Key result
Elevated uric acid independently predicted the composite of all-cause mortality or heart failure hospitalization in HFpEF patients (HR 3.76; 95% CI 1.19-11.85; P=0.024), whereas MPO did not.
Why the study?
Microvascular inflammation is proposed as an underlying mechanism in HFpEF, and MPO is associated with vascular dysfunction and prognosis in congestive HF.
Do MPO and related biomarkers predict all-cause mortality or HF hospitalization in patients with HFpEF?
Cohort (n=132)
Do MPO and related biomarkers predict all-cause mortality or HF hospitalization in patients with HFpEF?
Hazard Ratio: 3.76 (95% CI 1.19–11.85)
p-value: p=0.024
In HFpEF patients, MPO and related biomarkers of oxidative stress are elevated, with uric acid independently predicting the composite of all-cause mortality or HF hospitalization.
May inform HFpEF risk stratification; leaves open whether uric acid is a modifiable target.
Aims In heart failure (HF) with preserved ejection fraction (HFpEF), microvascular inflammation is proposed as an underlying mechanism. Myeloperoxidase (MPO) is associated with vascular dysfunction and prognosis in congestive HF. Methods and results MPO, MPO-related biomarkers, and echocardiography were assessed in 86 patients, 4–8 weeks after presentation with acute HF (EF ≥ 45%), and in 46 healthy controls. Patients were followed up for median 579 days (Q1;Q3 276;1178) regarding the composite endpoint all-cause mortality or HF hospitalization. Patients were 73 years old, 51% were female, EF was 64% (Q1;Q3 58;68), E/e′ was ratio 10.8 (8.3;14.0), and left atrial volume index (LAVI) was 43 mL/m2 (38;52). Controls were 60 (57;62) years old (vs. patients; P < 0.001), 24% were female (P = 0.005), and left ventricular EF was 63% (59;66; P = 0.790). MPO was increased in HFpEF compared with controls, 101 (81;132) vs. 86 (74;101 ng/mL, P = 0.015), as was uric acid 369 (314;439) vs. 289 (252;328 μmol/L, P < 0.001), calprotectin, asymmetric dimethyl arginine (ADMA), and symmetric dimethyl arginine (SDMA), while arginine was decreased. MPO correlated with uric acid (r = 0.26; P = 0.016). In patients with E/e′ > 14, uric acid and SDMA were elevated (421 vs. 344 μM, P = 0.012; 0.54 vs. 0.47 μM, P = 0.039, respectively), and MPO was 121 vs. 98 ng/mL (P = 0.090). The ratios of arginine/ADMA (112 vs. 162; P < 0.001) and ADMA/SDMA (1.36 vs. 1.17; P = 0.002) were decreased in HFpEF patients, suggesting reduced NO availability and increased enzymatic clearance of ADMA, respectively. Uric acid independently predicted the endpoint [hazard ratio (HR) 3.76 (95% CI 1.19–11.85; P = 0.024)] but not MPO [HR 1.48 (95% CI 0.70–3.14; P = 0.304)] or the other biomarkers. Conclusions In HFpEF, MPO-dependent oxidative stress reflected by uric acid and calprotectin is increased, and SDMA is associated with diastolic dysfunction and uric acid with outcome. This suggests microvascular neutrophil involvement mirroring endothelial dysfunction, a central component of the HFpEF syndrome and a potential treatment target.
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Hage et al. (2020) conducted a cohort in Heart failure with preserved ejection fraction (HFpEF) (n=132). Uric acid and Myeloperoxidase (MPO) vs. Healthy controls was evaluated on Composite of all-cause mortality or HF hospitalization (HR 3.76, 95% CI 1.19-11.85, p=0.024). Elevated uric acid independently predicted the composite of all-cause mortality or heart failure hospitalization in HFpEF patients (HR 3.76; 95% CI 1.19-11.85; P=0.024), whereas MPO did not.
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