Abstract 963: Metabolic Syndrome is Characterized by Ventriculo-Arterial Mismatch with Disproportionate Increase of End-systolic Ventricular Stiffness
Objective: Ventricular end-systolic stiffness (Ees) reflects the contractile behavior of the left ventricle, geometry and mass. In subjects without heart disease, Ees is matched to arterial load (arterial elastance, Ea) so that ventriculo-vascular coupling is preserved and cardiac performance optimized. However, it remains unknown whether metabolic syndrome (MS) affects the coupling ratio (Ees/Ea).
Methods: Ea and Ees were non-invasively estimated by single-beat methods based on resting echocardiography and blood pressure data from 176 participants (age 64±13 y, 51% females) in the Baltimore Longitudinal Study of Aging. Presence (+) or absence (−) of MS and the MS score were defined by ATP III-NCEP.
Results: MS+ subjects had higher Ees/Ea ratio than MS - (2.1 vs. 1.9, p=0.02) due to higher Ees (3.1 vs. 2.6 mmHg/ml, p=0.002), even if adjusted to body size. Vascular load (Ea, 1.5 vs. 1.4 mmHg/ml, p=0.07), LV mass, age, gender were similar (p>0.1) in both groups, but pulse pressure and relative LV wall thickness were higher in MS+. Ees/Ea and Ees correlated with MS score (r=0.18 and 0.27, p=0.02 and <0.001) and plasma leptin level (r=0.31 and 0.20, p<0.001 and 0.02). From individual MS components, Ees/Ea was most affected by waist circumferrence. Ees and Ees/Ea predicted attained peak VO2 (r= − 0.33 and − 0.29, p<0.001), being lower in MS+ (19±6 vs. 25±6 ml/kg/min, p<0.001).
Conclusions: In MS, ventricular end-systolic stiffening rises beyond that predicted by arterial load. Leptin and other endocrine factors related to central obesity may be implicated in disproportionate increase of Ees. Abnormal coupling and low systolic reserve likely contribute to exercise intolerance in MS.