Year

2021

Season

Spring

Paper Type

Master's Thesis

College

Brooks College of Health

Degree Name

Master of Science in Health Science (MSH)

Department

Clinical & Applied Movement Sciences

NACO controlled Corporate Body

University of North Florida. Department of Clinical & Applied Movement Sciences

First Advisor

Dr. James R. Churilla

Second Advisor

Dr. Michael R. Richardson

Rights Statement

http://rightsstatements.org/vocab/InC/1.0/

Third Advisor

Dr. Jasper Xu

Fourth Advisor

Dr. Hirofumi Tanaka

Fifth Advisor

Dr. Kevin S. Heffernan

Department Chair

Dr. Joel Beam

College Dean

Dr. Curt Lox

Abstract

Purpose: The aim of this study was to evaluate the association between total brachial artery reactivity (TBAR) and the cumulative risk of incident heart failure (HF), HF with reduced ejection fraction (HFrEF), and HF with preserved ejection fraction (HFpEF) in a community-based study. Methods: Sample included 5,499 participants (45-84 years of age) from the Multi-Ethnic Study of Atherosclerosis who were free of cardiovascular disease at baseline. Brachial artery ultrasound was performed after five minutes of cuff occlusion at the right forearm. TBAR was calculated as the difference between maximum and minimum brachial artery diameters following cuff release, divided by the minimum diameter multiplied by 100%. A dichotomous TBAR variable was created based on the median value (below or above 7.9%). Participants with EF≤40% were considered HFrEF and those with EF ≥ 50% were considered HFpEF. Cox proportional hazards regression models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI). Results: Over a mean follow-up period of 12.5 years, incident HF was diagnosed in 250 participants; 98 classified as HFrEF, 106 as HFpEF, and 46 with unknown or borderline EF (41-49%). Crude analysis revealed that those with TBAR below the median have significantly higher risk of HF (HR 1.46; 95% CI 1.13-1.88, pConclusion:Lower TBAR values were associated with higher rates of incident HF and HFrEF, suggesting a possible role of endothelial dysfunction in HF pathogenesis. The impact of other known HF risk factors may mediate this relationship, thus further research is warranted.

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