Prospective Analysis after Coronary-artery Bypass Grafting: Platelet GP IIIa Polymorphism (HPA-1b /PlA2) Is a Risk Factor for Bypass Occlusion, Myocardial Infarction, and Death

Rainer B. Zotz; Michael Klein; Hans Peter Dauben; Christiane Moser; Emmeran Gams; Rüdiger E. Scharf

doi:10.1055/s-0037-1613827

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2000; 83(03): 404-407
DOI: 10.1055/s-0037-1613827

Review Article

Schattauer GmbH

Prospective Analysis after Coronary-artery Bypass Grafting: Platelet GP IIIa Polymorphism (HPA-1b /Pl^A2) Is a Risk Factor for Bypass Occlusion, Myocardial Infarction, and Death

Rainer B. Zotz

¹From the Department of Haemostasis and Transfusion Medicine, Düsseldorf, Germany

,

Michael Klein

²Department of Thoracic and Cardiovascular Surgery, Heinrich Heine University Medical Center, Düsseldorf, Germany

,

Hans Peter Dauben

²Department of Thoracic and Cardiovascular Surgery, Heinrich Heine University Medical Center, Düsseldorf, Germany

,

Christiane Moser

²Department of Thoracic and Cardiovascular Surgery, Heinrich Heine University Medical Center, Düsseldorf, Germany

,

Emmeran Gams

²Department of Thoracic and Cardiovascular Surgery, Heinrich Heine University Medical Center, Düsseldorf, Germany

,

Rüdiger E. Scharf

¹From the Department of Haemostasis and Transfusion Medicine, Düsseldorf, Germany

› Author Affiliations

Abstract

Summary

Recently, we have demonstrated that human platelet antigen 1b (HPA-1b or Pl^A2) is a hereditary risk factor for platelet thrombogenicity leading to premature myocardial infarction in preexisting coronary artery disease. However, HPA-1b does not represent a risk factor for coronary artery disease itself. The aim of our present study was to evaluate the role of HPA-1b on the outcome in patients after coronaryartery bypass surgery. We prospectively determined the HPA-1 genotype in 261 consecutive patients prior to saphenous-vein coronaryartery bypass grafting. The patients were followed for one year. Among patients with bypass occlusion, myocardial infarction, or death more than 30 days after surgery, the prevalence of HPA-1b was significantly higher than among patients without postoperative complications (60 percent, 6/10, vs. 24 percent, 58/241, p <0.05, odds ratio 4.7). Using a stepwise logistic regression analysis with the variables HPA1b, age, sex, body mass index, smoking (pack-years), hypertension, diabetes, cholesterol and triglyceride concentration, only HPA-1b had a significant association with bypass occlusion, myocardial infarction, or death after bypass surgery (p = 0.019, odds ratio 4.7). This study shows that HPA-1b is a hereditary risk factor for bypass occlusion, myocardial infarction, or death in patients after coronary-artery bypass surgery.

Keywords

Coronary-artery bypass grafting - human platelet antigen 1 (HPA-1) - glycoprotein IIb-IIIa - inherited risk factor

