Homocysteine levels as a measure of myocardial damage
A recent study shows that homocysteine levels reflect the extent of myocardial damage in acute ischemia.
Plasma homocysteine levels are positively correlated with the extent of ischemic myocardial damage in patients presenting with acute coronary syndromes (ACS), a multicenter research team report in Journal of the American College of Cardiology.
Al-Obaidi and colleagues studied 390 consecutive patients who presented with acute myocardial infarction (MI) or unstable angina pectoris (UA). Analysis of clinical and biochemical parameters revealed that there was a significant increase in peak cardiac troponin T (cTnT) levels in the highest homocysteine quintile (7.85 μg/l, p<0.0001 for top versus bottom quintile). The authors also report a step-up in peak cTnT levels in the top homocysteine quintile, although this was restricted to UA patients (p<0.0001 for analysis of variance, p<0.0001 for top versus bottom quintile). Multivariate regression analysis showed that cTnT levels were influenced by greater age, thrombolysis and a final diagnosis of MI, as well as by homocysteine levels in the 5th quintile; however, the correlation between homocysteine levels and cTnT remained significant after adjusting for these confounders (p<0.0001). Subgroup analysis of UA patients found that homocysteine levels were significantly higher in patients with cTnT levels >0.1 μg/l, compared to those with levels below this value, at 13.8 vs 10.3 μmol/l, respectively, p=0.002. Al-Obaidi and colleagues conclude that threshold homocysteine values of 16.5 μmol/l in MI and 15.7 μmol/l in UA are "strong and independent predictors of ischemic myocardial necrosis" in patients with acute coronary ischemia.
The team also report that in patients who present with unstable angina, those at greatest risk of cardiovascular events can be identified by cTnT levels >0.2 μ/l, as intracoronary thrombosis leading to peripheral embolization causes cTnT release. This finding is of major clinical significance, as it identifies high-risk patients who would benefit from aggressive thrombolytic therapy (such as glycoprotein IIb/IIIa antagonism). The findings, if confirmed, raise the possibility of using either folic acid and/or vitamin B supplementation to limit myocardial damage during acute ischemic injury, the authors note.