SummaryBackgroundRemote ischaemic conditioning with transient ischaemia and reperfusion applied to the arm has been shown to reduce myocardial infarct size in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). We investigated whether remote ischaemic conditioning could reduce the incidence of cardiac death and hospitalisation for heart failure at 12 months.MethodsWe did an international investigator-initiated, prospective, single-blind, randomised controlled trial (CONDI-2/ERIC-PPCI) at 33 centres across the UK, Denmark, Spain, and Serbia. Patients (age >18 years) with suspected STEMI and who were eligible for PPCI were randomly allocated (1:1, stratified by centre with a permuted block method) to receive standard treatment (including a sham simulated remote ischaemic conditioning intervention at UK sites only) or remote ischaemic conditioning treatment (intermittent ischaemia and reperfusion applied to the arm through four cycles of 5-min inflation and 5-min deflation of an automated cuff device) before PPCI. Investigators responsible for data collection and outcome assessment were masked to treatment allocation. The primary combined endpoint was cardiac death or hospitalisation for heart failure at 12 months in the intention-to-treat population. This trial is registered with ClinicalTrials.gov (NCT02342522) and is completed.FindingsBetween Nov 6, 2013, and March 31, 2018, 5401 patients were randomly allocated to either the control group (n=2701) or the remote ischaemic conditioning group (n=2700). After exclusion of patients upon hospital arrival or loss to follow-up, 2569 patients in the control group and 2546 in the intervention group were included in the intention-to-treat analysis. At 12 months post-PPCI, the Kaplan-Meier-estimated frequencies of cardiac death or hospitalisation for heart failure (the primary endpoint) were 220 (8·6%) patients in the control group and 239 (9·4%) in the remote ischaemic conditioning group (hazard ratio 1·10 [95% CI 0·91–1·32], p=0·32 for intervention versus control). No important unexpected adverse events or side effects of remote ischaemic conditioning were observed.InterpretationRemote ischaemic conditioning does not improve clinical outcomes (cardiac death or hospitalisation for heart failure) at 12 months in patients with STEMI undergoing PPCI.FundingBritish Heart Foundation, University College London Hospitals/University College London Biomedical Research Centre, Danish Innovation Foundation, Novo Nordisk Foundation, TrygFonden.

Background and Purpose-The purpose of this study was to analyze the 30-day outcome after introduction of a rapid carotid endarterectomy (CEA) program. Reasons for delay in CEA and the incidence of early recurrence neurological symptoms were recorded. Methods-This is a prospective population-based study of delays to CEA and 30-day outcome in patients with symptomatic carotid stenosis. Neurological recurrence (NR) rate was determined after initiation of urgent best medical treatment (loading dose aspirin/clopidogrel and duel therapy with aspirin plus clopidogrel with a statin) until CEA and compared with NR ≤90 days prior index event.

Background: A new method was evaluated where local changes in oxygen tension were induced in a tissue while being studied under a microscope in vivo. We tested whether hypoxic vasodilation and hyperoxic vasoconstriction in arterioles in striated muscle are being propagated upstream, and whether the endothelium and smooth muscle cell layers are necessary components in the signaling pathway. Methods: The study was performed in mouse cremaster muscle superfused with Krebs buffer. A section of the capillary bed was then superfused with human red blood cell suspension equilibrated with either 95% nitrogen or 95% oxygen, and 5% carbon dioxide. Results: The superfusions caused a 12.9 ± 2.4% (p < 0.01) dilation and a 12.3 ± 2.7% (p < 0.01) constriction of the supplying non-exposed arteriole. Vasomotor responses could be detected 1 mm upstream of the stimulation site. The responses to hypoxia and hyperoxia were not affected by inhibition of nitric oxide (NO) synthases by L-NAME. Damage to the wall of an intervening segment of the arteriole abolished upstream changes. Conclusions: The method is capable of changing the oxygen tension locally in a membranous tissue and elicits NO-independent local and upstream vasomotor responses. Upstream responses were transmitted by a conducted vascular response.

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