the hypothesis that arterial vascular stiffening adversely influences in situ left ventricular contractile function and energetic efficiency. Ten reflex-blocked anesthetized dogs underwent a bypass operation in which a Dacron graft was sewn to the ascending aorta and connected to the infrarenal abdominal aorta via a plastic conduit. Flow was directed through either native aorta or plastic conduit by placement of vascular clamps. Arterial properties were measured from aortic pressure-flow data, and ventricular function was assessed by pressure-volume (PV) relations. Coronary sinus blood was drained via an extracorporeal circuit for direct measurement of myocardial O2 consumption (MV̇o2). Data at multiple steady-state preload volumes were combined to derive chamber function and energetics relations. Energetic efficiency was assessed by the inverse slope of the MV̇o2-PV area relation. Directing flow through plastic versus native aorta resulted in a 60-80% reduction in compliance but little change in mean resistance. Arterial pulse pressure rose from 34 to 99 mm Hg (p<0.001). Contractile function assessed by the end-systolic PV relation, stroke work-end-diastolic volume relation, and dP/dtmax at matched end-diastolic volume did not significantly change. However, MV̇o2 increased by 32% (p<0.01) and was matched by a rise in PV area, such that the MV̇o2-PV area relation and efficiency was unaltered. The MV̇o2 required to sustain a given stroke volume, however, increased from 20% to 40%, depending on the baseline level (p<0.001). Thus, whereas the contractile function and efficiency of normal hearts are not altered by ejection into a stiff vascular system, the energetic cost to the heart for maintaining adequate flow is increased. This suggests a mechanism whereby human vascular stiffening may yield little functional decrement at rest but limit reserve capacity under conditions of increased demand.
AB - This study tests the hypothesis that arterial vascular stiffening adversely influences in situ left ventricular contractile function and energetic efficiency. Ten reflex-blocked anesthetized dogs underwent a bypass operation in which a Dacron graft was sewn to the ascending aorta and connected to the infrarenal abdominal aorta via a plastic conduit. Flow was directed through either native aorta or plastic conduit by placement of vascular clamps. Arterial properties were measured from aortic pressure-flow data, and ventricular function was assessed by pressure-volume (PV) relations. Coronary sinus blood was drained via an extracorporeal circuit for direct measurement of myocardial O2 consumption (MV̇o2). Data at multiple steady-state preload volumes were combined to derive chamber function and energetics relations. Energetic efficiency was assessed by the inverse slope of the MV̇o2-PV area relation. Directing flow through plastic versus native aorta resulted in a 60-80% reduction in compliance but little change in mean resistance. Arterial pulse pressure rose from 34 to 99 mm Hg (p<0.001). Contractile function assessed by the end-systolic PV relation, stroke work-end-diastolic volume relation, and dP/dtmax at matched end-diastolic volume did not significantly change. However, MV̇o2 increased by 32% (p<0.01) and was matched by a rise in PV area, such that the MV̇o2-PV area relation and efficiency was unaltered. The MV̇o2 required to sustain a given stroke volume, however, increased from 20% to 40%, depending on the baseline level (p<0.001). Thus, whereas the contractile function and efficiency of normal hearts are not altered by ejection into a stiff vascular system, the energetic cost to the heart for maintaining adequate flow is increased. This suggests a mechanism whereby human vascular stiffening may yield little functional decrement at rest but limit reserve capacity under conditions of increased demand.
KW - Aortic input impedance
KW - Myocardial energetics
KW - Pressure-volume relations
KW - Ventricular function
KW - Ventriculovascular coupling
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U2 - 10.1161/01.RES.71.3.490
DO - 10.1161/01.RES.71.3.490
M3 - Article
C2 - 1386792
AN - SCOPUS:0026689951
SN - 0009-7330
VL - 71
SP - 490
EP - 502
JO - Circulation research
JF - Circulation research
IS - 3
ER -