Background— Nonserial observations have shown this bioresorbable scaffold to have no signs of area reduction at 6 months and recovery of vasomotion at 1 year. Serial observations at 6 months and 2 years have to confirm the absence of late restenosis or unfavorable imaging outcomes. Methods and Results— The ABSORB trial is a multicenter single-arm trial assessing the safety and performance of an everolimus-eluting bioresorbable vascular scaffold. Forty-five patients underwent serial invasive imaging, such as quantitative coronary angiography, intravascular ultrasound, and optical coherence tomography at 6 and 24 months of follow-up. From 6 to 24 months, late luminal loss increased from 0.16±0.18 to 0.27±0.20 mm on quantitative coronary angiography, with an increase in neointima of 0.68±0.43 mm 2 on optical coherence tomography and 0.17±0.26 mm 2 on intravascular ultrasound. Struts still recognizable on optical coherence tomography at 2 years showed 99% of neointimal coverage with optical and ultrasonic signs of bioresorption accompanied by increase in mean scaffold area compared with baseline (0.54±1.09 mm 2 on intravascular ultrasound, P =0.003 and 0.77±1.33 m 2 on optical coherence tomography, P =0.016). Two-year major adverse cardiac event rate was 6.8% without any scaffold thrombosis. Conclusions— This serial analysis of the second generation of the everolimus-eluting bioresorbable vascular scaffold confirmed, at medium term, the safety and efficacy of the new device. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00856856.
Journal Article Stenting of coronary arteries. Are we the sorcerer's apprentice? Get access P. W. SERRUYS, P. W. SERRUYS Thoraxcenter, Erasmus UniversityRotterdam, The Netherlands Address for correspondence: Patrick W. Serruys, Catheterisation Laboratory, Thoraxcenter, Erasmus University Rotterdam, P.O. Box 1738, 3000 DR Rotterdan, The Netherlands. Search for other works by this author on: Oxford Academic PubMed Google Scholar K. J. BEATT, K. J. BEATT Thoraxcenter, Erasmus UniversityRotterdam, The Netherlands Search for other works by this author on: Oxford Academic PubMed Google Scholar W. J. VAN DER GIESSEN W. J. VAN DER GIESSEN Thoraxcenter, Erasmus UniversityRotterdam, The Netherlands Search for other works by this author on: Oxford Academic PubMed Google Scholar European Heart Journal, Volume 10, Issue 9, September 1989, Pages 774–782, https://doi.org/10.1093/oxfordjournals.eurheartj.a059570 Published: 01 September 1989 Article history Received: 13 June 1989 Accepted: 21 June 1989 Published: 01 September 1989
Long-acting bronchodilators are the most effective treatments currently available for managing patients with COPD.Long-acting muscarinic antagonists and β 2 -agonists are equally effective in producing bronchodilation, reducing symptoms, improving quality of life, and preventing exacerbations and are well tolerated.They probably work mainly by relaxing smooth muscle of peripheral airways to reduce gas trapping.Although both drug classes have non-bronchodilator effects that might be beneficial, this has not been clearly established in COPD patients.Remarkably, long-acting β 2 -agonists and long-acting muscarinic antagonists have additive bronchodilator effects, although this has not always translated into greater clinical benefit.Nevertheless, long-acting β 2 -agonist/long-acting muscarinic antagonist fixed-dose combinations are more effective than the single components and inhaled-corticosteroid/long-acting β 2 -agonist combinations.Although there is some rationale for triple therapy with long-acting β 2 -agonist/long-acting muscarinic antagonist/inhaled-corticosteroid, it remains to be shown that this would be more effective than long-acting β 2 -agonist/long-acting muscarinic antagonist combinations, although may be indicated for COPD patients with frequent exacerbations and with overlapping features with asthma, including increased blood eosinophils.It is unlikely that new classes of bronchodilators will be developed for COPD and what is needed is effective and safe antiinflammatory treatments.(BRN Rev.
