Thromb Haemost 1993; 70(06): 0932-0936
DOI: 10.1055/s-0038-1649702
Original Article
Clinical Studies
Schattauer GmbH Stuttgart

“Spontaneous” Platelet Aggregation in Whole Blood in Diabetic and Non Diabetic Survivors of Acute Myocardial Infarction

Rosaire P Gray
The Department of Medicine, University College London Medical School, Whittington Hospital, Highgate Hill, London UK
,
Timothy J Hendra
The Department of Medicine, University College London Medical School, Whittington Hospital, Highgate Hill, London UK
,
David L H Patterson
1   The Department of Cardiology, Whittington Hospital, London, UK
,
John S Yudkin
The Department of Medicine, University College London Medical School, Whittington Hospital, Highgate Hill, London UK
› Author Affiliations
Further Information

Publication History

Received 28 April 1993

Accepted after revision 12 July 1993

Publication Date:
06 July 2018 (online)

Summary

There is increasing evidence that platelet thrombi play an important role in the pathogenesis of acute myocardial infarction (AMI). We compared “spontaneous” platelet aggregation in whole blood in 17 non-diabetic and 12 diabetic subjects on admission with AML There was no significant difference in the fall in platelet count between the two groups, expressed as platelets remaining (75.2 ± 7.9% vs 77.3 ± 6.9% at 10 min, 66.6 ± 8.9% vs 68.5 ± 6.3% at 20 min, 63.5 ± 8.2% vs 64.9 ± 6.7% at 30 min and 59.4 ± 10.3% vs 61.3 ± 7.6% at 60 min). The rate of “spontaneous” aggregation was increased in subjects with evidence of heart failure on admission compared to those without (59.9 ± 7.9% vs 66.2 ± 6.6% at 30 min [p = 0.05] and 55.4 ± 9.6% vs 63.1 ± 7.7% at 60 min [p = 0.04]). There was no correlation between the fall in platelet count and admission plasma glucose, glycated heaemoglobin or peak aspartate aminotransferase. The subjects studied on admission with AMI had greater rates of “spontaneous” aggregation than 8 subjects studied between 6 and 12 months after acute myocardial infarction (75.9 ± 7.4% vs 85.8 ± 5.4% at 10 min; p = 0.001 and 64.3 ± 7.5% vs 75.0 ± 7.8% at 30 min; p = 0.006) and compared to normal controls (90.7 ± 4.4% at 10 min; p <0.001 and 83.4 ± 6.5 at 30 min; p <0.001). This study provides evidence of increased “spontaneous” platelet aggregation in subjects admitted with acute myocardial infarction but no difference between diabetic and non-diabetic subjects was observed.

