tbuckley/cabot-search huggingface dataset:
Abstract 16780: Prevalence, Treatment, and Outcomes Among Asian Subgroups With Coronary Artery Disease
Authors: Lakshman Manjunath, Sukyung Chung, Jiang Li, Latha Palaniappan, Celina M Yong
Journal: Circulation (2018)

Introduction: Asians are the most rapidly growing minority population in the United States, yet coronary artery disease (CAD) treatment and outcomes among Asian subgroups remain poorly understood. Methods: We analyzed 772,882 patients receiving care from the Palo Alto Medical Foundation from 2006-2015 to determine whether CAD treatment and outcomes differ by race, including Asian subgroups, with adjustment for age, gender, household income and comorbidities. Results: Among the cohort, 219,150 patients were Asian (38.5% Asian Indian, 28.4% Chinese, 9.6% Filipino, 4.2% Japanese, 3.2% Korean, 2.1% Vietnamese, and 14.1% “Other Asian”). Among those who received angiogram, prevalence of CAD was highest among Asian Indian (81.3%), Chinese (83.3%), and Filipinos (82.4%). Compared to Non-Hispanic Whites (NHW), Chinese were more likely to receive a stent (50.9% vs 60.8%, adj OR 1.4 [95% CI 1.0 - 1.9], p = 0.005), while Filipinos were more likely to undergo CABG (6.9% vs 20.5%, adjusted OR 2.7 [CI 1.9 - 4.0], p &lt;0.0001). After stenting, Chinese, Filipinos, and Japanese were more likely to be prescribed clopidogrel compared to NHW (86.2%, 83.0%, and 91.4% vs 74.5%, adj ORs 1.8 [CI 1.1 - 3.0], 1.9 [CI 1.0 - 3.4], and 4.4 [CI 1.0 - 18.7] respectively, p &lt;0.0001) but there were no significant differences in prasugrel prescription by race. There were no significant differences by race in post-angiogram 1-year mortality, stroke, transient ischemic attack, or bleeding. However, Chinese and Asian Indians were more likely to be diagnosed with a myocardial infarction within 1 year following coronary angiography compared to NHW (15.6% and 17.4% vs 11.2%, adj ORs 1.5 [CI 1.0 - 2.2] and 1.7 [CI 1.2 - 2.3] respectively, p &lt;0.0001, see Figure). Conclusions: Disaggregation reveals significant diversity in CAD treatments and outcomes by Asian subgroup, highlighting potential opportunities to meet the needs of growing Asian populations in the United States.
Abstract 16642: Hyperkalemia is Associated With Increased Short and Long-Term Mortality Among Unselected Cardiac Intensive Care Unit Patients
Authors: Benjamin Brueske, Mandeep Sidhu, Joshua Schulman-Marcus, Kianoush Kashani, Gregory Barsness, Jacob Jentzer
Journal: Circulation (2018)

Introduction: Studies have demonstrated an association between hyperkalemia and increased mortality in patients with myocardial infarction, but limited data exist regarding hyperkalemia and associated death among unselected cardiac intensive care unit (CICU) patients. Hypothesis: Hyperkalemia is associated with mortality in CICU patients. Methods: Historical cohort of 9,681 CICU patients admitted from January 2007 to December 2015 with serum potassium measured on admission. Hyperkalemia was defined as admission potassium &gt;=5.0 mEq/L, normokalemia as admission potassium 3.5-4.9 mEq/L, and hypokalemia as admission potassium &lt;3.5 mEq/L. Multivariate logistic regression was used to determine predictors of hospital mortality. Post-discharge survival was assessed using Kaplan-Meier analysis and Cox proportional hazards models. Results: Mean age was 67±15 years with 3,629 (36%) females and hospital mortality of 9%. Hyperkalemia occurred in 1,187 (12.3%), and hypokalemia occurred in 719 (7.4%). Compared to normokalemic patients, both hyperkalemic patients (unadjusted OR 2.85, 95% CI 2.40-3.39; P&lt;.001) and hypokalemic patients (unadjusted OR 2.31, 95% CI 1.85-2.88; P&lt;.001) were at increased risk of hospital mortality. After adjustment for illness severity and renal function, only hyperkalemic patients were at increased risk of hospital death (adjusted OR 1.35, 95% CI 1.07-1.69; p = 0.01), while hypokalemic patients were not (P = NS). Among hospital survivors, hyperkalemic patients had lower post-discharge survival by Kaplan-Meier analysis (P &lt;0.001), while hypokalemic patients had similar survival compared to normokalemic patients (p = NS). After adjustment for illness severity and renal function, hospital survivors with hyperkalemia were at increased risk for post-discharge mortality compared with normokalemic patients (adjusted HR 1.16, 95% CI 1.05-1.28; p=.003). Conclusions: Hyperkalemia on CICU admission is associated with higher hospital and post-discharge mortality, independent of renal function and illness severity. This emphasizes the importance of potassium abnormalities as a risk predictor in patients admitted to the CICU.
Abstract 16927: Validation of CathPCI Bleeding Model in Transradial vs. Transfemoral PCI Patients
Authors: Shane P Flood, Kevin F Kennedy, David W Louis, Herbert D Aronow
Journal: Circulation (2018)

