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Aims: Phosphodiesterase‐5 inhibitors (PDE5I) are frequently implemented after left ventricular assist device (LVAD) implantation to improve haemodynamics in patients with early postoperative right ventricular (RV) failure. It is unknown if long‐term PED5I therapy beyond the early post‐operative period provides any clinical benefit in stable outpatients, who have recovered from post‐operative RV failure under univentricular device support. This study aimed to investigate the impact of PDE5I discontinuation on RV function and cardiopulmonary exercise capacity in patients on durable LVAD support. Methods and results: We enrolled 31 clinically stable LVAD recipients on long‐term oral PDE5I therapy. The mean age was 53 years, and 90% were male. Patients discontinued PDE5I and underwent cardiopulmonary exercise testing, echocardiography, LVAD interrogation, and biomarker analysis at baseline and 4 weeks after PDE5I withdrawal. At 4 weeks, no significant changes were observed in echocardiographic indices of RV morphology and function but an increase in peak tricuspid regurgitation velocity (2.1 vs. 2.4 m/s, P = 0.01). Peak oxygen consumption (11.4 vs. 11.8 mL/min/kg, P = 0.52), minute ventilation/carbon dioxide production slope (33 vs. 35, P = 0.56), N‐terminal pro‐brain natriuretic peptide (1455 vs. 1399 pg/mL, P = 0.55), flow and power readings of the device, and quality of life (Kansas City Cardiomyopathy Questionnaire score 78.3% vs. 77.5%, P = 0.62) exhibited no significant changes. We observed an increase in 6‐min walking distance (346 vs. 364 m, P = 0.03). Two patients were hospitalized for non‐cardiac reasons (subtherapeutic INR, driveline infection). No patient was hospitalized for cardiac decompensation. Conclusions: In LVAD patients with a history of early post‐operative RV failure, discontinuation of long‐term PDE5I therapy was not associated with deterioration of RV function, exercise capacity, and quality of life. PDE5I should be critically evaluated until more evidence regarding the net clinical benefit of this pharmacologic intervention becomes available. [ABSTRACT FROM AUTHOR]

(1) Background: The exercise capacity of patients with a left ventricular assist device (LVAD) remains limited despite mechanical support. Higher dead space ventilation (VD/VT) may be a surrogate for right ventricular to pulmonary artery uncoupling (RV–PA) during cardiopulmonary exercise testing (CPET) to explain persistent exercise limitations. (2) Methods: We investigated 197 patients with heart failure and reduced ejection fraction with (n = 89) and without (HFrEF, n = 108) LVAD. As a primary outcome NTproBNP, CPET, and echocardiographic variables were analyzed for their potential to discriminate between HFrEF and LVAD. As a secondary outcome CPET variables were evaluated for a composite of hospitalization due to worsening heart failure and overall mortality over 22 months. (3) Results: NTproBNP (OR 0.6315, 0.5037–0.7647) and RV function (OR 0.45, 0.34–0.56) discriminated between LVAD and HFrEF. The rise of endtidal CO2 (OR 4.25, 1.31–15.81) and VD/VT (OR 1.23, 1.10–1.40) were higher in LVAD patients. Group (OR 2.01, 1.07–3.85), VE/VCO2 (OR 1.04, 1.00–1.08), and ventilatory power (OR 0.74, 0.55–0.98) were best associated with rehospitalization and mortality. (4) Conclusions: LVAD patients displayed higher VD/VT compared to HFrEF. Higher VD/VT as a surrogate for RV–PA uncoupling could be another marker of persistent exercise limitations in LVAD patients. [ABSTRACT FROM AUTHOR]

