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Blood platelet response to plasma from patients with ischemic heart disease
Blood platelets change shape (from small round spheres to larger spread forms) as they participate in thrombosis. Using an electron microscopic technique, we surveyed 14 patients with both acute and chronic ischemic heart disease; each had increased spread platelet forms (69 plus and minus 22.2 [standard deviation] percent) when compared with 14 asymptomatic control subjects (P less than 0.001). When platelets from these 14 control subjects were exposed to plasma from the patients with ischemic heart disease, spread forms increased from 13.4 plus and minus 9.1 to 44.5 plus and minus 15.5 percent (P less than 0.001). There was no significant increase in spread platelets in these control subjects when their blood was mixed with plasma from another control group. Similar studies were performed in seriously ill noncardiac patients: 9 of 13 had increased spread platelet forms when compared with control subjects, but plasma from only 5 of these 9 subjects caused increased spread forms when mixed with platelets from normal subjects (P less than 0.05). Thus a factor existed in the plasma of these patients with ischemic heart disease that caused normal platelets to become spread. Similarly the plasma of some patients with serious noncardiac disease had a comparable effect on normal platelets. Although the identity of this factor is unknown, it is probably unrelated to hormonal or therapeutic influences occurring either during acute infarction or during the stress of serious illness because (1) the effect of the plasma from patients with acute ischemic heart disease was identical to that of patients with chronic ischemic heart disease, and (2) the effect was not present in all patients with serious noncardiac disease.
Blood platelets change shape (from small round spheres to larger spread forms) as they participate in thrombosis. Using an electron microscopic technique, we surveyed 14 patients with both acute and chronic ischemic heart disease; each had increased spread platelet forms (69 plus and minus 22.2 [standard deviation] percent) when compared with 14 asymptomatic control subjects (P less than 0.001). When platelets from these 14 control subjects were exposed to plasma from the patients with ischemic heart disease, spread forms increased from 13.4 plus and minus 9.1 to 44.5 plus and minus 15.5 percent (P less than 0.001). There was no significant increase in spread platelets in these control subjects when their blood was mixed with plasma from another control group. Similar studies were performed in seriously ill noncardiac patients: 9 of 13 had increased spread platelet forms when compared with control subjects, but plasma from only 5 of these 9 subjects caused increased spread forms when mixed with platelets from normal subjects (P less than 0.05). Thus a factor existed in the plasma of these patients with ischemic heart disease that caused normal platelets to become spread. Similarly the plasma of some patients with serious noncardiac disease had a comparable effect on normal platelets. Although the identity of this factor is unknown, it is probably unrelated to hormonal or therapeutic influences occurring either during acute infarction or during the stress of serious illness because (1) the effect of the plasma from patients with acute ischemic heart disease was identical to that of patients with chronic ischemic heart disease, and (2) the effect was not present in all patients with serious noncardiac disease.