tbuckley/cabot-search huggingface dataset:
Abstract 15311: Anomaly and Narrowing of Radial Artery and its Impact to the Transradial Angiography and Intervention
Authors: Yumiko Muta, Shigeyuki Watanabe, Masahiro Toyama, Eiji Ojima, Yasuhisa Kuroda, Yuta Oishi, Kazutaka Aonuma
Journal: Circulation (2015)

[Background] Increasing number of transradial coronary procedures are now performed because of the advantage of reduced access site complications. However, transradial approach sometimes ends in failure or vascular complication due to arterial anomaly or stenosis. [Objective] The objective of this study was to clarify the types and frequency of radial or brachial arterial anomaly and narrowing in patients who undergone cardiac catheterization. [Methods] Total of 1135 consecutive patients who underwent transradial cardiac angiography or intervention from Jan. 2013 to May 2015 were subjected. In all cases, angiography of radial and brachial arteries was performed through the inserted sheath. After removing the duplicating cases, we analyzed 826 arms of 786 patients. [Results] Of total 826 angiographies, 622 were identified as normal. There were 20 (2.4%) cases of 'high-bifurcation' in which radial artery originates proximal of the intercondylar line of the humerus. 'Radial loop' with a full 360 degree loop of the radial artery and accompanied by the recurrent artery which originates at the loop was identified in 9 (1.1%) cases. 'Radial simple loop' and 'brachial simple loop' with a full 360 degree loop without recurrent artery were observed in 5 (0.6%) and 6 (0.7%) cases, respectively. 'Radial or brachial tortuosity' with a bend of more than 90 degree existed in 64 (7.7%) and 45 (5.4%) cases, and 'narrow radial or brachial' with the vessel diameter &lt;2.0mm in 113 (13.7%) and 5 (0.6%) cases (some cases were duplicated). In high bifurcation, loop, or tortuosity cases, narrowing of the vessels of catheter route also coexisted in 20-89% cases. Cardiac catheterization ended in failure in 7 (1.1%) of normal radial and brachial artery cases, and in 31 (11.6%) cases of radial or brachial arterial abnormalities (p&lt;0.0001). Among the 31 failure cases with radial or brachial artery abnormalities, the cause of the failure was narrowing of a catheter route in 24 (77%) cases, and 1 case with both radial tortuosity and narrowing ended in radial artery perforation. [Conclusion] Radial artery anomaly and narrowing are not infrequent and often coexist, and lead to procedure failure or even vascular complications, indicating a need of confirmation of vascular anatomy by angiography.
Abstract 19158: MRI Based Non-Invasive Measures Correlates With Invasive Measurements of Left Atrial Diastolic Function in Atrial Fibrillation Patients
Authors: Irfan Khurram, Farhan Maqbool, Roy Beinart, Vadim Zipunnikov, Hugh Calkins, Saman Nazarian, Stefan L Zimmerman
Journal: Circulation (2013)

Background: Atrial fibrillation (AF) is associated with diminished cardiac functions. This study describes a novel methodology for non-invasive measurement of left atrial (LA) function in patients with AF. Methods: A total of 55 patients (81% male, 55% paroxysmal, 60.4±10.2 years) underwent cardiac MRI prior to AF ablation. Invasive LA pressure was measured during sinus rhythm following trans-septal puncture for AF ablation. LA pressure and volume (MRI derived) loops were prepared for all patients. LA diastolic function was defined as the ratio of the change in LA pressure to the change in LA volume during passive LA filling. Additionally, the ratio of pulmonary vein flow velocities during ventricular systole and diastole were obtained using phase contrast MRI (Figure top panel, S/D ratio). Patients with ventricular diastolic dysfunction (as seen by E/A ratio) were excluded. LA systolic functions were calculated from the active emptying fraction during atrial contraction. Diastolic dysfunction scores greater than the 90th %tile (&gt;1.6mmHg/ml) were considered to signify severe diastolic dysfunction. Results: The mean diastolic dysfunction score was 0.76±0.7 mmHg/ml. The score was higher in patients with persistent versus paroxysmal AF (1.0±0.9 vs. 0.60±0.5,p=0.02). The mean S/D ratio was 1.04±0.6; and was lower in patients with persistent versus paroxysmal AF (0.9±0.5 vs. 1.2±0.7, p=0.04). There was a negative linear association between diastolic dysfunction scores and S/D ratio measures (Figure bottom panel, p &lt;0.001). In a multivariate analysis adjusting for age, LA systolic function and CHADS2 score, the severe diastolic dysfunction was independently associated with lower S/D ratio (p-0.03). Conclusion: The non-invasive MRI derived ratio of pulmonary vein flow velocities during systole and diastole are associated with the MRI/invasive derived diastolic dysfunction score, and appear to be a fair surrogate of LA diastolic function.
