plotted on the y-axis and the PTRs using the local laboratory reagent are plotted on the x-axis, the slope of the line is known as the International Sensitivity Index (ISI). The INR is then the PTR found in the local laboratory raised to the power of the ISI.This system has improved anticoagulant control worldwide. However, it is important to realize that the straight-line relationship described above is only valid for patients stably anticoagulated with VKA, and therefore this manipulation of the PTR to the INR is only valid for these patients and not for patients with other coagulation defects. For example, the INR system is not valid for comparison of patients with liver impairment because different reagents do not give the same INR for the same sample [2]. The Haemostasis and Thrombosis Task Force of the British Committee for Standards in Haematology has noted that many UK laboratories now report all their PTs as INRs. We wish to discourage this practice, and for patients who are not on VKA, we prefer either the PT in seconds or the PTR, in both cases with a 95% reference range for comparison. In most cases, it is prolonged results that are of interest, so it would also be acceptable to report the result with the reference being given as less than the upper limit of the 95% reference range. We accept that if both the result and the local reference range are converted to an INR, then no information is lost; however, a spurious improvement is implied and we suggest that this should be avoided. Converting the result to an INR without providing a local reference range also converted to an INR is unhelpful.
Disclosure of Conflict of InterestsThe author states that he has no conflict of interest. Risk of acute ischemic heart disease in postmenopausal women depends on von Willebrand factor and fibrinogen concentrations, and blood group genotype Acute ischemic heart disease (IHD) is the major cause of death in developed countries. A crucial step in the development of acute IHD is platelet aggregate formation at the site of a ruptured atherosclerotic plaque [1]. The sensitivity for platelet aggregate formation depends on genetic variation in platelet glycoproteins (a 2 b 1 , GPIb, a IIb b 3 and GPVI) and on the availability of von Willebrand factor (VWF) and fibrinogen (reviewed in Ruggeri [2]). Furthermore, genetic coagulation markers -factor (F)V 1691GA and FII 20210GA -may be involved in the development of acute IHD. It is our hypothesis that subjects with high sensitivity to platelet aggregation (blood group A or B genotype, a 2 b 1 807T, GPIb -5T, a IIb b 3 Pl A2 , GPVI -13254T, high VWF levels and/or high fibrinogen levels) and high sensitivity to coagulation (FV 1691A and FII 20210A) are more prone to develop acute IHD than subjects who are less sensitive to platelet aggregation (blood group 0 genotype, a 2 b 1 C807, GPIb C-5, a IIb b 3 Pl A1 , GPVI -13254C, low VWF levels and/or low fibrinogen levels) and coagulation (FV G1691 and FII G20210).Until now, research on the contribution of platelet procoagulant ...