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We aimed to investigate the impact of lesion calcification on angiographic outcomes after Absorb everolimus-eluting bioresorbable vascular scaffold (BVS) implantation in comparison with those after cobalt-chromium everolimus-eluting stent (CoCr-EES) implantation.The present post hoc analysis of the ABSORB Japan randomised trial compared post-procedure and 13-month angiographic outcomes between patients implanted with BVS and CoCr-EES based on the presence or absence of calcification, excluding extremely heavily calcified lesions or lesions requiring rotational atherectomy. The study population comprised 384 patients with 384 lesions (including 114 lesions [29.7%] with moderate or severe calcification), classified into two subgroups: calcification, 114 (BVS: n=72 and CoCr-EES: n=42) and non-calcification, 270 (BVS: n=181 and CoCr-EES: n=89). Follow-up angiography was performed in 94.8% of patients. Both post-procedure and follow-up in-device minimal lumen diameters were comparable in both the BVS arm (calcification vs. non-calcification: 2.43±0.32 mm vs. 2.43±0.39 mm, p=0.91 and 2.17±0.49 mm vs. 2.27±0.47 mm, p=0.17) and in the CoCr-EES arm (2.68±0.34 mm vs. 2.65±0.42 mm, p=0.62 and 2.57±0.52 mm vs. 2.47±0.53 mm, p=0.36).Moderate or severe lesion calcification (excluding patients with extremely heavily calcified lesions or lesions requiring rotational atherectomy) does not negatively affect angiographic outcomes at both post-procedure and 13-month follow-up after BVS implantation.

The molecular regulation for the transition from stable to vulnerable plaque remains to be elucidated. Heme oxygenase 1 (HO-1) and its metabolites have been implicated in the cytoprotective defense against oxidative injury in atherogenesis. In this study, we sought to assess the role of HO-1 in the progression toward plaque instability in carotid artery disease in patients and in a murine model of vulnerable plaque development.Atherectomy biopsy from 112 patients with clinical carotid artery disease was collected and stratified according to characteristics of plaque vulnerability. HO-1 expression correlated closely with features of vulnerable human atheromatous plaque (P<0.005), including macrophage and lipid accumulation, and was inversely correlated with intraplaque vascular smooth muscle cells and collagen deposition. HO-1 expression levels correlated with the plaque destabilizing factors matrix metalloproteinase-9, interleukin-8, and interleukin-6. Likewise, in a vulnerable plaque model using apolipoprotein E(-/-) mice, HO-1 expression was upregulated in vulnerable versus stable lesions. HO-1 induction by cobalt protoporphyrin impeded lesion progression into vulnerable plaques, indicated by a reduction in necrotic core size and intraplaque lipid accumulation, whereas cap thickness and vascular smooth muscle cells were increased. In contrast, inhibition of HO-1 by zinc protoporphyrin augmented plaque vulnerability. Plaque stabilizing was prominent after adenoviral transduction of HO-1 compared with sham virus-treated animals, providing proof that the observed effects on plaque vulnerability were HO-1 specific.Here we demonstrate in a well-defined patient group and a murine vulnerable plaque model that HO-1 induction reverses plaque progression from a vulnerable plaque to a more stable phenotype as part of a compensatory atheroprotective response.

Objectives The aim of this study was to investigate the effect of complete, incomplete, and unsuccessful revascularization by percutaneous coronary intervention (PCI) on left ventricular ejection fraction (EF) in patients with multivessel disease and impaired left ventricular function and assess the diagnostic accuracy of cardiac magnetic resonance imaging (MRI) for improvement in EF. Background The effect of PCI for multivessel coronary artery disease on long-term myocardial function and the predictive value of cardiac MRI on global function are incompletely investigated. Methods Cardiac MRI was performed in patients with multivessel disease before and 6 months after complete revascularization (n = 34) or incomplete revascularization (n = 22) or in patients without successful revascularization (n = 15). For the prediction of recovery of EF, wall thickening was quantified on cine images at rest and during 5- and 10-μg/kg/min dobutamine. The transmural extent of infarction was quantified on delayed enhancement cardiac MRI. Results The EF improved significantly after complete revascularization (46 ± 12% to 51 ± 13%; p < 0.0001) but did not change after incomplete (49 ± 11% to 49 ± 10%; p = 0.88) or unsuccessful revascularization (49 ± 13% to 47 ± 13%; p = 0.11). Sensitivity, specificity, positive and negative predictive value for the prediction of improvement in EF of >4% after PCI were 100%, 75%, 74%, and 100%, respectively, for dobutamine-cardiac MRI and 70%, 77%, 70%, and 77%, respectively, for delayed enhancement-cardiac MRI. Conclusions Complete revascularization for multivessel coronary artery disease improves EF, whereas EF did not change in patients after incomplete or unsuccessful revascularization. Improvement in EF can be predicted by performing cardiac MRI before PCI.

