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Background Elevated arterial stiffness can contribute to cardiac and renal dysfunction. In heart failure with preserved ejection fraction (HFpEF), increased arterial afterload may drive disease progression through ventricular-arterial decoupling— distinguishing it from HF with reduced ejection fraction (HFrEF) which primarily stems from intrinsic myocardial disease. In the kidneys, this can impose excessive mechanical stress on glomerular cells and disrupt perfusion. Carotid-femoral pulse wave velocity (cf-PWV, normal <10m/s) is the gold-standard measure of arterial stiffness. This study evaluated cf-PWV differences between HFrEF, HFpEF and acute-on-chronic kidney disease (AKI on CKD) in decompensated and compensated states to elucidate the dynamic interplay between arterial stiffness and clinical stability.Methods This single-centre prospective study recruited 109 patients aged ≥60-years (from an initial 120, with 11 exclusions). Each participant underwent comprehensive assessment during hospitalisation (decompensated state) and at follow-up (compensated state), including blood tests, ECG, cf-PWV measurement using the SphygmoCor® tonometry device on the carotid and femoral arteries ( figure 1). Echocardiogram was performed if unavailable within 12 months. Statistical analysis used paired t-test, Chi-square test and repeated measures ANOVA to assess changes in PWV from decompensation to discharge, adjusting for covariates.Results Baseline characteristics are summarised in table 1. There were no significant differences in age, sex, body mass index and ethnicity. Cf-PWV differed significantly between groups (p=0.013), with HFpEF demonstrating the highest average PWV (13.9±4.4m/s, followed by AKI on CKD (11.7±3.7m/s) and HFrEF (10.9± 4.9m/s). All groups exhibited elevated PWV (>10m/s) during decompensation, with significant reductions observed in the compensated state for HFpEF (to 10.8±2.8m/s, p<0.001) and AKI on CKD (to 10.8±3.4m/s, p=0.04). Even in the compensated state, mean PWV remained >10m/s, unlike HFrEF which dropped below this threshold (9.8±3.1m/s). After adjusting for all cardiovascular medications, changes in weight, natriuretic peptides and systolic blood pressure on repeated measures ANOVA, the change in PWV over time was significant across all groups (p=0.011) and differed significantly between the groups (p=0.021).Conclusion Arterial stiffness plays a key role in the pathogenesis of decompensation in HFpEF and AKI on CKD. Despite clinical recovery, PWV remained elevated, reinforcing arterial stiffness as a chronic pathological driver in HFpEF and CKD. This suggests its contribution to both acute decompensation and sustained vascular dysfunction, predisposing patients to future instability. While our findings highlight the potential utility of PWV measurement in identifying patients at higher risk of decompensation—particularly in HFpEF—larger studies are needed to validate its role in risk stratification and clinical utility.Abstract 5-015 Table 1Comparison of baseline characteristics between the 3 groups HFrEF (n=37) HFpEF (n=36) AKI on CKD (n=36) p value Age – mean ± SD 75.4 ± 8.7 77.0 ± 7.5 75.6 ± 8.6 0.654 Female sex – n (%) 10 (27) 16 (44) 14 (39) 0.287 BMI – mean ± SD 29.6 ± 7.1 29.8 ± 6.8 27.6 ± 8.1 0.390 Ethnicity – n (%) Asian Black White Other 4 (11)3 (8)27 (73)3 (8) 2 (6)1 (3)30 (83)3 (8) 4 (11)2 (6)28 (77)2 (6) 0.837 Medical history – n (%) Atrial fibrillation Diabetes mellitus Hypertension IHD High cholesterol Valvular HD Stroke/ TIA Asthma/COPD 25 (68)12 (32)20 (54)14 (38)9 (24)5 (14)7 (19)10 (27) 24 (67)19 (53)23 (64)13 (36)9 (25)9 (25)5 (14)8 (22) 16 (45.7)18 (50)26 (72)12 (33)10 (28)05 (14)7 (19) 0.2790.1600.2720.4460.8850.0060.7440.591 NYHA Class – n (%) I II III IV 03 (8)18 (49)16 (43) 03 (8)12 (33)20 (56) N/A -- Medications – n (%) ACE inhibitors ARBs ARNI Amiodarone Beta-blockers Digoxin DHP CCB Non-DHP CCB Hydralazine Loop diuretics MRA Nitrates Statins SGLT2 inhibitors 6 (16)2 (5)23 (62)7 (19)34 (92)8 (22)2 (5)01 (3)34 (92)20 (54)016 (43)24 (65) 8 (22)2 (6)1 (3)1 (3)32 (89)7 (19)9 (25)1 (3)5 (14)32 (89)9 (25)4 (11)22 (61)13 (36) 10 (28)4 (11)01 (3)17 (47)1 (3)8 (22)1 (3)3 (8)19 (53)1 (3)2 (6)23 (64)9 (25) 0.4910.570<0.0010.015<0.0010.0460.1300.1300.222<0.001<0.0010.1150.1550.002 Biochemistry NT-proBNP- mean ± SD 1150.8 ± 858.9 792.8 ± 867.8 629.5 ± 753.2 0.027 Estimated GFR 51.3 ± 21.3 52.7 ± 22.0 38.6 ± 22.2 0.013 White cell count (x109/L) 8.2 ± 2.7 8.4 ± 4.0 10.9 ± 5.1 0.009 Haemoglobin 130 ± 16.7 120.5 ± 21.4 117.5 ± 22.8 0.027 Platelets – median (IQR) 210 (91.5) 231 (151.5) 243 (114) 0.409 Echocardiogram LVEF (%) 30.5 ± 11.5 54.5 ± 5.6 50.2 ± 10.5 - LVEDD (mm) 55.6 ± 10.8 47 ± 6.4 49.3 ± 5.3 <0.001 Indexed LV mass 125.0 ± 57.2 103.0 ± 32.8 91.4 ± 23.0 0.002 Average E/e’ – median (IQR) 13.0 (6.2) 15.7 (7.2) 11.7 (4.3) 0.033 TAPSE 16.3 ± 13.4 15.8 ± 5.4 15.9 ± 3.8 0.963 Haemodynamics Peripheral systolic BP 111.9 ± 14.9 121.5 ± 16.8 129.4 ± 23.4 <0.001 Peripheral diastolic BP 67.7 ± 9.4 68.2 ± 9.2 71.2 ± 9.8 0.227 Pulse wave velocity (m/s) 10.9 ± 4.9 13.9 ± 4.4 11.7 ± 3.7 0.013 Abbreviations: ACEi- angiotensin converting enzyme inhibitor; ARB- angiotensin receptor blocker; BMI- body mass index; BNP- B-type natriuretic peptide; CKD- chronic kidney disease; COPD- chronic obstructive pulmonary disease; (N)-DHP CCB- (non)-dihydropyridine calcium channel blockers; GFR- glomerular filtration rate; LVEDD- left ventricular end-diastolic diameter; LVEF- left ventricular ejection fraction; MRA- mineralocorticoid receptor antagonists; SGLT2i- sodium glucose co-transporter 2 inhibitor; TAPSE- tricuspid annular planar systolic exercise; TIA- transient ischaemic attackAbstract 5-015 Figure 1Comparison of pulse wave velocity at decompensated and compensated states in HFrEF, HFpEF and acute on chronic kidney disease