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The coagulation system is activated in idiopathic cardiomyopathy
K Yamamoto1, U Ikeda, K Furuhashi
1Department of Cardiology, Jichi Medical School, Tochigi, Japan.
Insights
This study reveals elevated markers of coagulation activation in hypertrophic and dilated cardiomyopathy patients. These changes may stem from left atrial dilation or left ventricular dysfunction, impacting thromboembolic risk.
Area of Science:
- Cardiology
- Hematology
- Biochemistry
Background:
- Thromboembolic events are significant complications in idiopathic cardiomyopathy.
- The precise triggers for coagulation system activation in these conditions remain under-investigated.
Purpose of the Study:
- To investigate plasma markers of platelet activity, thrombotic, and fibrinolytic status in hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM).
- To identify the site of coagulation activation in these cardiomyopathies.
Main Methods:
- Measured plasma levels of platelet factor 4, beta-thromboglobulin, fibrinopeptide A, thrombin-antithrombin III complex, D-dimer, and plasmin-alpha 2-plasmin inhibitor complex.
- Compared levels in 13 HCM patients, 17 DCM patients, and 20 healthy controls.
Main Results:
- Fibrinopeptide A and thrombin-antithrombin III complex were significantly elevated in both HCM and DCM groups compared to controls.
- D-dimer levels were higher in DCM patients than in HCM patients and controls.
- Specific correlations were found between coagulation markers and cardiac dimensions/function in both patient groups.
Conclusions:
- The coagulation system is activated in HCM and DCM.
- Left atrial dilation may trigger coagulation in HCM.
- Left ventricular enlargement and dysfunction may trigger coagulation in DCM.
Objectives:
We investigated the plasma levels of molecular markers for platelet activity and the thrombotic and fibrinolytic status in patients with hypertrophic cardiomyopathy and dilated cardiomyopathy to determine the activating site of coagulation in these disorders.
Background:
A thromboembolic event is a serious complication in patients with idiopathic cardiomyopathy. However, the activating site of the coagulation system in idiopathic cardiomyopathy has not been fully investigated.
Methods:
We determined the plasma levels of molecular markers for platelet activity (platelet factor 4 and beta-thromboglobulin), thrombotic status (fibrinopeptide A and thrombin-antithrombin III complex) and fibrinolytic status (D-dimer and plasmin-alpha 2-plasmin inhibitor complex) in 13 patients with hypertrophic cardiomyopathy, 17 patients with dilated cardiomyopathy and 20 normal subjects.
Results:
Plasma levels of platelet factor 4, beta-thromboglobulin and plasmin-alpha 2-plasmin inhibitor complex did not differ significantly among the three groups, whereas plasma levels of fibrinopeptide A and thrombin-antithrombin III complex in both patient groups were significantly higher than those in normal subjects. Plasma levels of D-dimer in patients with dilated cardiomyopathy were significantly higher than those in patients with hypertrophic cardiomyopathy and normal groups. In patients with hypertrophic cardiomyopathy, both fibrinopeptide A and thrombin-antithrombin III complex levels were significantly correlated with left atrial diameter. In patients with dilated cardiomyopathy, fibrinopeptide A and thrombin-antithrombin III complex levels showed a positive correlation with left ventricular end-diastolic volume and a negative correlation with fractional shortening of the left ventricle.
Conclusions:
The activated coagulation system in patients with hypertrophic and dilated cardiomyopathy may be triggered by left atrial dilation in hypertrophic cardiomyopathy and left ventricular enlargement and dysfunction in dilated cardiomyopathy.