ORCID Identifier(s)


Graduation Semester and Year




Document Type


Degree Name

Master of Science in Exercise Science



First Advisor

Michael D Nelson


Women with signs and symptoms of ischemia but no obstructive coronary artery disease (INOCA) are at increased risk of developing heart failure with preserved ejection fraction (HFpEF); however, the exact mechanism for HFpEF progression remains to be elucidated. Prior studies have focused specifically on impaired left ventricular diastolic function in INOCA. We hypothesized that extending our evaluation to include the left atrium (LA)— a key constituent of the transmitral pressure gradient and left ventricular filling— would provide additional, novel, pathophysiological insight. To extend our knowledge of the pathophysiologic mechanism(s) linking INOCA with HFpEF, we evaluated LA function across the heart failure continuum: (A) 12 reference controls, (B) 55 women with INOCA, and (C) 19 patients with HFpEF. In all subjects, LA function was analyzed (in duplicate) using commercially available software, with the strain profile divided into three distinct phases: (1) reservoir, passive expansion of the left atrium from the pulmonary circulation while the mitral valve is closed; (2) conduit, passive emptying of the atrium into the ventricle; and (3) booster, active emptying of the left atrium following atrial depolarization. Consistent with prior reports, left atrial reservoir strain was significantly lower in HFpEF vs. reference controls (19.8 + 1.5% vs. 25.8 + 1.3%, respectively; p=0.02) and tended to be lower compared to INOCA (23.9 + 0.8%, p=0.09); however, we observed no group differences in conduit or booster strain. Interestingly, conduit strain rate tended to be depressed in both the INOCA and HFpEF groups (-1.6 + 0.07 and -1.5 + 0.1%, respectively) compared to reference controls (-1.9 + 0.1%, p=0.07). To our knowledge, this is the first report of LA function in women with INOCA. That left atrial reservoir strain was reduced across the heart failure continuum, being lowest in HFpEF patients compared to either reference controls or INOCA supports our hypothesis that INOCA may contribute to HFpEF progression. The seemingly depressed conduit function between in INOCA and HFpEF, may reflect a reduced transmitral pressure gradient, secondary to impaired ventricular diastolic function. More work is needed to better understand the role of chronic ischemia on left atrial function and the interaction between the atria and ventricles.


Atrial strain, Left atrium, INOCA, HFpEF, Diastolic function


Kinesiology | Life Sciences


Degree granted by The University of Texas at Arlington

Included in

Kinesiology Commons