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Thromb Haemost 2003; 89(05): 892-903
DOI: 10.1055/s-0037-1613477
Vascular Development and Vessel Remodelling
Schattauer GmbH

Evidence of prolonged disturbances in the haemostatic, hemorheologic and inflammatory profiles in transmural myocardial infarction survivors

A 12-month follow-up study
Luis Sargento
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
,
Carlota Saldanha
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
,
José Monteiro
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
,
Carlos Perdigão
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
,
João Martins eSilva
1   Instituto de Bioquímica, Faculdade de Medicina de Lisboa. UTIC-AC, Serviço de Cardiologia, Hospital de Santa Maria, Lisboa, Portugal
› Author Affiliations
Further Information

Publication History

Received 14 November 2002

Accepted after revision 27 January 2003

Publication Date:
09 December 2017 (online)

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Summary

Haemostatic, hemorheologic and inflammatory disturbances have been associated with acute coronary syndromes. Most knowledge is reported in cross sectional studies and are without time dependent evolution of these profiles.

The aim of this study was to evaluate, during the first year, the evolution of the haemostatic, hemorheologic and inflammatory profiles determined at hospital discharge in survivors with transmural myocardial infarction (MI).

Eighty eight (79 male; 9 female) mean age of 58 ± 11 years, survivors of a transmural MI were prospectively studied at discharge, 6 months and one year after the event. Haemostatic (protein C, antithrombin III and plasminogen activator inhibitor 1), hemorheologic (blood fluidity and components) and inflammatory profiles (polymorphonuclear elastase and leukocyte count) were determined using standard methodology.

The results of the study can be summarized as follows: (1) Protein C decreased (p < 0.05) over time while PAI-1 only varied significantly until 6th month. (2) Plasma viscosity and fibrinogen (p < 0.001) decrease over time, while erythrocyte aggregation (p < 0.001) and haematocrit increased. Whole blood viscosity did not vary. (3) Leukocyte decreased (p < 0.001) and elastase did not (4). Those patients with cardiovascular events (n = 7) had higher PAI-1 concentration (p<0.05) and leukocyte count (p < 0.01), at discharge (5) Left ventricle ejection fraction correlated significantly with plasma viscosity (r = 0.35 p < 0.05). The results of this longitudinal study show dynamic modifications of the haemostatic, hemorheologic and inflammatory profiles during the first year of a transmural myocardial infarction. In addition, there are interrelations between them and the clinical profile that could help to explain the clinical evolution of this group of patients.

Keywords

Myocardial infarction - protein C - elastase - plasminogen inhibitor 1 and erythrocyte aggregation - longitudinal study
 

