Refining the Enrolment Process in Emergency Medicine Research

Research in the emergency setting involving patients with acute clinical conditions is needed if there are to be advances in diagnosis and treatment. But research in these areas poses ethical and practical challenges. One of these is the general inability to obtain informed consent due to the patient’s lack of mental capacity and insufficient time to contact legal representatives. Regulatory frameworks which allow this research to proceed with a consent ‘waiver’, provided patients lack mental capacity, miss important ethical subtleties. One of these is the varying nature of mental capacity among emergency medicine patients. Not only is their capacity variable and often unclear, but some patients are also likely to be able to engage with the researcher and the context to varying degrees. In this paper we describe the key elements of a novel enrolment process for emergency medicine research that refines the consent waiver and fully engages with the ethical rationale for consent and, in this context, its waiver. The process is verbal but independently documented during the ‘emergent’ stages of the research. It provides appropriate engagement with the patient, is context-sensitive and better addresses ethical subtleties. In line with regulation, full written consent for on-going participation in the research is obtained once the emergency is passed

Incidence and risk factors of post-operative arrhythmias and sudden cardiac death after atrioventricular septal defect (AVSD) correction: Up to 47 years of follow-up

Thoracic Surger

Simultaneous Endo-Epicardial Mapping of the Human Right Atrium: Unraveling Atrial Excitation

Background The significance of endo-epicardial asynchrony (EEA) and atrial conduction block (CB), which play an important role in the pathophysiology of atrial fibrillation (AF) during sinus rhythm is poorly understood. The aim of our study was therefore to examine 3-dimensional activation of the human right atrium (RA). Methods and Results Eighty patients (79% men

First Evidence of Atrial Conduction Disorders in Pediatric Patients With Congenital Heart Disease

This study sought to investigate whether pediatric patients with congenital heart disease (CHD) already have atrial conduction disorders early in life. The authors conducted first-in-children epicardial mapping in 10 pediatric patients with CHD undergoing primary open heart surgery. Areas of conduction delay (CD) and block (CB) were present in all patients and were particularly observed at Bachmann's bundle (CD: 4.9%; CB: 2.3%), followed by the right atrium (CD: 3.7%; CB: 1.6%) and, to a lesser degree, the left atrium (CD: 1.8%; CB: 1.0%). Conduction abnormalities may by aggravated over time (e.g., aging, residual lesions, or valvular dysfunction), predisposing these patients to atrial arrhythmias early in life

Simvastatin prevents inflammation-induced aortic stiffening and endothelial dysfunction

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Both acute and chronic inflammation are associated with aortic stiffening and endothelial dysfunction. • Statins have been shown to reduce inflammation and arterial stiffening and to improve endothelial function in patients with chronic inflammation. • In a model of acute-inflammation, statins have been shown to prevent endothelial dysfunction, but the effect on aortic stiffening is unknown. WHAT THIS STUDY ADDS • This study demonstrates, for the first time, that pre-treatment with simvastatin prevents inflammation-induced aortic stiffening, as well as endothelial dysfunction, in a cohort of healthy individuals. • It also shows that simvastatin prevents the inflammation-induced reduction in concentrations of apolipoprotein A-I. AIMS The aim of this study was to determine whether simvastatin would protect against inflammation-induced aortic stiffening and endothelial dysfunction. METHODS Aortic pulse wave velocity (aPWV) and flow-mediated dilatation (FMD) were assessed three times, at baseline, after a 14 day administration of simvastatin or placebo and 8 h after Salmonella typhi vaccination in 50 healthy subjects. RESULTS Following vaccination there was a significant increase in aPWV in the placebo group (5.80 ± 0.87 vs. 6.21 ± 0.97 m s−1, 95% CI 0.19, 0.62, P= 0.002) but not the simvastatin group (5.68 ± 0.73 vs. 5.72 ± 0.74 m s−1, 95% CI −0.19, 0.27, P= 0.9; P= 0.016 for comparison). Whereas FMD response was reduced in the placebo group (6.77 ± 4.10 vs. 5.27 ± 2.88%, 95% CI −2.49, −0.52, P= 0.02) but not in the simvastatin group (7.07 ± 4.37 vs. 7.17 ± 9.94%, 95% CI −1.1, 1.3. P= 0.9, P > 0.001 for comparison). There was no difference in the systemic inflammatory response between groups following vaccination. However, there was a significant reduction in serum apolipoprotein A-I (Apo A-I) in the placebo, but not in the simvastatin, group. CONCLUSIONS Simvastatin prevents vaccination-induced aortic stiffening and endothelial dysfunction. This protective mechanism may be due to preservation of the Apo A-I lipid fraction, rather than pleiotropic anti-inflammatory effects of statins

Hyperaemic microvascular resistance predicts clinical outcome and microvascular injury after myocardial infarction

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Relation Between Coronary Arterial Dominance and Left Ventricular Ejection Fraction After ST-Segment Elevation Acute Myocardial Infarction in Patients Having Percutaneous Coronary Intervention

Cardiolog