Shape and Spreading of Platelets from the Blood of Patients with Acute Myocardial Infarction

Summary

The shape of platelets in circulating blood and alterations of this shape after the contact of platelets with glass surfaces, as well as spontaneous platelet aggregation, were examined in patients with acute myocardial infarction (AMI) and in controls.

The shape of circulating platelets were studied by scanning electron microscopy and the spreading - by differential interference contrast microscopy.

Most platelets circulating in the blood of the patients with AMI had non-activated discoid shape; the percentage of these nonactivated platelets was similar to that in the control group. However, these platelets of many AMI patients acquired an increased ability to undergo morphological changes after contact with glass. The percentage of spread platelets in controls was never higher than 50%. In contrast, this percent was higher than 50% in 73% of patients with AMI. Increased spontaneous platelet aggregation was determined only in 30% of AMI patients.

Keywords

Platelets - DIC microscopy - SEM microscopy - Myocardial infarction

• References

• 1 Wu KK, Hoak JC. A new method for the quantitative detection of platelet aggregates in patients with arterial insufficiency. Lancet 1974; 2: 924-926
• 2 Mehta P, Mehta J. Platelet function studies in coronary artery disease. V. Evidence for enhanced platelet micro-thrombus formation activity in acute myocardial infarction. Am J Cardiol 1979; 43: 757-760
• 3 Gjesdal J. Platelet function and plasma free fatty acids during acute myocardial infarction and severe angina pectoris. Scand J Haematol 1976; 17: 205-212
• 4 Yamazaki H, Takahashi T, Sano T. Hyperaggregability of platelets in thromboembolic disorders. Thrombos Diathes Haemorrh 1975; 34: 90-105
• 5 Handin RI, McDonough M, Lesch M. Elevation of platelet factor four in acute myocardial infarction: measurement by radio-immunoassay. J Lab Clin Med 1978; 91: 340-349
• 6 Neri-Serneri GG, Gensini GF, Abbate R, Mugnaini C, Favilla S, Brunelli C, Chierchia S, Parodi O. Increased fibrinopeptide A formation and thromboxane A₂production in patients with ischemic heart disease: relationship with coronary pathoanatomy, risk factors and clinical manifestations. Am Heart J 1981; 101: 185-194
• 7 Barnhart M, Walsh RT, Robinson TA. A three dimensional view of platelet responses to chemical stimuli. Ann N Y Acad Sci 1972; 201: 360-390
• 8 Cooper HA, Mason RG, Brinkhous KM. The platelet: Membrane and surface reactions. Ann Rev Physiol 1976; 38: 504-535
• 9 Shatz JG, Riddle GM. Platelet surface activation and aggregation in myocardial infarction. Electron microscope observations Adv Cardiol 1970; 4: 143-160
• 10 Allen RD, Zacharski LR, Widirsky ST, Rosenstein R, Zaitlin LM, Burgess DR. Transformation and motility of human platelets. J Cell Biol 1979; 83: 126-142
• 11 Rosenstein R, Zacharski LR, Allen RD. Quantitation of human platelet transformation of siliconized glass: comparison of“normal” and“abnormal” platelets. Thromb Haemostas 1981; 46: 521-524
• 12 Boyde A, Vesely P. Comparison of fixation and drying procedures for preparation of some cultured cell lines for examination in the SEM. In: Scanning electron microscopy. Johari O. (ed) II T Research Institute; Chicago: 1972. pp 265-272