In conclusion, long-term trimetazidine improves functional class and left ventricular function in patients with HF. This benefit contrasts with the natural history of the disease, as shown by the decrease of EF in patients on standard HF therapy alone.

Trimetazidine improves functional class and LV function in patients with heart failure. These effects are associated to the observed trimetazidine-induced increase in the PCr/ATP ratio, indicating preservation of the myocardial high-energy phosphate levels.

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Objective-Regulatory T (Treg) cells play a protective role in experimental atherosclerosis. In the present study, we investigated whether the levels of circulating Treg cells relate to the degree of atherosclerosis in carotid and coronary arteries. Methods and Results-We studied 2 distinct populations: (1) 113 subjects, selected from a free-living population (carotid study), in which we measured the intima-media thickness of the common carotid artery, as a surrogate marker of initial atherosclerosis; and (2) 75 controls and 125 patients with coronary artery disease (coronary study): 36 with chronic stable angina, 50 with non-ST-elevation acute coronary syndrome, 39 with ST-elevation acute myocardial infarction. Treg-cell levels were evaluated by flow cytometry (Treg cells identified as CD3 ϩ CD4 ϩ CD25 high CD127 low ) and by mRNA expression of forkhead box P3 or of Treg-associated cytokine interleukin 10. In the carotid study, no correlation was observed between Treg-cell levels and intima-media thickness. No differences in Treg-cell levels were observed comparing rapid versus slow intima-media thickness progressors from a subgroup of patients (nϭ65), in which prospective data on 6-year intima-media thickness progression were available. In the coronary group, Treg-cell levels were not altered in chronic stable angina patients. In contrast, nonunivocal variations were observed in patients suffering an acute coronary syndrome (with a Treg-cell increase in ST-elevation acute myocardial infarction and a Treg-cell decrease in non-ST-elevation acute coronary syndrome patients). Key Words: regulatory T cells Ⅲ coronary artery disease Ⅲ flow cytometry Ⅲ carotid artery intima-media thickness Ⅲ acute coronary syndrome T cells play a role in atherosclerosis and in acute manifestation of plaque destabilization. 1 The activation of inflammatory pathways in atherosclerosis and in coronary artery disease (CAD) is not confined to coronary lesions but involves the activation of neutrophils, monocytes, and lymphocytes (ie, CD69 Conclusion-Theϩ , HLA-DR ϩ , and CD 137 ϩ T cells) in peripheral blood in particular during acute coronary syndromes (ACSs). [2][3][4] On the other hand, regulatory T (Treg) cells reduce the development of experimental atherosclerosis acting both systemically and within the lesion. 5,6 Immunostaining of human atherosclerotic plaques showed that Treg cells are present during all stages of plaque development in the intima and adventitia. 7 In general, Treg cells play a key role in the maintenance of immunologic self-tolerance and negative control of a variety of pathological immune responses. 8 Several subsets of Treg cells with distinct phenotypes and distinct mechanisms of action have been described (see Sakaguchi et al,8 Roncarolo et al, 9 and O'Garra and Vieira 10 for review). Treg cells mediate the immunoregulatory function by producing cytokines, such as interleukin (IL)-10 and See accompanying article on page 1679 ϩ Treg cells, which have increased ability of homing and trafficking to inflamed nonly...

Objective: The purpose of this study was (a) to study whether a folate and vitamin B12 treatment, aimed at decreasing homocysteine levels, might ameliorate insulin resistance and endothelial dysfunction in patients with metabolic syndrome according to the National Cholesterol Education Program-Adult Treatment Panel-III criteria and (b) to evaluate whether, under these metabolic conditions, there is a relationship between hyperhomocysteinemia and insulin resistance. Design and methods: A double-blind, parallel, identical placebo -drug, randomized study was performed for 2 months in 50 patients. Patients were randomly allocated to two groups. In group 1, patients were treated with diet plus placebo for 2 months. In group 2, patients were treated with diet plus placebo for 1 month, followed by diet plus folic acid (5 mg/day) plus vitamin B12 (500 mg/day) for another month. Results: In group 2, folate treatment significantly decreased homocysteine levels by 27.8% (12.2^1.2 vs 8.8^0.7 mmol/l; P , 0.01). A significant decrement was observed for insulin levels (19.9^1.7 vs 14.8^1.6 mU/ml; P , 0.01) accompanied by a 27% reduction in the homeostasis model assessment levels. A positive relationship was found between the decrement of homocysteine and insulin levels (r ¼ 0.60; P , 0.002). In parallel, endothelial dysfunction significantly improved in the treated group, since post-ischemic maximal hyperemic vasodilation increased by 29.8% and cGMP by 13.6% while asymmetrical dimethylarginine levels decreased by 21.7%. On the contrary, in group 1 patients, treated with placebo, no changes were shown in any of the variables. Conclusions: Folate and vitamin B12 treatment improved insulin resistance and endothelial dysfunction, along with decreasing homocysteine levels, in patients with metabolic syndrome, suggesting that folic acid has several beneficial effects on cardiovascular disease risk factors. European Journal of Endocrinology 151 483-489

Angioplasty of BTE vessels for CHI is a feasible and safe procedure with acceptable rates of technical success and hand healing. Poor digital run-off due to obstructive disease of the digital vessels can reduce the hand-healing rate after a successful PTA. Pure isolated BTE vessel disease seems to characterise patients with ESRD and diabetes mellitus.

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