Decreased platelet activation and endothelial dysfunction after percutaneous mitral balloon valvuloplasty.
OBJECTIVE
This study was conducted to assess the changes in platelet activation and endothelial dysfunction in patients with mitral stenosis (MS) and sinus rhythm (SR) following percutaneous mitral balloon valvuloplasty (PMBV).


BACKGROUND
Systemic thromboembolism is a serious complication in patients with valvular heart disease, and its incidence is highest in those with mitral stenosis. A hypercoagulable state has also been reported in patients with mitral stenosis and sinus rhythm. A recent study has shown that patients with previous PMBV had a lower incidence of thromboembolism.


RESULTS
The study was conducted in 21 patients (two men, 19 women, mean age=34+/-6 years) with mitral stenosis and sinus rhythm (SR) who underwent percutaneous mitral balloon valvuloplasty and 17 healthy control subjects (two men, 15 women, mean age=33+/-6 years). Biochemical markers of platelet activity (beta thromboglobulin, BTG, and soluble P-selectin, sPsel) and endothelial dysfunction (von Willebrand Factor, vWF) were measured in both control subjects' and patients' serum samples taken immediately before PMBV and 24 h after PMBV procedure. All patients underwent successful PMBV. Significant improvement of mitral valve area, pulmonary artery pressure, mean mitral gradients, and left atrial diameter were achieved in all patients after PMBV. Compared with control subjects, patients with MS had higher plasma levels of BTG (66+/-26 ng/ml vs. 14+/-6 ng/ml, P<0.001), vWF (177+/-67 units/dl vs. 99+/-37 units/dl, P<0.0001), sPsel (226+/-74 ng/ml vs. 155+/-66 ng/ml, P<0.001). There was a significant reduction of plasma levels of BTG (66+/-26 ng/ml vs. 48+/-20 ng/ml, P=0.002), vWF (177+/-67 units/dl vs. 134+/-60 units/dl, P=0.001) and P-selectin (226+/-74 ng/ml vs. 173+/-71 ng/ml, P=0.008,) 24 h after PMBV.


CONCLUSIONS
We have shown that patients with severe MS and SR have increased platelet activation and endothelial dysfunction compared with control subjects and PMBV results in decreased platelet activity and improvement of endothelial injury.
Yetkin
Ertan
E
Inonu University Faculty of Medicine, Department of Cardiology, Malatya, Turkey.
Erbay
A Riza
AR
Turhan
Hasan
H
Ileri
Mehmet
M
Ayaz
Selime
S
Atak
Ramazan
R
Senen
Kubilay
K
Cehreli
Sengul
S
D000328:Adult; D001022:Aortic Valve Insufficiency / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D002404:Catheterization; D004452:Echocardiography; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000503:physiopathology*; D005260:Female; D006329:Heart Conduction System / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D008297:Male; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D008946:Mitral Valve Stenosis / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000502:physiology*; D012214:Rheumatic Heart Disease / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000628:therapy; D012720:Severity of Illness Index; D012995:Solubility; D016896:Treatment Outcome; D001620:beta-Thromboglobulin / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
D015415:Biomarkers; D019007:P-Selectin; D001620:beta-Thromboglobulin; D014841:von Willebrand Factor