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Hemostatic risk factors in patients with vascular disease
Atherosclerosis, 93 (1992) 255-256 0 1992 Elsevier Scientific Publishers Printed and Published in Ireland
ATHERO
255 Ireland
Ltd. All rights reserved
0021-9150/92/$05.00
04800
Letter to the Editors
Hemostatic risk factors in patients with vascular disease A.D. Blann and C.N. McCollum Department of Chemical Pathology, University Hospital of South Manchester, Didsburv. Manchester M2V 8LR (UK) (Received 30 December. 1991) (Accepted 13 January, 1992)
Dear Editors,
We read with interest
the report by Cortellaro et al. (Atherosclerosis, 90 (1991) 109) on risk factors in vascular disease patients as we too are involved in similar studies. Our own approach (using comparable patients and criteria) includes measurement of von Willebrand factor antigen (vWFAg) and other risk factors, but our analysis has been hampered by the presence of more than one risk factor in patients with peripheral vascular disease (PVD). In an attempt to address this problem we have measured vWFAg in each risk factor in isolation, and have found increased levels in smoking [l], hypertension [2] and in familial hypercholesterolaemia [3] in the absence of vascular disease, and others have reported raised vWFAg in uncomplicated diabetes 141. Many of the patients studied by Cortellaro et al. already have these risk factors. We therefore aimed to ask if vWFAg in PVD would remain increased in the absence of risk factor. We studied 45 non-diabetic patients with PVD (claudication, superficial femoral disease etc., of Correspondence to: A.D. Blann, Pathology, University Hospital Didsbury.
Manchester
Department of South
M20 8LR, UK.
of Chemical Manchester,
whom 29 smoked), finding a higher mean systolic blood pressure (150 f 20 mmHg vs. 133 f 9 P = 0.0001 (t-test) to 14 age- and sex-matched controls), higher diastolic blood pressure (87 f 11 vs. 72 f 10, P = 0.0001) and higher cholesterol (5.9 f 1.3 mmol/l vs. 4.5 f 1.2, P = 0.012). Using an ELISA, vWFAg was higher in PVD than in controls (143 + 41 international unitsjdecilitre (IU/dl) vs. 99 f 39, P = 0.0021) broadly confirming the findings of Cortellaro. In order to test the influence of risk factors, we classified these patients into two groups depending on the presence or absence of hypertension (> 140 and > 90 mmHg) and/or hypercholesterolaemia (cholesterol > 7 mmol/l). There were 29 patients with these risk factors (of whom 18 were smokers) and 16 (11 smokers) who were normotensive and normocholesterolaemic, and no difference in ages between the two groups (mean 65 years vs. 64 years, respectively). The patients in the risk group had higher systolic and diastolic blood pressures and cholesterol than patients without risks (all P < O.OOOl), whose indices were in turn not raised relative to the normal controls. This separation of patients according to risk factors failed to result in differences in vWFAg. In the presence of risk factors, vWFAg was 138 ?? 37 (P = 0.006 to normal
256 controls) and in the absence of risk factors it was 152 f 48 (not significant to risk group but P = 0.0003 to normal controls). Analysis according to smoking did not influence these results. There is clearly a role for vWFAg in atherosclerosis since it seems to be a useful marker of damage to the endothelium and may have a role in thrombus formation by aggregating platelets and modulate their adherence to the subendothelium [5]. Cortellaro et al. have shown raised levels of vWFAg in PVD. We have demonstrated that this remains following correction for the influences of hypertension, smoking and hypercholesterolaemia. It would be interesting to learn if Cortellaro et al. also came to the same conclusion by performing multi-variate analysis.
References Blann, A.D., Increased circulating levels of von Willebrand factor antigen in smokers may be due to lipid peroxides, Med. Sci. Res., I9 (1991) 535. Naqvi, T.Z., Waite, M., Blann, A.D. and McCollum, C.N., von Willebrand factor antigen levels in hypertension, Eur. Heart. J., 12 Suppl. (1991) 241. Duffy, A., Blann, A.D.. Anderson, J., Miller, P., Gowland, E. and McCollum, C.N., Increased von Willebrand factor antigen in familial hypercholesterolaemia with or without vascular disease, Atherosclerosis, 90 (1991) 226. Boneu, B., Abbal, M.. Plante, J. and Bierme, R., Factor VIII complex and endothelial damage, Lancet, i (1975) 1430. Wagner, D.D., Cell biology of von Willebrand nu. Rev. Cell Biol., 6 (1990) 217.
