End-tidal capnography provides reliable ventilatory monitoring for non-intubated patients presenting after sedative overdose to the emergency department.

OBJECTIVE: To assess the ability of end-tidal capnography to provide continuous ventilatory monitoring in sedated, non-intubated ED patients following sedative overdose. METHODS: Observational study undertaken in a tertiary hospital ED. Patient ventilation was assessed using capnography over 60 min. RESULTS: Capnography provided uninterrupted monitoring for 99% of total study time. Capnography detected all episodes of hypoxia detected by SpO2 monitoring. Changes in capnography preceded 70% of hypoxic episodes detected by SpO2 . There were no major adverse events or incidents of device failure. CONCLUSION: Capnography provided reliable measurement of ventilatory function in sedated non-intubated, poisoned ED patients.

Psychological interventions for depression in adolescent and adult congenital heart disease.

BACKGROUND: Adult and adolescent congenital heart disease is increasing in prevalence as better medical care means more children are surviving to adulthood. People with chronic disease often also experience depression. There are several non-pharmacological treatments that might be effective in treating depression and improving quality of life for adults and young adults with congenital heart disease. The aim of this review was to assess the effects of treatments such as psychotherapy, cognitive behavioural therapies and talking therapies for treating depression in this population. OBJECTIVES: To update the previous review on the effects (both harms and benefits) of psychological interventions for treating depression in young adults and adults with congenital heart disease. Psychological interventions include cognitive behavioural therapy, psychotherapy, or 'talking/counselling' therapy for depression. SEARCH METHODS: We updated the searches of the Cochrane Central Register of Controlled Trials (CENTRAL) on The Cochrane Library (Issue 1, 2013), MEDLINE (OVID, 1946 to January week 4 2013), EMBASE (OVID, 1980 to 2013 week 05), PsycINFO (OVID, 1806 to January week 5 2013), the Database of Abstracts of Reviews of Effectiveness (DARE) on The Cochrane Library (Issue 1, 2013), BIOSIS (Thomson Reuters, 1969 to 21 February 2013), and CINAHL (January 1980 to February 2013) on 5 February 2013. We did not search abstracts from national and international cardiology and psychology conferences and dissertation abstracts for this update. No language restrictions were applied. SELECTION CRITERIA: Randomised controlled trials comparing psychological interventions with no intervention for people over 15 years with depression who have congenital heart disease. DATA COLLECTION AND ANALYSIS: Two review authors independently screened titles and abstracts of studies that were potentially relevant to the review. We rejected studies that were clearly ineligible. Two review authors independently assessed the abstracts or full papers for inclusion criteria. We sought further information from the authors where papers contained insufficient information to make a decision about eligibility. MAIN RESULTS: We did not identify any randomised controlled trials that met the inclusion criteria. AUTHORS' CONCLUSIONS: Depression is common in people with congenital heart disease and can exacerbate the physical consequences of the illness. There are effective pharmacological and non-pharmacological treatments for depression, but we have not been able to identify any trials showing the effectiveness of non-pharmacological treatments. A well-designed randomised controlled trial is needed to assess the effects of psychological interventions for depression in congenital heart disease.

Eosinophil count predicts mortality following percutaneous coronary intervention.

INTRODUCTION: Several inflammatory markers have been shown to be independent predictors for both the development of clinically significant atherosclerosis and for adverse outcome in patients with symptomatic coronary artery disease (CAD). We investigated the prognostic role of eosinophil count in low to intermediate risk patients with CAD. METHODS: We studied 909 patients admitted for elective or urgent percutaneous coronary intervention (PCI) from April 2002 to December 2004, and measured pre-procedural total and differential white blood cell (WBC) counts. Inter-tertile WBC differences in short (6months) and long term (up to 74months) mortality were analysed after adjusting for differences in baseline characteristics. RESULTS: Over a median period of 54months (inter-quartile range 47-65), a total of 138 deaths (15.2%) occurred, of which 24 were in the first 6months of follow-up. Cox regression analysis showed that high pre-procedural eosinophil count (top tertile) was associated with improved outcome within the first 6months (OR=0.23 [0.06-0.84]; p=0.03) but after this period there was an increased risk of mortality (OR=2.21, [1.26-3.88]; p=0.006). CONCLUSIONS: Eosinophil count is a novel biomarker for risk stratification of CAD patients, which was associated initially with reduced mortality, but after 6months with increased mortality.

Impaired glucose tolerance and endothelial damage, as assessed by levels of von Willebrand factor and circulating endothelial cells, following acute myocardial infarction.

