tbuckley/cabot-search huggingface dataset:
Abstract 9578: Normal Ranges of Right Ventricular Strain in Children: A Systematic Review and Meta-Analysis
Authors: Philip T Levy, Aura A Sanchez-Mejia, Susan Fowler, Mark R Holland, Gautam K Singh
Journal: Circulation (2013)

Background: Establishment of the range of normal values and associated variations of two-dimensional speckle-tracking echocardiography (2DSTE) derived right ventricular (RV) strain is a prerequisite for its routine clinical application in children. The objectives of this study were to perform a meta-analysis of normal ranges of RV longitudinal strain measurements derived by 2DSTE in children and identify confounders that may contribute to differences in reported measures.[[Unable to Display Character: ]] Methods: A systematic review was launched in PubMed, Embase, Scopus, and Cochrane. Search hedges were created to cover the concepts of pediatrics, speckle-tracking, and right ventricle. Two investigators independently identified and included studies if they reported the 2DSTE derived RV strain measures: RV global longitudinal strain (GS), systolic strain rate (GSRs), early diastolic strain rate (GRSe), late diastolic strain rate (GSRa), or segmental LS at the apical, mid, and basal ventricular levels in healthy children. The weighted mean was estimated by using random-effects with 95% confidence intervals (CI), heterogeneity was assessed by the Cochran’s Q statistic and the inconsistency index (I2), and publication bias was evaluated by funnel plots and the Egger test. Effects of demographic, clinical, and equipment/software variables were assessed in a meta-regression.[[Unable to Display Character: ]] Results: The search identified 229 children from 10 studies. Normal values varied for GS from -21% to -34% (mean -29%, CI, -32% to -27%), GSRs from -1.3 to -2.4 (mean -1.9, CI, -2.1 to -1.6), GSRe from 1.7 to 2.7 (mean, 2.3, CI, 2.0 to 2.7), and GSRa from 1.0 to 1.3 (mean, 1.2, CI, 1.04 to 1.3). A significant base-to-apex segmental strain gradient (p &lt;0.05) was observed in the RV free wall. There was significant between-study heterogeneity and inconsistency (I2&gt;89% and p&lt;0.01 for each strain measure), which was not explained by age, gender, body surface area, heart rate, frame rate or equipment/software. The meta-regression showed that these effects were not significant determinants of variations among normal ranges of strain values. There was no evidence of publication bias (Egger, p=0.6).[[Unable to Display Character: ]] Conclusions: This study is the first to define normal values of RV strain in children on the basis of a meta-analysis.
Abstract 9955: Echocardiographic Markers of Right Ventricular Function, Body-Mass Index, and Sleep Apnea in the Wisconsin Sleep Cohort
Authors: Claudia E Korcarz, Jodi H Barnet, K. M Hla, Terry B Young, Paul E Peppard, James H Stein
Journal: Circulation (2013)

