Diastolic Ventricular Interaction in Heart Failure With Preserved Ejection Fraction

Background Exercise-induced pulmonary hypertension is common in heart failure with preserved ejection fraction ( HF p EF ). We hypothesized that this could result in pericardial constraint and diastolic ventricular interaction in some patients during exercise. Methods and Results Contrast stress ech...

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Published inJournal of the American Heart Association Vol. 8; no. 7; p. e010114
Main Authors Parasuraman, Sathish K., Loudon, Brodie L., Lowery, Crystal, Cameron, Donnie, Singh, Satnam, Schwarz, Konstantin, Gollop, Nicholas D., Rudd, Amelia, McKiddie, Fergus, Phillips, Jim J., Prasad, Sanjay K., Wilson, Andrew M., Sen‐Chowdhry, Srijita, Clark, Allan, Vassiliou, Vassilios S., Dawson, Dana K., Frenneaux, Michael P.
Format Journal Article
LanguageEnglish
Published England John Wiley and Sons Inc 02.04.2019
Wiley
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ISSN2047-9980
2047-9980
DOI10.1161/JAHA.118.010114

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Summary:Background Exercise-induced pulmonary hypertension is common in heart failure with preserved ejection fraction ( HF p EF ). We hypothesized that this could result in pericardial constraint and diastolic ventricular interaction in some patients during exercise. Methods and Results Contrast stress echocardiography was performed in 30 HF p EF patients, 17 hypertensive controls, and 17 normotensive controls (healthy). Cardiac volumes, and normalized radius of curvature ( NRC ) of the interventricular septum at end-diastole and end-systole, were measured at rest and peak-exercise, and compared between the groups. The septum was circular at rest in all 3 groups at end-diastole. At peak-exercise, end-systolic NRC increased to 1.47±0.05 ( P<0.001) in HF p EF patients, confirming development of pulmonary hypertension. End-diastolic NRC also increased to 1.54±0.07 ( P<0.001) in HF p EF patients, indicating septal flattening, and this correlated significantly with end-systolic NRC (ρ=0.51, P=0.007). In hypertensive controls and healthy controls, peak-exercise end-systolic NRC increased, but this was significantly less than observed in HF p EF patients ( HF p EF , P=0.02 versus hypertensive controls; P<0.001 versus healthy). There were also small, non-significant increases in end-diastolic NRC in both groups (hypertensive controls, +0.17±0.05, P=0.38; healthy, +0.06±0.03, P=0.93). In HF p EF patients, peak-exercise end-diastolic NRC also negatively correlated ( r=-0.40, P<0.05) with the change in left ventricular end-diastolic volume with exercise (ie, the Frank-Starling mechanism), and a trend was noted towards a negative correlation with change in stroke volume ( r=-0.36, P=0.08). Conclusions Exercise pulmonary hypertension causes substantial diastolic ventricular interaction on exercise in some patients with HF p EF , and this restriction to left ventricular filling by the right ventricle exacerbates the pre-existing impaired Frank-Starling response in these patients.
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Dr Parasuraman and Dr Loudon contributed equally to this work.
ISSN:2047-9980
2047-9980
DOI:10.1161/JAHA.118.010114