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"Insulin resistance and CVD" Groups 3&4 (biography)
English - 2003-03-29 - 22 minutes
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Summary :
Group 3: The purpose of this workshop was to assess the data supporting IR as the cause of atherosclerosis, and determine if and/or when an IR treatment strategy can be used to manage metabolic syndrome. There is epidemiological data suggesting a link between IR and atherosclerosis, and carotid IMT evidence of improvement of atherosclerosis with insulin sensitizers. So should we be using TZDs in non-diabetic syndrome X i.e., in patients who do not yet have abnormalities in glucose homeostasis? The current clinical opinion and behaviour is that we’re not pushing lifestyle intervention enough, we need more information, better endpoints, and we need to be more aggressive in treatment, earlier on. We need to further evaluate current therapy to get the hard end points, to see if the effects of TZDs and of treating IR do translate into decreased cardiovascular events.
Group 4: This workshop was held to discuss whether IR or hyperinsulinemia is the primary culprit in the development of CVD in type 2 diabetes, and how this might influence management, i.e., use of a secretagogue? Epidemiological studies show that high insulin levels are associated with CVD, but these studies are confounded because of high insulin due to IR. Other studies using insulin show that there is no increase or even a decrease in CVD, suggesting that IR is more likely the causative factor. In terms of current clinical opinion and behaviour, doctors in the U.S. are using TZDs more in relation to patients with CVD, whereas in Canada we face some hurdles including cost and coverage among other issues. There is a need to re-evaluate current therapy, but we can’t make any firm recommendations until seeing the outcome data from present and future studies.
Learning objectives :
The participant will gain an understanding of the current state of decision making on prescribing insulin sensitizers to reduce cardiovascular events in type 2 diabetics:
- There is a need to further evaluate current therapy
- Outcome studies are needed to clarify whether treating IR does in fact decrease cardiovascular events
Bibliographic references :
Association between insulin resistance and carotid arteriosclerosis in subjects with normal fasting glucose and normal glucose tolerance.
Ishizaka N, Ishizaka Y, Takahashi E, Unuma T, Tooda E, Nagai R, Togo M, Tsukamoto K, Hashimoto H, Yamakado M.
Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, Japan. nobuishizka-tky@umin.ac.jp
OBJECTIVE: We examined the possible association between insulin resistance and carotid arteriosclerosis in subjects who had both normal fasting glucose and normal glucose tolerance after intake of a glucose load. METHODS AND RESULTS: Our subjects were individuals who underwent general health screening at our institute, which included carotid ultrasound and oral glucose tolerance testing. Of the 1238 subjects enrolled in our study, 738 (60%) were classified as normal, defined as a normal fasting glucose level and normal glucose tolerance, and 334 (27%) and 166 (13%) were classified as borderline and diabetic, respectively, according to the criteria of the Japan Diabetes Society. The homeostasis model assessment of insulin resistance (HOMA-IR) was used as the index to measure insulin resistance. In normal-type subjects, univariate analysis showed that insulin resistance, but not insulin secretion, was associated with the presence of carotid plaque. Multivariate analysis showed that HOMA-IR was positively associated with carotid plaque in normal-type subjects, with an odds ratio of 1.19 (95% confidence interval, 1.00 to 1.41; P<0.05). CONCLUSIONS: These data suggest the possibility that the presence of higher insulin resistance could be a risk factor for carotid arteriosclerosis in subjects with normal fasting glucose and normal glucose tolerance.
Arterioscler Thromb Vasc Biol 2003 Feb 1;23(2):295-301
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