BACKGROUND: Impaired glucose tolerance (IGT) following acute myocardial infarction (AMI) increases the incidence of major adverse cardiac events. We hypothesized that endothelial damage following AMI, as assessed by levels of von Willebrand factor (vWF) and circulating endothelial cells (CECs), would be more pronounced in patients with IGT compared to those with normal glucose tolerance (NGT). METHODS: We studied non-diabetic patients with AMI (n=125; 107 (86%) male; mean age 59 years (SD 12.5)) who underwent oral glucose tolerance testing 3-5 days after admission. We measured vWF (enzyme-linked immunosorbent assay) and CECs (CD146 immunobead capture) in the fasting state and at 2 h post glucose load. RESULTS: Base-line vWF and CEC levels were higher in IGT patients versus those with NGT and healthy controls (HC) (P<0.001). The acute increase in vWF and CECs in response to the glucose load was significantly higher in the IGT group compared to those with NGT and HC (P<0.01)-an increase on a par with that seen in newly diagnosed diabetics. CONCLUSION: The degree of endothelial damage post AMI in patients with IGT is greater than NGT, and comparable to that seen in frank diabetes mellitus. Subjects with IGT therefore need to be as actively sought and managed.

Vascular damage in impaired glucose tolerance: an unappreciated phenomenon?

Impaired glucose tolerance (IGT) is an independent risk predictor for cardiovascular morbidity and mortality, as well as for total mortality, independent of the subsequent development of overt diabetes mellitus. Increased rates of major adverse cardiac event and shorter survival in subjects with IGT who are post acute myocardial infarction have also been observed. The aim of this review article is to provide an overview of the pathophysiological basis of IGT and the actual mechanism(s) of vascular damage, accounting for its impact in cardiovascular disease (CVD). We focus on endothelial damage, aberrant angiogenesis and apoptosis-the three important pathophysiological mechanisms responsible for most long term complications in frank diabetes. However, on this occasion we evaluate these mechanisms in the milieu of IGT (post prandial hyperglycaemia or post challenge hyperglycaemia) rather than frank diabetes per se. A better understanding of the actual mechanisms of vascular damage in IGT may not only enhance our understanding about the disease process but may also facilitate implementation of appropriate therapeutic measures.

Kounis syndrome presenting as ST-segment elevation myocardial infarction following a hymenoptera (bee) sting.

We described a patient presenting with acute myocardial infarction after sustaining a hymenoptera (bee) sting. Cardiac catheterisation confirmed significant intra-coronary thrombosis in the left anterior descending artery with minimal underlying plaque disease. A unifying diagnosis of Kounis syndrome secondary to hymenoptera envenomation was made. This is followed by a brief review of the pathophysiology of acute myocardial infarction in the context of Kounis syndrome.

Patients with chest pain and occult gastroesophageal reflux demonstrate visceral pain hypersensitivity which may be partially responsive to acid suppression.

OBJECTIVES: Mechanisms of chest pain in gastroesophageal reflux disease (GERD) are poorly understood. The recent demonstration in healthy subjects that lower esophageal acid exposure induces pain hypersensitivity within the non-acid-exposed upper esophagus (secondary allodynia) raises the possibility that an increase in spinal neuronal excitability (i.e., central sensitization) contributes to chest pain in GERD. The aim of this study was to determine whether in patients with unexplained chest pain, acid reflux contributes to esophageal pain hypersensitivity. METHODS: In 14 patients with chest pain and GERD and 8 healthy volunteers, electrical pain thresholds (PT) were recorded from the upper esophagus before, and then repeatedly for 90 min after either hydrochloric acid (0.15 M) or saline (0.15 M) infusion into the lower esophagus. Six patients underwent a repeat study after 6 wk of high-dose proton pump inhibitor (PPI) therapy. RESULTS: GERD patients had lower resting upper esophageal PT than in healthy subjects (40.8 +/- 9 mA and 70.4 +/- 11 mA, respectively; p= 0.018). Acid infusion reduced PT in the non-acid-exposed upper esophagus in healthy subjects, but not in the patients (area under curve [AUC] - 304 +/- 333 and 786 +/- 464; p= 0.03, respectively). Following PPI therapy, resting PT increased (34.65 +/- 13.4 to 40.5 +/- 12.5 mA; p= 0.03), and a reduction in PT now occurred in acid infusion (AUC - 369 +/- 321; p= 0.03). CONCLUSIONS: Patients with unexplained chest pain and occult GERD have esophageal pain hypersensitivity that is PPI responsive. The increase in resting PT and secondary allodynia only following PPI therapy suggests that pain hypersensitivity in these GERD patients may partially be the result of central sensitization.