In Vivo Platelet Activation Following Myocardial Infarction and Acute Coronary Ischaemia

Abstract

SummaryForty-seven patients presenting with acute chest pain had in vivo platelet activity assessed by measuring plasma levels of the platelet-specific protein beta thromboglobulin (BTG), and by screening for the presence of circulating platelet aggregates. Nineteen patients with transmural myocardial infarction (MI), 21 patients with acute coronary ischaemia (CI), and 7 patients with non-cardiac chest pain (NCCP) were investigated in a serial study and compared with a normal control group. The means of all BTG determinations in the MI (34, ± SD = 21-57) and CI (33, ± SD = 19-57) groups were significantly higher than those in the NCCP group (24, ± SD = 17-34; p Ã0.01) and normal subjects (22,5, ± SD = 14-37; p Ã0.001). There was no difference in BTG between those with MI or CI, nor between the NCCP group and normal subjects. Raised numbers of circulating platelet aggregates could not be detected in either MI or CI. The mean BTG levels in both MI and CI patients were significantly raised, compared to normal subjects, on the first day of admission to hospital and remained so on each of the subsequent nine days. Neither heparin plus warfarin nor sulphinpyrazone had any significant effect in lowering BTG levels. 15/40 patients (37.5%) following MI and CI had repeatedly raised BTG levels throughout the study period, and it is suggested that these patients represent an “at risk” group that may benefit from anti-platelet therapy in secondary prevention studies.

The Role of the Platelet in the Pathogenesis of Atherothrombosis

“…[74] Post-mortem and angioniques and can be used as platelet activation markers. [84] Other scopic studies in patients with unstable angina have shown that platelet activation assays are based upon quantification of platelet-rich thrombi are common in the coronary vessels. [19,75] In thromboxane B2 levels in plasma and urine.…”

Impaired fibrinolysis determines the outcome of percutaneus transluminal coronary angioplasty (PTCA)

“…It is believed that these factors penetrate the vascular wall, where they render smooth muscle cells susceptible to stimulation by PDGF, while progression to the active phase of replication depends on the synthesis of insulin‐like growth factor (IGF‐1). In the presence of both these growth factors, smooth muscle cells are stimulated to migrate and proliferate, encouraging the formation of a new fibrocellular stenotic lesion [13–21]. The main line of defence of this process is fibrinolysis, which removes fibrin deposited on the initial acute thrombus.…”

Effect of parathyroid-hormone-related protein on human platelet activation

“…This is accompanied by an inflammatory response which is responsible for most acute coronary syndromes. In fact, increased plasma levels of inflammatory markers have been detected in this scenario, and the degree of inflammation has been associated with the outcome of these patients [12,13,33,34].…”

“…As mentioned above, platelet activation is a key process related to both plaque instability and the compromised blood flow after coronary ischaemia [12,13]. To our knowledge, there are no current data on a possible effect of PTHrP on platelet activation, but some investigators have reported some conflicting effects of PTH in platelets.…”