factor,
An-
ATHERO
255 Ireland
Ltd. All rights reserved
0021-9150/92/$05.00
04800
Letter to the Editors
Hemostatic risk factors in patients with vascular disease A.D. Blann and C.N. McCollum Department of Chemical Pathology, University Hospital of South Manchester, Didsburv. Manchester M2V 8LR (UK) (Received 30 December. 1991) (Accepted 13 January, 1992)
Dear Editors,
We read with interest
the report by Cortellaro et al. (Atherosclerosis, 90 (1991) 109) on risk factors in vascular disease patients as we too are involved in similar studies. Our own approach (using comparable patients and criteria) includes measurement of von Willebrand factor antigen (vWFAg) and other risk factors, but our analysis has been hampered by the presence of more than one risk factor in patients with peripheral vascular disease (PVD). In an attempt to address this problem we have measured vWFAg in each risk factor in isolation, and have found increased levels in smoking [l], hypertension [2] and in familial hypercholesterolaemia [3] in the absence of vascular disease, and others have reported raised vWFAg in uncomplicated diabetes 141. Many of the patients studied by Cortellaro et al. already have these risk factors. We therefore aimed to ask if vWFAg in PVD would remain increased in the absence of risk factor. We studied 45 non-diabetic patients with PVD (claudication, superficial femoral disease etc., of Correspondence to: A.D. Blann, Pathology, University Hospital Didsbury.
Manchester
Department of South
M20 8LR, UK.
of Chemical Manchester,
whom 29 smoked), finding a higher mean systolic blood pressure (150 f 20 mmHg vs. 133 f 9 P = 0.0001 (t-test) to 14 age- and sex-matched controls), higher diastolic blood pressure (87 f 11 vs. 72 f 10, P = 0.0001) and higher cholesterol (5.9 f 1.3 mmol/l vs. 4.5 f 1.2, P = 0.012). Using an ELISA, vWFAg was higher in PVD than in controls (143 + 41 international unitsjdecilitre (IU/dl) vs. 99 f 39, P = 0.0021) broadly confirming the findings of Cortellaro. In order to test the influence of risk factors, we classified these patients into two groups depending on the presence or absence of hypertension (> 140 and > 90 mmHg) and/or hypercholesterolaemia (cholesterol > 7 mmol/l). There were 29 patients with these risk factors (of whom 18 were smokers) and 16 (11 smokers) who were normotensive and normocholesterolaemic, and no difference in ages between the two groups (mean 65 years vs. 64 years, respectively). The patients in the risk group had higher systolic and diastolic blood pressures and cholesterol than patients without risks (all P < O.OOOl), whose indices were in turn not raised relative to the normal controls. This separation of patients according to risk factors failed to result in differences in vWFAg. In the presence of risk factors, vWFAg was 138 ?? 37 (P = 0.006 to normal
256 controls) and in the absence of risk factors it was 152 f 48 (not significant to risk group but P = 0.0003 to normal controls). Analysis according to smoking did not influence these results. There is clearly a role for vWFAg in atherosclerosis since it seems to be a useful marker of damage to the endothelium and may have a role in thrombus formation by aggregating platelets and modulate their adherence to the subendothelium [5]. Cortellaro et al. have shown raised levels of vWFAg in PVD. We have demonstrated that this remains following correction for the influences of hypertension, smoking and hypercholesterolaemia. It would be interesting to learn if Cortellaro et al. also came to the same conclusion by performing multi-variate analysis.
References Blann, A.D., Increased circulating levels of von Willebrand factor antigen in smokers may be due to lipid peroxides, Med. Sci. Res., I9 (1991) 535. Naqvi, T.Z., Waite, M., Blann, A.D. and McCollum, C.N., von Willebrand factor antigen levels in hypertension, Eur. Heart. J., 12 Suppl. (1991) 241. Duffy, A., Blann, A.D.. Anderson, J., Miller, P., Gowland, E. and McCollum, C.N., Increased von Willebrand factor antigen in familial hypercholesterolaemia with or without vascular disease, Atherosclerosis, 90 (1991) 226. Boneu, B., Abbal, M.. Plante, J. and Bierme, R., Factor VIII complex and endothelial damage, Lancet, i (1975) 1430. Wagner, D.D., Cell biology of von Willebrand nu. Rev. Cell Biol., 6 (1990) 217.
factor,
An-