Full Text

References

References
1 Fuster V. Prevention of atherosclerosis in coronary-artery bypass grafts. N Engl J Med 1997; 336: 212-3.
2 Pearson T, Rappaport E, Criqui M, Furberg C, Fuster V, Hiratzka L, Little W, Ockene I, Williams G. Optimal risk factor management in the patient after coronary revascularization. Circulation 1994; 90: 3125-33.
3 Lie JT, Lawrie GM, Morris Jr GC. Aortocoronary bypass saphenous vein graft atherosclerosis: anatomic study of 99 vein grafts from normal and hyperlipoproteinemic patients up to 75 months postoperatively. Am J Cardiol 1977; 40: 906-14.
4 Neitzel GF, Barboriak JJ, Pintar K, Qureshi I. Atherosclerosis in aortocoronary bypass grafts: morphologic study and risk factor analysis 6 to 12 years after surgery. Arteriosclerosis 1986; 06: 594-600.
5 Palac RT, Meadows WR, Hwang MH, Loeb HS, Pifarre R, Gunnar RM. Risk factors related to progressive narrowing in aortocoronary vein grafts studied 1 and 5 years after surgery. Circulation. 1982 66. (Suppl I): I-40-4.
6 Campeau L, Enjalbert M, Lesperance J, Bourassa MG, Kwiterovich P, Wacholder S, Sniderman A. The relation of risk factors to the development of atherosclerosis in saphenous-vein bypass grafts and the progression of disease in the native circulation: a study 10 years after aortocoronary bypass surgery. surgery. N Engl J Med 1984; 311: 1329-32.
7 Campeau L, Knatterud G, Domanski M, Hunninghake D, White CW, Geller NL, Rosenberg Y. The Effect of Aggressive Lowering of Low-Density Lipoprotein Cholesterol Levels and Low-Dose Anticoagulation on Obstructive Changes in Saphenous-Vein Coronary-Artery Bypass Grafts. N Engl J Med 1997; 336: 153-62.
8 Badimon L, Badimon JJ, Turitto VT, Vallabhajosula S, Fuster V. Platelet thrombus formation on collagen type 1: a model of deep vessel injury: influence of blood rheology, von Willebrand factor, and blood coagulation. Circulation 1988; 78: 1432-42.
9 Badimon L, Badimon JJ. Mechanism of arterial thrombosis in nonparallel streamlines: platelet thrombi grow at the apex of stenotic severely injured vessel wall: experimental study in the pig model. J Clin Invest 1989; 84: 1134-44.
10 Fernandez-Ortiz A, Badimon JJ, Falk E, Fuster V, Meyer B, Mailhac A, Wenig D, Shah PK, Badimon L. Characterization of relative thrombogenicity of atherosclerotic plaque components: implications for consequences of plaque rupture. J Am Coll Cardiol 1994; 23: 1564-9.
11 Drake TA, Morrissey JH, Edgington TS. Selective cellular expression of tissue factor in human tissue: implication for disorders of hemostasis and thrombosis. Am J Pathol 1989; 134: 1087-97.
12 Serneri GGN, Gensini GF, Poggesi L, Modesti PA, Rostagno C, Boddi M, Gori AM, Martini F, Ieri A, Margheri M, Abbate R. The role of dual thromboxane A2 inhibitor: importance of activated monocytes. Coronary Art Dis 1994; 05: 137-45.
13 Henderson WG, Goldman S, Copeland JG, Moritz TE, Harker LA. Antiplatelet or anticoagulant therapy after coronary artery bypass surgery: a meta-analysis of clinical trials. Ann Intern Med 1989; 111: 743-50.
14 Fremes SE, Levington C, Naylor CD, Chen E, Christakis GT, Goldman BS. Optimal antithrombotic therapy following aortocoronary bypass: a metaanalysis. Eur J Cardiothorac Surg 1993; 07: 169-80.
15 Kunicki TJ, Newman PJ. The molecular immunology of human platelet proteins. Blood 1992; 80: 1386-404.
16 Weiss EJ, Bray PF, Tayback M, Schulman SP, Kickler TS, Becker LC, Weiss JL, Gerstenblith G, Goldschmidt-Clermont PJ. A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis. N Engl J Med 1996; 334: 1090-4.
17 Carter AM, Ossei-Gerning N, Wilson IJ, Grant PJ. Association of the platelet PlA polymorphism of glycoprotein IIb/IIIa and the fibrinogen Bβ448 polymorphism with myocardial infarction and extent of coronary artery disease. Circulation 1997; 96: 1424-31.
18 Zotz RB, Winkelmann BR, Nauck M, Giers G, Maruhn-Debowski B, März W, Scharf RE. Polymorphism of platelet membrane glycoprotein IIIa: Human platelet antigen 1b (HPA-1b/Pl^A2) is an inherited risk factor for premature myocardial infarction in coronary artery disease. Thromb Haemost 1998; 79: 731-5.
19 Marian AJ, Brugada R, Kleiman NS. Platelet glycoprotein IIIa PLA polymorphism and myocardial infarction. (Letter) N Engl J Med 1996; 335: 1071-2.
20 Ridker PM, Hennekens CH, Schmitz C, Stampfer M, Lindpaintner K. Pl^A1/A2 polymorphism of platelet glycoprotein IIIa and risks of myocardial infarction, stroke, and venous thrombosis. Lancet 1997; 349: 385-8.
21 Osborn SV, Hampton KK, Smillie D, Channer KS, Daly ME. Platelet glycoprotein IIIa gene polymorphism and myocardial infarction. Lancet 1996; 348: 1309-10.
22 Herrmann SM, Poirer O, Marques-Vidal P, Evans A, Arveiler D, Luc G, Emmerich J, Cambien F. The Leu33/Pro polymorphism (PlA1/PlA2) of the glycoprotein IIIa (GPIIIa) receptor is not related to myocardial infarction in the ECTIM study. Thromb Haemost 1997; 77: 1179-81.
23 Klein M, Dauben HP, Schulte HD, Gams E. Centrifugal pumping during routine open heart surgery improves clinical outcome. Artif Organs 1998; 22: 326-36.
24 Zotz RB, Giers G, Maruhn-Debowski B, Scharf RE. Genetic typing of human platelet antigen 1 (HPA-1) by oligonucleotide ligation assay in a specific and reliable semi-automated system. Brit J Haematol 1997; 96: 198-203.
25 Solymoss BC, Nadeau P, Millette D, Campeau L. Late thrombosis of saphenous vein coronary bypass grafts related to risk factors. Circulation. 1988 78. (Suppl II): I-140-3.
26 Komiyama N, Nakanishi S, Nishiyama S, Seki A. Intravascular imaging of serial changes of disease in saphenous vein grafts after coronary artery bypass grafting. Am Heart J 1996; 132: 30-40.
27 Fuster V, Badimon L, Badimon JJ, Chesebro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med. 1992 326. 242-50, 310-8.
28 Chesebro JH, Webster MWI, Zoldhelyi P, Roche PC, Badimon L, Badimon JJ. Antithrombotic therapy and progression of coronary artery disease: antiplatelet versus antithrombins. Circulation. 1992 86. (Suppl III): III-100-10.
29 Goldman S, Copeland J, Moritz T, Henderson Zadina K, Ovitt T, Kern KB, Sehti G, Sharma GVRK, Khuri S, Richards K, Grover F, Morrison D, Whitman G, Chesler E, Sako Y, Pacold I, Montoya A, DeMots H, Floten S, Doherty J, Read R, Scott S, Spooner T, Masud Z, Haakenson C, Kim T, Harker LA. Long-term graft patency (3 years) after coronary artery surgery: effects of aspirin: results of a VA cooperative study. Circulation 1994; 89: 1138-43.
30 Scharf RE, Deitenbeck R, Giers G, Zotz RB. Increased binding of soluble fibrinogen to the platelet glycoprotein (GP) IIb-IIIa receptor related to the polymorphism of the GPIIIa gene (HPA-1b/PL^A2). Blood. 1997 90. (Suppl 1, Part 1 of 2) 256a.