Background: Estimation of bleeding risk in patients undergoing PCI informs the use of bleeding avoidance strategies, allows for personalized consent, and supports quality improvement efforts. The CathPCI Bleeding Model (CPBM) was developed in patients undergoing PCI between 2008 and 2011, when PCI was performed predominantly via transfemoral (TF) access. Whether this model functions equally well in transradial (TR) PCI is unclear. Objectives: This study sought to determine if the CPBM behaves differently for PCI performed via TF vs TR access. Methods: Patients who underwent PCI between Q4 2010 and Q4 2016 were identified from an institutional CathPCI Registry. The primary outcome was post-PCI bleeding within 72 hours or before hospital discharge. A logistic regression model was created predicting CPBM on the 10-variable reduced model. Interactions between each variable and access site were tested. Using the CPBM integer scoring system, the interaction between low, moderate, and high risk groups with the access site was tested. Results: TR access increased from 14% in 2010 to 60% in 2016. Major bleeding was lower for TR than TF PCI (2.5% vs 7.3%, p &lt; 0.001). Prior PCI was protective of bleeding in the TF, but predictive of bleeding in the TR group. There was no significant interaction between access site and all remaining variables (Fig. 1). There was no difference in the discriminative capacity of the CPBM between TR and TF access (Fig. 1). The CPBM integer score behaved similarly between groups, without significant interaction, p = 0.53 (Fig. 2). Conclusions: The CPBM may be used to estimate patients’ bleeding risk regardless of PCI access site.
Abstract 16654: The Role of Glycolytic ATP Generation in the Restoration of Vascular Endothelial Barrier Function
Authors: Priyanka Gajwani, Li Wang, Pallavi Chaturvedi, Sarah Krantz, Asrar Malik, Andrei Karginov, Jalees Rehman
Journal: Circulation (2018)

Introduction: Acute Lung Injury (ALI) is characterized by endothelial barrier dysfunction of the lung vasculature, leading to disassembly of endothelial adherens junctions, increased vascular permeability and fluid accumulation in the lungs. Little is known about the bioenergetics of the barrier disruption and repair processes. The glycolysis regulatory enzyme PFKFB3 has recently been identified as a key mediator of endothelial glucose metabolism and could thus serve as a potential mediator of barrier repair. Methods and Results: To quantitatively measure metabolic changes in response to an inflammatory stimulus, we performed a Seahorse bioenergetic flux assay using human lung microvascular endothelial cells (HLMVECs). Glycolysis, as measured by the extracellular acidification rate, increased acutely by 36% (from 9.1 to 12.4 mpH/min) following treatment with the inflammatory mediator TNFα. This upregulation was abolished in the presence of PFK15, a specific inhibitor of PFKFB3. PFKFB3 activity was also necessary for barrier restoration of HLMVECs following injury, as measured by a transendothelial electrical resistance (TER) assay (p&lt;0.0001). Live cell microscopy of endothelial cells expressing the ATP biosensor Perceval HR revealed that ATP is generated at cell junctions following TNFα treatment. Additionally, controlled translocation of PFKFB3 to the plasma membrane resulted in enhanced barrier restoration after injury, both in terms of the extent of barrier integrity as well as the rate of recovery (p&lt;0.0001). Finally, PFKFB3 was pharmacologically inhibited in vivo following lung injury with the bacterial toxin LPS in mice. This inhibition resulted in significantly impaired recovery of lung vascular barrier function as measured by an Evans blue albumin (EBA) permeability assay (p&lt;0.001). Endothelial cell-specific overexpression of PFKFB3 in mice by liposomal delivery resulted in an enhanced rate of recovery from LPS mediated injury. Lung vascular leakiness decreased from 29.0 to 18.3 ng EBA/g body weight at two days following the LPS injury (p&lt;0.001), thus achieving pre-injury levels of barrier function. Conclusions: Glycolytic ATP generation regulated by PFKFB3 is essential for restoration of the endothelial barrier after inflammatory injury. A better understanding of the endothelial barrier bioenergetics could allow for the development of novel therapeutic approaches which enhance barrier function in severe diseases such as acute lung injury.
Abstract 16625: Electrical Activity in the Blind Spot of Lasso Guided PVI
Authors: Guenter Stix, Marianne Gwechenberger, Laura Stix
Journal: Circulation (2018)

