Thromb Haemost 2008; 100(05): 899-904
DOI: 10.1160/TH07-10-0650
Cardiovascular Biology and Cell Signalling
Schattauer GmbH

The effects of exercise capacity and sedentary lifestyle on haemostasis among middle-aged women with coronary heart disease

Edit Nagy
1   Karolinska Institutet, Division of Medicine, Cardiology Unit, Stockholm, Sweden
,
Imre Janszky
2   Department of Public Health Sciences, Division of Preventive Medicine, Karolinska Institutet, Stockholm, Sweden
3   Institute of Behavioural Sciences, Semmelweis University, Budapest, Hungary
,
Margita Eriksson-Berg
4   Department of Emergency Medicine, Karolinska University Hospital, Solna, Stockholm, Sweden
,
Faris Al-Khalili
5   Karolinska Institutet, Department of Clinical Sciences, Division of Cardiology, Danderyds University Hospital, Stockholm, Sweden
,
Karin Schenck-Gustafsson
1   Karolinska Institutet, Division of Medicine, Cardiology Unit, Stockholm, Sweden
› Author Affiliations
Financial support: This work was supported by grants from ALF:academic money from Stockholm County Council.
Further Information

Publication History

Received 31 October 2007

Accepted after major revision 19 August 2008

Publication Date:
22 November 2017 (online)

Summary

Previous studies have established a link/relationship between haemostatic factors and increased risk of cardiovascular disease. In addition, physical conditioning is associated with lower coronary heart disease risk. The purpose of this study was to assess the association between physical exercise and haemostatic factors among middle-aged women surviving an acute coronary event. The Stockholm Female Coronary Risk Study included 292 women aged < 65 years, resident in the greater Stockholm area, who were hospitalized for an acute coronary syndrome. Extensive clinical screening including exercise testing, and blood tests were performed 3–6 months after the coronary event. Self-reported physical activity was assessed by a WHO questionnaire. Patients on warfarin treatment were excluded from our analyses. Haemostatic factors were generally higher among physically inactive patients when compared to physically active women in our univariate models. Exercise capacity had a statistically significant relationship with factor VII antigen (p=0.039) and vWFag (p=0.038) even in our multiadjusted analyses. Physical inactivity and poor physical fitness are associated with a potentially prothrombotic blood profile in middle aged women with coronary heart disease.

