title: Homocysteine increase after acute myocardial infarction--can it explain the differences between case-control and cohort studies?
abstract: Several case-control studies agree that elevated homocysteinemia (HC) is a risk factor for cardiovascular disease, particularly for acute myocardial infarction (AMI). However, this agreement does not extend to prospective studies--some of which confirm and others (MRFIT and Karelia) reject this relation. After an AMI there are significant changes in biochemical and laboratory parameters, including a decrease in cholesterolemia, which takes several months to return to baseline levels. The evolution of HC after AMI is still unknown. In this work we set out to evaluate the evolution of homocysteinemia values after acute myocardial infarction. We evaluated fasting homocysteinemia in 34 sequential patients after admission to the Intensive Care Unit and after confirmation of acute myocardial infarction (26 male; mean age 63.8 +/- 13.9 years) in the first 36 hours, between the 3rd and 6th day, and one month after AMI. Simultaneously, we studied traditional risk factors and performed routine laboratory tests. The mean values found for HC were 13.85 +/- 5.46 mol/l in the first 36 hours after AMI, 16.16 +/- 6.63 mol/l between the 3rd and the 6th day, and 16.27 +/- 7.27 mol/l one month after myocardial infarction. The difference between the first and the second, and between the first and the third measurements, was significant (p < 0.05). The HC values found 3-6 days and one month after myocardial infarction were similar (p = 0.88). A highly significant correlation was found between HC values assessed in the first and second (correlation coefficient [CC] = 0.62) and in the second and third measurements (CC = 0.57), both with p = 0.001. We can conclude that HC levels increase significantly 36 hours after an acute myocardial infarction, an increase of around 20%, which is maintained until at least one month after the infarction. In these circumstances the difference in the vascular risk of HC found between case-control and prospective studies may be explained, at least partially, by the HC increase after AMI.
authors.affiliation: Serviço de Cardologia do Hospital Pulido Valente, Lisboa, Portugal.
authors.forename: Eustáquio
authors.initials: E
authors.lastname: Gomes
authors.forename: Rita
authors.initials: R
authors.lastname: Duarte
authors.forename: R Palma
authors.initials: RP
authors.lastname: Reis
authors.forename: António
authors.initials: A
authors.lastname: Cândido
authors.forename: Nuno
authors.initials: N
authors.lastname: Cardim
authors.forename: Maria João
authors.initials: MJ
authors.lastname: Correia
authors.forename: Susana
authors.initials: S
authors.lastname: Castela
authors.forename: Rui
authors.initials: R
authors.lastname: Cordeiro
authors.forename: Alexandra
authors.initials: A
authors.lastname: Ramos
authors.forename: Judite Lima
authors.initials: JL
authors.lastname: Lobo
authors.forename: J F Martins
authors.initials: JF
authors.lastname: Correia
mesh_terms: D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D015331:Cohort Studies; D005215:Fasting / Q000097:blood; D005260:Female; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D013997:Time Factors
chemical_list: D015415:Biomarkers; D006710:Homocysteine