Introduction The SYNTAX III REVOLUTION trial demonstrated that clinical decision-making between coronary artery bypass graft (CABG) and percutaneous coronary intervention (PCI) based on coronary artery computed tomography (CCTA) and predicting four years mortality according to the SYNTAX score II had a high agreement with the treatment decision derived from invasive coronary angiography (ICA). The agreement of the novel SYNTAX score 2020 (SS-2020) based on CCTA and ICA has not yet been evaluated in a prospective fashion. Methods This study included 54 consecutive patients in the ongoing FASTTRACK CABG trial that investigates decision making, planning and procedural CABG guidance based solely on CCTA and FFRct. All the patients underwent CCTA and ICA, and SS-2020 was calculated based on the results of anatomical SYNTAX score derived from either CCTA or ICA, and the respective scores were compared by using paired t-test. Results The mean age was 67.3±9.7, and 48 were men (88.9%). Anatomical SYNTAX score derived from CCTA was assessed in the 54 cases (analysability 100%). Anatomical SYNTAX scores based on CCTA and ICA were 34.3±9.3, and 35.5±11.3, respectively (P=0.480). As shown in the table predicted 5 years major adverse cardiac and cerebrovascular events (MACCE) following either PCI or CABG, as well as predicted 10 years mortality following CABG differed significantly. However the absolute risk differences (ARD) in 5 years MACCE and 10 years mortality following either PCI or CABG, were comparable. Conclusions High agreements were confirmed in the calculations of anatomical SYNTAX scores with CCTA and ICA. Despite significant differences in predicted MACCE rates at 5 years and mortalities at 10 years, the ARD in MACCE rates and mortality were comparable. In terms of treatment decision-making, SS-2020 calculations based on CCTA is a non-invasive predictive tool comparable to the one based on ICA. Funding Acknowledgement Type of funding sources: None.

Sensory nerves regulate central and local reflexes such as airway plasma leakage, and cough and their function may be enhanced during inflammation. Evidence suggests that dopamine receptor agonists may inhibit sensory nerve‐mediated responses. In this study dopamine inhibited vagal sensory nerve induced microvascular leakage in the rat. In order to characterize the receptor involved rat vagus preparations were utilized. Quinagolide (D 2/3 agonist), ropinirole (D 2/3/4 agonist), SKF 38393 (D 1/5 agonist), AR‐C68397AA (Viozan™) (dual D 2 /B 2 agonist) and dopamine inhibited hypertonic saline induced depolarization by approximately 50%. Data suggests that AR‐C68397AA and quinagolide also inhibited depolarization of the human vagus. The quinagolide response was blocked by sulpiride (D 2/3 antagonist) but not SCH 23390 (D 1/5 antagonist); ropinirole was partially blocked by sulpiride, totally blocked by spiperone (at a concentration that blocks all dopamine receptors) but not by SCH 23390. The response to SKF 38393 was not blocked by sulpiride but was by SCH 23390. The inhibition evoked by AR‐C68397AA was only partially blocked by SCH 23390 but not by sulpiride or spiperone whereas dopamine was blocked by spiperone. The effect of dopamine was not stimulus‐specific as it inhibited capsaicin‐induced depolarization of the rat vagus in a spiperone sensitive manner. In conclusion, dopamine receptor ligands inhibit depolarization of the rat and human vagus. These data suggest that dopamine receptor agonists may be of therapeutic benefit in the treatment of symptoms such as cough and mucus secretion which are evident in respiratory diseases such as asthma and chronic obstructive pulmonary disease. British Journal of Pharmacology (2002) 136 , 620–628; doi: 10.1038/sj.bjp.0704758