The coagulation system is activated in idiopathic cardiomyopathy.
OBJECTIVE
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.
Yamamoto
K
K
Department of Cardiology, Jichi Medical School, Tochigi, Japan.
Ikeda
U
U
Furuhashi
K
K
Irokawa
M
M
Nakayama
T
T
Shimada
K
K
D000933:Antifibrinolytic Agents; D000990:Antithrombin III / Q000032:analysis; D016279:Atrial Function, Left / Q000502:physiology; D001777:Blood Coagulation / Q000502:physiology*; D001779:Blood Coagulation Factors / Q000032:analysis*; D002311:Cardiomyopathy, Dilated / Q000097:blood* / Q000000981:diagnostic imaging; D002312:Cardiomyopathy, Hypertrophic / Q000097:blood* / Q000000981:diagnostic imaging; D016022:Case-Control Studies; D004452:Echocardiography; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005341:Fibrinolysin / Q000032:analysis; D005344:Fibrinopeptide A / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000032:analysis; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000000981:diagnostic imaging; D000979:alpha-2-Antiplasmin / Q000032:analysis; D001620:beta-Thromboglobulin / Q000032:analysis
D000933:Antifibrinolytic Agents; D001779:Blood Coagulation Factors; D005338:Fibrin Fibrinogen Degradation Products; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; D001620:beta-Thromboglobulin; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; D005344:Fibrinopeptide A; D000990:Antithrombin III; D010447:Peptide Hydrolases; D005341:Fibrinolysin