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Archived Comments for: Relevance of hemostatic risk factors on coronary morphology in patients with diabetes mellitus type 2

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  1. Hypercoagulability, a physiological reaction to increased blood viscosity due to hypovolaemia

    Simon Thornton, Université Henri Poincaré

    14 May 2009

    Dear Sir,

    I was very interested to read the recent article by Jax et al., (1) in the journal Cardiovascular Diabetology (2009; 8 (1): 24) entitled “Relevance of hemostatic risk factors on coronary morphology in patients with diabetes mellitus type 2” where the authors clearly show an increased thrombogenic state in diabetes associated with an increase in blood viscosity. Similar risk factors have been reported with hypertension and when this disease state is associated with diabetes the risk is even further increased (2). It is important to note that plasma viscosity correlates to the progression of coronary and peripheral artery diseases (3). Now the question could be asked whether the hypercoagulability is a symptom of the two disease states or a reaction to the problem of viscosity ?

    I have already published a letter on a common link between hypertension and diabetes and that being the hormone angiotensin (4), released in physiological response to a hypovolaemic state associated with these problems. This could suggest that with hypovolaemia not only blood perfusion could become a serious problem but also red blood cell volume, and thus the heart would need to work more to pump thickening blood around the body thus affecting tissue perfusion (5). A further adaptation to a reduced blood volume that would allow easier blood flow is a decrease in the number of red blood cells, which would induce also a state of mild hypoxia (6). But what about the increase in coagulability; I would like to suggest that this is a normal physiological reaction simply to aid the fluidity of the blood.

    Furthermore, it has been shown that anti-hypertensive treatments, especially antagonists of the renin-angiotensin system, can have a positive effect on these haemorheological disturbances (2). With colleagues I have a letter (7) concerning the use of antagonists of the renin angiotensin system and obesity where we comment on the decreases in body weight seen in obese animals. We suggest that this is due to the increased drinking observed in these animals with the use of the antagonists. This would tend to reinforce the idea that it is the correction of the hypovolaemia that leads to correction of the haemorheological disturbances.

    In the future then it would appear important to suggest that fluid, especially water, consumption be monitored, if not encouraged, in all human studies on haemostatic risk factors in patients with diabetes and/or hypertension.


    1. Jax TW, Peters AJ, Plehn G, Schoebel FC. Relevance of hemostatic risk factors on coronary morphology in patients with diabetes mellitus type 2. Cardiovasc Diabetol. 2009; 8 (1): 24.
    2. Kearney-Schwartz A, Virion JM, Stoltz JF, Drouin P, Zannad F. Haemorheological disturbances in hypertensive type 2 diabetic patients--influence of antihypertensive therapy. Fundam Clin Pharmacol. 2007; 21 (4): 387-396.
    3. Késmárky G, Kenyeres P, Rábai M, Tóth K. Plasma viscosity: a forgotten variable. Clin Hemorheol Microcirc. 2008; 39 (1-4): 243-246.
    4. Thornton SN. Angiotensin, the hypovolaemia hormone, aggravates hypertension, obesity, diabetes and cancer. J Intern Med. 2009; 265(5):616-7.
    5. Baskurt OK, Meiselman HJ. Blood rheology and hemodynamics. Semin Thromb Hemost. 2003; 29 (5): 435-450.
    6. Thornton SN. Hypovolaemia-induced mild hypoxia produces subchronic metabolic dysfunction. Int J Obes (Lond). 2009; 33 (5): 605.
    7. Thornton SN, Even PC, van Dijk G. Hydration increases cell metabolism. Int J Obes (Lond). 2009; 33 (3): 385.

    Competing interests