  • References

  • 1 Heller RF, Chinn S, Tunstall-Pedor H, Rose G.. How well can we predict coronary heart disease? Findings in the United Kingdon Heart Disease Prevention Project. Br Med J 1984; 288: 1409-11.
    CrossrefPubMedGoogle Scholar
  • 2 Principal investigators of the MONICA Project. Geographic variation in mortality from cardiovascular diseases. World Health Stat Q 1987; 40: 171-84.
    PubMedGoogle Scholar
  • 3 Koenig JW, Sund M, Lowe GDO, Lee AJ, Resch KL, Tunstall-Pedoe H, Keil U, Ernst E.. Geographical variations in plasma viscosity and relation to coronary event rates. Lancet 1994; 334: 711-4.
    PubMedGoogle Scholar
  • 4 Buffon A, Biasucci L, Liuzzo G, D’Onofrio G, Crea F, Maseri A.. Widespread coronary inflammation in unstable angina. N Engl J Med 2002; 347: 5-12.
    CrossrefPubMedGoogle Scholar
  • 5 Erikssen G, Liestol K, Bjonholt JV, Stormorken H, Thaulow E, Erikssen J.. Erythrocyte sedimentation rate: a possible marker of atherosclerosis and a strong predictor of coronary heart disease mortality. Eur Heart J 2000; 21: 1614-20.
    CrossrefPubMedGoogle Scholar
  • 6 Falk E, Fuster V.. Angina pectoris and disease progression. Circulation 1995; 92: 2033-5.
    CrossrefPubMedGoogle Scholar
  • 7 Baker I, Pickering J, Elwood P, Bayer A, Ebrahim S.. Fibrinogen, viscosity and white blood cell count predict myocardial, but not cerebral infarction: Evidence from the Caerphilly and Speedwell cohort. Thromb Haemost 2002; 87: 421-5.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 8 Lowe G, Rumley A, Norrie J, Shepherd J, Cobbe S, Macfarlane P, Packard C.. WOSKOPS. Blood rheology, cardiovascular risk factors and cardiovascular disease: The West of Scotland Coronary Prevention Study. Thromb Haemost 2000; 84: 553-8.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 9 Sargento L, Saldanha C, Monteiro J, Ribeiro C Martins e Silva.. Biohemorheologic factors and the cardiovascular events curve in trans-mural myocardial infarction survivors. 24 months of clinical follow-up. Rev Port Cardiol 2002; 21: 165-71.
    PubMedGoogle Scholar
  • 10 Koenig W, Sund M, Filipiak B, Doring A, Lowel H, Ernst E.. Plasma viscosity and the risk of coronary heart disease. Results from the MONICA-Augsburg cohort study. Arterioscler Thromb Vasc Biol 1998; 18: 768-72.
    CrossrefPubMedGoogle Scholar
  • 11 Bagkurt OK, Levi E, Çaglayan S, Dikmenoglu N, Uçer O, Gtiner R, Yõriikan S.. The role of hemorheologic factors in the coronary circulation. Clin Hemorheol 1991; 11: 121-7.
    PubMedGoogle Scholar
  • 12 Saldanha C, Sargento L, Monteiro J, Ribeiro C, Martins e Silva J.. Impairment of the erythrocyte membrane fluidity in survivors of acute myocardial infarction. A prospective study. Clin Hemorheol Microc 1999; 20: 111-6.
    PubMedGoogle Scholar
  • 13 Sargento L, Zabala L, Saldanha C, SouzaRamalho P, Martins e Silva J.. Sodium fluorescein influence on the hemorheological profile of non-insulin dependent diabetes mellitus patients. Clin Hemorheol Microcirc 1999; 20: 77-84.
    PubMedGoogle Scholar
  • 14 Mulvihill NT, Foley JB, Murphy R, Crean P, Walsh M.. Evidence of prolonged inflammation in unstable angina and non-q wave myocardial infarction. JACC 2000; 36: 1210-6.
    CrossrefPubMedGoogle Scholar
  • 15 Juhan-Vague I, Pyke SD, Alessi MC, Jespersen J, Haverkate F, Thompson SG.. Fibrinolytic factors and the risk of myocardial infarction or sudden death in patients with angina pectors. ECAT Study group. European concerted action on Thrombosis and Disabilities. Circulation 1996; 94: 2057-63.
    CrossrefPubMedGoogle Scholar
  • 16 Thompson SG, Kienast J, Stephen DM, Pyke S, Haverkate F, Jurgen CW, Van de Loo.. Hemostatic factors and the risk of myocardial infarction and sudden death in patients with angina pectoris. N Engl J Med 1995; 332: 635-41.
    CrossrefPubMedGoogle Scholar
