Relationship between control of ventricular rate in atrial fibrillation and systemic coagulation activation in patients with mitral stenosis.
OBJECTIVE
Systemic thromboembolism is a major complication in patients with mitral stenosis (MS), especially in those who have atrial fibrillation (AF). It has been suggested that systemic coagulation activity may be increased in these patients. The study aim was to investigate the relationship between control of ventricular rate and systemic coagulation factors in patients with MS and AF by measuring plasma levels of prothrombin fragment (PF) 1+2, thrombin-antithrombin III complex (TAT) and plasminogen activator inhibitor-1.


METHODS
Fifty-four consecutive patients with moderate to severe MS and AF were included in the study. Patients with resting heart rates < 100 beats per min were considered as having a controlled ventricular response rate (group A; n = 28) and those with > 100 beats per min as an uncontrolled ventricular response rate (group B; n = 26).


RESULTS
Group A patients had a lower mean mitral gradient and pulmonary artery pressure than group B patients (11 +/- 6 versus 15 +/- 5 and 35 +/- 7 versus 39 +/- 8; p < 0.05, respectively). Plasma concentrations of PF 1+2 (4.17 +/- 2.1 versus 2.95 +/- 1.21; p < 0.01) and TAT III (4.61 +/- 1.75 versus 3.12 +/- 1.01; p < 0.01) were elevated in group B compared with group A. Similarly, group B patients had higher plasminogen activator inhibitor-1 levels than group A patients (7.87 +/- 3.8 versus 5.8 +/- 2.9; p < 0.05). A significant correlation was found between heart rate and plasma PF 1+2 and TAT levels. Multiple logistic regression analysis revealed that heart rate and mean mitral gradient were independent predictors of systemic coagulation activation.


CONCLUSIONS
Besides contributing towards hemodynamic and symptomatic relief, the control of AF rate in MS patients induces a drastic decline in coagulation activation, and may also reduce the incidence of thromboembolism.
Atak
Ramazan
R
Department of Cardiology, Turkiye Yuksek Ihtisas Hospital, Ankara, Turkey. hratak@yahoo.com
Turhan
Hasan
H
Senen
Kubilay
K
Yalta
Kenan
K
Ayaz
Selime
S
Alyan
Omer
O
Basar
Nurcan
N
Demirkan
Deniz
D
D000293:Adolescent; D000328:Adult; D000990:Antithrombin III; D001022:Aortic Valve Insufficiency / Q000097:blood / Q000503:physiopathology; D001281:Atrial Fibrillation / Q000097:blood* / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000502:physiology*; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000097:blood / Q000503:physiopathology; D008946:Mitral Valve Stenosis / Q000097:blood* / Q000503:physiopathology*; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011237:Predictive Value of Tests; D011516:Prothrombin; D012044:Regression Analysis; D012720:Severity of Illness Index; D013223:Statistics as Topic
D015415:Biomarkers; D010446:Peptide Fragments; D017395:Plasminogen Activator Inhibitor 1; C046193:antithrombin III-protease complex; C045879:prothrombin fragment 1.2; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases