https://doi.org/10.1007/s00392-025-02625-4
1Universitätsmedizin Göttingen Herzzentrum, Klinik für Kardiologie und Pneumologie Göttingen, Deutschland; 2Kerckhoff Klinik GmbH Abteilung für Kardiologie Bad Nauheim, Deutschland; 3Georg-August Universität Göttingen Fakultät für Mathematik und Informatik Göttingen, Deutschland; 4Forum Radiology Rosdorf, Deutschland; 5Forum Medizin GbR Kardiologie Rosdorf, Deutschland
Background
Right ventricular (RV) dysfunction has prognostic relevance in patients with heart failure with preserved ejection fraction (HFpEF). As RV functional impairment in HFpEF is a result to increased transpulmonary gradients and subsequent pulmonary vascular remodelling over time, we hypothesized that pulmonary artery (PA) compliance is an early indicator of adverse haemodynamical coupling in HFpEF-patients with normal RV function.
Methods
75 patients with signs of diastolic dysfunction (NYHA≥II, left ventricular (LV) ejection fraction (EF)≥ 50%, E/e’≥8) were prospectively recruited and underwent comprehensive rest and stress right heart catheterization (RHC) with simultaneous echocardiography. Within 24h, patients received exercise stress cardiovascular magnetic imaging (CMR) using the same exercise protocol as during RHC. All patients had normal RV function as measured by CMR-derived RV EF. HFpEF was diagnosed according to invasive measurements of pulmonary capillary wedge pressure (PCWP)≥15mmHg at rest or ≥ 25mmHg during exercise stress. Remaining patients were categorized as non-cardiac dyspnoea (NCD). PA compliance was non-invasively assessed by measuring main pulmonary artery pulsatility (MPAPuls) in real-time phase contrast images at rest and during exercise stress over five consecutive cardiac cycles. MPAPuls was calculated as relative area change ((Amax-Amin/Amin)*100). Patients had systematic follow-up via telephone contact and hospital chart review after 48 months. The occurrence of cardiovascular events was defined as the clinical endpoint.
Results
A total of 63 patients (66±9years, 39 (61.9%) female) were eligible for final analyses. There was no difference in RV EF between patients with HFpEF and NCD (64% (60;68) vs. 67% (63,71); p=0.104) or RV end diastolic and end systolic dimensions. Furthermore, RV output at rest and during exercise stress was similar in both groups (RV stroke volume rest: 41.2ml/m2 (34.2;49.6) vs. 44.4ml/m2 (34.6;52.5); p=0.459), RV stroke volume stress: (43.7ml/m2 (38.5;52.5) vs. 44.4ml/m2 (36.1;50.8); p=0.815). However, while patients with HFpEF and NCD had similar MPAPuls at rest (20% (15;23.5) vs. 20% (15;20); p=0.793), MPAPuls decreased during exercise stress in HFpEF patients, but not NCD (13% (11.5;21) vs. 20% (16;25); p<0.001).
Decreasing MPAPuls during exercise stress correlated with impaired CMR-derived left atrial (LA) function (LA LAS rest: R=0.499, p<0.001; LA LAS stress: R=0.439, p<0.001) and increased PCWP (PCWP rest: R=-0.444, p<0.001; PCWP stress: R=-0.492, p<0.001). An optimal cut-off for outcome prediction was found at an exercise MPAPuls of 22.5% using Youden’s index. Patients with decreased MPAPuls during exercise stress had worse long-term outcome after 4 years follow up (HR 6.0 (95%CI: 1.4-25.9); p=0.016) with 45% vs. 9.5% (p=0.006 in log-rank testing) of patients experiencing cardiovascular events in the low MPAPuls group (see Figure 1).
Conclusion
Decreased PA compliance during exercise stress is associated with worse outcomes in HFpEF patients with normal RV function. Hereby, non-invasively calculated PA compliance may serve as an early marker of worsening biventricular coupling prior to RV functional impairment.
Figure 1: Long-term prognosis of patients with high (>22.5%) and low (≤22.5%) MPAPuls during exercise stress. MPAPuls – Main pulmonary artery pulsatility