Background: Sleep-disordered breathing (SDB) is associated with increased cardiovascular disease risk and adverse cardiac remodeling due to increased sympathetic activity, oxidative stress and intermittent hypoxia. We characterized echocardiographic markers of right ventricular (RV) function in a large cohort with SDB. Methods: Between 2009 and 2012, transthoracic echocardiography was performed in a population-based cohort study evaluating the association of SDB and cardiovascular disease risk. Overnight polysomnography was performed ~1 month prior. SDB was characterized by the apnea-hypopnea index (AHI, events/hour). Participants on continuous positive airway pressure were excluded. RV systolic function was assessed from apical views and described by RV fractional area change (RVFAC), RV free wall strain (%) and strain rate (s -1 ), Tricuspid Annular Plane Systolic Excursion (TAPSE, mm), and qualitatively by an experienced echocardiographer. Associations between echocardiographic markers and AHI were adjusted for covariates in multivariable linear and logistic regression models. Results: The 352 subjects were mean (standard deviation) 64.6 (7.3) years old (49% female). They had a body-mass index (BMI) of 30.5 (6.4) kg/m 2 , systolic blood pressure (SBP) of 127 (13.6) mmHg, and ejection fraction of 61.4 (5.8) %. 52% had hypertension. Mean AHI was 5.8 (7.8) events/hour; 7.7% had moderate-severe SDB (AHI ≥15 events/hour). After adjustment for age, sex, BMI, smoking status, lung disease, SBP and use of antihypertensive medications, subjects with higher AHI had lower global RV strain rate (β=-0.12 s -1 /events/hour, p=0.03) and TAPSE (β=-0.07 mm/events/hour, p=0.03). Increased AHI was a significant predictor of visually assessed RV systolic dysfunction, but only in models that did not include BMI (OR=1.04; 95% confidence interval 1.01 -1.08 events/hour; p=0.015). RVFAC (p=0.20) and RV free wall global strain (p=0.21) were not associated with AHI. Conclusion: SDB is associated with RV dysfunction independent of its associations with obesity and hypertension. Quantification of RV global strain rate and TAPSE permit more objective assessment of RV function and are less sensitive to the confounding effects of BMI.
Abstract 9683: Leisure-time Physical Inactivity and Risk of Myocardial Infarction and All-cause Mortality: a Case-control Study
Authors: Fredrik Calais, Ole Fröbert, Andreas Rosenblad, Pär O Hedberg, Kristian Wachtell, Jerzy Leppert
Journal: Circulation (2013)

Background: Physical inactivity has pandemic qualities, with major impacts on cardiovascular morbidity and death. However, it is unclear whether the association is affected by extra-cardiac atherosclerotic disease (EAD) and in what ways physical inactivity before myocardial infarction (MI) affects post-MI prognosis. Our hypothesis is that leisure time physical inactivity (LTPI) is an important independent risk factor for MI, and that a sedentary lifestyle is associated with a less favorable outcome after MI. Methods and results: The study included patients (n=734) with acute myocardial infarction (MI), and, for each patient, an age, gender, and city-of-residence matched control with no history of MI. Baseline physical activity level was compared between patients and controls and results were adjusted for medical history and clinical data including objective measures of EAD. All-cause mortality in both patients and controls during the course of the study was stratified according to level of physical activity : Leisure time physical inactivity was associated with a more than 2-fold risk of MI [unadjusted odds ratio (OR) 3.4, 95% confidence interval (CI) 2.59-4.45, P &lt;0.001, adjusted OR 2.1, CI 1.45-2.91, P &lt;0.001]. Survival at 6 years for LTPI vs. active patients was 70% vs. 90% ( P &lt;0.001) and for LTPI vs. active controls 81% vs. 95% ( P =0.002). The unadjusted risk of death from all causes during follow-up was significantly higher in the LTPI group compared to the active group both for patients [hazard ratio (HR) 3.9, CI 2.57-6.01, P &lt;0.001], and controls (unadjusted HR 3.3, CI 1.46-7.34, P =0.004). After adjustment the HR remained significantly elevated for patients (HR 2.3, CI 1.48-3.73, P &lt;0.001) but not for controls (HR 1.7, CI 0.66-4.26, P =0.27). Conclusion: Leisure time physical inactivity is independently associated with MI and death after MI.
Abstract 9441: Three-Dimensional Speckle Tracking Echocardiography for Evaluating Left Ventricular Rotation: An in vitro Validation Study using a Rotational Phantom Model
Authors: Austin Park, Meihua Zhu, Sumito Kimura, Rosie Bleck, Kacie Amacher, Cole Streiff, Sreyas Ravi, Shahryar Ashraf, Muhammad Ashraf, David J Sahn
Journal: Circulation (2013)

