Stent thrombosis in the era of drug eluting stents.

Despite a marked reduction in restenosis and the need for repeat revascularization procedures with the use of drug-eluting stents (DES), the risk for stent thrombosis remains of serious concern. Although the safety profiles of DES dose not seem to differ from those of bare metal stent (BMS) in the acute and subacute phases following coronary intervention, recent data suggest a potential increase of thrombotic events late after DES deployment. The main factors associated with late stent thrombosis remain elusive. Delayed re-endothelialization, hypersensitivity reaction, technical and mechanical factors and hypercoagulability have all been proposed as contributing factors. It is unlikely that any of these variables alone can cause stent thrombosis, as the incidence of each factor is much higher than the currently known rates of DES thrombosis. Further, temporal appearances of the thrombotic events represent a challenge to our understanding of re-endothelialization, as one would expect that endothelial coverage would be higher in the later phases after treatment. New expanded definitions of stent thrombosis, which also include events secondary to repeat revascularization, have been proposed to provide a better comparative endpoint between BMS and DES. Such clinical attempt to characterize stent thrombosis is valuable, but does not provide much insight into the pathophysiology and intrinsic thrombotic risk of each device. A true progress in this field will only be possible after we improve our understanding of the patho-physiology of very late stent thromboses, which may differ from events occurring earlier after treatment. The incidence of stent thrombosis remains rare, but its potential catastrophic consequences should remind clinicians and scientists to make every effort to develop strategies and technologies for its prevention. The topic of stent thrombosis in the era of DES will be reviewed in this article.

Percutaneous coronary intervention of bifurcation coronary disease.

Bifurcation coronary artery disease is a frequent problem faced by interventional cardiologists and it affects approximately 15-20% of patients undergoing percutaneous coronary intervention (PCI). The application of drug-eluting stents (DES) technology to prevent restenosis after PCI represents one of the success stories in cardiology, but DES have not resolved the bifurcation PCI challenge. Bifurcation PCI remains associated with higher procedural failure and worse outcomes compared with PCI of non-bifurcated lesions even in DES era. A dependable strategy for PCI of bifurcation lesions has yet to be established, which is likely due to the paucity of studies evaluating the anatomical intricacies of the bifurcation as well as the lack of large scale randomized therapeutic trials. Further, bifurcation has many anatomical variants and it is unlike that one technique will fit all. Currently, we are left with the option of a tailor-made strategy for each patient and bifurcation anatomy and make the most of the limited evidence available to support our therapeutic decisions. In this review, we attempted to describe the current understanding of bifurcation anatomy and corresponding PCI strategies.

Usefulness of cardiac magnetic resonance imaging for coronary artery disease detection.

Cardiac magnetic resonance imaging (cMRI) is a promising non-invasive technique to assess the presence of coronary artery disease (CAD), which is free of ionizing radiation and iodine contrast. cMRI can detect CAD by angiographic methods or indirectly by perfusion stress techniques. While coronary angiography by cMRI remains limited to research protocols, stress perfusion cMRI is currently being applied worldwide in the clinical setting. Studies have shown good correlation between adenosine-induced stress myocardial perfusion cMRI and single-photon-emission computed tomography or positron emission tomography to detect CAD. Quantitative methods to analyze cMRI perfusion data have been developed in an attempt to provide a more objective imaging interpretation. Standardization of such quantitative methods, with minimal operator dependency, would be useful for clinical and research applications. Myocardial perfusion reserve (MPR), calculated using Fermi deconvolution technique, has been compared with well established anatomical and physiological CAD detection techniques. MPR appears to be the most accurate quantitative index to detect anatomical and hemodynamically significant CAD. Beyond physiological assessment of CAD, cMRI provides information regarding regional and global left ventricular function and morphology, myocardial infarction size, transmurality and viability. Such comprehensive information would require the performance of multiple tests if other modalities were used. This article describes current applications of cMRI for evaluation of patients with CAD.

cis Element decoy against nuclear factor-kappaB attenuates development of experimental autoimmune myocarditis in rats.

Nuclear factor-kappaB (NFkappaB) plays a significant role in the coordinated transactivation of cytokine, inducible NO synthase (iNOS), and adhesion molecule genes. Although inflammation is an essential pathological feature of myocarditis, the role of NFkappaB in this process remains obscure. We examined the role of NFkappaB in the progression of rat experimental autoimmune myocarditis (EAM) and tested the hypothesis that NFkappaB blockade with a decoy against the cis element of NFkappaB can prevent the progression of EAM. Lewis rats were immunized with purified porcine cardiac myosin to establish EAM on day 0. NFkappaB decoy was infused into the rat coronary artery on day 0 (group NF0), 7 (group NF7), or 14 (group NF14) and harvested on day 21. Scrambled decoy was infused on day 0 (group SD0), 7 (group SD7), or 14 (group SD14) and served for control groups. The ratios of myocarditis-affected areas to the ventricular cross-sectional area of all treatment groups were significantly lower than those of the control groups (group NF0, 33+/-18% versus SD0, 53+/-14%; group NF7, 19+/-15% versus SD7, 50+/-16%; and group NF14, 34+/-10% versus SD14, 52+/-14%). Immunohistochemical and immunoblot analyses showed expression of ICAM-1, iNOS, IL-2, and TNFalpha in myocardium of scrambled decoy groups, and this expression was effectively suppressed by NFkappaB decoy treatment. Thus, we found that NFkappaB is a key regulator in the progression of EAM and that in vivo transfection of NFkappaB decoy reduces the severity of EAM.