OBJECTIVE-Diabetic patients may have a higher prevalence of platelet aspirin resistance than nondiabetic patients. Our goal was to analyze platelet aspirin responsiveness to various aspirin doses in diabetic and nondiabetic patients. RESEARCH DESIGN AND METHODS-We examined the effect of aspirin (81, 162, and 325 mg/day for 4 weeks each) on platelet aspirin responsiveness in 120 stable outpatients (30 diabetic patients and 90 nondiabetic patients) with coronary artery disease (CAD) using light transmittance aggregometry (LTA), VerifyNow, platelet function analyzer (PFA)-100, and levels of urinary 11-dehydro-thromboxane B 2 (11-dh-TxB 2 ).RESULTS-In the total group, a low prevalence (0 -2%) of aspirin resistance was observed with all aspirin doses as determined by arachidonic acid-induced LTA. Aspirin resistance was higher at the 81-mg dose in diabetic versus nondiabetic patients using collagen-induced LTA (27 vs. 4%, P ϭ 0.001), VerifyNow (13 vs. 3%, P ϭ 0.05), and urinary 11-dh-TxB 2 (37 vs. 17%, P ϭ 0.03). Diabetic patients treated with 81 mg exhibited higher platelet function measured by VerifyNow, collagen-and ADP-induced LTA, and 11-dh-TxB 2 levels (P Յ 0.02 for all comparisons). Higher aspirin doses significantly inhibited platelet function and decreased aspirin resistance in diabetic patients (P Ͻ 0.05).CONCLUSIONS-Diabetic patients with CAD treated with 81 mg aspirin exhibit a higher prevalence of aspirin resistance and have significantly higher ADP-and collagen-induced platelet aggregation, 11-dh-TxB 2 levels, and aspirin reaction units measured by VerifyNow than nondiabetic patients. Increased aspirin dosing resulted in similar rates of resistance and platelet function levels between groups. These findings indicate that diabetic patients exhibit a global high platelet reactivity phenotype that may be partially overcome by higher aspirin doses. Diabetes 56: 3014-3019, 2007

One week of DC ingestion improved lipid profiles and decreased platelet reactivity within the total group while reducing inflammation only in women. Regular dark chocolate ingestion may have cardioprotective properties. Further long-term research is warranted to evaluate the effect of flavonoids on cardiovascular health and to determine whether DC's beneficial effects are related to flavonoids or some yet unknown component. This research is based on a larger study which was presented at the American Heart Association Scientific Sessions 2007.

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As a result of ambiguous results from several recent trials in diabetes, scrutiny has focused on the potential effects of insulin and its role in atherosclerosis. This article reviews the premise that anti-diabetes therapy (type 2 diabetes) with insulin causes vascular impairment that leads to atherothrombosis and compromises vascular integrity, which may further potentiates cardiovascular morbidity and mortality. Underlying mechanisms are discussed, including metabolic derangements (blood pressure, lipids, body weight, and glucose) and how these factors trigger insulin-like growth factor (IGF) receptors, leading to cancer. Cellular and molecular mechanisms are discussed, as well as whether the negative results seen in recent glucose trials support this premise. As with most drug therapy, aggressive therapies designed to reach glucose control targets trigger multiple and inter-related mechanisms that, in many cases, go far beyond the pre-determined physiologic targets. From a clinical perspective, physicians should always stress lifestyle modifications, including physical exercise and diet, to their patients who show the first signs of metabolic impairment. Yet even within this context, diet and exercise should be the cornerstone of good therapy when pharmacotherapy is necessary. Given the amount of evidence seen to date with existing agents and the amount of information we do not yet know, patient-centered approaches to modifying behavior before intensive drug therapy are needed should be stressed.

The thrombotic risk profile between premenopausal and postmenopausal women is similar. However, improved management of cholesterol may be of clinical benefit. Large-scale studies are required to validate these findings.