Evidence suggests that γ‐aminobutyric acid (GABA) and its receptors are present in the peripheral nervous system. We have now investigated the effect of GABA and related substances on non‐adrenergic, non‐cholinergic (NANC) neurally‐evoked bronchoconstriction in the anaesthetised guinea‐pig. Bilateral vagal stimulation (5 V, 5 ms, 3 or 5 Hz) for 30 s, after propranolol (1 mg kg −1 i.v.) and atropine (1 mg kg −1 i.v.) evoked a NANC bronchoconstrictor response manifest as a mean tracheal pressure rise of 21.9 ± 1.04 cmH 2 O ( n = 70). The bronchoconstrictor response was reproducible for any given animal. GABA (10 μg‐10 mg kg −1 i.v.) did not alter basal tracheal pressure but reduced the NANC bronchoconstrictor response to vagal stimulation in a dose‐dependent manner (ED 50 = 186 μg kg −1 with a maximal inhibition of 74 ± 3.4% at 10 mg kg −1 ). Neither the opioid antagonist naloxone (1 mg kg −1 i.v.) nor the α‐adrenoceptor antagonist phentolamine (2.5 mg kg −1 i.v.) had any significant effect on the inhibitory response produced by GABA (500 μg kg −1 ). GABA‐induced inhibition was not antagonised by the GABA A ‐antagonist bicuculline (2 mg kg −1 i.v.). The GABA B ‐agonist baclofen (10 μg‐3 mg kg −1 i.v.) caused a dose‐dependent inhibition of the NANC response (ED 50 = 100 μg kg −1 with a maximal inhibition of 35.5 ± 2.8% at 3 mg kg −1 ). The GABA A ‐agonist, 4,5,6,7‐tetrahydroisoxazolo[5,4‐C] pyridin‐3‐ol (THIP), also inhibited the NANC bronchoconstrictor response. However, the dose of THIP required for this effect was high (3 mg kg −1 ) and the effect (< 10% inhibition) was small. Substance P (SP; 5 μg kg −1 or 25 μg kg −1 ), produced a bronchoconstrictor response equivalent to that produced by NANC vagal stimulation. This response was significantly increased by injection of GABA. Baclofen had no significant effect on responses evoked by exogenous SP. We conclude that GABA inhibits the release of transmitter from NANC nerves via an action at GABA B receptors and that GABA might play a role in the regulation of neurogenic responses in the airways.
Chronic obstructive pulmonary disease (COPD) is a major cause of ill health and is increasing in many parts of the world. It is one of the commonest causes of death and the only common cause of death which is increasing. COPD is characterised by a slowly progressive irreversible airflow obstruction that is due to a loss of lung elasticity resulting from parenchymal destruction and peripheral airflow obstruction. Cigarette smoking is currently a causal factor in more than 90% of patients in westernised societies, so environmental factors are clearly very important in the disease.1However, in Caucasians only 10–20% of chronic heavy cigarette smokers develop symptomatic COPD, suggesting that genetic factors are likely to be important in determining which cigarette smokers are at risk from developing airflow obstruction. Furthermore, some patients develop airflow obstruction at an earlier age, again suggesting that genetic factors may determine the progression of COPD. Patients who have a genetic deficiency in the anti-protease α1-antitrypsin (α1-AT) have a very high risk of developing emphysema at an early age if they smoke, indicating the importance of genetic factors in some patients with COPD. Despite the clinical importance of COPD, relatively few studies have searched for genetic factors using modern molecular genetic techniques. There may also be differences in the prevalence of COPD in different ethnic groups, but these are difficult to separate from lifestyle factors. For example, the prevalence of COPD is apparently low in China and this cannot be entirely accounted for by a lower tobacco consumption.2 Anecdotally, COPD is uncommon in Chinese living in the USA which suggests that there may be genetic differences in the factors that protect against COPD. In Hawaii, the prevalence of COPD in Japanese-Americans smoking more than 20 cigarettes daily was 7.9% compared with 16.7% …