Background: Left ventricular (LV) rotation provides an index of regional and global LV function. Two-dimensional (2D) speckle tracking imaging (STI) has been used to calculate rotation, but is subject to computational errors due to through plane myocardial motion; 3D STI is not subject to such limitations. We qualitatively evaluated the accuracy of a new 3D wall-motion tracking program (3D-WMT) in terms of physiologically relevant degrees of LV rotation in a digitally controlled phantom. Methods: Eleven pig hearts with a fixed left ventricular volume of 60mL were passively rotated using a custom apparatus in a water bath. Each heart was mounted on a rotary actuator with the apex externally fixed to optimize the imaging angle and rotated at 0°, 3°, 5°, 7°, 10°, and 15°. Full-volume 3D image loops were acquired on a Toshiba Applio Artida™ ultrasound system. 3D-WMT values were compared to the angle of rotation of the phantom as defined by the actuator. Results: Linear regression between phantom rotation and 3D-WMT derived values demonstrated a strong correlation as rotation increased (R 2 = 0.93, P &lt; 0.001). The mean and standard deviation for 3D-WMT derived rotation for 0° was 0.020° ± 0.016°, 3° was 0.228° ± 0.298°, 5° was 2.073° ± 1.031°, 7° was 4.590° ± 1.391°, 10° was 8.142° ± 1.173°, 12° was 10.289° ± 0.934°, and 15° was 13.059° ± 0.647°. Bland-Altman analysis showed 98% of data points within 95% CI. Conclusion: The Toshiba 3D-WMT program may be able to track LV rotation at physiologically relevant degrees of rotation.
Abstract 9446: Periodic Acceleration (pGz) Preserves Heart Rate Variability After Cardiac Arrest
Authors: Jose A Adams, Arkady Uryash, Paul Kurlansky
Journal: Circulation (2013)

Heart Rate Variability (HRV) and lack thereof is important in predicting neurological outcome after brain injury and cardiac arrest (CA). The post CA period has decreased HRV compared to pre-arrest, and interventions such hypothermia may preserve HRV. Periodic acceleration (pGz) the sinusoidal head to foot motion of the supine body with a motion platform increases endothelial derived NO (eNO) and neuronal nitric oxide (nNOS) in heart via pulsatile shear stress, and preconditions from global and focal ischemia reperfusion injury (I/R). NO has a facilitator role on vagal chronotropism and inhibition of nNOS reduces HRV. CA is a model of whole body I/R. This study tests whether pGz applied prior to whole body I/R preserves HRV in a pig model of CA. Fourteen male swine (40-50lbs) were anesthetized, intubated and instrumented to measure EKG and hemodynamics. They were placed on a motion platform and randomized to 1 hr of pGz (180 cpm and Gz ± 0.4) or none control (C). VF was electrically induced and unsupported for 8 min, followed by chest compression and defibrillation until return of spontaneous circulation (ROSC) or 10 min. Short term HRV (excluding ectopic beats) was measured including; time domain; SDNN (standard deviation of normal to normal intervals), RMSSD (square root of the mean squared differences of successive normal to normal intervals) and frequency domain, at baseline (BL1), after pGz or C (BL2) and 30, to 180 mins after ROSC (ROSC30, 60,120,180 ). All animals had ROSC after a median of 4 defibrillation attempts. There were no differences between groups in defibrillation attempts, time to ROSC, arterial blood gases or hemodynamics over time. pGz animals had less hemodynamically significant arrhythmias in the first 30 mins ROSC; C (35) vs pGz (7) (p&lt; 0.05) Data mean ±SEM * p &lt; 0.05 C vs pGz. pGz applied prior to I/R in addition to being cardioprotective preserves HRV and is a novel non invasive method to preserve autonomic nervous system output and precondition the myocardium.
Abstract 9982: Long-term Administration of Type-I Interferon Leads to Premature Atherosclerosis
Authors: Yanpeng Diao, Pui Lee, Larysa Sautina, Rajesh Mohandas, Mark Segal
Journal: Circulation (2013)

