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Published on: August 13, 2015
Platelet and leukocyte activation after myocardial infarction. Influence of enalapril
C Sylvén1, I Hagerman, K E Karlberg
1Karolinska Institute, Department of Medicine, Huddinge University Hospital, Stockholm, Sweden.
Insights
Platelet and leukocyte activation persist for 6 months post-myocardial infarction, suggesting ongoing atherosclerosis. Enalapril showed minimal impact on these inflammatory markers.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Acute myocardial infarction (AMI) triggers inflammatory responses.
- Persistent inflammation post-AMI may indicate ongoing atherosclerotic processes.
- Understanding these reactivities is crucial for patient management.
Purpose of the Study:
- To investigate the temporal patterns of platelet and leukocyte activation after AMI.
- To evaluate the effect of enalapril on these inflammatory markers.
- To determine if persistent activation correlates with ongoing atherosclerosis.
Main Methods:
- Double-blind, placebo-controlled study involving 74 patients post-AMI.
- Measurements of fibrinogen, leukocytes, elastase, B beta 30-43 peptide, and platelet angiotensin converting enzyme activity at multiple time points (0-180 days).
- Comparison of enalapril group versus placebo group.
Main Results:
- Platelet and leukocyte activation were observed within the first 7 days post-AMI.
- Fibrinogen, leukocytes, elastase, and B beta 30-43 remained elevated in a significant proportion of patients for 6 months.
- Enalapril did not significantly alter fibrinogen, leukocyte count, or elastase levels; B beta 30-43 peptide showed a decrease but without significant group difference compared to placebo.
- No detectable angiotensin converting enzyme activity in platelets was found.
Conclusions:
- Platelet activation is transient (first week post-AMI), while fibrinogen and leukocyte activation persist for 6 months.
- Persistent inflammatory markers suggest an ongoing atherosclerotic process after AMI.
- Enalapril demonstrated limited efficacy in modulating these specific inflammatory reactivities in the post-AMI period.
Abstract:
In this double-blind placebo-controlled study with enalapril, 74 patients with acute myocardial infarction were followed at 0, 7, 30, 60 and 180 days after the event. Platelets and leukocytes were activated during the first 7 days. During the 6-month period fibrinogen, leukocytes, elastase, and B beta 30-43 remained elevated in 50, 15, 30 and 80% of the patients, respectively, but there was no detectable angiotensin converting enzyme activity in platelets. Enalapril did not modulate fibrinogen, leukocyte count or elastase, while B beta 30-43 peptide showed decreased levels, although the proportion of patients with values above the reference limit did not differ from placebo. In conclusion, in the 6-month post acute myocardial infarction period, while platelet function is activated only during the first week after acute myocardial infarction, fibrinogen and leukocyte function continue to be activated throughout the 6 months in a considerable proportion of patients. These signs may indicate an ongoing atherosclerotic process. Enalapril has no major influence on these reactivities.
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