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May 1995, Volume 45, Issue 5

Editorial

Haemorrheologic and Haemostatic Factors in Ischaemic Heart Disease

Shoaib Tauheed  ( Department of Physiology, Dow Medical College, Karachi. )

Clinicians specially dealing with cardiovascular or circulatoiy problems, generally overlook the importance of blood and its constituents which are therapeutically modifi­able as compared to other anatomical cardiovascular struc­tures. Measurements of the flow behaviour of blood orplasma in vitro can be perfonned for one of the two reasons; for the diagnosis and monitoring of disease, or for the prediction and study of blood flow in vivo1. Routine haemorrheological tests for the former include ESR and plasma viscosity. For prediction and study of the blood flow invivo measurement of whole blood viscosity and the deformability of red and white cells in small bore capillaries can be performed. The arterial and venous occlusive diseases being of major medical importance haemorrheology is establishing its rightful place along side perfusion pressure and vessel diameter in the triad of determinants of blood flow and tissue perfusion2,3.
Most workers accept that in the aetiology of coronary heart disease, there are two elements, atherogenesis and thrombogenesis. However, for more than 30 years atherosclemtic research became almost synonymous with researches on lipid and lipoprotein metabolismbutpartplayed by thrombi and hemostatic factors have not been the main-stream topics for investigations and most clinical trials and experimental tools were designed to produce gross hyper­cholesterolaemia4. Lately this imbalance was partly redressed by the publication of early results of the North Park Prospec­tive Heart Study (NPHS) on haemostatic function and cardiovascular death5, which showed the association of cardiovascular death with raised fibrinogen level was atleast as strong as that with raised cholesterol. Association of IRD with fibrinogen is also shown by some other authors6-9. It is known that elevation of fibnnogen levels increases blood viscosity which may further enhance the risk of thrombus formation. Fibrinogen is a major determinant of blood viscosity which if increased has a casual role in IHD10. Fibnnogen levels are also found to be higher in smokers4-8,11-13 and hence the increase in blood viscosity. Much of the association between smoking and IHD may be mediatedby raisedfibnnogen levels and increased blood viscosity.
Primarily haematocrit and plasma viscosity are impor­tant determinants in the rate of oxygen transport and delivery in the circulation and coronary blood flow14. According to the Gordon’s equation14 oxygen delivery is inversely propor­tional to the haematocnt and plasma viscosity. Other haemo­static factors7.as well as haematocrit15-18 have also beenfound to be associated with IHD. Hypercoagulable states as well as thrombogenic stimuli can be reversed easily as compared to relatively irreversible atherosclerotic changes. Despite adequate control and increasing efforts to reduce the elevated levels of lipids, the incidence of LHD is constantly on rise. Therefore, inclusion of rheologic and haemostatic factors in coronary risk profile will have salutary effects.

References

1. Lowe, G. D. 0. Blood rheology and hyperviscosity syndromes. Bailliere’s clinical haematology, London, Bailliere Trindal, 1987, P. 597.
2. Humphrey, P. R. D., Marshal, J., Russel, R. W. R. et at. Cerebral blood flow and viscosity in relative polycythemia. Lancet, 1979;ii:8 73-76.
3. Hudak, M. L., Kochler, R. C., Rosenber, A. A. et a!. Effect of haematocrit on cerebral blood flow Am. 5. Physiol., 1986;251:63-70.
4. Anonymous (Editorial). Haemostatic factors and coronary heart disease. Lancet, 1981;1 :22-23.
5. Meade, T. W., Chakrabarty, R., Haines, A.P. et al. Haemostatic function and cardiovascular death. Early results of a prospective study. Lancet. 1980:1: 1050­-53.
6. Wilhelmsen, L., Svardusdd,K.,Bengsten,K. K. et al. Fibrinogen as a risk factor for stroke and myocardial infarction. N. EngI. J. Med., 1984;311:501-505.
7. Stone, M. C. and Throp, J. M. Plasma fibrinogen a major coronary risk factor. J. P. Colt. Gen. Tract., 1985;35:565-69.
8. Meade, T. W., Brozovick, M., Chakarbarty, R. et at. Haemostatic function and cardiovascular death. Principle results of North Wick Park Heart Study. Lancet, 1986;ii:533-37.
9. Tauheed, S. and Shoaib, S. Importance of plasma fibrinogen in IHD. Ann. Dow Med. Coil., 1991;1:53-55.
10. Lowe, G. D. 0., Drummond, M. M., Lorimer, A. R. et al. Relation between extentofcoronary artery diseaseand bloodviscosity. Br. Med. J., 1980;i:673-74.
11. Powel, J. T., Sian, M., Wiseman, S. et at. Fibrmogen and carboxyhaemoglobin in peripheral arterial disease Lancet, 1988;1: 121.
12. Wilkes,C. H., Keileher, C. and Meade, T. W. Smoking and plasma Fibrinogen. Lancet, 1988;i:307-308.
13. Tauheed, S., Shoaib, S. and Kamat, A. Haemogiobin, haematocrit and plasma fibrinogen in cigarette smokers. J. Pak. Med. Assoc., 1992;42:162-63.
14. Gordon, R. J., Synder, G. K., Trital, H. et al. Potential significance of plasma viscosity and haematocrit variations in Myocardial ischaemia. Am. Heart J., 1974;87: 175-82.
15. Mayer, G. A. Haematocrit and coronary heart disease. Can. Med. Assoc. J., 1965;93:1151-53.
16. Cullen, K. J., Stenhouse, N. S. and Weame, K. L. Raised haemoglobin and the risk of cardiovascular disease. Lancet, 1981 ;ii: 1288-89.
17. Tauheed, S., Shoaib, S. and Kamal, A. Haematocrit values in ischaemic heart disease. J. Pak. Med. Assoc., 1993;43:34-35.

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