Abstract
BackgroundBetaine insufficiency is associated with unfavourable vascular risk profiles in metabolic syndrome patients. We investigated associations between betaine insufficiency and secondary events in acute coronary syndrome patients.MethodsPlasma (531) and urine (415) samples were collected four months after discharge following an acute coronary event. Death (34), secondary acute myocardial infarction (MI) (70) and hospital admission for heart failure (45) events were recorded over a median follow-up of 832 days.Principal FindingsThe highest and lowest quintiles of urinary betaine excretion associated with risk of heart failure (p = 0.0046, p = 0.013 compared with middle 60%) but not with subsequent acute MI. The lowest quintile of plasma betaine was associated with subsequent acute MI (p = 0.014), and the top quintile plasma betaine with heart failure (p = 0.043), especially in patients with diabetes (p<0.001). Top quintile plasma concentrations of dimethylglycine (betaine metabolite) and top quintile plasma homocysteine both associated with all three outcomes, acute MI (p = 0.004, <0.001), heart failure (p = 0.027, p<0.001) and survival (p<0.001, p<0.001). High homocysteine was associated with high or low betaine excretion in >60% of these subjects (p = 0.017). Median NT-proBNP concentrations were lowest in the middle quintile of plasma betaine concentration (p = 0.002).ConclusionsBetaine insufficiency indicates increased risk of secondary heart failure and acute MI. Its association with elevated homocysteine may partly explain the disappointing results of folate supplementation. In some patients, especially with diabetes, elevated plasma betaine also indicates increased risk.
Highlights
Betaine (N,N,N-trimethylglycine) is an essential osmolyte and methyl group donor [1,2,3,4] that affects lipid partitioning [5]
Low plasma betaine is common in subjects with an unfavourable vascular risk profile [7,8], but plasma betaine is only modestly correlated with tissue betaine [9]; because of its role as an osmolyte, betaine concentrations are much higher in most tissues than in blood [9]
The strong homeostatic control of plasma and urine betaine [12,13,14] is only minimally affected by osmotic changes, despite large changes in tissue betaine concentrations, and there is no correlation between plasma betaine concentrations and urinary betaine excretions
Summary
Betaine (N,N,N-trimethylglycine) is an essential osmolyte and methyl group donor [1,2,3,4] that affects lipid partitioning [5]. Crosssectional data [6,7,8] hint that betaine insufficiency may be associated with vascular disease, especially in subjects with the metabolic syndrome [3], but the evidence is circumstantial. Low plasma betaine is common in subjects with an unfavourable vascular risk profile [7,8], but plasma betaine is only modestly correlated with tissue betaine [9]; because of its role as an osmolyte, betaine concentrations are much higher in most tissues than in blood [9]. Other crosssectional evidence has associated elevated plasma betaine with vascular disease [15] This presumably reflects a different pathology; the plasma betaine concentrations in this study were still well below tissue concentrations and the elevations could reflect (for example) defective retention of intracellular betaine in some tissues. Betaine insufficiency is associated with unfavourable vascular risk profiles in metabolic syndrome patients. We investigated associations between betaine insufficiency and secondary events in acute coronary syndrome patients
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