Introduction: Disease states such as SLE, CMV, and HIV are associated with elevated type I interferon (IFN-I) and increased cardiovascular risk. Previously we have demonstrated that IFN-I has detrimental effects on endothelial progenitor cells that could contribute to the atherosclerosis. However, the relationship between IFN-I and smooth muscle progenitor cells (SMPC), cells derived from the bone marrow that can differentiate into mature SMC, has not been determined. We hypothesized that IFN-I could induce premature atherosclerosis by increasing the number of SMPC in the bloodstream and increasing the number of immature SMC within the vasculature. Methods: In vitro, SMPC isolated from wild-type (WT) and IFN receptor knock-out (IFNR-KO) animals, were cultured in medium plus or minus IFN-1. In vivo, two mice models of long-term IFN-I exposure (electroporation of an IFN-I plasmid, or Q 3 day IFN-I i.p. injection for 3 months) were studied and the number of SMPC and degree of atherosclerosis were analyzed. Results: The number of SMPC from WT animals was significantly increased when cultured in medium plus IFN-I. However, IFN-I had no effect in the SMPC from IFNR-KO mice. Increased SMPC numbers were also observed in mice treated with or that expressed IFN-I. In addition, atherosclerotic-like lesions were found in the arterial wall in WT mice expressing IFN-I. Within the lesions we observed CD34+/smooth muscle α-actin+ expressing cells (Fig). These cells did not express smooth muscle myosin heavy chain, suggesting that they were immature SMC. Conclusions: For the first time we demonstrated that elevated IFN-I levels, found in a number of disease states, could lead to an atherosclerosis-like lesion. In concert with our previous work, this work suggests a complex interplay between the bone marrow, circulating cells, and the vessel wall leading to IFN-I mediated atherosclerosis. This has profound implications for cardiovascular disease in a number of disease states.
Abstract 9855: Presence of J-waves or Slurs in Chest Pain Patients Predicts Higher Mortality in those Diagnosed as Acute Myocardial Infarction
Authors: Roger Abächerli, Raphael Twerenbold, Tobias Reichlin, Hans-Jakob Schmid, Vic Frölicher, Stefan Osswald, Christian Müller
Journal: Circulation (2013)

BACKGROUND: Although early repolarization is known as a benign, J-waves or slurs on the R wave downslope have recently been associated with sudden cardiac death. We investigated the presence and prognostic significance of R wav downslope phenomena in patients presenting chest pain at the emergency department. METHODS: We performed a retrospective study of 747 chest pain patients. The presence of a J-wave or slurs in the 12-lead resting ECG recorded at the emergency department was defined as a QRS notching and or QRS slurring of more than 0.1mV relative to the PR-interval (QRSonset) as coded by a single observer using enhanced imaging (RA). Final diagnosis was adjudicated by two independent cardiologists having access to all acquired data including a 2 year follow-up period. Results: Of the participants (mean of age 61.9, 67.1% males), 16% had an acute myocardial infarction, 17% an unstable angina, 12% with cardiac symptoms other than CAD, 46% non-cardiac symptoms and 9% symptoms of unknown origin. There was a significant correlation between patients presenting J-waves/slurs and days in hospital (p=0.04), know hypertonia (p=0.003), known CAD (p=0.05), prior MI (p=0.04), and presence of T negativity (p=0.005) but no significant correlation with ST-segment elevation or depression. There was a significant lower survival rate (0.90 versus 0.94, p=0.03, HR=1.81) in presence of J-waves primarily due to the AMI subgroup (0.72 versus 0.94, p=0.002, HR=4.71). CONCLUSIONS: From this analysis we found an overall association between comorbidities and the presence of J-waves or slurs at the emergency department. A significant higher mortality rate in patients J-waves or slurs was only found in patients who evolved AMI.
Abstract 9273: Meta-Analysis of Stroke After Transradial Versus Transfemoral Artery Catheterization
Authors: Vishal G Patel, Kimberly M Brayton, Dharam J Kumbhani, Subhash Banerjee, Emmanouil S Brilakis
Journal: Circulation (2013)

