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Endocardial injury and the pathogenesis of mural thrombosis in the left ventricle
1Department of Pathology, University of Auckland, School of Medicine, New Zealand.
Insights
Lactic acid damages heart endocardium, causing cell rupture and exposing underlying tissue. This endocardial injury promotes platelet aggregation and thrombosis, particularly on exposed collagen, complicating myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Biochemistry
- Pathology
Background:
- Myocardial infarction (MI) can lead to complications like mural thrombosis.
- The role of metabolites, such as lactic acid, in endocardial injury during ischemia is not fully understood.
Purpose of the Study:
- To investigate the direct effects of lactic acid on endocardial tissue.
- To elucidate the interaction between blood components and lactic acid-damaged endocardium.
Main Methods:
- Isolated, perfused, beating rat hearts were exposed to lactic acid (33 µmol/mL, pH 6.4) for 0-4 hours.
- Endocardial surfaces were subsequently exposed to heparinized blood and buffer.
- Microscopic examination assessed endothelial damage and thrombus formation.
Main Results:
- Lactic acid induced endothelial cell membrane rupture, intercellular separation, and exfoliation.
- Exposed basal lamina showed multilayered platelet aggregation.
- Fibrin deposition and blood cell incorporation occurred primarily in thrombi on exposed collagen.
Conclusions:
- Lactic acid, a metabolite accumulating in ischemic myocardium, directly injures endocardial endothelium.
- This injury creates a prothrombotic surface, increasing the risk of mural thrombosis post-myocardial infarction.
Abstract:
To define the interactions between blood and endocardium damaged by lactic acid, the left ventricles of 48 isolated continuously perfused and beating hearts were exposed for 0-4 hours to Krebs Henseleit buffer (KHB) with or without 33 mumol.ml-1 of lactic acid (pH 6.4). After excising its apex, the left ventricle was flushed with KHB, followed by 10 ml of lightly heparinised blood, and then by a further 10 ml of KHB. Lactic acid caused endothelial cell membrane rupture, intercellular separation, and exfoliation with exposure of the basal lamina and underlying connective tissue. Whereas multilayered platelet aggregations formed on exposed basal lamina, fibrin deposition and incorporation of blood cells were only observed in the larger thrombi which formed on exposed collagen. These findings indicate that a metabolite which accumulates in ischaemic myocardium can cause endocardial injury which would predispose to the mural thrombosis which can complicate myocardial infarction.