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Abnormal right ventricular reserve capacity in patients with heart failure and preserved biventricular function is caused by ventricular stiffness, impaired relaxation and vascular stiffness.

Session Poster session 1

Speaker Karl-Philipp Rommel

Congress : ESC Congress 2016

  • Topic : imaging
  • Sub-topic : Echocardiography: Systolic and Diastolic Function
  • Session type : Poster Session
  • FP Number : P778

Authors : KP Rommel (Leipzig,DE), M Von Roeder (Leipzig,DE), K Latuscynski (Leipzig,DE), C Oberueck (Leipzig,DE), S Blazek (Leipzig,DE), C Besler (Leipzig,DE), S Sandri (Leipzig,DE), C Luecke (Leipzig,DE), M Gutberlet (Leipzig,DE), G Schuler (Leipzig,DE), P Lurz (Leipzig,DE)

Authors:
K.P. Rommel1 , M. Von Roeder1 , K. Latuscynski1 , C. Oberueck1 , S. Blazek1 , C. Besler1 , S. Sandri1 , C. Luecke2 , M. Gutberlet2 , G. Schuler1 , P. Lurz1 , 1Heart Center of Leipzig, Internal Medicine/Cardiology - Leipzig - Germany , 2Heart Center of Leipzig, Radiology - Leipzig - Germany ,

Citation:
European Heart Journal ( 2016 ) 37 ( Abstract Supplement ), 128

Background: Right ventricular (RV) dysfunction has been shown to be a potent predictor for adverse outcomes in patients with Heart Failure and Preserved Ejection Fraction (HFpEF). However, little is known about RV function abnormalities during exercise which might manifest prior to RV dysfunction at rest in patients with preserved biventricular function.

Invasive tracings of pressure-volume relations provide the unique opportunity to directly assess mechanical properties of the right ventricle under different loading conditions.

Purpose: To invasively assess right ventricular stiffness and right ventricular function in HPpEF patients compared to patients without heart failure symptoms.

Methods: We performed cardiac magnetic resonance imaging to evaluate cardiac dimension and biventricular function in 18 HFpEF patients and 9 patients without heart failure symptoms. Pressure volume loops were obtained with a conductance catheter during basal conditions and handgrip exercise. Transient preload reduction was used to extrapolate the RV end systolic elastance and diastolic stiffness constant.

Results: HFpEF patients and controls showed similar left ventricular (LV) and RV dimensions and LV ejection fraction while RV ejection fraction was even higher in HFpEF patients (p=0.04) Invasively determined load-independent systolic RV function (p=0.8) was comparable between groups. In contrast, HFpEF patients demonstrated an elevated load-independent passive RV stiffness constant β (p<0.01).

While RV active relaxation, filling pressures, arterial elastance and cardiac output where similar at baseline; HFpEF patients demonstrated a blunted increase in cardiac output under exercise (p<0.01) resulting from a longer active RV relaxation (p=0.01), higher RV-filling pressures (p<0.01) with a marked rise in the enddiastolic-pressure-volume relationship (p<0.01) and increased pulmonary artery elastance (p=0.05).

Conclusion: In HFpEF patients with preserved RV function increased intrinsic RV myocardial stiffness, impairment of active RV relaxation and increased pulmonary artery stiffness lead to a blunted increase in cardiac output during exertion. These functional abnormalities can be unmasked by exercise testing and possibly precede overt RV dysfunction at rest.



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