Background and aims Heart failure with preserved ejection fraction (HFpEF) is a syndrome with a heterogeneous presentation. This study provides an in-;depth description of haemodynamic and metabolic alterations revealed by systematic assessment through cardiopulmonary exercise testing combined with exercise echocardiography (CPETecho) within a dedicated dyspnoea clinic. Methods and results Consecutive patients (n = 297), referred to a dedicated dyspnoea clinic using a standardized workup including CPETecho, with HFpEF diagnosed through a H2FPEF score ≥6 or HFA-PEFF score ≥5, were evaluated. A median of four haemodynamic/metabolic alterations was uncovered per patient: impaired stroke volume reserve (73%), impaired chronotropic reserve (72%), exercise pulmonary hypertension (65%), and impaired diastolic reserve (64%) were the most frequent cardiac alterations. Impaired peripheral oxygen extraction and a ventilatory limitation were present in 40% and 39%, respectively. In 267 patients (90%), 575 further diagnostic examinations were recommended (median of two tests per patient). Cardiac magnetic resonance imaging, coronary or amyloidosis workup, ventilation–perfusion scanning, and pulmonology referral were each recommended in approximately one out of three patients. In 293 patients (99%), 929 cardiovascular drug optimizations were performed (median of 3 modifications per patient). In 110 patients (37%), 132 cardiovascular interventions were performed, with ablation as the most frequent procedure. Conclusion Holistic workup of HFpEF patients within a multidisciplinary, dedicated dyspnoea clinic, including systematic implementation of CPETecho reveals various haemodynamic/metabolic alterations, leading to further diagnostic testing and potential treatment changes in the majority of cases.

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Aim To compare the cardiac function and pulmonary vascular function during exercise between dyspneic and non-dyspneic patients with type 2 diabetes mellitus (T2DM). Methods 47 T2DM patients with unexplained dyspnea and 50 asymptomatic T2DM patients underwent exercise echocardiography combined with ergospirometry. Left ventricular (LV) function (stroke volume, cardiac output, LV ejection fraction, systolic annular velocity (s’)), estimated LV filling pressures (E/e’), mean pulmonary arterial pressures (mPAP) and mPAP/COslope were assessed at rest, low- and high-intensity exercise with colloid contrast. Results Groups had similar patient characteristics, glycemic control, stroke volume, cardiac output, LV ejection fraction and E/e’ (p > 0.05). The dyspneic group had significantly lower systolic LV reserve at peak exercise (s’) (p = 0.021) with a significant interaction effect (p < 0.001). The dyspneic group also had significantly higher mPAP and mPAP/CO at rest and exercise (p < 0.001) with significant interaction for mPAP (p < 0.009) and insignificant for mPAP/CO (p = 0.385). There was no significant difference in mPAP/COslope between groups (p = 0.706). However, about 61% of dyspneic vs. 30% of non-dyspneic group had mPAP/COslope > 3 (p = 0.009). The mPAP/COslope negatively predicted V̇O2peak in dyspneic group (β= -1.86, 95% CI -2.75, -0.98; multivariate model R²:0.54). Conclusion Pulmonary hypertension and less LV systolic reserve detected by exercise echocardiography with colloid contrast underlie unexplained exertional dyspnea and reduced exercise capacity in T2DM.

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Funding Acknowledgements Type of funding sources: None. Background Aortic valve stenosis (AS) and heart failure with preserved ejection fraction (HFpEF) present with similar cardiac alterations, but their overlap is poorly understood.(1–3). Purpose To study left ventricular (LV) hypertrophy, diastolic dysfunction, left atrial (LA) dysfunction, hemodynamics, and exercise capacity according to HFpEF status versus AS severity. Methods Patients (n=206) with at least moderate AS (aortic valve area ≤0.85 cm2/m2) and discordant symptoms underwent cardiopulmonary exercise testing with simultaneous echocardiography. The population was stratified according to the probability of underlying HFpEF by the H2FPEF score [0–5 (AS/HFpEF-) vs. 6–9 points (AS/HFpEF+)] and AS severity (Moderate vs. Severe). Results Mean age was 73±10 years with 40% women. Stratification yielded 41 AS/HFpEF+ (20%) versus 165 AS/HFpEF- (80%) and 139 Severe (67%) versus 67 Moderate (33%) AS patients. AS/HFpEF+ patients had a lower LV global longitudinal strain, impaired diastolic function, reduced LV compliance, and more pronounced LA dysfunction compared to AS/HFpEF- patients. The mean pulmonary arterial pressure-cardiac output (mPAP/CO) slope was significantly higher in AS/HFpEF+ versus AS/HFpEF- (5.4±3.1 vs. 3.9±2.2 mmHg/L/min, respectively; p = 0.003), mainly driven by impaired cardiac output (CO) reserve and chronotropic incompetence, with signs of right ventricular-pulmonary arterial (RV-PA) uncoupling. AS/HFpEF+ versus AS/HFpEF- was associated with a lower peak aerobic capacity (11.5±3.7 vs. 15.9±5.9 mL/min/kg, respectively; p<0.0001), but did not differ between Moderate and Severe AS (14.7±5.5 vs. 15.2±5.9mL/min/kg, respectively; p = 0.6). Conclusions A high H2FPEF score is associated with a reduced exercise capacity and adverse hemodynamics in patients with moderate to severe AS. Both exercise performance and hemodynamics correspond better with intrinsic cardiac dysfunction than AS severity itself.