Compared with femoral access, radial access reduces mortality and MACE and improves safety, with reductions in major bleeding and vascular complications across the whole spectrum of patients with CAD.

No abstract

This preliminary study supports the utility of the PTFE-covered stent for the nonsurgical treatment of vessel ruptures.

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...

Direct stenting without predilation in selected lesions seems to be a safe and successful procedure that provides a way to contain cost and to shorten radiation exposure time.

This preliminary series supports the feasible use of the PercuSurge GuardWire for retrieval of plaque debris and prevention of embolization in degenerated SVGs. The good tolerance of temporary occlusions without angiographic or clinical evidence of distal embolization represents encouraging early findings.

Background-Experimental studies have demonstrated that intravenous ␤-blocker administration before coronary artery occlusion significantly reduces myocardial injury. Clinical studies have shown that intracoronary (IC) propranolol administration before percutaneous coronary intervention (PCI) delays myocardial ischemia. The present study tested the hypothesis that IC propranolol treatment protects ischemic myocardium from myocardial damage and reduces the incidence of myocardial infarction (MI) and short-term adverse outcomes after PCI. Methods and Results-Patients undergoing PCI (nϭ150) were randomly assigned in a double-blind fashion to receive IC propranolol (nϭ75) or placebo (nϭ75). Study drug was delivered before first balloon inflation via an intracoronary catheter with the tip distal to the coronary lesion. Biochemical markers were evaluated through the first 24 hours and clinical outcomes to 30 days. Evidence of MI with creatine kinase-MB elevation after PCI was seen in 36% of placebo and 17% of propranolol patients (Pϭ0.01). Troponin T elevation was seen in 33% of placebo and 13% of propranolol patients (Pϭ0.005). At 30 days, the composite end point of death, postprocedural MI, non-Q-wave MI after PCI hospitalization, or urgent target-lesion revascularization occurred in 40% of placebo versus 18% of propranolol patients (hazard ratio 2.14, 95% CI 1.24 to 3.71, Pϭ0.004). Conclusions-IC

This case illustrates that a 2-stage combined endovascular and surgical approach may be a safe and effective alternative to reoperation for recurrent TAAA.