  • 17 Wiman B, Anderson T, Hallqvist J, Reuterwall C, Ahlbom A, deFaire U.. Plasma levels of tissue plasminogen activator / plasminogen activator inhibitor-1 complex and von Willibrand factor are significant risk factors for recurrent myocardial infarction in the Stockholm Heart Epidemology Program (SHEEP) study. Arterioscler Thromb Vasc Biol 2000; 20: 2019-23.
    CrossrefPubMedGoogle Scholar
  • 18 Yamada S, Yamada R, Ishii A, Ashikawa K, Kawamitsu H, Fujita K.. Evaluation of tissue plasminogen activator and plasminogen activator inhibitor-I levels in acute myocardial infarction. J Cardiol 1996; 27: 171-8.
    PubMedGoogle Scholar
  • 19 Cushman M., Lemaitre Kuller LH, Psaty BM, Macy EM, Sharrett AR, Tracy RP.. Fibrinolytic activation markers predict myocardial infarction in the elderly. The Cardiovascular Health Study. Arterioscler Thromb Vasc Biol 1999; 19: 493-8.
    CrossrefPubMedGoogle Scholar
  • 20 Danesh J, Collins R, Peto R, Lowe GDC.. Hematocrit, viscosity, erythrocyte sedimentation rate: meta-analysis of prospective studies of coronary heart disease. Eur Heart J 2000; 21: 515-20.
    CrossrefPubMedGoogle Scholar
  • 21 Dietzel J, Bang HO, Thorsen N.. Myocardial infarction and whole blood viscosity. Acta Med Scand 1968; 183: 577-9.
    PubMedGoogle Scholar
  • 22 Lowe GDO.. Blood Rheology, haemostasis and vascular disease. In Bloom AL, Forbes CD, Thomas DP, Tuddenham EGD.. Eds. Haemostasis and Thrombosis, 3rd Ed Edinburgh: Churchill Livingstone; 1994: 1169-88.
    Google Scholar
  • 23 Esmon CT.. Protein C anticoagulant pathway and its role in controlling microvascular thrombosis and inflamation. Crit Care Med 2001; 29: S48-S51.
    CrossrefPubMedGoogle Scholar
  • 24 Spaan JAE, Breals NPW, Laird JD.. Diastolicsystolic coronary flow differences are caused by intramyocardial pump action in the anesthetized dog. Circ Res 1981; 49: 584-93.
    CrossrefPubMedGoogle Scholar
  • 25 Ridker PM, Hennekens CH, Manson JT, Vaughan DE.. Prospective study of endogenous tissue plasminogen activator and the risk of stroke. Lancet 1994; 343: 940-3.
    CrossrefPubMedGoogle Scholar
  • 26 Thompson SG, Kienast J, Pyke SDM, Haverkate F, Van der Loo JCW.. for the European Action on thrombosis and disabilities angor pectoris study group. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1993; 88: 1030-4.
    PubMedGoogle Scholar
  • 27 Jansson JH, Olofsson BO, Nilsson TK.. Predictive value of tissue plasminogen activator mass concentration on long term mortality, in patients with coronary artery disease: A seven year follow-up. Circulation 1993; 88: 2030-4.
    CrossrefPubMedGoogle Scholar
  • 28 Grzywacz A, Elikowski W, Psuja P, Zozulinska M, Zawilska K.. Impairment of plasma fibrinolysis in young survivors of myocardial infarction with silent ische-mia. Blood Coagul Fibrinolysis 1998; 9: 245-9.
    CrossrefPubMedGoogle Scholar
  • 29 Sinkovic A.. Prognostic role of plasminogen activator inhibitor 1 levels in treatment with streptokinase of patients with acute myocardial infarction. Clin Cardiol 2000; 23: 486-9.
    CrossrefPubMedGoogle Scholar
  • 30 Ganapathyraman L, Shanthi P, Baba Krishnan K, Madhavan M, Lakshmikanthan C.. Protein C levels in ischemic heart disease. Indian Heart J 1996; 48: 125-7.
    PubMedGoogle Scholar
  • 31 Peyrou V, Lormeau JC, Hérault JP, Gaich C, Pflirgger AM, Herbert JM.. Contribution of erythrocytes to thrombin generation in whole blood. Thromb Haemost 1999; 81: 400-6.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 32 Smith FB, Fowkes FG, Rumley A, Lee AJ, Lowe GD, Hau CM.. Tissue plasminogen activator and leukocyte elastase as predictors of cardiovascular events in subjects with angina pectoris: Edinburgh Artery Study. Eur Heart J 2000; 21: 1607-13.
    CrossrefPubMedGoogle Scholar
  • 33 Mulvihill N, Foley JB, Murphy R, Crean P, Walsh M.. Evidence of prolonged inflammation in unstable angina and Non Q wave myocardial infarction. J Am Coll Cardiol 2000; 36: 1210-6.
