Does any therapy really work for neurocardiogenic syncope?

Effectiveness of a treatment for neurocardiogenic syncope can be defined in terms of symptom response, quality-of-life, healthcare utilization, treatment side effects and cost-effectiveness. Most trials have focused on syncope recurrence or burden, without assessing quality-of-life formally. Drug and device interventions are characterized by a dearth of randomized controlled trials, with those few of robust design demonstrating little impact on recurrence of syncope. General advice includes hydration, trigger recognition and counter pressure maneuvers to attenuate episodes. Lifestyle recommendations have limited comparative effectiveness evidence, but are favored due to lack of side effects and low cost. The frequency of syncope improves in many patients regardless of the intervention, although ultimate recurrence of syncope remains high. In the minority of patients seeking treatment due to recurrence, midodrine has reasonable supporting evidence for effectiveness with some evidence for beta-blockers in older age patients. Emerging evidence favors pacing in patients with asystole during spontaneous (as opposed to provoked) syncope. Combining long-term implantable cardiac monitoring, tilt and adenosine triphosphate testing may yet accurately define the optimal minority who benefit from pacing. In the remaining majority, pharmacologic and device interventions should be used sparingly until clear benefits are established. Better understanding of patient fears, beliefs and behaviors may help develop cognitive therapies and improve quality-of-life alongside the focus on physical symptoms

Sewage sludge biochars as effective PFAS-sorbents

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How to diagnose the cause of sudden cardiac arrest

Sudden cardiac death or sudden cardiac arrest (SCA) is defined as natural death that occurs within an hour of the onset of acute symptoms or during sleep due to a primary cardiac cause. Most cases of SCA are attributable to coronary artery disease, with occult cardiomyopathy or inheritable arrhythmic syndromes accounting for a minority of SCA. Diagnosing the cause of SCA has potential implications for the patient and the family, and demands a comprehensive approach. This review summarizes the potential causes of SCA and outlines a systematic diagnostic approach to the SCA survivor. (Cardiol J 2011; 18, 2: 210-216

Progression to chronic atrial fibrillation after pacing: the Canadian Trial of Physiologic Pacing

AbstractOBJECTIVESThis study examined the effect of physiologic pacing on the development of chronic atrial fibrillation (CAF) in the Canadian Trial Of Physiologic Pacing (CTOPP).BACKGROUNDThe role of physiologic pacing to prevent CAF remains unclear. Small randomized studies have suggested a benefit for patients with sick sinus syndrome. No data from a large randomized trial are available.METHODSThe CTOPP randomized patients undergoing first pacemaker implant to ventricular-based or physiologic pacing (AAI or DDD). Patients who were prospectively found to have persistent atrial fibrillation (AF) lasting greater than or equal to one week were defined as having CAF. Kaplan-Meier plots for the development of CAF were compared by log-rank test. The effect of baseline variables on the benefit of physiologic pacing was evaluated by Cox proportional hazards modeling.RESULTSPhysiologic pacing reduced the development of CAF by 27.1%, from 3.84% per year to 2.8% per year (p = 0.016). Three clinical factors predicted the development of CAF: age ≥74 years (p = 0.057), sinoatrial (SA) node disease (p < 0.001) and prior AF (p < 0.001). Subgroup analysis demonstrated a trend for patients with no history of myocardial infarction or coronary disease (p = 0.09) as well as apparently normal left ventricular function (p = 0.11) to derive greatest benefit.CONCLUSIONSPhysiologic pacing reduces the annual rate of development of chronic AF in patients undergoing first pacemaker implant. Age ≥74 years, SA node disease and prior AF predicted the development of CAF. Patients with structurally normal hearts appear to derive greatest benefits

Health-state utilities in a prisoner population : a cross-sectional survey

Background: Health-state utilities for prisoners have not been described. Methods: We used data from a 1996 cross-sectional survey of Australian prisoners (n = 734). Respondent-level SF-36 data was transformed into utility scores by both the SF-6D and Nichol's method. Socio-demographic and clinical predictors of SF-6D utility were assessed in univariate analyses and a multivariate general linear model. Results: The overall mean SF-6D utility was 0.725 (SD 0.119). When subdivided by various medical conditions, prisoner SF-6D utilities ranged from 0.620 for angina to 0.764 for those with none/mild depressive symptoms. Utilities derived by the Nichol's method were higher than SF-6D scores, often by more than 0.1. In multivariate analysis, significant independent predictors of worse utility included female gender, increasing age, increasing number of comorbidities and more severe depressive symptoms. Conclusion: The utilities presented may prove useful for future economic and decision models evaluating prison-based health programs