Heart failure with preserved (HFpEF), mildly reduced (HFmrEF) and reduced (HFrEF) ejection fraction (EF) remains a controversial categorization. Whether these three categories reflect a distinct pattern of exercise limitation in cardiopulmonary exercise testing (CPET) needs to be investigated. We aimed to analyze whether CPET variables differ between all heart failure categories (HF). We analyzed CPET variables of stable HFpEF (n = 123), HFmrEF (n = 31), and HFrEF (n = 153; 74 patients with and 79 patients without left ventricular assist device, LVAD) patients. The association between HF and peak oxygen consumption (VO 2peak) was used as a primary outcome, while the association between HF, oxygen uptake efficiency slope (OUES), and increase of O 2 pulse (ΔO 2 pulse) were analyzed as secondary outcomes. VO 2peak displayed a consistent decline across all HF categories (19.8 ml ± 6.2/kg/min vs. 17.5 ± 7.9 ml/kg/min vs. 13.7 ± 4.0 ml/kg/min, p < 0.001). OUES only showed differences between HFpEF and HFrEF (1.8 ± 0.6 vs. 1.4 ± 0.5, p < 0.001) as well as HFmrEF and HFrEF (1.9 ± 0.9 vs. 1.4 ± 0.5, p = 0.004). ΔO 2 pulse differed between HFpEF and HFrEF (7.7 ± 3.5 ml/beat/kg*100 vs. 5.5 ± 3.0 ml/beat/kg*100, p < 0.001) as well as HFpEF and HFmrEF (7.7 ± 3.5 ml/beat/kg*100 vs. 6.3 ± 4.1 ml/beat/kg*100, p = 0.049). Outcome variables did not differ between HFrEF with and without LVAD support (VO 2peak : p = 0.364, OUES: p = 0.129, ΔO 2 pulse: p = 0.564). HF did not display a distinct CPET profile. Thus, EF-based categorization does not entirely reflect exercise limitations. CPET variables could contribute to better characterize HF phenotypes. Differential response of variables of cardiopulmonary exercise testing across ejection fraction in heart failure. HFpEF: Heart failure with preserved ejection fraction. HFmrEF: Heart failure with mildly reduced ejection fraction. HFrEF+/-LVAD: Heart failure with reduced ejection fraction with/without left ventricular assist device. VO 2peak : Peak oxygen consumption. OUES: Oxygen uptake efficiency slope. ΔO 2 pulse: Difference between resting and peak O 2 pulse. [Display omitted] • VO2peak declines with HF category. • ΔO2 pulse and OUES show a differential response in HF categories. • Variables of cardiopulmonary exercise testing should be used to delineate exercise limitations of heart failure phenotypes. [ABSTRACT FROM AUTHOR]

Background: Exercise oscillatory ventilation (EOV), indicating pathological fluctuations on pulmonary arterial pressure, is associated with mortality in patients with heart failure (HF). Whether left ventricular assist device (LVAD)‐induced ventricular unloading can reverse EOV and may prevent short‐term rehospitalization has not been investigated. Methods: We performed a retrospective single‐center in‐ and outpatient analysis of patients with (n = 20, LVAD) and without (n = 27, HF) circulatory support and reduced ejection fraction (EF, 22.8 ± 7.9%). The association of cardiopulmonary exercise testing (CPET) variables and 3 months‐rehospitalization (3MR) as a primary outcome was analyzed. Furthermore, CPET variables were compared regarding the presence of EOV (+/−). Results: Lower VO2peak (11.6 ± 4.9 ml/kg/min vs. 14.4 ± 4.3 ml/kg/min, p = 0.039), lower increase of PETCO2 (CI = 0.049–1.127; p = 0.068), and higher VE/VCO2 (43.8 ± 9.5 vs. 38.3 ± 10.6; p = 0.069) were associated with 3MR. Flattening of O2 pulse (CI = 0.139–2.379; p = 0.487) had no impact on 3MR. EOV was present in 59.5% (n = 28/47) of patients, without a significant difference between LVAD and HF patients (p = 0.959). Patients with HF/EOV+ demonstrated significantly lower VO2peak compared with HF/EOV− (p = 0.039). LVAD/EOV+ displayed significantly lower EF (p = 0.004) and fewer aortic valve opening than LVAD/EOV− (p = 0.027). Conclusions: Lower VO2peak, but not EOV, was associated with 3MR. EOV occurred at a similar rate in LVAD and HF patients, which may illustrate insufficient unloading during exercise in chronic LVAD therapy and may contribute to the limited exercise capacity following LVAD implantation. Simultaneous CPET and right heart catheterization studies are needed to elucidate whether EOV may serve as a non‐invasive predictor of insufficient LV unloading necessitating LVAD reprograming. [ABSTRACT FROM AUTHOR]