Age-related changes in venticular-arterial coupling: pathophysiologic implications.
The interaction of the heart with the systemic vasculature, termed ventricular-arterial coupling, is a central determinant of net cardiovascular performance. The capacity of the body to augment cardiac output, regulate systemic blood pressure, and respond appropriately to elevations in heart rate and venous filling volume is related as much to the properties of the heart as it is the vasculature into which the heart ejects. With aging, changes in the arterial system associated with vascular stiffening and a reduction in peripheral vasomotor regulation can profoundly affect this coupling by imposing far greater pulsatile and late-systolic loads on the heart. This is accompanied by tandem increases in left ventricular end-systolic stiffness (end-systolic chamber elastance) and reduced diastolic compliance. Altered coupling related to combined ventricular-vascular stiffening increases blood pressure lability for a given change in hemodynamic loading and heart rate (i.e. under stress demands), as well as reduces the capacity to enhance cardiac output without greatly increasing cardiac wall stress. Furthermore, such coupling influences myocardial perfusion by elevating the proportion of coronary flow during the systolic time period. This more closely links ventricular systolic function with myocardial flow, and can compromise flow reserve and exacerbate ischemic dysfunction when ventricular systolic function declines, such as with concomitant heart failure or acute regional ischemia. This article reviews the theory behind ventricular-arterial coupling analysis, the changes in coupling that occur with age and their impact on normal reserve mechanisms, and the likely role of these changes have on heart failure and ischemic heart disease and disease therapy in the elderly.
Kass
David A
DA
Division of Cardiology, Department of Medicine, Professor of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21287, USA.
D000368:Aged; D000375:Aging / Q000502:physiology*; D002319:Cardiovascular System / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008955:Models, Cardiovascular; D016276:Ventricular Function / Q000502:physiology*