Thromb Haemost 1979; 42(02): 752-756
DOI: 10.1055/s-0038-1666913
Original Article
Schattauer GmbH Stuttgart

Inhibition of ADP-Induced Platelet Aggregation by Dipyrone in Patients with Acute Myocardial Infarction

Itzhak Weinberger
The Clinical Laboratory, The Israel and lone Massada Center for Heart Diseases, Department of Medicine B, Beilinson Medical Center, Petah-Tikva and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
,
Henry Joshua
The Clinical Laboratory, The Israel and lone Massada Center for Heart Diseases, Department of Medicine B, Beilinson Medical Center, Petah-Tikva and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
,
Jacov Friedmann
The Clinical Laboratory, The Israel and lone Massada Center for Heart Diseases, Department of Medicine B, Beilinson Medical Center, Petah-Tikva and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
,
Saadia Rahamim
The Clinical Laboratory, The Israel and lone Massada Center for Heart Diseases, Department of Medicine B, Beilinson Medical Center, Petah-Tikva and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
,
Jacob Agmon
The Clinical Laboratory, The Israel and lone Massada Center for Heart Diseases, Department of Medicine B, Beilinson Medical Center, Petah-Tikva and Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
› Author Affiliations
Further Information

Publication History

Received 20 May 1978

Accepted 16 August 1978

Publication Date:
23 August 2018 (online)

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Summary

ADP induced platelet aggregation was investigated in 48 patients within three days of the first signs of acute myocardial infarction (AMI). Thirty six of them received 1 gram of dipyrone. Twelve patients who did not receive dipyrone served as controls.

Platelet aggregation was found severely inhibited in 11 patients who had received dipyrone up to 12 hours before investigation and moderately inhibited among 25 patients who were given the drug 12-24 hours prior to the investigation.

All the patients with AMI who did not receive dipyrone, exhibited a state of hyper- aggregability evidenced by the presence of a second phase of aggregation even with 0.5 μM ADP.

The inhibitory activity of dipyrone on the second phase of platelet aggregation resembles that of other non steroidal anti-inflammatory drugs.

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