    CrossrefPubMedGoogle Scholar
  • 34 Joanassen L, Holm J Skalli, Bandjers G, Hansson G.. Regional accumulation of T-cells, macrophages and smooth muscle cells in human atherosclerotic plaque. Atherosclerosis 1986; 6: 131-8.
    PubMedGoogle Scholar
  • 35 Mazzone A, De Servi S, Riavuti G.. Increased expression of neutrophil and monocyte adhesion molecules in unstable coronary artery disease. Circulation 1993; 88: 358-63.
    CrossrefPubMedGoogle Scholar
  • 36 Hirsh P, Hillis L, Campbell W, Firth B, Willerson J.. Release of prostaglandins and thnromboxane into the coronary circulationin patients with ischemic heart disease. N Engl J Med 1981; 304: 685-91.
    CrossrefPubMedGoogle Scholar
  • 37 Jang Y, Lincoff A, Plow E, Topol E.. Cell adhesion molecules in coronary artery disease. J Am Coll Cardiol 1994; 24: 1591-601.
    CrossrefPubMedGoogle Scholar
  • 38 Ault KA, Cannon CP, Mitchell J.. Platelet activation in patients after an acute coronary syndrome: results from the Timi 12 trial. J Am Coll Cardiol 1999; 33: 634-9.
    CrossrefPubMedGoogle Scholar
  • 39 Goldstein JA, Demetriou D, Grines OL, Pica M, Shoukkfeh M, O’Neill WW.. Multiple complex coronary plaques in patients with AMI. N Engl J Med 2000; 343: 915-22.
    CrossrefPubMedGoogle Scholar
  • 40 Nosh GB.. White blood cell rheology and atherosclerotic ischemic disease. Clin Hemorheol 1992; 12: 57-67.
    PubMedGoogle Scholar
  • 41 Wolin MS, Rodenberg JM, Messina EJ, Kaley G.. Oxygen metabolites and vasomotor mechanisms in rat cremasteric arterioles. Am J Physiol 1987; 252: H1159-H1163.
    PubMedGoogle Scholar
  • 42 Kmithof EKO, Ransign A, Bachmann F.. Inhibition of tissue plasminogen activator by human plasma. In Davidson JF, Bachmann F, Bouvier CA, Kmithof EKO.. Eds. Progress in fibrinolysis Edinburgh, Scotland: Churchill Livingstone; 1983: 362-6.
    Google Scholar
  • 43 Chandler WL.. A kinetic model of the circulatory regulation of tissue plasminogen activator. Thromb Haemost 1991; 66: 321-8.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 44 Hamsten A, Wiman B, de Faire U, Blomback M.. Increased plasma levels of a rapid inhibitor of tissue plasminogen activator in young survivors of myocardial infarction. N Engl J Med 1985; 313: 1557-63.
    CrossrefPubMedGoogle Scholar
  • 45 Hamsten A, de Faire U, Walldius G, Dahlen G, Szamosi A, Landre L, Blomback M, Wiman B.. Plasminogen activator inhibitor in plasma: risk factor for recurrent myocardial infarction. Lancet 1987; 2: 3-9.
    PubMedGoogle Scholar
  • 46 Espana F, Vaya A, Mira Y, Medina P, Estelles A, Villa P, Falco C, Aznar J.. Low level of circulating activated protein C is a risk factor for venous tromboembolism. Thromb Hemost 2001; 86: 1368-71.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 47 Watanabe R, Wada H, Sakakura M, Nakasaki T, Okugawa Y, Gabazza EC, Hayashi T, Nishioka J, Suzuki K, Shiku H, Nobori T.. Plasma levels of activated protein C inhibitor complex in patients with hypercoagulable states. Am J Hematol 2000; 65: 35-40.
    CrossrefPubMedGoogle Scholar
  • 48 Rosendaal FR, Sisconick DS, Schwartz SM, Beverly RK, Psaty BM, Longstreth WT, Raghnathan TE, Koeprell TD, Reitsma PH.. Factor V Leiden (resistance to activated protein C) increases the risk of myocardial infarction in young women. Blood 1997; 89: 2817-21.
    PubMedGoogle Scholar
  • 49 Rivard GE, David M, Farrell C, Schwarz HP.. Treatment of purpura fulminants in meningococcemia with protein C concentrates. J Pediatr 1995; 126: 646-52.
    CrossrefPubMedGoogle Scholar
  • 50 Powards D, Larsen R, Johnson J, Hubert T, Sun T, Patch MJ, Francis R, Chan L.. Epidemic meningococcemia and purpura fulminants with induced protein C deficiency. Clin Infect Dis 1993; 17: 254-61.
    CrossrefPubMedGoogle Scholar
