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[Platelet activation in the early phases of acute myocardial infarction]
A Salvioni1, F Giraldi, E Assanelli
1Istituto di Cardiologia, Università degli Studi, Centro di Studio per le Ricerche Cardiovascolari del CNR, IRCCS, Milano.
Insights
Platelet activation increases early after myocardial infarction and is affected by thrombolytic treatment timing. Aspirin shows limited effect on platelet activity within the first 48 hours post-thrombolysis.
Area of Science:
- Cardiology
- Hematology
- Pharmacology
Background:
- Myocardial infarction (MI) and thrombolysis are linked to platelet activation.
- The precise timing of platelet activation relative to symptom onset and thrombolysis, and aspirin's effect, require further definition.
Purpose of the Study:
- To measure platelet activity in early MI patients receiving thrombolysis.
- To evaluate the impact of streptokinase versus recombinant tissue-type plasminogen activator (rt-PA) on platelet activation.
- To assess the effectiveness of aspirin in counteracting thrombolysis-induced platelet activation.
Main Methods:
- Studied 41 MI patients undergoing thrombolysis with streptokinase or rt-PA.
- Administered aspirin intravenously before thrombolysis and orally thereafter to a subset of patients.
- Measured Beta-thromboglobulin (BTG) levels at admission, post-thrombolysis, and up to 48 hours.
Main Results:
- Thrombolysis increased platelet activity similarly in both groups, peaking at 3 hours.
- BTG levels were higher in the streptokinase group from 24 hours onwards.
- Aspirin's significant effect on BTG levels was observed only at 48 hours post-thrombolysis.
- Earlier symptom onset correlated with higher admission BTG levels; thrombolysis increased activity less in these patients.
Conclusions:
- Platelet activation is greater early in MI and influenced by admission delay.
- Streptokinase and rt-PA cause similar initial platelet activation, but streptokinase's effect is more persistent.
- Aspirin's antiplatelet effect becomes significant after 48 hours in this context.
Abstract:
Myocardial infarction and thrombolysis are proven to be associated with platelet activation. However, the time relationship of platelet activation with the onset of symptoms and with thrombolysis, and the response to aspirin are not well defined. In this study we measured platelet activity in the early phase of myocardial infarction treated with either streptokinase or recombinant tissue-type plasminogen activator (rt-PA) and evaluated whether and to what extent it may be counteracted by aspirin. Fourty-one patients (mean age 57 +/- 6 years) received thrombolytic therapy after coronary occlusion: 1.5 million units of streptokinase (Group 1; 21 patients) or 100 mg of rt-PA (Group 2; 20 patients). Ten randomly selected patients in either group were given 500 mg aspirin i.v. prior to infusion of the thrombolytic compound and, then, 325 mg/die of aspirin orally. Beta-thromboglobulin (BTG), a marker of platelet activity, was determined at admission, after thrombolysis and in the subsequent 48 hours. At admission, BTG plasma levels averaged 125 +/- 31 IU/ml in Group 1 and 134 +/- 35 IU/ml in Group 2 (NS). Thrombolysis produced a similar increase in platelet activity in both groups, and maximal values were reached at the third hour (196 +/- 43 IU/ml in Group 1 and 192 +/- 39 in Group 2, p < 0.001 vs baseline and NS between groups). Levels of BTG were higher in streptokinase-treated group starting from 24 hours (p < 0.05). Differences in BTG levels between aspirin-treated and aspirin-untreated patients became significant at 48 hours after thrombolysis in both groups. An inverse correlation was found between time elapsed from onset of symptoms and BTG value on admission (r = -0.86, p < 0.001); in patients admitted within 2 hours after the beginning of symptoms, and having the higher BTG levels, thrombolysis did not induce a significant increase in platelet activity; this, on the contrary, was observed in patients admitted later. Platelet activation is greater early after myocardial infarction and is differently influenced by thrombolytic treatment, depending on the delay of the patient's admission. Streptokinase and rt-PA induce a similar increase in platelet activity which is more persistent after streptokinase; cycloxygenase inhibition with aspirin seems to influence platelet activity only starting from the second day.