CirculatingAggregatedPlatelets,Numberof Plateletsper Aggregate,and PlateletSize During Acute MyocardialInfarction ltzhak Weinberger, MD, Jacob Fuchs, MD, Ehud Davidson, MD, and Zvi Rotenberg, MD
P
revious studies’-” have emphasized the role of
platelets in the development and course of acute Circubting aggregated ptatdets (total, reversfbly myocardial infarction (AMI). Colman5 suggestand irreverdbly aggregated), the number of plateed that platelets have a central role in coronary thromlets per aggregate and *‘big” platelets were meabosis through releasing thromboxane AZ, causing corosured by a modification of the Wu and Hoak methnary vasoconstriction and platelet aggregation. AM1 od in 42 patients on the first, second and fifth day was induced in animals by infusing adenosine diphosof acute myocardial infarction (AM). Among phate which provoked platelet aggregation in the microthem, 30 had an uncomplicated course and 12 pacirculation.* Other investigators*-4 found an increased tients had complkations that occurred between number of platelet aggregates in the myocardial microthe 5th and 19thday of hospitalization (7 patients circulation of patients who died suddenly of coronary had rehtfarction and 5 died). In all patients the artery disease. An increased number of circulating agmeasured parameters were elevated compared gregated platelets, mostly in the reversible form, were with those of control subjects. There was a signifialso found in patients with AMI. The number of platecant increase, especially after the first observation lets per aggregate was also emphasized in patients with day, in the values of total aggregated platelets (37 ischemic heart disease.12 Trowbridge,i3 Cameron14 and f 11% vs 26 f 1296, p
P
revious studies’-” have emphasized the role of
platelets in the development and course of acute Circubting aggregated ptatdets (total, reversfbly myocardial infarction (AMI). Colman5 suggestand irreverdbly aggregated), the number of plateed that platelets have a central role in coronary thromlets per aggregate and *‘big” platelets were meabosis through releasing thromboxane AZ, causing corosured by a modification of the Wu and Hoak methnary vasoconstriction and platelet aggregation. AM1 od in 42 patients on the first, second and fifth day was induced in animals by infusing adenosine diphosof acute myocardial infarction (AM). Among phate which provoked platelet aggregation in the microthem, 30 had an uncomplicated course and 12 pacirculation.* Other investigators*-4 found an increased tients had complkations that occurred between number of platelet aggregates in the myocardial microthe 5th and 19thday of hospitalization (7 patients circulation of patients who died suddenly of coronary had rehtfarction and 5 died). In all patients the artery disease. An increased number of circulating agmeasured parameters were elevated compared gregated platelets, mostly in the reversible form, were with those of control subjects. There was a signifialso found in patients with AMI. The number of platecant increase, especially after the first observation lets per aggregate was also emphasized in patients with day, in the values of total aggregated platelets (37 ischemic heart disease.12 Trowbridge,i3 Cameron14 and f 11% vs 26 f 1296, p