 
  • References

  • 1 Hu G, Tuomilehto J, Silventoinen K. et al. Joint effects of physical activity, body mass index, wait circumference and waist-to-hip ratio with the risk of cardiovascular disease among middle-aged Finnish men and women. Eur Heart J 2004; 25: 2212-2219.
  • 2 Stevens J, Cai J, Evenson KR. et al. Fitness and fatness as predictors of mortality from all causes and from cardiovascular disease in men and women in the lipid research clinics study. Am J Epidemiol 2002; 156: 832-841.
  • 3 Barengo NC, Hu G, Timo Lakka TA. et al. Low physical activity as a predictor for total and cardiovascular disease mortality in middle-aged men and women in Finland. Eur Heart J 2004; 24: 2204-2211.
  • 4 Panagiotakos DB, Pitsavos C, Chrysohoou C. et al. The associations between leisure-time physical activity and inflammatory and coagulation markers related to cardiovascular disease: the ATTICA study. Prev Med 2005; 40: 432-437.
  • 5 Stevenson ET, Davy KP, Seals DR. Hemostatic, metabolic, and androgenic risk factors for coronary heart disease in physically active and less active postmenopausal women. Arterioscler Thromb Vasc Biol 1995; 15: 669-677.
  • 6 Szymanski LM, Kessler CM, Fernhall B. Relationship of physical fitness, hormone replacement therapy, and hemostatic risk factors in postmenopausal women. J Appl Physiol 2005; 98: 1341-1348.
  • 7 Niessner A, Richter B, Penka M. et al. Endurance training reduces circulating inflammatory markers in persons at risk of coronary event: Impact on plaque stabilization?. Atherosclerosis 2006; 186: 160-165.
  • 8 Yusuf S, Hawken S, Ounpuu S. et al. INERTHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 2004; 364: 937-952.
  • 9 Kannel WB, Wolf PA, Castelli WP. et al. Fibrinogen and risk of cardiovascular disease: the Framingham Study. J Am Med Assoc 1987; 258: 1183-1186.
  • 10 Yarnell JW, Baker IA, Sweetnam PM. et al. Fibrinogen, viscosity and white cell count are major risk factors for ischemic heart disease. The Caerphilly and Speedwell collaborative heart disease studies. Circulation 1991; 83: 836-844.
  • 11 Feinbloom D, Bauer KA. Assessment of hemostatic risk factors in predicting arterial thrombotic events. Arterioscler Thromb Vasc Biol 2005; 25: 2043-2053.
  • 12 Whincup PH, Danesh J, Walker M. et al. von Willebrand factor and coronary heart disease. Prospective study and meta-analysis. Eur Heart J 2002; 23: 1764-1770.
  • 13 El-Sayed MS, El-Sayed Ali Z, Ahmadizad S. Exercise and training effects on blood haemostasis in health and disease: an update. Sports Med 2004; 34: 181-200.
  • 14 Meade TW, Mellows S, Brozovic M. et al. Haemostatic function and ischaemic heart disease: principal results of the Northwick Park Heart Study. Lancet 1986; 02: 533-537.
  • 15 Folsom AR, Wu KK, Rosamond WD. et al. Prospective study of haemostatic factors and incidence of coronary heart disease: the Atherosclerosis Risk in Communities (ARIC) study. Circulation 1997; 96: 1102-1108.
  • 16 Wiman B, Andersson T, Hallqvist J. et al. Plasma levels of tissue plasminogen activator/plasminogen activator inhibitor-1 complex and von Willebrand factor are significant risk markers for recurrent myocardial infarction in the Stockholm Heart Epidemiology Program (SHEEP) study. Arterioscler Thromb Vasc Biol 2000; 20: 2019-2023.
  • 17 Levi M, van der Poll T, Buller HR. Bidirectional relation between inflammation and coagulation. Circulation 2004; 109: 2698-2704.
  • 18 Thorand B, Baumert J, Döring A. et al. Association of cardiovascular risk factors with markers of endothelial dysfunction in middle-aged men and women. Results from the MONICA/KORA Augsburg Study. Thromb Haemost 2006; 95: 131-141.
  • 19 Stramba-Badiale M, Fox KM, Prior SG. et al. Cardiovascular disease in women: a statement from the policy conference of the European Society of Cardiology. Eur Heart J 2006; 27: 994-1005.
  • 20 Vaccarino V, Krumholz HM, Yarzebski J. et al. Sex differences in 2-year mortality after hospital discharge for myocardial infarction. Ann Intern Med 2001; 134: 173-181.
  • 21 Vaccarino V, Rathore SS, Wegner NK. et al for the National Registry of Myocardial Infarction Investigators. Sex and racial differences in the management of acute myocardial infarction, 1994 through 2002. N Engl J Med 2005; 353: 671-682.
  • 22 Gillum R, Fortman S, Princas R. et al. International diagnostic criteria for acute myocardial infarction and stroke. Am Heart J 1984; 108: 150-158.
  • 23 Braunwald E. Unstable angina: a classification. Circulation 1989; 80: 410-414.
  • 24 Morrissey JH, Macik BG, Neuenschwander PF. et al. Quantitation of activated factor VII levels in plasma using a tissue factor mutant selectively deficient in promoting factor VII activation. Blood 1993; 81: 734-744.
  • 25 Al-Khalili F, Janszky I, Andersson A. et al. Physical activity and exercise performance predict long-term prognosis in middle-aged women surviving acute coronary syndrome. J Int Med 2007; 261: 178-187.
  • 26 Baecke JA, Burema J, Frijters JE. A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr 1982; 36: 936-942.
  • 27 Grundy SM. Metabolic syndrome: Connecting and reconciling cardiovascular and diabetes worlds. J Am Coll Cardiology 2006; 47: 1093-1100.
  • 28 Silveira A, Green F, Karpe F. et al. Elevated levels of factor VII activity in postprandial state: effect of the factor VII arg-Gln polymorphism. Thromb Haemost 1994; 72: 734-739.
  • 29 Blann AD. Plasma von Willebrand factor, thrombosis and the endothelium: The first 30 years. Thromb Haemost 2006; 95: 49-55.
  • 30 Eriksson-Berg M, Silveira A, Orth-Gomer K. et al. Coagulation factor VII in middle-aged women with and without coronary heart disease. Thromb Haemost 2001; 85: 787-792.
  • 31 Silveira A, Karpe F, Johnsson H. et al. In vivo demonstration in humans that large postprandial triglyceride-rich lipoproteins activate coagulation factor VII through the intrinsic coagulation pathway. Arterioscler Thromb Vasc Biol 1996; 16: 1333-1339.
  • 32 Eriksson-Berg M, Egberg N, Wamala S. et al. Relationship between plasma fibrinogen and coronary heart disease in women. Arterioscler Thromb Vasc Biol 1999; 19: 67-72.
  • 33 Juhan-Vague I, Pyke SDM, Alessi MC. et al. bon behalf of the ECAT Study Group. Fibrinolytic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. Circulation 1996; 94: 2057-2063.
  • 34 Hoekstra T, Geleijnse J, Schouten EG. et al. Plasminogen activator inhibitor-type I: its plasma determinants and relation with cardiovascular risk. Thromb Haemost 2004; 91: 861-872.
  • 35 Hamsten A, de Faire U, Walldius G. et al. Plasminogen activator inhibitor in plasma: risk factor for recurrent myocardial infarction. Lancet 1987; 02: 3-9.
  • 36 Rega G, Kaun C, Weiss TW. et al. Inflammatory cytokines interleukin-6 and oncostatin M induce plasminogen activator inhibitor-1 in human adipose tissue. Circulation 2005; 111: 1938-1945.