Qualitative methods are increasingly recognized as valuable, yet practitioners face difficult decisions in their choice of method and the process of analysis. The nominal group technique combines quantitative and qualitative data collection in a group setting, and avoids problems of group dynamics associated with other group methods such as brainstorming, Delphi and focus groups. Idea generation and problem solving are combined in a structured group process, which encourages and enhances the participation of group members. The stages involved in conducting a nominal group are described, and practical problems of its use in a health care setting are discussed with reference to a study of the priorities of care of diabetic patients, carers and health professionals. Some potential applications of the technique in audit and exploratory research are also outlined.
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.
Abstract-The inactivation of glycogen synthase kinase-3 (GSK-3) is proposed as the event integrating protective pathways initiated by preconditioning and other interventions. The inactivation of GSK-3 is thought to decrease the probability of opening of the mitochondrial permeability transition pore. The aim of this study was to verify the role of GSK-3 using a targeted mouse line lacking the critical N-terminal serine within GSK-3 (Ser9) and the highly homologous GSK-3␣ (Ser21), which when phosphorylated results in kinase inactivation. Postconditioning with 10 cycles of 5 seconds of reperfusion/5 seconds of ischemia and preconditioning with 6 cycles of 4 minutes of ischemia/6 minutes of reperfusion, similarly reduced infarction of the isolated perfused mouse heart in response to 30 minutes of global ischemia and 120 minutes of reperfusion. Preconditioning caused noticeable inactivating phosphorylation of GSK-3. However, both preconditioning and postconditioning still protected hearts of homozygous GSK-3 double knockin mice. Moreover, direct pharmacological inhibition of GSK-3 catalytic activity with structurally diverse inhibitors before or after ischemia failed to recapitulate conditioning protection. Nonetheless, cyclosporin A, a direct mitochondrial permeability transition pore inhibitor, reduced infarction in hearts from both wild-type and homozygous GSK-3 double knockin mice. Furthermore, in adult cardiac myocytes from GSK-3 double knockin mice, insulin exposure was still as effective as cyclosporin A in delaying mitochondrial permeability transition pore opening. Our results, which include a novel genetic approach, suggest that the inhibition of GSK-3 is unlikely to be the key determinant of cardioprotective signaling in either preconditioning or postconditioning in the mouse. (Circ Res. 2008;103:307-314.)Key Words: postconditioniong Ⅲ preconditioning Ⅲ GSK-3 Ⅲ mPTP I schemic preconditioning is a powerful and established modulator of intrinsic myocardial resistance to lethal ischemia. 1 Its clinical application in patients with acute myocardial infarction is limited as a result of the inability to predict the moment of coronary artery occlusion. More recently, Zhao et al described the concept of postconditioning as a novel strategy for protecting the heart against reperfusion-injury. 2 They demonstrated that a similar regimen of brief periods of ischemia after a lethal index ischemic insult was as protective as preconditioning. This phenomenon has subsequently been confirmed in a variety of animal models, both in vivo and in isolated heart preparations, 3 as well as in preliminary clinical interventional studies. 4,5 The endogenous cellular and molecular mechanisms involved in cardioprotection against ischemia have been extensively investigated in the field of preconditioning. 6 Because pre-and postconditioning are temporally remote, the signaling pathways might be expected to differ considerably. 2,7 However, recent evidence suggests that the early reperfusion phase after lethal ischemia is crucial i...
Aim This paper reports on one review of four rapid reviews undertaken to explore the relationships between oral health and general medical conditions, in order to support teams within Public Health England, health practitioners and policy makers. This review aimed to explore the most contemporary evidence on whether poor oral health and cardiovascular disease occurs in the same individuals or populations, to outline the nature of the relationship between these two health outcomes and to discuss the implication of any findings for health services and future research.Methods The review was undertaken by a group comprising consultant clinicians from medicine and dentistry, trainees, public health and academics. The methodology involved a streamlined rapid review process and synthesis of the data.Results The results identified a number of systematic reviews of low to high quality, which suggests that there is: (1) fairly robust evidence of an increased risk of atherosclerotic vascular disease (ASVD) amongst individuals with chronic periodontitis, independent of other established cardiovascular risk factors; (2) there is some evidence that the incidence of caries and tooth loss is higher in patients with cardiovascular disease; and (3) that orofacial pain can presents as the sole symptom of stroke in some patients. The findings are discussed in relation to implications for service and future research.Conclusion There is high quality evidence to support an association between cardiovascular disease and oral health. This evidence is mainly related to the association between chronic periodontitis and atherosclerotic heart disease, and is independent of confounding factors as drawn from epidemiological observational studies.
