[Increased thrombocyte activation in dilated cardiomyopathy: a risk factor for development of ventricular thrombosis despite anticoagulant therapy?].
METHODS
A 48-year-old patient with dilated cardiomyopathy complained of dyspnea at rest, severe sleeplessness and a slight pain in the stomach. The clinical examination was normal except for a murmur at the apex of the heart. There was no evidence of edema or congestion of the jugular veins.


METHODS
The echocardiography demonstrated a dilated left ventricle with severely compromised function. No ventricular thrombi were present at this time. Coronary artery disease was excluded by coronary angiography. Endomyocardial biopsies were obtained from the right ventricular septum. The immunohistological analysis of the endomyocardial biopsy specimens revealed pathologically increased lymphocytic infiltrates and increased expression of interstitial and endothelial MHC I and II antigens. Flow cytometric analysis of platelets surface antigens (P-selectin, GP53, thrombospondin) was performed as a measure for intravasal platelet activation. Our patient compared to a healthy control group (> 4 SD) and to other patients with dilated cardiomyopathy (> 2 SD). A high grade increase of platelet activation was found.


METHODS
ACE inhibitor, diuretics, spironolactone and digitalis were used to treat the heart insufficiency. Due to the severe left ventricular dysfunction phenprocoumone and aspirin were also prescribed. A follow-up echocardiography was performed 6 months later. Comparable to the first examination left ventricular contractility was found to be severely reduced. In addition, a marginal thrombus was now present in the left ventricle despite antithrombotic therapy.


CONCLUSIONS
An increased platelet activation was found in the peripheral circulation of our patient with dilated cardiomyopathy. After 6 months, ventricular thrombi were found in the dilated ventricle, although aspirin and phenprocoumone had been administred. We speculate that an additional thrombotic treatment with clopidogrel is necessary in patients with dilated cardiomyopathy and increased platelet activation.
Weikert
U
U
Klinikum Benjamin Franklin Medizinische Klinik II Kardiologie und Pulmologie Freie Universität Berlin Hindenburgdamm 30 12200 Berlin, Germany.
Rauch
U
U
Kühl
U
U
Hohmann
C
C
Jaster
M
M
Pauschinger
M
M
Schwimmbeck
P L
PL
Schultheiss
H P
HP
D000925:Anticoagulants / Q000008:administration & dosage* / Q000009:adverse effects; D001241:Aspirin / Q000008:administration & dosage* / Q000009:adverse effects; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy*; D002317:Cardiovascular Agents / Q000008:administration & dosage / Q000009:adverse effects; D004359:Drug Therapy, Combination; D006333:Heart Failure / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D008297:Male; D008875:Middle Aged; D010644:Phenprocoumon / Q000008:administration & dosage* / Q000009:adverse effects; D015539:Platelet Activation / Q000187:drug effects*; D012307:Risk Factors; D013927:Thrombosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy*; D017211:Treatment Failure; D014463:Ultrasonography
D000925:Anticoagulants; D002317:Cardiovascular Agents; D010644:Phenprocoumon; D001241:Aspirin