Heterogeneity of platelet aggregation and major surface receptor expression in patients with acute myocardial infarction

V. L. Serebruany, P. A. Gurbel, A. R. Shustov, E. M. Ohman, E. J. Topol

Research output: Contribution to journalArticle

Abstract

Background: Platelets play an important role in the natural history of acute myocardial infarction (AMI). Methods and Results: Platelet aggregation and receptor expression were studied in 23 patients with AMI before reperfusion therapy and compared with 10 healthy control subjects. Platelet aggregation was induced with 5 μmol/L adenosine 5'-diphosphate, 10 μmol/L ADP, 1 μg/mL collagen, 1 mg/mL thrombin, and 1.25 mg/mL ristocetin. Receptor expression was measured by flow cytometry with monoclonal antibodies to p24 (CD9), Ib (CD42b), IIb (CD41 b), IIIa (CD61), IIb/IIIa (CD41b/CD61), very late antigen-2 (CD49b), P-selectin (CD62p), platelet/endothelial cell adhesion molecule-1 (CD31); and vitronectin (CD51/CD61). The percentage of platelet aggregation was higher in patients with AMI when induced by 5 μmol/L ADP (64.1 ± 12.7 vs 52.0 ± 6.7; P = .04), by 10 μmol/L ADP (71.7 ± 13.0 vs 59.2 ± 7.2, P = .003), by thrombin (75.8 ± 10.9 vs 60.5 ± 6.9, P = .01), and by ristocetin (92.5 ± 7.8 vs 71.3 ± 7.4, P = .0001). Collagen-induced platelet aggregation did not differ between groups. Expression of P-selectin (log amplification of fluorescence intensity) (31.5 ± 5.0 vs 25.1 ± 2.6, P = .003) and platelet/endothelial cell adhesion molecule-1 (56.8 ± 17.7 vs 44.5 ± 3.7, P = .04) were significantly increased in patients with AMI. The expression of IIb (28.4 ± 2.5 vs 37.2 ± 1.7, P = .0001) and Ib (103.6 ± 29.9 vs 133.8 ± 8.0, P = .007) were reduced in patients with AMI. Conclusions: Platelets are not necessarily systemically activated during the prereperfusion phase of AMI. For each agonist used and surface antigen measured, there was a cohort of patients with AMI within the normal or even below normal range of platelet status.

Original languageEnglish (US)
Pages (from-to)398-405
Number of pages8
JournalAmerican Heart Journal
Volume136
Issue number3
DOIs
StatePublished - 1998

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Platelet Aggregation
Myocardial Infarction
Adenosine Diphosphate
CD31 Antigens
Ristocetin
P-Selectin
Blood Platelets
Thrombin
Integrin alpha2beta1
Collagen
Vitronectin
Surface Antigens
Reperfusion
Healthy Volunteers
Flow Cytometry
Reference Values
Fluorescence
Monoclonal Antibodies

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Heterogeneity of platelet aggregation and major surface receptor expression in patients with acute myocardial infarction. / Serebruany, V. L.; Gurbel, P. A.; Shustov, A. R.; Ohman, E. M.; Topol, E. J.

In: American Heart Journal, Vol. 136, No. 3, 1998, p. 398-405.

Research output: Contribution to journalArticle

Serebruany, V. L. ; Gurbel, P. A. ; Shustov, A. R. ; Ohman, E. M. ; Topol, E. J. / Heterogeneity of platelet aggregation and major surface receptor expression in patients with acute myocardial infarction. In: American Heart Journal. 1998 ; Vol. 136, No. 3. pp. 398-405.
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abstract = "Background: Platelets play an important role in the natural history of acute myocardial infarction (AMI). Methods and Results: Platelet aggregation and receptor expression were studied in 23 patients with AMI before reperfusion therapy and compared with 10 healthy control subjects. Platelet aggregation was induced with 5 μmol/L adenosine 5'-diphosphate, 10 μmol/L ADP, 1 μg/mL collagen, 1 mg/mL thrombin, and 1.25 mg/mL ristocetin. Receptor expression was measured by flow cytometry with monoclonal antibodies to p24 (CD9), Ib (CD42b), IIb (CD41 b), IIIa (CD61), IIb/IIIa (CD41b/CD61), very late antigen-2 (CD49b), P-selectin (CD62p), platelet/endothelial cell adhesion molecule-1 (CD31); and vitronectin (CD51/CD61). The percentage of platelet aggregation was higher in patients with AMI when induced by 5 μmol/L ADP (64.1 ± 12.7 vs 52.0 ± 6.7; P = .04), by 10 μmol/L ADP (71.7 ± 13.0 vs 59.2 ± 7.2, P = .003), by thrombin (75.8 ± 10.9 vs 60.5 ± 6.9, P = .01), and by ristocetin (92.5 ± 7.8 vs 71.3 ± 7.4, P = .0001). Collagen-induced platelet aggregation did not differ between groups. Expression of P-selectin (log amplification of fluorescence intensity) (31.5 ± 5.0 vs 25.1 ± 2.6, P = .003) and platelet/endothelial cell adhesion molecule-1 (56.8 ± 17.7 vs 44.5 ± 3.7, P = .04) were significantly increased in patients with AMI. The expression of IIb (28.4 ± 2.5 vs 37.2 ± 1.7, P = .0001) and Ib (103.6 ± 29.9 vs 133.8 ± 8.0, P = .007) were reduced in patients with AMI. Conclusions: Platelets are not necessarily systemically activated during the prereperfusion phase of AMI. For each agonist used and surface antigen measured, there was a cohort of patients with AMI within the normal or even below normal range of platelet status.",
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T1 - Heterogeneity of platelet aggregation and major surface receptor expression in patients with acute myocardial infarction

AU - Serebruany, V. L.