  • 51 Sargento L, Monteiro J, Saldanha C, Perdigão C, Ribeiro C, Martins e Silva J.. Blood fluidity in survivors of acute myocardial infarction. Prospective study. XIX Congress of the European Society of Cardiology. Eur Heart J 1997; 18: 63.
    CrossrefPubMedGoogle Scholar
  • 52 Sargento L, Saldanha C, Martins e Silva e J.. Fibrinogen and the Erythrocyte Membrane. Biorheology 1999; 36: 128 [Abstract from International Conference of Clinical Hemorheology]
    PubMedGoogle Scholar
  • 53 Folson AR, Wu KK, Rosamond WD, Sharrett AR, Chambless LE.. Prospective study of hemostatic factors and incidence of coronary heart disease: The atherosclerotic risk in communities (ARIC) study. Circulation 1997; 96: 1102-8.
    CrossrefPubMedGoogle Scholar
  • 54 Blake GJ, Ridker PM.. Novel markers of vascular wall inflammation. Circ Res 2001; 89: 763-771.
    CrossrefPubMedGoogle Scholar
  • 55 Lagrand WK, Visser CA, Hermens WT, Niessen HW, Verheugt FWA, Wolbink G, Hack E.. C-Reactive protein as cardiovascular risk factor. More than an epiphenomenon?. Circulation 1999; 100: 96-102.
    CrossrefPubMedGoogle Scholar
  • 56 Pietila KO, Harmoinen AP, Jokiniitty J, Pasternack AI.. Serum C-reactive protein concentration in acute myocardial infarction and its relationship to mortality during 24 months of follow-up in patients under thrombolytic treatment. Eur Heart J 1996; 17: 1345-9.
    CrossrefPubMedGoogle Scholar
  • 57 Haverkate F, Thompson SG, Pyke SDM, Gallimore JR, Pepys MB.. Production of C reactive protein and risk of coronary events in stable and unstable angina. Lancet 1997; 349: 462-6.
    CrossrefPubMedGoogle Scholar
  • 58 Margaglione M, Cappucci G, Colaizzo D, Vecchione G, Grandone E, Di Minno G.. C-reactive protein of offspring is associated with the occurrence of myocardial infarction in first-degree relatives. Arterioscler Thromb Vasc Biol 2000; 20: 198-203.
    CrossrefPubMedGoogle Scholar
  • 59 Bogaty P, Poirier P, Simard S, Boyer L, Solymoss S, Dagenais GR.. Biological profiles in subjects with recurrent aciute coronary events compared with subjects with long standing stable angina. Circulation 2001; 103: 3062-8.
    CrossrefPubMedGoogle Scholar
  • 60 Andreotti F, Hacket DR, Haider AW, Roncaglioni MC, Davies GJ, Beacham JL, Kluft C, Maseri A.. Von Willibrand factor, plasminogen activator inhibitor 1 and c reactive protein are markers of thrombolytic efficacy in acute myocardial infarction. Thromb Haemost 1992; 68: 678-82.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 61 Burke AP, Tracy RP, Kolodgie F, Malcom GT, Zieske A, Kutys R, Pestaner J, Smialek J, Virmani R.. Elevated c-reactive protein values and atherosclerosis in sudden coronary death: association with different pathologies. Circulation 2002; 105: 2019-23.
    CrossrefPubMedGoogle Scholar
  • 62 Becker A, Van Hinsbergh VW, Jager A, Kostense PJ, Dekker JM, Nijpels G, Heine RJ, Bouter LM, Stehouwer CD.. Why is soluble intercellular adhesion molecule-1 related to cardiovascular mortality?. Eur J Clin Invest 2002; 32: 1-8.
    PubMedGoogle Scholar
  • 63 Murphy RT, Foley JB, Mulvihill N, Crean P, Walsh MJ.. Endothelial inflammation and thrombolysis resistance in acute myocardial infarction. Int J Cardiol 2002; 83: 227-31.
    CrossrefPubMedGoogle Scholar
  • 64 Ridker PM, Rifai N, Clearfield M, Downs JR, Weiss SE, Miles JS, Gotto AM.. Measurement of C reactive protein fot the targeting of statin therapy in the primary prevention of acute coronary events. N Engl J Med 2001; 344: 1959-65.
    CrossrefPubMedGoogle Scholar
  • 65 Ford ES.. Body mass index, diabetes and c-reactive protein among US adults. Diabetes Care 1999; 22: 1971-7.
    CrossrefPubMedGoogle Scholar
  • 66 Bem Ami R, Barshtein G, Zeltser D.. et al. Parameters of red blood cell aggregation as correlates of the inflammatory state. Am J Physiol Heart Circ Physiol 2001; 280: H1982-H1988.
    CrossrefPubMedGoogle Scholar