Objectives: To assess the risk of stroke after transradial (TR) versus transfemoral (TF) artery cardiac catheterization. Background: TR catheterization is gaining popularity due to its association with lower bleeding and access site complications, improved patient comfort, and lower costs compared to TF catheterization; however, there is concern that TR catheterization may be associated with an increased risk of neurological complications. Methods: We conducted a meta-analysis of randomized studies published until 2013 reporting risk of stroke in TR vs. TF catheterization. Results: Data from 11,273 patients in 13 studies were collated. The majority of patients were men, and 8,987 (79.7%) were enrolled in acute coronary syndrome trials. Very few patients had a history of prior coronary artery bypass grafting, and approximately 2/3 of patients underwent percutaneous coronary intervention. Stroke occurred in 25 of 5,659 patients in the TR group, vs. 24 of 5,614 patients in the TF group. There was no difference in stroke rates between the TR and TF groups ( Figure , risk difference 0.00%, 95% confidence interval -0.29% - 0.25%, p=0.88). This finding was consistent in a number of sensitivity analyses (excluding non-ST elevation acute coronary syndrome (ACS) trials, non-ACS trials, trials reporting in-hospital events or 30-day events, trials requiring radial expertise). Conclusions: TR catheterization is not associated with a significant increase in stroke compared to TF catheterization.
Abstract 9814: Nf-?B Inhibition Prevents Vascular Obliteration and Improves Immune Regulation in Severe Pulmonary Arterial Hypertension
Authors: Daniela Farkas, Aysar A Alhussaini, Donatas Kraskauskas, Vita Kraskauskiene, Mark R Nicolls, Norbert F Voelkel, Ramesh Natarajan, Laszlo Farkas
Journal: Circulation (2013)

Nuclear factor-κB (NF-κB) and interleukin-6 (IL-6), a NF-κB downstream mediator, play a central role in inflammatory response and vascular cell growth. Inflammation and a dysregulated immune response are found in many forms of severe pulmonary arterial hypertension (PAH), but how the NF-κB pathway contributes to PAH development is unclear. The SU5416 and chronic hypoxia (Su/Hx) rat PAH model is, like severe human PAH, characterized by obliterative pulmonary vascular lesions and right ventricular failure. We hypothesized that activation of the classical NF-κB pathway in severe PAH promotes ongoing vascular lesion cell apoptosis and proliferation, as well as dysregulation of the immune system. We aimed to determine the role of NF-κB in severe PAH induced by Su/Hx in rats. PAH was induced by a single injection of SU5416 and exposure to chronic hypoxia. Su/Hx rats were treated from day 1-21 with the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) and/or anti-IL-6 antibody. After hemodynamic assessment at day 21, cytokine/chemokine expression, NF-κB activation, lymphocyte accumulation, as well as pulmonary arterial cell apoptosis and proliferation were evaluated by Western blot, Flow cytometry and immunohistochemistry. The classical NF-κB pathway was activated in pulmonary arterial lesions SuHx rats. NF-κB inhibition with PDTC prevented the development of pulmonary arterial obliteration and in part PAH without reducing muscularization. However, the elevated lung levels of IL-6 were not reduced in PDTC-treated SuHx animals. Apoptosis of pulmonary artery wall cells and pulmonary arterial obliteration was prevented by PDTC or by PDTC+IL-6 inhibition and partially by IL-6 inhibition alone. Pulmonary arterial media wall thickness was not affected by any of these treatments. In Su/Hx rats, CD4 + T cells were reduced and perivascular CD8 + T lymphocytes and CD45RA + B lymphocytes were increased. NF-κB inhibition promoted immune regulation by increasing the number of perivascular CD4 + T cells and reducing the number of perivascular CD8 + T lymphocytes and CD45RA + B lymphocytes. Inhibition of NF-κB may represent a therapeutic option for pulmonary arterial obliteration via reduced vessel wall cell apoptosis and improved immune regulation.
Abstract 89: Nitrite After Cardiac Arrest Has Mitochondrial Antioxidant Effects Reducing Reperfusion Cerebral Hyperemia
Authors: Cameron Dezfulian, Amalea Misse, Jason P Stezoski, Elizabeth Kenny, Patrick M Kochanek, Hulya Bayir, Robert S Clark
Journal: Circulation (2013)