Abstract 19187: Impact of a Tailored Behavioral Intervention on Lowering Sodium Intake in Adults With Uncontrolled Hypertension
Authors: Gertraud Stadler, Ming-Chin Yeh, Binhuan Wang, Jennifer Friedberg, Sundar Natarajan
Journal: Circulation (2013)

Introduction: : Sodium is related to elevated blood pressure (BP) and reducing sodium intake is a key non-pharmacological approach to lowering BP. We conducted a randomized controlled trial testing whether a tailored or non-tailored behavioral intervention would lead to lower BP. Sodium intake was one of the key dietary behaviors targeted. METHODS: This 3-arm randomized controlled trial evaluated the effectiveness of two active interventions, each compared to the usual care (UC) control group. Participants in the active intervention groups received either a tailored stage-matched intervention (SMI) based on the transtheoretical model (TTM) or a non-tailored health education intervention (HEI) to lower BP through six monthly telephone calls targeting diet, exercise and medication adherence. Participants were adult patients with repeated uncontrolled blood pressure. Urinary sodium levels were measured at baseline and post-intervention (6 months). We indexed sodium intake using urinary sodium-to-creatinine ratio to standardize for time and urine volume since last urination. To compare the two intervention groups with the usual care group at the 6-month follow-up we conducted planned contrasts comparing SMI and HEI with UC in a robust regression model adjusting for baseline sodium-to-creatinine ratio. RESULTS: At baseline, there were no differences between the groups with the median sodium-to-creatinine ratios being 9.28 for SMI, 10.08 for HEI and 8.99 for UC. At the 6-month follow-up, the median sodium-to-creatinine ratio was 7.99 for SMI, 8.76 for HEI and 9.39 for UC. Participants in the SMI group showed on average lower sodium-to-creatinine ratio than participants in the usual care group (SMI-UC contrast: p = .04). Participants in the HEI group did not differ from participants in the usual care group (HEI-UC contrast: p = .45). CONCLUSIONS: A TTM-based tailored behavioral intervention leads to lower sodium intake. Such an intervention shows promise for lowering sodium intake in adults with uncontrolled hypertension.
