Open AccessDiastolic Ventricular Interaction in Heart Failure With Preserved Ejection Fraction
Author(s) -
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.,
SenChowdhry Srijita,
Clark Allan,
Vassiliou Vassilios S.,
Dawson Dana K.,
Frenneaux Michael P.
Publication year - 2019
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.118.010114
Subject(s) - medicine , cardiology , diastole , ejection fraction , interventricular septum , heart failure , systole , diastolic heart failure , blood pressure , ventricle
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.