Rapid Fire Abstracts
Jan Sebastian Wolter
physician
Kerckhoff-Klinik, Germany
Jan Sebastian Wolter
physician
Kerckhoff-Klinik, Germany
Alexander Schulz, MD
Dr.
Harvard Medical School / BIDMC, Germany
Torben Lange, MD
Resident
University Medical Center Göttingen, Germany, Germany
Steffen D Kriechbaum, MD
physician
Kerckhoff-Klinik, Germany
Maren Weferling, MD
Senior Physician
Kerckhoff Klinik, Germany
Shelby Kutty, MD
Dr.
Taussig Heart Center, USA
Johannes Kowallick, MD
Prof.
University Medical Center Göttingen, Germany, Germany
Julia Treiber, MD
senior physician
Kerckhoff Klinik, Germany
Andreas Rolf, MD
Senior Cardiologist
Kerckhoff Klinikum Bad Nauheim, Germany
Samuel Sossalla, MD
chief medical officer
Kerckhoff Klinik, Germany
Gerd Hasenfuß, MD
Prof
University Medical Center Göttingen, Germany, Germany
Andreas Schuster, MD, PhD
Cardiologist
University Medical Center Göttingen, Germany
Sören Backhaus, MD
Consultant Cardiologist
Department of Cardiology, Heart Centre, Kerckhoff-Clinic Bad Nauheim, Germany
The pathophysiology of heart failure with preserved ejection fraction (HFpEF) reaches beyond left ventricular function including pulmonary vascular remodelling and right ventricular (RV) involvement. Consequently, we sought to investigate the significance of non-invasive cardiovascular magnetic resonance (CMR) derived RV loading conditions.
Methods:
Patients with exertional dyspnoea and diastolic dysfunction (E/e' >8, LVEF >50%) were enrolled and underwent rest and exercise-stress echocardiography, right heart catheterisation and CMR. HFpEF was defined by pulmonary capillary wedge pressure (≥15mmHg at rest (overt) or ≥25mmHg during exercise-stress (masked)). CMR-derived RV haemodynamic indices were defined as follows: Afterload Ea= End-systolic pressure (ESP)/Stroke volume (SV), contractility Ees= ESP/left ventricular end-systolic volume and RV/pulmonary artery coupling as Ea/Ees.
Results:
The final population consisted of n=34 HFpEF and n=34 non-cardiac dyspnoea (NCD) patients. HFpEF patients showed increased afterload and contractility at rest (Ea 1.20 vs 0.85, p=0.001, Ees 0.61 vs 0.37, p< 0.001) and during exercise (Ea 2.48 vs 1.53, Ees 1.00 vs 0.74, p< 0.001) compared to NCD. However, the relative increase of contractility from rest to stress was smallest in overt HFpEF (overt 1.40 vs masked 1.86, p=0.001) and highest in NCD (HFpEF 1.56 vs NCD 1.97, p=0.022) (figure 1A). The out of proportion increase in afterload over contractility in HFpEF was reflected in a statistical trend towards increased coupling index Ea/Ees from rest to stress in HFpEF (p=0.078) whilst Ea/Ees decreased in NCD (p=0.002) (figure 1B). Indeed, patients with resting Ea or Ees above the median showed lower increase in cardiac index comparing rest to exercise-stress (Ea: below: 2.8 vs above: 2.2, p=0.031; Ees: below: 2.9, above: 2.1, p< 0.001) (figure 1C and 1D).
Conclusion:
Resting afterload elevation in HFpEF results in a compensatory increase in contractility. However, out-of-proportion increase of afterload in HFpEF paralleled by inadequate increase in contractility results in failure to increase cardiac output. This may be a feature of HFpEF pathophysiology associated to exertional functional failure.
