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.

European Heart Journal
|December 1, 1995
PubMed

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.

Related Concept Videos

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Blood Studies for Cardiovascular System I: Cardiac Biomarkers01:20

Blood Studies for Cardiovascular System I: Cardiac Biomarkers

Cardiac biomarkers are enzymes, proteins, and hormones released into the blood when cardiac cells are injured. They are powerful tools for triaging.
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Myocarditis III: Medical Management01:14

Myocarditis III: Medical Management

Myocarditis: Comprehensive Medical ManagementMyocarditis, the heart muscle inflammation, requires a comprehensive medical management strategy that addresses the underlying cause, provides supportive care, manages symptoms, and reduces cardiac workload.Infections and Autoimmune CausesAdminister appropriate antimicrobial therapy when an infectious agent causes myocarditis. For instance, penicillin treats infections caused by Group A Streptococcus. In cases where autoimmune processes are...