First-pass contrast-enhanced myocardial perfusion MRI in rodents has so far not been possible due to the temporal and spatial resolution requirements. We developed a new first-pass perfusion MR method for rodent imaging on a clinical 3.0-T scanner (Philips Healthcare, Best, The Netherlands) that employed 10-fold k-space and time domain undersampling with constrained image reconstruction, using temporal basis sets (k-t principle component analysis) to achieve a spatial resolution of 0.2 × 0.2 × 1.5mm3 and an acquisition window of 43 msec. The method was successfully tested in five healthy and four infarcted mice (C57BL/6J) at heart rates of 495.1 ± 45.8 beats/min. Signal-intensity-time profiles showed a percentage myocardial signal increase of 141.3 ± 38.9% in normal mice, compared with 44.7 ± 32.4% in infarcted segments. Mean myocardial blood flow by Fermi function for constrained deconvolution in control mice was 7.3 ± 1.5 mL/g/min, comparable to published literature, with no significant differences between three myocardial segments. In infarcted segments, myocardial blood flow was significantly reduced to 1.2 ± 0.8 mL/g/min (P < 0.01). This is the first report of first-pass myocardial perfusion MR in a mouse model on a clinical 3-T MR scanner and using a k-t undersampling method. Data were acquired on a 3-T scanner, using an approach similar to clinical acquisition protocols, thus facilitating translation of imaging findings between rodent and human studies. Magn Reson Med, 2010. © 2010 Wiley-Liss, Inc.
IntroductionTroponin T (cTnT) elevation is common in patients in the Intensive Care Unit (ICU) and associated with morbidity and mortality. Our aim was to determine the epidemiology of raised cTnT levels and contemporaneous electrocardiogram (ECG) changes suggesting myocardial infarction (MI) in ICU patients admitted for non-cardiac reasons.MethodscTnT and ECGs were recorded daily during week 1 and on alternate days during week 2 until discharge from ICU or death. ECGs were interpreted independently for the presence of ischaemic changes. Patients were classified into four groups: (i) definite MI (cTnT ≥15 ng/L and contemporaneous changes of MI on ECG), (ii) possible MI (cTnT ≥15 ng/L and contemporaneous ischaemic changes on ECG), (iii) troponin rise alone (cTnT ≥15 ng/L), or (iv) normal. Medical notes were screened independently by two ICU clinicians for evidence that the clinical teams had considered a cardiac event.ResultsData from 144 patients were analysed (42% female; mean age 61.9 (SD 16.9)). A total of 121 patients (84%) had at least one cTnT level ≥15 ng/L. A total of 20 patients (14%) had a definite MI, 27% had a possible MI, 43% had a cTNT rise without contemporaneous ECG changes, and 16% had no cTNT rise. ICU, hospital and 180-day mortality was significantly higher in patients with a definite or possible MI.Only 20% of definite MIs were recognised by the clinical team. There was no significant difference in mortality between recognised and non-recognised events.At the time of cTNT rise, 100 patients (70%) were septic and 58% were on vasopressors. Patients who were septic when cTNT was elevated had an ICU mortality of 28% compared to 9% in patients without sepsis. ICU mortality of patients who were on vasopressors at the time of cTnT elevation was 37% compared to 1.7% in patients not on vasopressors.ConclusionsThe majority of critically ill patients (84%) had a cTnT rise and 41% met criteria for a possible or definite MI of whom only 20% were recognised clinically. Mortality up to 180 days was higher in patients with a cTnT rise.
Objectives We aimed to validate the Society for Cardiovascular Angiography and Interventions (SCAI) classification to evaluate association with outcome in a real‐world population and effect of invasive therapies. Background Cardiogenic shock is common after Out of Hospital Cardiac Arrest (OOHCA) but is often multifactorial and challenging to stratify. Methods The SCAI shock grade was applied to an observational registry of OOHCA patients on admission to our center between 2012 and 2017. The primary end‐point was 30‐day mortality and secondary end‐points were mode of death and 12‐month mortality. Provision of early CAG and mechanical circulatory support (MCS) was evaluated by SCAI shock grade using logistic regression. Results Three hundred and ninety‐three patients (median age 64.3 years (24.9% females) were included. One hundred and seven patients (27.2%) were in Grade A, 94 (23.9%) in Grade B, 66 (16.8%) in Grade C, 91 (23.2%) in Grade D, and 35 (8.9%) in Grade E. There was a step‐wise significant increase in 30‐day mortality with increasing shock grade (A 28.9% vs. B 33.0% vs. C 54.5% vs. D 59.3% vs. E 82.9%; p < .0001). With worsening shock grade, requirement for renal replacement therapy and mortality from multiorgan dysfunction syndrome and cardiogenic causes increased. Early CAG was performed equally in all groups but was significantly associated with reduced mortality in SCAI grade D only (OR 0.26 [CI 0.08–0.91], p = .036). Conclusions Increasing SCAI shock grade after OOHCA is associated with 30‐day mortality, requirement for renal replacement therapy and mortality attributed to multiorgan dysfunction syndrome and cardiac etiology death.
Objectives -To identify issues that patients and professionals consider important in diabetes care and differences in their priorities for care and to determine patients' and professionals'
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