Abstract 239: Initial Cytokine Levels Are Associated With Outcome After Cardiac Arrest
Authors: Mary Ann Peberdy, Joseph P Ornato, Shirley L Helm, Leroy R Thacker, Clifton W Callaway, Jon C Rittenberger, Michael N Cocchi, David F Gaieski, Benjamin S Abella, Michael W Donnino
Journal: Circulation (2013)

Background: The post arrest syndrome is characterized, in part, by a systemic inflammatory state whose molecular mechanisms and association with survival remain poorly understood. A deeper understanding of cytokine activity post arrest may identify an early biomarker for outcomes as well as a potential therapeutic target. Hypothesis: Cytokine elevation is associated with survival after cardiac arrest (CA) and ROSC. Methods: One hundred eleven consecutive patients (pts) enrolled in the multicenter Characterization of Mitochondrial Injury after Cardiac Arrest (COMICA) study underwent serial serum measurements for IL-6, IL-8, IL-10, and TNFα via a Millipore Multiplex Human Cytokine Panel at Time 0 (T0) defined as upon arrival to the hospital, and 12, 24, 36, and 48 hours post ROSC. We assessed the ability (sensitivity, specificity, and area under the receiver operating curve (ROC)) of these cytokines drawn at T0 to predict survival to hospital discharge. A repeated measures ANOVA was fit with a between subjects factor (Group: Survived, Expired), a within subjects factor (Time: 0, 12, 24, 38, 48) and the interaction between these two factors. Values are presented as mean ± SEM. Results: The areas under the ROC [sensitivity, specificity] were: IL-6= .894 [.732, .837]; IL-8= .800 [.851, .696]; IL-10= .738 [.738, .745]; and TNFα= .512 [.975, .143]. The repeated measures ANOVA analysis for IL-6, which had the best predictive value, is shown in the Figure. There was a significant Group x Time interaction (p=0.0022) and post-hoc tests revealed a significant difference in Log(IL6) at T0 (p 6.72 at baseline is approximately 19 times (OR=18.68, 95% CI (6.60, 52.90)) more likely to die before being discharged than a pt with Log(IL6) &lt; 6.72. Conclusion: Early IL-6 levels are strongly associated with outcome after CA. Further investigation is needed to determine molecular mechanisms and potential for use as an early marker of outcome in post arrests pts.
Abstract 15209: Endotoxemia as Mechanism for Platelet Aggregation in Patients With Pneumonia
Authors: Cristina Nocella, Roberto Carnevale, Simona Bartimoccia, Daniele Pastori, Pasquale Pignatelli, Franecesco Violi
Journal: Circulation (2015)

Introduction: Patients with community-acquired pneumonia (CAP) are at increased risk of cardiovascular events; platelet activation has been suggested to play a role but the underlying mechanism is still unclear. Hypothesis: Our study hypothesis was that endotoxins (bacterial lipopolysaccharide, LPS) might play a role. Methods: Patients (n=100) with diagnosis of community-acquired pneumonia (CAP) through the emergency department (ED) and healty subjects (n=50) were consecutively recruited. Categorical variables were reported as counts (percentage) and continuous variables as means ± standard deviation (SD). The study was comprised 3 parts: 1) analysis of serum endotoxins in CAP patients versus controls; 2) ex vivo platelets aggregation in CAP patients and controls; 3) in vitro experiments to assess if LPS, in a range of concentrations detected in the blood of CAP patients, was capable of activating platelets. Results: CAP patients showed higher serum LPS and ex vivo platelet aggregation (PA) compared to controls. In in vitro study LPS, in a concentration (15-100 pg/ml) similar to that detected in human circulation of CAP patients, no changes of PA were detected. Conversely, LPS elicited PA if incubated with platelets stimulated with sub-threshold concentration of collagen or ADP; this effect was blunted in platelets pre-incubated with an inhibitor of toll-like receptor 4 (TLR4bp). LPS-mediated PA was associated with over-production of thromboxane (Tx) A2 and 8-iso-PGF2α-III, and was inhibited by aspirin or a TxA2 receptor antagonist. Platelet oxidative stress as assessed by measuring reactive oxygen species such as H 2 O 2 , and Nox2 activation was enhanced in LPS-treated platelets and reduced by the TLR4bp. Similarly, TLR4bp blunted the up-regulation of PLA2 phosphorylation, which was observed in LPS-treated platelets. Analysis of up-stream signaling potentially responsible for Nox2 and PLA2 activation demonstrated that LPS-mediated PA was associated with phosphorylation of AKT, p38 and p47 phox translocation. Conclusion: Together these data show that LPS amplifies the platelet response to common agonists via TLR4-mediated eicosanoid production and suggest endotoxemia as a potential trigger for PA in patients with pneumonia.