 
  • References

  • 1 Hirsh J. Hyperreactive platelets and complications of coronary artery disease. N Engl J Med 1987; 316: 1543-1544
  • 2 Tofler GH, Brezinski D, Schafer AJ, Czeisler CA, Rutherford JD, Willich SN, Gleason RE, Williams GH, Muller JE. Concurrent morning increase in platelet aggregability and the risk of myocardial infarction and sudden death. N Engl J Med 1987; 316: 1514-1518
  • 3 Mikhailidis DP, Barradas MA, Mier A, Boag F, Jeremy JY, Havard CWH, Dandona P. Platelet function in patients admitted with a diagnosis of myocardial infarction. Angiology 1987; 38: 36-43
  • 4 Erickson LA, Ginsberg MH, Loskutoff DJ. Detection and partial characterisation of an inhibitor of plasminogen activator in human platelets. J Clin Invest 1984; 74: 1465-1472
  • 5 Kruithof EKO, Tran-Thang C, Bachmann F. Studies on the release of a plasminogen activator inhibitor by human platelets. Thromb Haemostas 1986; 55: 201-205
  • 6 Plow EF, Collen D. The presence and release of alpha2antiplasmin from human platelets. Blood 1981; 58: 1069-1074
  • 7 Yudkin JS, Oswald GA. Determinants of hospital admission and case fatality in diabetic patients with myocardial infarction. Diabetes Care 1988; 11: 351-358
  • 8 Gwilt DJ. Why do diabetics die after myocardial infarction?. Practical Diabetes 1984; 1: 36-39
  • 9 Mustard JF, Packham MA. Platelets and diabetes mellitus. N Engl J Med 1984; 311: 665-667
  • 10 Pengo V, Boschello M, Prandoni P, Schiavon R, Bellotto F, Schivazappa L, Dalla Volta S. Enhanced “in vitro” release of platelet alpha granules after acute myocardial infarction. Thromb Haemostas 1985; 54: 544-546
  • 11 Pumphrey CW, Dawes J. Plasma betathromboglobulin as a measure of platelet activity. Effect of risk factors and findings in ischemic heart disease and after acute myocardial infarction. Am J Cardiol 1982; 50: 1258-1261
  • 12 Smitherman TC, Milam M, Woo J, Willerson JT, Frenkel EP. Elevated betathromboglobulin in peripheral venous blood of patients with acute myocardial infarction. Am J Cardiol 1981; 48: 395-402
  • 13 Oswald GA, Smith CCT, Betteridge DJ, Yudkin JS. Raised concentrations of glucose and adrenaline and increased in vivo platelet activation after myocardial infarction. Br Heart J 1988; 59: 663-671
  • 14 Knudsen JB, Gormsen J, Skagen K, Amtorp O. Changes in platelet function, coagulation and fibrinolysis in uncomplicated cases of acute myocardial infarction. Thromb Haemostas 1979; 42: 1513-1522
  • 15 McDaniel HG, Maddox WT, Poon MC, Rogers WJ, Rackley CE. Platelet function abnormalities in response to arachidonic acid in the acute phase of myocardial infarction. Am J Cardiol 1983; 52: 965-968
  • 16 O’Brien JR, Etherington MD, Shuttleworth RD, Calwell WH. Platelet function in acute myocardial infarction compared with controls. Thromb Haemostas 1980; 44: 96-99
  • 17 Fox SC, Burgess-Wilson M, Heptinstall S, Mitchell JRA. Platelet aggregation in whole blood determined using the Ultra-Flo platelet counter. Thromb Haemostas 1982; 48: 327-329
  • 18 Cho NH, Becker D, Dorman JS, Wolfson S, Kuller LH, Drash AL, Follansbee WF, Kelsey SF, Orchard TJ. Spontaneous whole blood platelet aggregation in insulin-dependent diabetes mellitus: an evaluation in an epidemiologic study. Thromb Haemostas 1989; 61: 127-130
  • 19 Hendra TJ, Yudkin JS. “Spontaneous” platelet aggregation in whole blood in diabetic patients with and without microvascular disease. Diabetic Medicine 1992; 9: 247-251
  • 20 World Health Organisation Regional Office for Europe. Public health in Europe 5. Myocardial infarction community registers. Annexe 1; Copenhagen, Denmark: 1976
  • 21 Killip T, Kimball JT. Treatment of myocardial infarction in a coronary care unit. Am J Cardiol 1967; 20: 457-464
  • 22 Oswald GA, Smith CCT, Betteridge DJ, Yudkin JS. Determinants and importance of stress hyperglycaemia in non-diabetic patients with myocardial infarction. Br Med J 1986; 293: 917-922
  • 23 Hendra TJ, Oughton J, Smith CCT, Betteridge D, Yudkin JS. Exercise induced changes in platelet aggregation: a comparison of whole blood and platelet-rich plasma techniques. Thromb Res 1988; 52: 443-451
  • 24 Saniabadi AR, Lowe GDO, Barbanel JC, Forbes CD. Further studies on the role of red blood cells in spontaneous platelet aggregation. Thromb Res 1985; 38: 225-232
  • 25 ISIS-2 Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin or both or neither among 17,187 cases of suspected acute myocardial infarction. Lancet 1988; 2: 349-360
  • 26 Fitzgerald DJ, Catella F, Roy L, FitzGerald GA. Marked platelet activation in vivo after intravenous streptokinase in patients with acute myocardial infarction. Circulation 1988; 77: 142-150
  • 27 Kerins DM, Roy L, FitzGerald GA, Fitzgerald DJ. Platelet and vascular function during coronary thrombolysis with tissue plasminogen activator. Circulation 1989; 80: 1718-1725
  • 28 Ostermann H, Van de Loo J. Factors of the haemostatic system in diabetic patients. A survey of controlled studies. Haemostasis 1986; 16: 386-416
  • 29 Lawson JL, Brash AR, Doran J, FitzGerald GA. Measurement of urinary 2,3 dinor-thromboxane B2and thromboxane B2using bondedphase phenylboronic acid columns and capillary gas chromatographynegative-ion chemical ionization mass spectrometry. Anal Biochem 1985; 150: 463-470
  • 30 Henriksson P, Wennmalm A, Edhag O, Vesterqvist O, Green K. In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction. Br Heart J 1986; 55: 543-548
  • 31 Fitzgerald DJ, Wright F, FitzGerald GA. Increased thromboxane biosynthesis during coronary thrombolysis. Circ Res 1989; 65: 83-94
  • 32 Thomas DP. Effect of catecholamines on platelet aggregation caused by thrombin. Nature 1967; 215: 298-299
  • 33 Mills DCB, Roberts GCK. Effects of adrenaline on human blood platelets. J Physiol (Lond) 1967; 193: 443-453
  • 34 Thomas DP. The role of platelet catecholamines in the aggregation of platelets by collagen and thrombin. Exp Biol Med 1967; 3: 129-134
  • 35 Saniabadi AR, Lowe GDO, Barbenel JC, Forbes CD. A comparison of spontaneous platelet aggregation in whole blood with platelet-rich plasma, additional evidence for the role of ADP. Thromb Haemostas 1984; 51: 115-118
  • 36 Hendra TJ, Wickens DJ, Dormandy TL, Yudkin JS. Platelet function and conjugated diene concentrations in diabetic and non-diabetic survivors of acute myocardial infarction. Cardiovas Res 1991; 25: 676-683
  • 37 Harrison MJG, Weisblatt E. A sex difference in the effect of aspirin on “spontaneous” platelet aggregation in whole blood. Thromb Haemostas 1983; 50: 773-774
  • 38 Trip MD, Cats VM, van Capelle FJL, Vreeken J. Platelet hyperactivity and prognosis in survivors of myocardial infarction. N Engl J Med 1990; 332: 1549-1554