Platelet aggregation in aortic and coronary venous blood in patients with and without coronary disease. 3. Role of tachycardia stress and propranolol.
We studied 16 patients with coronary artery disease (CAD) to evaluate platelet aggregation in blood samples withdrawn simultaneously from the aorta and coronary sinus. At rest, mean platelet aggregation in coronary venous blood was significantly lower than that in aortic blood. Platelet counts in coronary venous blood were also lower than in the aortic blood in each of the six CAD patients in whom counts were done. Platelet aggregation was lower in seven patients who were taking propranolol than in the remaining nine who were not taking propranolol. During tachycardia stress, platelet aggregation increased in all patients, but the magnitude of increase was greater in patients not taking propranolol. In four other patients without CAD, platelet aggregation and counts were also studied in the same fashion and were similar in both the aortic and coronary venous blood. These data suggest that in certain CAD patients, platelet consumption or destruction within atherosclerotic vasculature may occur. Propranolol may reduce platelet aggregation at rest and modify excessive aggregation during tachycardia stress in certain CAD patients.
D001011:Aorta; D001772:Blood Cell Count; D001792:Blood Platelets; D001800:Blood Specimen Collection; D006328:Cardiac Catheterization; D002304:Cardiac Pacing, Artificial; D003326:Coronary Circulation; D003327:Coronary Disease / Q000097:blood*; D006801:Humans; D008722:Methods; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D011433:Propranolol / Q000627:therapeutic use*; D013610:Tachycardia / Q000097:blood* / Q000209:etiology; D014680:Veins
D011433:Propranolol