Investigating the efficacy of chest pressure for direct current cardioversion in atrial fibrillation: a randomised control trial protocol (Pressure-AF).

INTRODUCTION: Atrial fibrillation (AF) is the most common sustained arrhythmia worldwide. Direct current cardioversion is commonly used to restore sinus rhythm in patients with AF. Chest pressure may improve cardioversion success through decreasing transthoracic impedance and increasing cardiac energy delivery. We aim to assess the efficacy and safety of routine chest pressure with direct current cardioversion for AF. METHODS AND ANALYSIS: Multicentre, double blind (patient and outcome assessment), randomised clinical trial based in New South Wales, Australia. Patients will be randomised 1:1 to control and interventional arms. The control group will receive four sequential biphasic shocks of 150 J, 200 J, 360 J and 360 J with chest pressure on the last shock, until cardioversion success. The intervention group will receive the same shocks with chest pressure from the first defibrillation. Pads will be placed in an anteroposterior position. Success of cardioversion will be defined as sinus rhythm at 1 min after shock. The primary outcome will be total energy provided. Secondary outcomes will be success of first shock to achieve cardioversion, transthoracic impedance and sinus rhythm at post cardioversion ECG. ETHICS AND DISSEMINATION: Ethics approval has been confirmed at all participating sites via the Research Ethics Governance Information System. The trial has been registered on the Australia New Zealand Clinical Trials Registry (ACTRN12620001028998). De-identified patient level data will be available to reputable researchers who provide sound analysis proposals.

Cardiac Myeloid Sarcoma: A 1-kg Heart.

A 53-year-old man with a background of acute myelomonocytic leukemia in remission presented with pleurisy. Repeat transthoracic echocardiography over several weeks revealed thickening left ventricular walls and decreasing systolic function. He died of decompensated heart failure due to cardiac myeloid sarcoma, with autopsy revealing an enlarged heart weighing >1 kg. (Level of Difficulty: Intermediate.).

Combining structured and unstructured data in EMRs to create clinically-defined EMR-derived cohorts.

BACKGROUND: There have been few studies describing how production EMR systems can be systematically queried to identify clinically-defined populations and limited studies utilising free-text in this process. The aim of this study is to provide a generalisable methodology for constructing clinically-defined EMR-derived patient cohorts using structured and unstructured data in EMRs. METHODS: Patients with possible acute coronary syndrome (ACS) were used as an exemplar. Cardiologists defined clinical criteria for patients presenting with possible ACS. These were mapped to data tables within the production EMR system creating seven inclusion criteria comprised of structured data fields (orders and investigations, procedures, scanned electrocardiogram (ECG) images, and diagnostic codes) and unstructured clinical documentation. Data were extracted from two local health districts (LHD) in Sydney, Australia. Outcome measures included examination of the relative contribution of individual inclusion criteria to the identification of eligible encounters, comparisons between inclusion criterion and evaluation of consistency of data extracts across years and LHDs. RESULTS: Among 802,742 encounters in a 5 year dataset (1/1/13-30/12/17), the presence of an ECG image (54.8% of encounters) and symptoms and keywords in clinical documentation (41.4-64.0%) were used most often to identify presentations of possible ACS. Orders and investigations (27.3%) and procedures (1.4%), were less often present for identified presentations. Relevant ICD-10/SNOMED CT codes were present for 3.7% of identified encounters. Similar trends were seen when the two LHDs were examined separately, and across years. CONCLUSIONS: Clinically-defined EMR-derived cohorts combining structured and unstructured data during cohort identification is a necessary prerequisite for critical validation work required for development of real-time clinical decision support and learning health systems.

The nitric oxide donor sodium nitroprusside stimulates the Na+-K+ pump in isolated rabbit cardiac myocytes.

Nitric oxide (NO) affects the membrane Na(+)-K(+) pump in a tissue-dependent manner. Stimulation of intrinsic pump activity, stimulation secondary to NO-induced Na(+) influx into cells or inhibition has been reported. We used the whole-cell patch clamp technique to measure electrogenic Na(+)-K(+) pump current (I(p)) in rabbit ventricular myocytes. Myocytes were voltage clamped with wide-tipped patch pipettes to achieve optimal perfusion of the intracellular compartment, and I(p) was identified as the shift in holding current induced by 100 microm ouabain. The NO donor sodium nitroprusside (SNP) in concentrations of 1, 10, 50 or 100 microm induced a significant increase in I(p) when the intracellular compartment was perfused with pipette solutions containing 10 mm Na(+), a concentration near physiological levels. SNP had no effect when the pump was near-maximally activated by 80 mm Na(+) in pipette solutions. Stimulation persisted in the absence of extracellular Na(+), indicating its independence of transmembrane Na(+) influx. The SNP-induced pump stimulation was abolished by inhibition of soluble guanylyl cyclase (sGC) with 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one, by inhibition of protein kinase G (PKG) with KT-5823 or by inhibition of protein phosphatase with okadaic acid. Inclusion of the non-hydrolysable cGMP analogue 8pCPT-cGMP, activated recombinant PKG or the sGC-activator YC-1 in patch pipette filling solutions reproduced the SNP-induced pump stimulation. Pump stimulation induced by YC-1 was dependent on the Na(+) concentration but not the K(+) concentration in pipette filling solutions, suggesting an altered sensitivity of the Na(+)-K(+) pump to intracellular Na(+).