Abstract 19155: Multiple Arterial Grafting Confers Survival Advantage Compared to Percutaneous Intervention With Drug-Eluting Stents in Multivessel Coronary Artery Disease. A Propensity Score Adjusted Analysis
Authors: Shahzad Raja, Umberto Benedetto, Dimple Chudasama, Siobhan Daley, Fabio De Robertis, Charles I lsley, Mohamed Amrani
Journal: Circulation (2013)

Background: Despite increasing recognition that coronary artery bypass grafting (CABG) compared to percutaneous coronary intervention (PCI) significantly reduces the need for repeat revascularization in multivessel coronary disease (MVD), overall late mortality has been shown comparable for the two strategies. This perception supports PCI as an acceptable alternative to conventional CABG particularly when drug eluting stents (DES) are used. On the other hand, multiple arterial grafting (MAG) confers improved patency and survival benefits compared with conventional CABG utilizing single internal mammary artery. We aimed to investigate whether MAG offers survival benefit over DES-PCI in MVD. Methods and Results: A total of 5686 patients with MVD (≥2 vessel) underwent CABG (n=4256) or PCI (n=1430) at a single institution. MAG was performed in 1264 CABG cases and DES where implanted in 1180 PCI cases. Propensity score adjusted analysis was performed to investigate the potential survival advantage of MAG over PCI. Mean follow-up was 4.6±2.9 years. Risk for late death was comparable after DES-PCI versus conventional CABG in the overall population (adjusted HR 1.11; 95%CI 0.9 to 1.33; P=0.25). However DES-PCI was associated with an increased risk for late death when compared to MAG (HR 1.86; 95% CI 1.45 to 2.40; P&lt;0.0001) and this advantage persisted when elective cases only where included (HR 1.67; 95%CI 1.23 to 2.26, Figure). DES-PCI was associated with a 3.35 fold increased risk for repeat revascularization over MAG (95%CI 2.38 to 4.71; P&lt;0.0001) and 2.94 fold increased risk for repeat revascularization over conventional CABG (95%2.27 to 3.81; P&lt;0.0001). Conclusions: Compared to conventional CABG, MAG improved late survival when compared to DES-PCI. When feasible, MAG should be strongly recommended in patients with MVD.
Abstract 19149: Pulmonary Oxidative Stress, Reperfusion Injury and Lung Tissue Damage During Cardiac Surgery: The Outcome of an Experimental Trial in a Porcine Model
Authors: Ishtiaq Rahman, Laura Walker, Guillaume Chanoit, Pamela Murison, James Hillier, Joya Pawade, Kim Dora, Timea Beleznai, Gianni Angelini, Saadeh Suleiman, Raimondo Ascione
Journal: Circulation (2013)

Background and Objective: The incidence of pulmonary complications following cardiac surgery remains high and is associated with increased in-hospital mortality and costs. Established surgical practice predominantly regards diverting the pulmonary circulation and deflating the lungs from mechanical ventilator (to facilitate surgical exposure) as a safe approach during the period of cardiopulmonary bypass (CPB) and cardioplegic arrest (CA). In this experimental trial we investigate for the first time the incidence of pulmonary dysfunction, ischemia, oxidative stress, and lung tissue damage associated with cardiac surgery in a porcine experimental model and CPB and CA. Methods: Landrace white female pigs (~60kg) were randomised to either median sternotomy alone (Control; n=6) or with CPB (80 minutes) and CA with intermittent antegrade cold blood cardioplegia delivered at 20 minutes intervals (CPB+CA; n=7). Standardised anaesthetic, surgical and perfusion protocols were used in accordance with Home Office Guidance. During CPB the lungs were left deflated as per routine surgical practice. Serial blood samples and lung biopsies were collected at baseline, prior weaning CPB (ischemia), and 1 hour following CPB weaning (recovery). Functional, inflammatory, oxidative, histo-pathological, micro-vascular permeability and apoptosis variables were compared. Results: In the CPB+CA group there was marked functional deterioration (respiratory index and alveolar-arterial oxygenation gradients; both p&lt;0.05), significant pulmonary ischemia (reduced ATP/ADP and ATP/AMP ratios; both p&lt;0.05), evidence of lung apoptosis (caspase-3 activity), increased pulmonary micro-vascular leakage (p&lt;0.05) and pulmonary tight junctions fragmentation (immunohistochemistry). None of these findings was observed in the Control group. Conclusions: The established practice of cardiac surgery does not protect the lungs during CPB and CA and it is associated with pulmonary dysfunction, ischaemia, apoptosis, and marked lung tissue damage. Novel interventions of lung protection during cardiac surgery are required to minimise these detrimental effects.