Background: Nitrite confers neuroprotection after asphyxial cardiac arrest (ACA) through uncertain mechanisms though others have demonstrated antioxidant effects and improved blood flow after ischemia. We hypothesized that nitrite would modulate reperfusion blood flow and reduce reactive oxygen species (ROS). Methods: Adult male SD rats were intubated and catheterized. Cardiac output (CO) was measured using an ultrasonic flow probe (ascending aorta), cortical blood flow (CBF) was measured using laser speckle imaging (5mm craniotomy). 5m post-ROSC from 8m ACA, animals were randomized to a 500 ul 10m infusion of 8 uM nitrite or plasmalyte placebo. Physiology was measured for 1h and normalized to pre-arrest baseline. Brains were removed at 1h and homogenized for ascorbate measurement (ac-TEMPO). Separately, brains removed 15m post-ROSC had mitochondria isolated by Percoll gradient. Respiration was measured using a Clark electrode and ROS generation quantified by Amplex Red fluorescence +/- UV pretreatment to lyse S-nitrosothiols. Pyruvate/malate or succinate +/- ADP were the substrates. Results: Animals had similar baseline physiology. In placebo animals, post-RSOC hypertension resulted in significant increases in CBF (187%) compared to nitrite treated animals (136%; p&lt;0.01; Figure): This difference persisted until 20 min after ROSC at which point groups converged. Nitrite treated animals had significantly higher levels of ascorbate (33.09 nmol/mg protein) compared to placebo treated animals (26.17; p=0.027). ROS generation with pyruvate substrate was reduced with nitrite therapy with minimal effects on respiration ( Figure ). This difference was reversed with UV pretreatment and not present with succinate. Conclusion: Nitrite is antioxidant after ROSC, preserving ascorbate, reducing mitochondrial ROS generation at complex I presumably via S-nitrosation and blunting loss of autoregulation and hyperemia.
Abstract 9841: Expression of Mitochondrial Fusion Proteins is Increased in Hibernating Hearts Following Bypass Surgery
Authors: Eric K Long, Tammy A Butterick, Cayla Duffy, Jesús A Cabrera, Meghan Lindsey, Christopher T Holley, Herbert B Ward, Edward O McFalls, Rosemary F Kelly
Journal: Circulation (2013)

Background: Based on clinical studies, regional function within hibernating myocardium may not return to normal immediately following successful bypass surgery (CABG). We hypothesized that the mitochondrial proteome within chronically ischemic hibernating hearts does not fully recover early post-CABG and may in part, contribute to submaximal myocardial oxygen expenditure. Methods: Twelve pigs underwent thoracotomy with placement of a constrictor around the LAD artery and had reduced regional function 12 weeks later. Six pigs then underwent sternotomy and off-pump revascularization with a left internal mammary artery graft to the LAD just beyond the chronic stenosis. A patent graft was confirmed by CTA at 4 weeks post-CABG. Five additional pigs underwent a SHAM operation and served as controls. Prior to sacrifice, regional blood flows by μspheres were determined at baseline and during high dose dobutamine (40 μg/kg/min). Post-sacrifice, the content of mitochondrial electron transport chain (ETC) and fusion proteins was determined by western gels. Results: In the hibernating regions that underwent CABG, maximal blood flow during dobutamine was lower than Control hearts (2.5±0.2 vs 3.5±0.2 ml/min/g; NS). As shown in the Figure, the content of mitochondrial ETC proteins, when normalized to SHAM hearts, did not recover in hibernating hearts that had undergone CABG. Compared with non-revascularized hibernating hearts however, hearts that had undergone CABG demonstrated increased expression of fusion proteins. Conclusion: Despite successful revascularization of hibernating heart tissue, maximal blood flow in response to a catecholamine challenge is submaximal at 4 weeks following CABG, at a time that the expression of ETC proteins has not recovered to normal. Mitochondrial fusion proteins are increased however, and may be an important dynamic mitochondrial process to restore maximal energetics of hibernating hearts following CABG.