Why the study?
Is plasma homocysteine concentration elevated in horses with atrial fibrillation and does it predict AF recurrence?
Is plasma homocysteine concentration elevated in horses with atrial fibrillation and does it predict AF recurrence?
Unlike in humans, plasma homocysteine concentrations are not elevated in horses with atrial fibrillation and do not predict AF recurrence.
Does not support homocysteine as an AF biomarker in horses; leaves open species-specific mechanisms versus humans.
Homocysteine (HCY) is an amino acid produced from methionine metabolism. Plasma homocysteine concentrations ([HCY]p) are elevated (>13 μmol/L) in people with atrial fibrillation (AF) and can predict the recurrence of AF after cardioversion. This study aimed to validate a commercially available human HCY assay for use in horses to develop reference intervals for [HCY]p and compare [HCY]p in healthy horses and horses with AF. Healthy horses (n = 27) and horses with AF (n = 55, 34 of which were cardioverted using transvenous electrical cardioversion). Blood samples were analysed for HCY using an automated enzyme-cycling assay (Homocysteine Cobas C, Integra, Roche) and creatinine (compensated Jaffe method). Assay linearity and precision were assessed, reference intervals calculated and [HCY]p and creatinine compared between groups. The assay was precise (coefficient of variation 1.6–4.3%, n = 10 repetitions) and provided linear results (r = 0.99 for spiked and natural samples) for a range of [HCY]p. The reference interval for [HCY]p was 1.5–7.8 μmol/L. The plasma concentration of homocysteine was 4.65 ± 1.5 μmol/L (mean ± standard deviation) in healthy horses and 4.65 ± 1.72 μmol/L in horses with AF (p=0.99); [HCY]p was not associated with recurrence of AF (n = 18, p=0.97). A weak, positive correlation between plasma creatinine and [HCY]p was detected (r = 0.295, p=0.008, r2 = 0.11). This assay allows precise measurement of [HCY]p in horses. Unlike in people, [HCY]p is not increased in horses with AF and cannot predict AF recurrence. This might be due to differences in the underlying pathological mechanisms of AF development in people and horses.
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Mitchell et al. (2018) studied this question.
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