Erschienen in:
03.05.2019 | Original Paper
Right atrial–right ventricular coupling in heart failure with preserved ejection fraction
verfasst von:
Maximilian von Roeder, Johannes Tammo Kowallick, Karl-Philipp Rommel, Stephan Blazek, Christian Besler, Karl Fengler, Joachim Lotz, Gerd Hasenfuß, Christian Lücke, Matthias Gutberlet, Holger Thiele, Andreas Schuster, Philipp Lurz
Erschienen in:
Clinical Research in Cardiology
|
Ausgabe 1/2020
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Abstract
Background
Right ventricular (RV) function is prognostically relevant in heart failure with preserved ejection fraction (HFpEF) but data on profound assessment of RV and right atrial (RA) interaction in HFpEF are lacking. The current study characterizes RV and RA interaction using invasive pressure–volume-loop analysis and cardiac magnetic resonance imaging (CMR) data.
Methods and results
We performed CMR and myocardial feature-tracking in 24 HFpEF patients and 12 patients without HFpEF. Invasive pressure–volume-loops were obtained to evaluate systolic and diastolic RV properties. RV early filling was determined from CMR RV volume–time curves. RV systolic function was slightly increased in HFpEF (RV EF 68 ± 8 vs. 60 ± 9%, p = 0.01), while no differences in RV stroke volume were found (45 ± 7 vs 42 ± 9 ml/m2, p = 0.32). RV early filling was decreased in HFpEF (21 ± 11 vs. 40 ± 11% of RV filling volume, p < 0.01) and RV early filling was the strongest predictor for VO2max even after inclusion of invasively derived RV stiffness and relaxation constant (Beta 0.63, p < 0.01). RA conduit-function was lower in HFpEF (RA conduit-strain − 11 ± 5 vs. − 16 ± 4%, p < 0.01) while RA booster-pump-function was increased (RA active-strain − 18 ± 6 vs. − 12 ± 6%, p = 0.01) as a compensation. RV filling was associated with RA conduit-function (r = − 0.55, p < 0.01) but not with invasively derived RV relaxation constant.
Conclusion
In compensated HFpEF patients RV early filling was impaired and compensated by increased RA booster pump function, while RV systolic function was preserved. Impaired RV diastology and RA–RV interaction were linked to impaired exercise tolerance and RA–RV-coupling seems to be independent of RV relaxation, suggestive of an independent pathophysiological contribution of RA dysfunction in HFpEF.
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