Abstract P059: Arterial Thickness and Stiffness are Independent Predictors of Myocardial Strain
Vascular dysfunction is associated with cardiac dysfunction, a precursor of CV events (MI,CHF) in adults. We hypothesized that abnormalities in vascular structure and function are associated with cardiac systolic dysfunction as measured by cardiac strain and strain rate in young adults.
Carotid ultrasound and echocardiography were performed on 338 subjects (22.2 + 3.7 years; 38% male (M); 63% non-white (NW); 33% lean, 36% obese and 31% T2DM). CIMT was traced along the far wall of the distal CCA, bulb, and proximal ICA. Stiffness measures included carotid-femoral pulse wave velocity (PWVf), brachial distensibility (BrachD) and Peterson’s Elastic Modulus in the CCA (PEM). LV systolic function was assessed by global longitudinal (4-chamber) strain (GS) and strain rate in systole (GSRs). Anthropometry, BP, HR, fasting lipids, CRP, and glucose were collected. Correlations were calculated between vascular measures and cardiac strain. General linear models were constructed to determine if vascular measures were independent predictors of GS and GSRs. Covariates included age, sex, race, BMI z-score, MAP, group, TG, HDL, LDL, insulin, glucose, and CRP.
GS and GSRs correlated with peripheral arterial stiffness (lower BrachD, higher PEM, higher PWVf) and structure (thicker CIMT), all p<.01 (Figure). After adjusting for other risk factors, BrachD was an independent predictor of poorer GSRs: GSRs=-1.1611 -.13*BrachD + .05 (if M) + .06 (if NW) + .004*MAP - .0003*glucose + .07*Insulin. CCA IMT independently predicted both GS and GSRs: GS=-.26 + 4.6* CCA + .92 (if M) + .58*BMIZ + .56*MAP- .03*HDL + 1.06*insulin; GSRs= -1.4 + .26*CCA+ .05 (if M) + .03*BMIZ + .003*MAP - .0003*glucose + .06*Insulin. All factors were significant at p<.05 in these models.
We conclude that adverse pre-clinical vascular and cardiac findings are present in youth simultaneously and may increase risk for future CV events. Assessment of vascular structure and function may add incremental benefit in stratifying risk in young adults for future CV events.
Author Disclosures: C.E. McCoy: None. P.R. Khoury: None. S.N. Stewart: None. L.E. Longhshore: None. N.L. Madsen: None. L.M. Dolan: B. Research Grant; Modest; R01 HL105591-01. T.R. Kimball: B. Research Grant; Modest; R01 HL105591-01. E.M. Urbina: B. Research Grant; Significant; R0 1HL105591-01.
- © 2015 by American Heart Association, Inc.