The Cypher and Taxus DES result in delayed arterial healing when compared with BMS of similar implant duration. The cause of DES LST is multifactorial with delayed healing in combination with other clinical and procedural risk factors playing a role.

The present study marks the first comparator analysis of endothelial coverage in leading polymeric DES, supporting disparities in arterial healing based on endothelial regrowth and recovery, favoring newer designs over the current generation of FDA-approved stents.

Background-Although effective coverage of challenging coronary lesions has warranted the use of overlapping drug-eluting stents, the histopathological response to stent overlap is unknown. Methods and Results-The arterial reaction to overlapping Cypher or Taxus drug-eluting stents was examined in rabbits with bare metal stents, BxVelocity or Express, serving as controls. Single iliac artery balloon injury was followed by placement of 2 overlapping 3.0-mm-diameter drug-eluting stents or bare metal stents in 60 animals (mean length of overlap, 9.8Ϯ3.6 mm). Stented arteries were harvested at 28 and 90 days for histology. Overlapped segments exhibited delayed healing compared with proximal and distal nonoverlapping sites at 28 days. Overlapped segments in Taxus stents induced significantly more luminal heterophils/eosinophils and fibrin deposition than Cypher; peristrut giant cell infiltration, however, was more frequent in the latter. Overlapping bare metal stents also showed mild delayed healing compared with nonoverlapped segments, but not to the same extent as drug-eluting stents. Although neointimal thickness within the overlap was similar in 28-and 90-day Cypher stents, there was a significant increase with Taxus (Pϭ0.03). Conclusions-Compared

Objective-Although lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) has received recent attention as a biomarker of inflammation and risk for acute coronary events, its relative expression in coronary plaque phenotypes, including unstable lesions, has not been established. Methods and Results-Coronary segments (nϭ30) were prospectively collected from 25 sudden coronary death patients for immunolocalization of Lp-PLA 2 . Lesion morphologies were classified as pathologic intimal thickening, fibroatheromas, thin-cap fibroatheromas (fibrous cap thicknesses Ͻ65 m), and rupture. The expression of Lp-PLA 2 was detected using a specific monoclonal antibody. Apoptosis was identified by DNA end-labeling using terminal deoxynucleotidyl transferase (TdT). Lp-PLA 2 staining in early plaques was absent or minimally detected. In contrast, thin-cap fibroatheromas and ruptured plaques showed intense Lp-PLA 2 expression within necrotic cores and surrounding macrophages including those in the fibrous cap. T he natural history of atherosclerosis in humans is a dynamic process involving the progression of early lesions to more complex plaques that are responsible for the majority of acute ischemic coronary and stroke events. Throughout lesion progression, there are transitional plaque phenotypes ranging from early lipid pools to those characterized by a dense fibrous cap of connective tissue and a strong collagen matrix overlying a core of lipids and necrotic debris, and ultimately, to plaques with large necrotic cores and thin fibrous caps invaded by macrophages, referred to as thin-cap fibroatheromas (TCFAs). 1 TCFAs are characterized by a thin fibrous cap (Ͻ65 m), a large necrotic core, an abundance of macrophages, and limited luminal narrowing. 2 It is widely held that the instability of the TCFA gives rise to the main clinical complications associated with rupture and thrombosis; however, there are important morphological differences between TCFA and ruptured plaques. 2 Ruptured plaques demonstrate even thinner fibrous caps (23Ϯ19 m), larger necrotic cores, and greater macrophage infiltrates compared with TCFAs. 2 In this context a better understanding of the biology of rupture-prone plaques has the potential to reduce the morbidity and mortality associated with atherothrombotic disease. See page 2417 and coverInflammation plays a primary role in the progression of human atheroma based on the local and systemic inflammatory responses observed throughout the spectrum of atherosclerotic disease-from initial lesion formation to plaque destabilization and rupture. 3 The key role of inflammation in atherosclerosis also is evidenced by numerous epidemiology studies indicating an association between inflammatory markers (eg, C-reactive protein [CRP], interleukin [IL]-6) and risk of future cardiovascular events. However, considerably less is known about whether the various inflammatory markers represent similar pathophysiologic processes or Original