Abstract 19253: Chronic Hypobaric Hypoxia and Chronic Intermittent Hypobaric Hypoxia in Rats Leads to a Mismatch in the ADMA-NO Pathway
Authors: Nicole Lueneburg, Patricia Siques, Julio Brito, Karem Arriaza, Eduardo Pena, Hans Klose
Journal: Circulation (2013)

Introduction: Chronic Hypoxia (CH) as well as chronic intermittent hypoxia (CIH) are associated with pathophysiological conditions like acute/chronic mountain sickness and pulmonary hypertension. In the manifestation of these diseases the endothelium and the L-arginine/NO pathway plays a crucial role. Asymmetric dimethylarginine (ADMA) is an endogenous formed NO synthase (NOS) inhibitor and well known as a risk factor for respiratory diseases associated with an endothelial dysfunction in the pulmonary circulation. ADMA is metabolized by dimethylarginine dimethylaminohydrolases (DDAH). In order to have a broader view of the involvement and behavior of ADMA and DDAH under CH as well as CIH our study was aimed to assess the changes in ADMA levels and the underlying molecular mechanisms. Methods: Wistar rats were maintained under conditions of CIH (2 days of hypobaric hypoxia followed by 2 days of normoxia (NX) for 30 days (428 torr), CH (30 days, 428 torr) and a control group maintained under NX (n=8 within each group). Systemic blood pressure (SBP) was measured by tail cuff plethysmography. ADMA concentration and DDAH activity were measured in lung tissue by a LC-MS/MS assay. Vascular oxidative stress response was determined by expression of Nox4 and the formation of malondialdehyde. Results: Hemodynamic measurements showed an increase in SBP in CH compared to NX (171.9±1.2 mmHg vs 176.7±4.6 mmHg; p=0.037). CH and CIH led to the development of a moderate right ventricular hypertrophy. ADMA concentrations in the lung were increased under hypoxia (P(NX vs CIH)=0.01 (85.3±66.3 nM vs 140.3±46.7 nM); P(NX vs CH)=0.007 (85.3±66.3 nM vs 197.1±56.0 nM) although it was more pronounced in CH (P=0.04). Hypoxia increased oxidative stress in the lung in combination with a reduced DDAH activity, more pronounced in CH. Expression of the endothelial NOS was increased but NO bioavailability was reduced in CH and CIH. Conclusion: The increase of ADMA might be one reason for impaired NO bioavailability in CH and CIH, resulting in an endothelial dysfunction. Likewise, oxidative stress seems to be another main cause of the mismatch in the ADMA-NO pathway.
