title: Arterial-ventricular coupling: mechanistic insights into cardiovascular performance at rest and during exercise.
abstract: Understanding the performance of the left ventricle (LV) requires not only examining the properties of the LV itself, but also investigating the modulating effects of the arterial system on left ventricular performance. The interaction of the LV with the arterial system, termed arterial-ventricular coupling (E(A)/E(LV)), is a central determinant of cardiovascular performance and cardiac energetics. E(A)/E(LV) can be indexed by the ratio of effective arterial elastance (E(A); a measure of the net arterial load exerted on the left ventricle) to left ventricular end-systolic elastance (E(LV); a load-independent measure of left ventricular chamber performance). At rest, in healthy individuals, E(A)/E(LV) is maintained within a narrow range, which allows the cardiovascular system to optimize energetic efficiency at the expense of mechanical efficacy. During exercise, an acute mismatch between the arterial and ventricular systems occurs, due to a disproportionate increase in E(LV) (from an average of 4.3 to 13.2, and 4.7 to 15.5 mmHg.ml(-1).m(-2) in men and women, respectively) vs. E(A) (from an average of 2.3 to 3.2, and 2.3 to 2.9 mmHg.ml(-1).m(-2) in men and women, respectively), to ensure that sufficient cardiac performance is achieved to meet the increased energetic requirements of the body. As a result E(A)/E(LV) decreases from an average of 0.58 to 0.34, and 0.52 to 0.27 in men and women, respectively. In this review, we provide an overview of the concept of E(A)/E(LV), and examine the effects of age, hypertension, and heart failure on E(A)/E(LV) and its components (E(A) and E(LV)) in men and women. We discuss these effects both at rest and during exercise and highlight the mechanistic insights that can be derived from studying E(A)/E(LV).
authors.affiliation: Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, 3001 S. Hanover Street, Baltimore, MD 21225, USA.
authors.forename: Paul D
authors.initials: PD
authors.lastname: Chantler
authors.forename: Edward G
authors.initials: EG
authors.lastname: Lakatta
authors.forename: Samer S
authors.initials: SS
authors.lastname: Najjar
mesh_terms: D000367:Age Factors; D000375:Aging / Q000473:pathology; D000818:Animals; D001158:Arteries / Q000473:pathology / Q000503:physiopathology*; D004548:Elasticity; D004734:Energy Metabolism; D015444:Exercise; D005260:Female; D006333:Heart Failure / Q000473:pathology / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008955:Models, Cardiovascular; D016277:Ventricular Function, Left