6,963 publications from this institution
‘Continuous improvement of devices and techniques has progressed from the limited treatment of single, simple lesions to the extensive management of multiple and severely complex stenoses.’ Sophia Vaina, Keiichi Tsuchida and Patrick W Serruys Author for correspondence Erasmus Medical Center, Thoraxcenter, Ba 583, Dr Molewaterplein 40, 3015 GD Rotterdam,The Netherlands Tel.: +31 104 635 260 Fax: +31 104 369 154 p.w.j.c.serruys@erasmusmc.nl Expert Rev. Cardiovasc. Ther. 4(2), 143–147 (2006)
Objectives We studied the effect of drug-eluting stent implantation for chronic total coronary occlusion (CTO) on left ventricular volumes and function and assessed the predictive value of magnetic resonance imaging (MRI) performed before revascularization. Background The effect of recanalization of CTO on long-term left ventricular function and the value of myocardial viability assessment with MRI is incompletely understood. Methods Twenty-seven patients underwent contrast-enhanced MRI before and five months after successful drug-eluting stent implantation for CTO. A CTO was defined as a complete occlusion of a major epicardial coronary artery existing for at least six weeks (mean, 7 ± 5 months). Myocardial wall thickening and left ventricular volumes were quantified on cine-images, and the transmural extent of infarction (TEI) was scored on delayed-enhancement images. Results A significant decrease in mean end-systolic volume index (34 ± 13 ml/m2to 31 ± 13 ml/m2; p = 0.02) and mean end-diastolic volume index (84 ± 15 ml/m2to 79 ± 15 ml/m2; p < 0.002) was observed, whereas the mean ejection fraction did not change significantly (61 ± 9% to 62 ± 11%; p = 0.54). The extent of the left ventricle that was dysfunctional but viable before revascularization was related to improvement in end-systolic volume index (R = 0.46; p = 0.01) and ejection fraction (R = 0.49; p = 0.01) but not to the end-diastolic volume index (R = 0.10; p = 0.53). Segmental wall thickening improved significantly in segments with <25% TEI (21 ± 15% to 35 ± 25%; p < 0.001), tended to improve in segments with 25% to 75% TEI (18 ± 22% to 27 ± 22%; p = 0.10), whereas segments with >75% TEI did not improve (4 ± 14% to −9 ± 14%; p = 0.54). Conclusions Drug-eluting stent implantation for a CTO has a beneficial effect on left ventricular volumes and function that can be predicted by performing MRI before revascularization.
The global prevalence of chronic obstructive pulmonary disease (COPD) has increased markedly in recent decades. Given the scarcity of resources available to address global health challenges and respiratory medicine being relatively under-invested in, it is important to define research priorities for COPD globally. In this paper, we aim to identify a ranked set of COPD research priorities that need to be addressed in the next 10 years to substantially reduce the global impact of COPD.
The purpose of this study was to determine acute recoil of the vessel wall immediately after Wiktor stent implantation in native coronary arteries of 77 consecutive patients and to assess whether there was compression or “late recoil” of the stent itself at long‐term follow‐up. Furthermore, the relationship between recoil and a number of clinical, angiographic, and procedural variables was studied in addition to the relation between acute recoil renarrowing or restenosis was assessed. All angiograms were analyzed with the Cardiovascular Angiography Analysis System using automated edge detection. Acute recoil was defined by the difference between the mean diameter of the fully expanded balloon on which the stent was mounted and the mean diameter of the stented segment. Late recoil was calculated by comparing the mean diameter of the stent itself immediately after implantation and at follow‐up without opacification of the vessel. Acute recoil amounted to 0.25 ± 0.32 mm or 8.2%. Multivariate analysis identified sex (coefficient = –0.20, p = 0.04) and stent/artery ratio (coefficient = 0.99, p = 0.0001) as the only independent predictors of acute recoil. “Late recoil” of the stent itself was not observed. The overall difference between the mean diameter of the stent itself immediately after implantation and at follow‐up was –0.15 ± 0.33 mm, suggesting an overall increase in diameter of 5.0%. There was no relation between acute recoil and late restenosis. On the contrary, there was a trend towards a greater degree of recoil in patients without restenosis. Moreover, linear regression analysis disclosed a weak but negative correlation between acute recoil and a loss in minimal luminal diameter (coefficient: –0.55, p = 0.04). The Wiktor stent effectively scaffolds the instrumented vessel. Only a minimal amount of acute recoil was noted, which did not contribute to late luminal renarrowing or restenosis. In addition, no late compression of the stent itself was observed. These data suggest that tissue ingrowth into the lumen of the stented segment is the main cause of late luminal renarrowing after stent implantation. © 1994 Wiley‐Liss,Inc..
Much of the research in asthma has focused on the multiple proinflammatory mechanisms involved in this complex inflammatory disease (1). Much less attention has been paid to endogenous antiinflammatory mechanisms that may counteract or limit the inflammatory process in asthma. It is possible that these inhibitory mechanisms might be defective, resulting in increased or more prolonged inflammation. Such mechanisms, if deficient, might also be important in determining the severity of asthma, which differs markedly and inexplicably between patients. Little is understood about the factors that determine severity in chronic inflammatory diseases, such as asthma, but it is possible that endogenous inhibitory mechanisms may be of critical importance. There has been relatively little research into endogenous inhibitory mechanisms in asthma, but it is likely that understanding these processes may give a better understanding of disease severity. This may also lead to novel therapeutic approaches, such as drugs that increase the release of endogenous inhibitors or mimic their effects. Such therapeutic approaches are attractive since they may restore antiinflammatory mechanisms to normal and thus carry a lower risk of adverse effects in the long term.
Despite the enormous global impact of COPD and the increasing investment in research, there are no current therapies that have been shown to prevent the inevitable progression of the disease. However, as exemplified in this volume, there is now an increasing understanding of the cellular and molecular mechanisms involved in COPD (1) and this has identified many new targets and will lead to the development of new therapies in the future (2,3) (Table 1).
