P182Does platelet dysfunction account for thrombolysis-related upper gastrointestinal bleeding (UGB) in STEMI patients? A 4year prospective study in Constanta County, Romania

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Abstract

Background

In Constanţa County, Romania, coronary reperfusion in acute STEMI is achieved only by pharmacological therapy. UGB represents a major and potentially fatal haemorrhagic complication of thrombolysis.

Aim

To evaluate the possible etiology of STEMI-related UGBs.

Method

All STEMI patients who underwent thrombolysis in Constanţa County ICCU during 4 years (2006−2009) were assessed for platelet function using platelet count and optical aggregometry. During heparin therapy aPTT was evaluated every 12 hours. Fibrinolysis was assessed by monitoring fibrinogen and D-dimer levels 6 hours after thrombolysis.

Results

618 STEMI patients underwent thrombolysis during the study period. UGB occured exclusively after thrombolysis in 42 cases (6.79%). Among UGB patients: 2 (4.76%) had mild thrombocytopenia (100,000/dl≤Plt≤150,000/dl), 2 (4.76%) were aspirin-resistant (defined as ≥20% platelet aggregation with 1mg/ml arachidonic acid in aspirin-treated patients) and no patient had platelet dysfunction (hypoaggregation), while in non-UGB group 29 patients had mild thrombocytopenia (5.03%), 32 were aspirin resistant (5.55%) and 3 patients had platelet dysfunction (0.52%). There was no significant difference between UGB and non-UGB patients concerning platelet dysfunction (p=0.1). In the UGB group 4 patients (9.52%) had an aPTT > 80sec during the first 12 hours of heparin therapy, comparing with 54 (9.37%) from the non-UGB group for the same interval (p=0.9768). Fibrinogen depletion rate 6 hours after thrombolysis was 54% ± 12% in the streptokinase (SK) group and 29% ± 13% in the reteplase (r-PA) group for UGB patients, similar with the rate in non-UGB patients (51% ± 10% in the SK group and 28% ± 12% in the r-PA group). Even though fibrinogen depletion was more important (p=0.0002) for SK patients, for the same pharmacologic agent there was no significant difference between UGB and non-UGB patients (p=0.7826). Mean plasmatic D-dimer levels 6 hours after thrombolysis were 16.52μg/ml ± 4.36μg/ml in SK group and 5.22μg/ml ± 0.86μg/ml in r-PA group for UGB patients, similar with the levels for non-UGB patients (15.8μg/ml ± 5.27μg/ml in SK group and 4.65μg/ml ± 1,22μg/ml in r-PA group). Even though D-dimer levels were significantly higher after SK (p=0.0017), for the same agent there was no difference between UGB and non-UGB patients (p=0.3187).

Conclusions

Among STEMI-related UGBs we didn't find out any patient with platelet dysfunction (with optical aggregometry method). We couldn't establish a significant etiologic relationship between fibrinogen depletion level and postthrombolysis UGB

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