In patients with STEMI and multivessel coronary artery disease undergoing infarct-artery PCI, preventive PCI in noninfarct coronary arteries with major stenoses significantly reduced the risk of adverse cardiovascular events, as compared with PCI limited to the infarct artery. (Funded by Barts and the London Charity; PRAMI Current Controlled Trials number, ISRCTN73028481.).

In a registry of all comers to PCI, transradial access was associated with a halving of the transfusion rate and a reduction in 30-day and 1-year mortality.

High procedure and patient success rates, combined with a low event rate and improved procedural characteristics, support further use of the hybrid algorithm for a broad community of appropriately trained CTO operators.

Abstract-Metalloproteinase secretion by macrophages is believed to play a key role in the matrix degradation that underlies atherosclerotic plaque instability and aneurysm formation. We studied the hypothesis that nuclear factor-B (NF-B), a transcription factor, is necessary for metalloproteinase secretion and, hence, is a target for pharmacological intervention. Key Words: macrophages Ⅲ foam cells Ⅲ metalloproteinases Ⅲ nuclear factor-B R upture of the fibrous cap of the atherosclerotic plaque is a key event in triggering coronary thrombosis and acute coronary syndromes. Two characteristic pathological features of the rupture-prone plaque are increased macrophage density and reduced collagen content, associated with reduced tensile strength. 1,2 Overexpression of several matrix-degrading metalloproteinases (MMPs), including MMP-1, MMP-3, and MMP-9, has been demonstrated in human atherosclerotic plaques and in animal models 3,4 and is particularly associated with macrophages. Therefore, excessive production of macrophage-derived MMPs probably links increased macrophage density and loss of collagen. Consequently, inhibition of MMP production from macrophages could prove a valuable strategy for promoting plaque stability. Our recent work 5,6 has shown that inhibiting nuclear factor-B (NF-B), a transcription factor, prevents upregulation of MMP-1, MMP-3, and MMP-9 secretion from fibroblasts and vascular smooth muscle cells (SMCs). However, it is unknown whether this strategy would also reduce MMP secretion from macrophages. To investigate this possibility, we subjected human monocyte-derived macrophages to adenovirus-mediated overexpression of the inhibitory subunit, I-B␣, which has been shown previously to inhibit the secretion of tumor necrosis factor (TNF)-␣, interleukin (IL)-1␤, IL-6, and IL-8 from macrophages. 7 Although several available agents, including aspirin, statins, fibrates, and thiazolidinediones, probably exert part of their effects though reducing NF-B activity, there are presently no highly selective inhibitors that can be used in vivo. As a surrogate to evaluate the likely impact of NF-B inhibition in vivo, we extended our study of I-B␣ overexpression to the established model 8 of foam cells elicited in cholesterol-fed rabbits.