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Homocysteine increase after acute myocardial infarction--can it explain the differences between case-control and
Eustáquio Gomes1, Rita Duarte, R Palma Reis
1Serviço de Cardologia do Hospital Pulido Valente, Lisboa, Portugal.
Insights
Homocysteine (HC) levels significantly increase by 20% within 36 hours after acute myocardial infarction (AMI) and remain elevated for at least one month. This post-AMI HC rise may explain discrepancies in studies assessing its cardiovascular disease risk.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Clinical Pathology
Background:
- Elevated homocysteinemia (HC) is a suspected risk factor for cardiovascular disease, particularly acute myocardial infarction (AMI).
- Conflicting results exist between case-control and prospective studies regarding the association between HC and cardiovascular risk.
- The temporal changes in HC levels following an AMI have not been well-characterized.
Purpose of the Study:
- To investigate the evolution of homocysteinemia (HC) levels in patients after experiencing an acute myocardial infarction (AMI).
- To determine if HC levels change significantly in the period following an AMI and if these changes persist.
Main Methods:
- Fasting homocysteinemia (HC) was measured in 34 patients at three time points after acute myocardial infarction (AMI): within 36 hours, between days 3-6, and one month post-AMI.
- Traditional cardiovascular risk factors and routine laboratory tests were also assessed simultaneously.
- Statistical analysis, including correlation coefficients, was used to evaluate changes and relationships in HC levels.
Main Results:
- Mean HC levels increased significantly from 13.85 ± 5.46 mol/l within 36 hours to 16.16 ± 6.63 mol/l between days 3-6 post-AMI (p < 0.05).
- HC levels remained elevated and similar at one month post-AMI (16.27 ± 7.27 mol/l), showing no significant difference from the 3-6 day measurements (p = 0.88).
- A significant positive correlation was observed between HC measurements at all time points (CC = 0.62 and CC = 0.57, both p = 0.001).
Conclusions:
- Homocysteinemia (HC) levels significantly increase approximately 36 hours after acute myocardial infarction (AMI) and this elevation is sustained for at least one month.
- The observed increase in HC post-AMI may contribute to the differing conclusions on its role as a cardiovascular risk factor found in various study designs.
- Understanding HC dynamics after AMI is crucial for accurately assessing its impact on cardiovascular health.
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.