Document Detail

Relationship between control of ventricular rate in atrial fibrillation and systemic coagulation activation in patients with mitral stenosis.
MedLine Citation:
PMID:  15086252     Owner:  NLM     Status:  MEDLINE    
BACKGROUND AND AIM OF THE STUDY: 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. CONCLUSION: 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.
Ramazan Atak; Hasan Turhan; Kubilay Senen; Kenan Yalta; Selime Ayaz; Omer Alyan; Nurcan Basar; Deniz Demirkan
Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  The Journal of heart valve disease     Volume:  13     ISSN:  0966-8519     ISO Abbreviation:  J. Heart Valve Dis.     Publication Date:  2004 Mar 
Date Detail:
Created Date:  2004-04-16     Completed Date:  2004-11-06     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9312096     Medline TA:  J Heart Valve Dis     Country:  England    
Other Details:
Languages:  eng     Pagination:  159-64     Citation Subset:  IM    
Department of Cardiology, Turkiye Yuksek Ihtisas Hospital, Ankara, Turkey.
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MeSH Terms
Antithrombin III
Aortic Valve Insufficiency / blood,  physiopathology
Atrial Fibrillation / blood*,  physiopathology*
Biological Markers / blood
Blood Coagulation / physiology*
Heart Rate / physiology*
Heart Ventricles / physiopathology
Middle Aged
Mitral Valve Insufficiency / blood,  physiopathology
Mitral Valve Stenosis / blood*,  physiopathology*
Peptide Fragments / blood
Peptide Hydrolases / blood
Plasminogen Activator Inhibitor 1 / blood
Predictive Value of Tests
Regression Analysis
Severity of Illness Index
Statistics as Topic
Reg. No./Substance:
0/Biological Markers; 0/Peptide Fragments; 0/Plasminogen Activator Inhibitor 1; 0/antithrombin III-protease complex; 0/prothrombin fragment 1.2; 9000-94-6/Antithrombin III; 9001-26-7/Prothrombin; EC 3.4.-/Peptide Hydrolases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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