apyrase and Angina-Pectoris

apyrase has been researched along with Angina-Pectoris* in 2 studies

Other Studies

2 other study(ies) available for apyrase and Angina-Pectoris

Article	Year
Relation of CD39 to plaque instability and thrombus formation in directional atherectomy specimens from patients with stable and unstable angina pectoris. The American journal of cardiology, 2005, Mar-01, Volume: 95, Issue:5 To determine whether the expression of CD39 in coronary atherosclerotic lesions is related to plaque instability and thrombus formation, we assessed directional coronary atherectomy (DCA) specimens from patients with stable and unstable angina pectoris. CD39 immunoreactivity was decreased in culprit lesions in patients with unstable angina pectoris compared with those with stable angina pectoris, and was reduced in DCA specimens with thrombus formation. These results suggest that CD39 expressed in atheromatous plaque plays an important role in preventing acute coronary syndromes. Topics: Adenosine Triphosphatases; Angina Pectoris; Angina, Unstable; Antigens, CD; Apyrase; Atherectomy, Coronary; Coronary Restenosis; Coronary Thrombosis; Female; Humans; Immunoenzyme Techniques; Male; Middle Aged; Risk Factors	2005
Spontaneous platelet aggregation in arterial insufficiency: mechanisms and implications. Thrombosis and haemostasis, 1976, Jun-30, Volume: 35, Issue:3 To investigate the clinical implications and mechanisms of spontaneous platelet aggregation (SPA) in man, 150 normal subjects, 22 patient controls and 130 patients with vascular insufficiency were studied. SPA was negative in normal subjects and patient controls whereas it was positive in 36 of 66 (54%) patients with transient ischemic attacks, 6 of 32 (19%) patients with stable angina, 7 of 10 (70%) patients with acute myocardial infarction and 11 of 14 (80%) patients with acute peripheral arterial insufficiency. The SPA was inhibited with aspirin in vivo, and inhibited competitively in vitro by low concentrations of aspirin, 2-chloroadenosine, prostaglandin E1 or apyrase but only by high concentrations of heparin or hirudin. Addition of platelet-poor plasma from patients with positive SPA did not cause normal platelets to aggregate. Treatment of patients who had acute peripheral arterial insufficiency with aspirin and dipyridamole prevented SPA with notable clinical improvement of the ischemic changes. Topics: Adenosine; Adult; Aged; Angina Pectoris; Apyrase; Arterial Occlusive Diseases; Aspirin; Coronary Disease; Dipyridamole; Heparin; Hirudins; Humans; Ischemic Attack, Transient; Middle Aged; Myocardial Infarction; Platelet Aggregation; Prostaglandins E	1976

Article

Year

Relation of CD39 to plaque instability and thrombus formation in directional atherectomy specimens from patients with stable and unstable angina pectoris.

The American journal of cardiology, 2005, Mar-01, Volume: 95, Issue:5

To determine whether the expression of CD39 in coronary atherosclerotic lesions is related to plaque instability and thrombus formation, we assessed directional coronary atherectomy (DCA) specimens from patients with stable and unstable angina pectoris. CD39 immunoreactivity was decreased in culprit lesions in patients with unstable angina pectoris compared with those with stable angina pectoris, and was reduced in DCA specimens with thrombus formation. These results suggest that CD39 expressed in atheromatous plaque plays an important role in preventing acute coronary syndromes.

Topics: Adenosine Triphosphatases; Angina Pectoris; Angina, Unstable; Antigens, CD; Apyrase; Atherectomy, Coronary; Coronary Restenosis; Coronary Thrombosis; Female; Humans; Immunoenzyme Techniques; Male; Middle Aged; Risk Factors

2005

Spontaneous platelet aggregation in arterial insufficiency: mechanisms and implications.

Thrombosis and haemostasis, 1976, Jun-30, Volume: 35, Issue:3

To investigate the clinical implications and mechanisms of spontaneous platelet aggregation (SPA) in man, 150 normal subjects, 22 patient controls and 130 patients with vascular insufficiency were studied. SPA was negative in normal subjects and patient controls whereas it was positive in 36 of 66 (54%) patients with transient ischemic attacks, 6 of 32 (19%) patients with stable angina, 7 of 10 (70%) patients with acute myocardial infarction and 11 of 14 (80%) patients with acute peripheral arterial insufficiency. The SPA was inhibited with aspirin in vivo, and inhibited competitively in vitro by low concentrations of aspirin, 2-chloroadenosine, prostaglandin E1 or apyrase but only by high concentrations of heparin or hirudin. Addition of platelet-poor plasma from patients with positive SPA did not cause normal platelets to aggregate. Treatment of patients who had acute peripheral arterial insufficiency with aspirin and dipyridamole prevented SPA with notable clinical improvement of the ischemic changes.

Topics: Adenosine; Adult; Aged; Angina Pectoris; Apyrase; Arterial Occlusive Diseases; Aspirin; Coronary Disease; Dipyridamole; Heparin; Hirudins; Humans; Ischemic Attack, Transient; Middle Aged; Myocardial Infarction; Platelet Aggregation; Prostaglandins E

1976