Abstract
BackgroundDiscrimination of heart failure with preserved ejection fraction with pulmonary hypertension (HFpEF-PH) from pulmonary arterial hypertension (PAH) is crucial for clinical management but may be challenging due to similarities in clinical and comorbid characteristics. We aimed to investigate tumour and metabolism related proteins in differentiating HFpEF-PH from PAH. MethodsSixty-nine tumour and metabolism plasma proteins were analysed with proximity extension assay in heathy controls (n = 20), patients with PAH (n = 48) and LHF-PH (n = 67) [HFpEF-PH (n = 31) and HF reduced EF-PH (n = 36)]. Haemodynamics were assessed with right heart catheterization. ResultsThe plasma levels of alpha-1-microglobulin/bikunin precursor (AMBP) and lipoprotein lipase (LPL), were higher in HFpEF-PH compared to healthy controls (p < 0.01), HFrEF-PH (p < 0.05), and PAH (p < 0.001). Glyoxalase I levels were higher in HFpEF-PH and HFrEF-PH compared to controls (p < 0.001) and PAH (p < 0.001). Each of plasma AMBP, LPL, and glyoxalase I, adjusted for age and sex in multivariable logistic regression models, could differentiate HFpEF-PH from PAH, with areas under the receiver operating characteristic curve (AUC) of 0.81, 0.84 and 0.79, respectively. The combination of AMBP, LPL and glyoxalse I yielded the largest AUC of 0.87 [95% confidence interval (0.79–0.95)] in discriminating HFpEF-PH from PAH, with a sensitivity of 87.1% and a specificity of 85.4%. In HFpEF-PH, the plasma levels of AMBP correlated with pulmonary arterial wedge pressure (rs = −0.42, p = 0.018). ConclusionsPlasma AMBP, LPL and glyoxalase I may facilitate the distinction of HFpEF-PH from PAH. Larger clinical studies are encouraged to confirm and validate our findings.
Highlights
Heart failure (HF) with preserved ejection fraction (HFpEF) accounts for approximately 40-50% of all incident cases of HF and is driven by a complex interplay of molecular and structural cardiac alterations.[1]
In previous studies of heart transplanted patients with pulmonary hypertension (PH), we found that several tumour- and metabolism-related biomarkers were associated with the reversal of HF and PH after heart transplantation and to improved pulmonary and cardiac haemodynamics.[15, 16]
According to the aforementioned eligibility criteria, the 36 proteins were classified into either i.) HFpEF-PH specific (n=3) or ii.) LHF-PH specific (n=34) (p
Summary
Heart failure (HF) with preserved ejection fraction (HFpEF) accounts for approximately 40-50% of all incident cases of HF and is driven by a complex interplay of molecular and structural cardiac alterations.[1]. Pulmonary arterial hypertension (PAH, group I PH) arises due to pre-capillary PH and is, pathologically a distinct entity, characterized by vasoconstriction and structurally obliterated and remodelled pulmonary arteries, precipitating maladaptive right ventricular remodelling and failure.[5, 6] Compared to PAH, patients with HFpEF-PH are generally older and more multimorbid, frequently presenting with systemic hypertension, obesity, diabetes mellitus and coronary artery disease.[7]. Discrimination of heart failure with preserved ejection fraction with pulmonary hypertension (HFpEF-PH) from pulmonary arterial hypertension (PAH) is crucial for clinical management but may be challenging due to similarities in clinical and comorbid characteristics. Results: The plasma levels of alpha-1-microglobulin/bikunin precursor (AMBP) and lipoprotein lipase (LPL), were higher in HFpEF-PH compared to healthy controls (p
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