Aerobic as well as resistance exercises are good for patients with type 1 diabetes.

AIMS: To assess whether aerobic or resistance training has greater benefits in non-physically active men with a long lasting type 1 diabetes. The effects of exercise were evaluated in terms of diabetes control and risk factors for cardiovascular complications. METHODS: 21 male participants (mean age: 37 yrs, diabetes duration: 23 yrs, mean HbA1c: 7.4%) randomly assigned to 2 groups: 1-aerobic training (n = 10) and 2-resistance training (n = 11). All subjects participated in 60-min training sessions, either aerobic or resistance, twice a week for three months. At baseline and after 3 months: echocardiography, ECG and incremental exercise test, ECG and blood pressure monitoring, lipid profile, lactate and diabetes control parameters were assessed in all patients. RESULTS: Baseline HbA1c was 7.44% in aerobic group and 7.36% in resistance group (p = 0.84). After 3 months there was no significant change in HbA1c value in any exercise group but a non-statistically significant downward trend was seen particularly in aerobic exercise group (p = 0.07) vs the resistance group (p = 0.15). There was no significant difference in body mass, risk of hypoglycemia and cardiovascular risk factors. CONCLUSIONS: Both forms of exercise are safe in terms of glycemic control and cardiovascular risk factors in patients with quite well-controlled type 1 diabetes without advanced late complications.

Thrombin generation and platelet reactivity at hospital discharge and 6-month outcome after the acute coronary syndrome in diabetic and nondiabetic patients.

OBJECTIVES: Increased plasma thrombogenesis and blood platelet reactivity are associated with a worse outcome in patients with the acute coronary syndrome (ACS). The aim of this study was to test the clinical utility of combining a thrombin generation test and platelet aggregation in predicting future ischemic events after ACS. METHODS: The study included patients hospitalized due to ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention with stent implantation. Blood for platelet aggregation and thrombin generation was collected at hospital discharge. We performed whole-blood platelet aggregation with arachidonic acid (AA), collagen, adenosine diphosphate and thrombin receptor-activating peptide (TRAP) as agonists and the thrombin generation test using a fluorescence method. Patients were followed for up to 6 months. The combined end point of the study consisted of death, stroke, myocardial infarction or repeated target vessel revascularization. RESULTS: The study enrolled 161 patients. The end point occurred in 30 patients (18.6%). Thrombin generation showed a significantly prolonged lag time, time to thrombogram peak and start of the tail of the thrombogram in diabetic patients who reached the study end point but not in nondiabetics. End point occurrence was not connected with platelet reactivity at hospital discharge in the whole group. In the diabetic subgroup, increased platelet aggregation induced with AA and TRAP at hospital discharge was connected with a more frequent occurrence of the study end point. CONCLUSIONS: In diabetic patients after STEMI, thrombin generation measures as well as TRAP- and AA-induced platelet aggregation at hospital discharge are associated with an ensuing ischemic event during the 6-month follow-up.

Effect of glycemic control on response to antiplatelet therapy in patients with diabetes mellitus and ST-segment elevation myocardial infarction.

Impaired glycemic control (GC) is a troubling clinical condition with an unclear prognostic value that is frequent in diabetics, especially in the setting of acute coronary syndrome. Residual platelet reactivity can be also affected by GC. We evaluated the relation between response to dual antiplatelet therapy and GC in diabetics with STEMI treated with primary coronary angioplasty (PCI). Sixty diabetic patients were prospectively enrolled in the study. All patients were treated with clopidogrel and aspirin. Platelet reactivity (whole blood aggregation and phosphorylation of vasodilator-stimulated phosphoprotein, VASP) were assessed serially before and 24 hours, 7 days, and 30 days after the PCI. Blood glucose >8.5 mmol/L on admission was an independent predictor of a impaired clopidogrel response measured with platelet reactivity index (PRI) >50% on admission (OR 7.8, 95% CI 1.4-17.7, p<0.02) and 24 hours after PCI (OR 13.1, 95% CI 3.4-28.1, p<0.01). In conclusion, diabetic patients with STEMI and glycemia >8.5 mmol/L on admission is related to a poorer response to clopidogrel. There were no interaction between glycated hemoglobin level or glycemia on admission and platelet reactivity measured with collagen, arachidonic acid or thrombin receptor agonist peptide-induced aggregation. Further clinical studies of the role of GC in the efficacy of antiplatelet agents are warranted.

Effects of platelet and inflammatory system activation on outcomes in diabetic patients with ST segment elevation myocardial infarction treated with primary percutaneous coronary intervention.

BACKGROUND: Recurrent myocardial ischaemia and restenosis are more common in diabetic patients treated with primary percutaneous coronary intervention (PCI) due to an acute coronary syndrome (ACS) compared to patients without diabetes. Diabetes is also associated with increased residual platelet activity during dual antiplatelet treatment. In recent reports, platelet reactivity has been linked to outcomes after ACS. Appropriate platelet inhibition might lead to improved outcomes in this patient population. To this end, newest methods to evaluate platelet function may prove helpful. AIM: To evaluate 6-month outcomes in diabetic patients treated with primary PCI due to ST segment elevation myocardial infarction (STEMI) in relation to platelet reactivity evaluated at discharge. METHODS: The study included 120 diabetic patients treated with primary PCI due to STEMI. Patients received loading doses of acetylsalicylic acid (ASA, 300 mg) and clopidogrel (600 mg) on admission, and later were treated with maintenance doses of 75 mg of ASA and clopidogrel. Blood for platelet aggregation testing was collected at discharge. We used whole blood impedance aggregometry using the Multiplate aggregometer with arachidonic acid (AA), adenosine diphosphate (ADP), collagen, and thrombin receptor peptide agonist (TRAP) as agonists. Six-month follow-up was based on telephone contact and hospital discharge summaries if hospitalisation occurred. The primary combined endpoint included recurrent ACS and restenosis. RESULTS: The primary combined endpoint occurred in 28 (23%) patients. Among patients with the primary endpoint, we found significantly higher platelet reactivity as evaluated by aggregation testing using AA and TRAP at discharge following the initial infarction compared to patients without the primary endpoint (area under aggregation curve 1137.4 ± 198.5 vs 833.5 ± 253.4; p = 0.013 for TRAP-induced aggregation, and 333.0 ± 263.8 vs 186.9 ± 105.4; p = 0.019 for AA-induced aggregation). We found no relationship between ADP- and collagen-induced aggregation at discharge and the occurrence of the primary endpoint. CONCLUSIONS: Increased platelet reactivity evaluated by TRAP-induced aggregation is related to a higher rate of restenosis and recurrent ACS during a 6-month follow-up of diabetic STEMI patients treated with PCI.