Abstract 222: Cerebral Performance Category at Hospital Discharge Predicts Long-Term Survival of Cardiac Arrest Patients Who Received Targeted Temperature Management
Authors: Cindy H Hsu, Jiaqi Li, Marisa J Cinousis, Benjamin Abella, Marion Leary
Journal: Circulation (2013)

Background: Little is known about the correlation between cerebral performance category (CPC) score and long-term survival of post-cardiac arrest survivors who received targeted temperature management (TTM). Methods: We performed retrospective chart review of initial cardiac arrest survivors at two tertiary academic centers from 5/2005 to 12/2012. The CPC scores at hospital discharge were determined by three independent abstractors. The 1-month, 6-month, and 12-month survival of these patients were determined by reviewing hospital records, querying the Social Security Death Index, and follow-up telephone calls. Kaplan-Meier survival estimates were calculated to compare unadjusted rates of long-term survival as well as log rank statistic to determine whether differences in survival were statistically significant. Results: Of the 2,417 identified cardiac arrest patients, 24.1% (582/2417) survived, of which 24.1% (140/582) received post-arrest TTM. The mean age of the TTM cohort was 54.4±15.7 yrs; 64.3% (90/140) were male, 43.6% (61/140) had initial shockable rhythms, and 55.7% (78/140) experienced out-of-hospital cardiac arrests. Overall, 42.9% (60/140) were discharged with CPC 1, 27.1% (38/140) with CPC 2, 18.6% (26/140) with CPC 3, and 11.4% (16/140) with CPC 4. The survival percentages of each CPC group and of the overall cohort were calculated . CPC 1 survivors had the highest long-term survival followed by CPC 2 and 3, with CPC 4 having the lowest long-term survival (p &lt; 0.001, log-rank test). Conclusion: Patients with different CPC scores at discharge have significantly divergent survival trajectories. Favorable CPC at hospital discharge predicts better long-term outcomes of cardiac arrest survivors who received TTM than those with less favorable CPC scores. Further studies and neurocognitive testing of these survivors may help to predict the duration and types of outpatient resources necessary after their hospital discharge.
Abstract 19260: Prothrombotic Activity and Reduction in Coronary Flow Reserve Associated With Therapeutic Intracoronary Delivery of Bone Marrow-Derived Mesenchymal Stem Cells is Ameliorated by Heparin Co-Administration in a Porcine Myocardial Infarction Model
Authors: Birgitta M Gleeson, Kenneth Martin, Arun H Kumar, Mohammed T Ali, Frank P Barry, Timothy O’Brien, Noel M Caplice
Journal: Circulation (2013)

Cell therapy remains an evolving therapeutic option for cardiac repair in the case of acute myocardial infarction (AMI) associated with significant cardiomyocyte death. Mesenchymal stem cells (MSCs) are promising candidates for promoting myocardial salvage post AMI, but concerns regarding the safety of intracoronary MSC delivery remain. Surface expression of tissue factor (TF), a key initiator of the soluble coagulation cascade, has recently been implicated as a possible cause of MSC procoagulant activity. This study aimed to characterize the prothrombotic activity of MSC and identify means of managing any thrombotic side effects during therapeutic intracoronary delivery post AMI. Expression of TF on MSC was detected by immunoflourescence, flow cytometry and immunoblotting. TF antigen was catalytically active (252.4 ± 8.3 pM/2 x 105 MSC) and capable of supporting thrombin generation in vitro. Addition of MSCs to whole citrated blood enhanced platelet-driven thrombus deposition on collagen at arterial shear flow (12.67 ± 1.0% untreated vs 18.9 ± 0.9% surface coverage with MSC, p&gt;0.001), an effect abolished by heparin co-administration (p&lt;0.01 vs MSC alone). Infusion of 25 x 106 MSC via an intracoronary route in a porcine AMI model was associated with a decrease in coronary flow reserve when delivered during reperfusion (-0.7 ± 0.05) but not when coadministered with heparin (0.1 ± 0.02, p&lt;0.01). Heparin also reduced MSC-associated thrombosis incorporating platelets and vWF in the microvasculature (p&lt;0.05). Therapeutic MSC delivery was able to reduce apoptosis in the infarct border zone 24 post AMI (p&lt;0.01). Procoagulant activity associated with therapeutic MSCs is independently associated with reduction in myocardial perfusion when delivered I.C. which may be successfully managed with heparin co-administration. This study highlights an important mechanistic insight into safety concerns associated with therapeutic intracoronary MSC delivery for AMI.