AU - Gurbel, P. A.

AU - Shustov, A. R.

AU - Ohman, E. M.

AU - Topol, E. J.

PY - 1998

Y1 - 1998

N2 - Background: Platelets play an important role in the natural history of acute myocardial infarction (AMI). Methods and Results: Platelet aggregation and receptor expression were studied in 23 patients with AMI before reperfusion therapy and compared with 10 healthy control subjects. Platelet aggregation was induced with 5 μmol/L adenosine 5'-diphosphate, 10 μmol/L ADP, 1 μg/mL collagen, 1 mg/mL thrombin, and 1.25 mg/mL ristocetin. Receptor expression was measured by flow cytometry with monoclonal antibodies to p24 (CD9), Ib (CD42b), IIb (CD41 b), IIIa (CD61), IIb/IIIa (CD41b/CD61), very late antigen-2 (CD49b), P-selectin (CD62p), platelet/endothelial cell adhesion molecule-1 (CD31); and vitronectin (CD51/CD61). The percentage of platelet aggregation was higher in patients with AMI when induced by 5 μmol/L ADP (64.1 ± 12.7 vs 52.0 ± 6.7; P = .04), by 10 μmol/L ADP (71.7 ± 13.0 vs 59.2 ± 7.2, P = .003), by thrombin (75.8 ± 10.9 vs 60.5 ± 6.9, P = .01), and by ristocetin (92.5 ± 7.8 vs 71.3 ± 7.4, P = .0001). Collagen-induced platelet aggregation did not differ between groups. Expression of P-selectin (log amplification of fluorescence intensity) (31.5 ± 5.0 vs 25.1 ± 2.6, P = .003) and platelet/endothelial cell adhesion molecule-1 (56.8 ± 17.7 vs 44.5 ± 3.7, P = .04) were significantly increased in patients with AMI. The expression of IIb (28.4 ± 2.5 vs 37.2 ± 1.7, P = .0001) and Ib (103.6 ± 29.9 vs 133.8 ± 8.0, P = .007) were reduced in patients with AMI. Conclusions: Platelets are not necessarily systemically activated during the prereperfusion phase of AMI. For each agonist used and surface antigen measured, there was a cohort of patients with AMI within the normal or even below normal range of platelet status.

AB - Background: Platelets play an important role in the natural history of acute myocardial infarction (AMI). Methods and Results: Platelet aggregation and receptor expression were studied in 23 patients with AMI before reperfusion therapy and compared with 10 healthy control subjects. Platelet aggregation was induced with 5 μmol/L adenosine 5'-diphosphate, 10 μmol/L ADP, 1 μg/mL collagen, 1 mg/mL thrombin, and 1.25 mg/mL ristocetin. Receptor expression was measured by flow cytometry with monoclonal antibodies to p24 (CD9), Ib (CD42b), IIb (CD41 b), IIIa (CD61), IIb/IIIa (CD41b/CD61), very late antigen-2 (CD49b), P-selectin (CD62p), platelet/endothelial cell adhesion molecule-1 (CD31); and vitronectin (CD51/CD61). The percentage of platelet aggregation was higher in patients with AMI when induced by 5 μmol/L ADP (64.1 ± 12.7 vs 52.0 ± 6.7; P = .04), by 10 μmol/L ADP (71.7 ± 13.0 vs 59.2 ± 7.2, P = .003), by thrombin (75.8 ± 10.9 vs 60.5 ± 6.9, P = .01), and by ristocetin (92.5 ± 7.8 vs 71.3 ± 7.4, P = .0001). Collagen-induced platelet aggregation did not differ between groups. Expression of P-selectin (log amplification of fluorescence intensity) (31.5 ± 5.0 vs 25.1 ± 2.6, P = .003) and platelet/endothelial cell adhesion molecule-1 (56.8 ± 17.7 vs 44.5 ± 3.7, P = .04) were significantly increased in patients with AMI. The expression of IIb (28.4 ± 2.5 vs 37.2 ± 1.7, P = .0001) and Ib (103.6 ± 29.9 vs 133.8 ± 8.0, P = .007) were reduced in patients with AMI. Conclusions: Platelets are not necessarily systemically activated during the prereperfusion phase of AMI. For each agonist used and surface antigen measured, there was a cohort of patients with AMI within the normal or even below normal range of platelet status.

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