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Relation between mitral regurgitation and platelet activation
1Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong.
Objectives:
This study sought to examine the effect of mitral regurgitation (MR) on platelet activation in patients with mitral valve prolapse (MVP) or rheumatic MR.
Background:
MVP and rheumatic MR are associated with an increased incidence of thromboembolic events. Although the underlying causes are not clear, increased platelet activation has been suggested as one of the pathogenic mechanisms. Results of previous studies that have investigated the relation between MVP and platelet activation are controversial. Whether the presence of MR in patients with mitral valve disease is associated with platelet activation remains unclear.
Methods:
We studied platelet activation by measuring the plasma level of platelet factor 4 (PF4) and beta-thromboglobulin (BTG) in 16 patients with MVP, 12 patients with rheumatic MR and 25 control subjects. A detailed echocardiographic examination, including M-mode measurement and color Doppler flow mapping to detect the presence and severity of MR was performed.
Results:
Patients and control subjects were matched for gender, age and left ventricular ejection fraction. Eight (50%) of 16 patients with MVP had MR. Patients with MVP and MR and patients with rheumatic MR had a significantly larger left atrial diameter. Mean log plasma levels of PF4 and BTG were significantly higher in patients with MVP and MR and patients with rheumatic MR than in control subjects (1.17 +/- 0.22 and 0.93 +/- 0.23 IU/ml vs. 0.52 +/- 0.34 IU/ml, p < 0.01; 1.70 +/- 0.21 and 1.53 +/- 0.15 IU/ml vs. 1.37 +/- 0.15 IU/ml, p < 0.05, respectively) but were comparable in patients with MVP and no MR and control subjects. Plasma levels of PF4 and BTG were positively correlated with the severity of MR, as assessed by a semiquantitative method (r = 0.59, p = 0.0001; r = 0.60, p = 0.0001, respectively). Increasing age and left atrial enlargement were not related to platelet activation.
Conclusions:
MR in mitral valve disease was associated with systemic platelet activation. MVP itself was not associated with increased platelet activation. The degree of platelet activation was positively correlated with the severity of MR and was independent of the underlying etiology of mitral valve disease, age and left atrial size. The possibility of a higher incidence of thromboembolism and the role of antiplatelet agents in such patients will require further studies to determine.
Insights
Mitral regurgitation (MR) in mitral valve disease activates platelets, but mitral valve prolapse (MVP) alone does not. Platelet activation correlates with MR severity, suggesting a role in thromboembolism.
Area of Science:
- Cardiology
- Hematology
- Biomedical Science
Background:
- Mitral valve prolapse (MVP) and rheumatic mitral regurgitation (MR) are linked to increased thromboembolic events.
- The exact causes are unknown, but heightened platelet activation is a suspected pathogenic mechanism.
- Previous studies on MVP and platelet activation yield conflicting results, and the association between MR and platelet activation in mitral valve disease remains unclear.
Purpose of the Study:
- To investigate the impact of mitral regurgitation (MR) on platelet activation in patients with mitral valve prolapse (MVP) or rheumatic MR.
- To determine if MVP itself is associated with increased platelet activation.
- To explore the relationship between the severity of MR and the degree of platelet activation.
Main Methods:
- Platelet activation was assessed by measuring plasma levels of platelet factor 4 (PF4) and beta-thromboglobulin (BTG).
- The study included 16 patients with MVP, 12 with rheumatic MR, and 25 controls.
- Echocardiography was used to evaluate the presence and severity of MR.
Main Results:
- Patients with MVP and MR, and those with rheumatic MR, exhibited significantly higher plasma levels of PF4 and BTG compared to controls.
- Platelet activation markers (PF4 and BTG) were positively correlated with the severity of MR.
- MVP without MR was not associated with increased platelet activation compared to controls.
Conclusions:
- Mitral regurgitation (MR) in mitral valve disease is linked to systemic platelet activation.
- Mitral valve prolapse (MVP) in the absence of significant MR is not associated with heightened platelet activation.
- The degree of platelet activation correlates with MR severity and is independent of disease etiology, age, or left atrial size, warranting further investigation into thromboembolic risk and antiplatelet therapy.
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