Introduction: The primary goal of AF ablation are complete and durable lesions in a circumferential line around all ipsilateral pulmonary veins. But there is a highly complex and multilayered arrangement of myocardial fibers around the orifice of the pulmonary veins, allowing for unpredictable ways of electrical conduction in this area. Hypothesis: The Lasso-catheter records signals at least one or more millimeters inside the pulmonary veins, but PVI usually is intended by a circumferential line at least several millimeters outside the veins. High density mapping was used to determine whether electrical activity can be detected in the blind spot between the circumferential ablation line on the atrial side and the site of the Lasso-catheter in the pulmonary veins. Methods: Patients scheduled for their first PVI underwent a circumferential radiofrequency ablation of the ipsilateral pulmonary veins. The PVI was verified by 1) an exit- and entryblock via all 20 electrodes of the Lasso 2515 variable, 2) a negative adenosine test and 3) unexcitability along the ablation line. After successfully completing all 3 tests an additional high density mapping with was performed. Results: We included 34 consecutive patients (61 +/- 10 years, 9 females), 28 patients had paroxysmal and persistent AF, 6 patients longstanding persistent AF. Complete PVI was achieved in all patients, verified by all 3 tests. Additional high density mapping with 7023 +/- 645 EGMs per left atrium revealed no electrical activity within the circumferential ablation line in 13 patients (38%), but in a majority of 21 patients (62%) electrical activity beyond the circumferential ablation line could be detected: in 12 of these patients (57%) in one region and in further 9 patients (43%) in several regions. The carina between the right pulmonary veins was the region were residual electrical activity was detected most frequently (15 patients, 71%). The pulmonary veins themselves appeared isolated in all 34 patients (100%) in the high density mapping. Conclusions: High density mapping appeared to detect electrical activity in a hitherto blind spot of Lasso-controlled PVI. Ablation of this discrete electrical activity beyond the circumferential lines might be of additional importance for durable PVI.
Abstract 16586: Parasympathetic Stimulation via Muscarinic Receptor 2 (M2R) is Mediated by Nitric Oxide (NO) Signaling in Cardiomyocytes
Authors: Stephen Baine, Ingrid Bonilla, Cynthia Carnes, Sandor Gyorke
Journal: Circulation (2018)

Several decades of evidence has shown a strong role of the sympathetic nervous system in the pathogenesis of HF. However, much less is known about the influence of the parasympathetic nervous system and HF. Recent data from our group suggests that parasympathetic stimulation by the muscarinic agonist carbachol (CCh) creates “smart” regulation of the cardiac ryanodine receptor 2 (RyR2); a major participant in excitation-contraction coupling (ECC) in the heart. Carbachol mediates phosphorylation of serine- 2808 through muscarinic receptor subtype 2 (M2R). Previous studies from our group have shown that a downstream effector of M2, PKG, is involved in increasing phosphorylation of ser-2808 of RyR2. Therefore, we hypothesized that pharmacological blockade of NOS1 would reduce NO levels and thus decrease RyR ser-2808 phosphorylation. Pharmacological inhibition of NOS1 through S-Methyl-L-Thiocitrulline was employed to investigate the role of NOS1 in CCh mediated RyR2 ser-2808 phosphorylation. Experimental data suggests that inhibition of NOS1 with 300nM SMLT is sufficient to prevent an increase in CCh mediated RyR2 ser-2808 phosphorylation. To further investigate the role of NO in CCh mediated parasympathetic stimulation, we used fluorescent DAF-FM diacetate dye to measure NO levels in isolated cardiomyocytes. In response to 10uM CCh; NO levels increased significantly vs. control (baseline) conditions. Following CCh treatment, cells were treated with Spermine NONOate as a positive control for maximal response. However, if cells were treated with a M2R receptor antagonist atropine (10uM) in the presence of CCh, NO levels decreased significantly vs. control conditions. These experiments support the role of the M2R-NO signaling axis in CCh mediated parasympathetic stimulation. Finally, a transverse aortic constriction model of heart failure in mice was used to investigate the role of CCh mediated parasympathetic stimulation in heart failure. We found that in failing cardiomyocytes, CCh fails to significantly increase levels of NO suggesting a role for impaired parasympathetic and NO signaling in heart failure. These pathways may contribute to the impaired contractility and adverse structural remodeling which are hallmarks of heart failure.
Abstract 12351: Perioperative Interventions for Prevention of Postoperative Atrial Fibrillation After Cardiac Surgery: A Systematic Review and Network Meta-Analysis
Authors: Zhongchen Li, Zhiwei Zeng, Shuo Yuan, Xingyi Zhang, Zhe Zheng
Journal: Circulation (2021)

Background: Postoperative atrial fibrillation (POAF) is the most common complication of cardiac surgery, which increases the risk of stroke and death, the length of hospital stays, and costs. Guidelines recommendations on the use of β-blockers (BBs) have only a modest influence on overall rates of POAF. The key clinical outcomes such as stroke and death have not been improved. The best approach to prophylaxis remains obscure. Method: We used Bayesian network meta-analysis to synthesize evidences from randomized controlled trials (RCTs) that compared interventions for POAF prophylaxis. The primary outcomes were incidence of POAF hypotension and bradycardia. Results: We included 262 RCTs with 52636 participants (age &gt; 18, undergoing CABG, valvular or combined surgery), in which 14 different interventions were investigated. For the incidence of POAF, sotalol, amiodarone, BBs, posterior pericardiotomy, atrial pacing, magnesium, polyunsaturated fatty acids, colchicine, glucocorticoid and statin had positive results compared to placebo with statistical significance. The best three therapeutics were sotalol (OR 0.29, 95% CI 0.21-0.41; probability of being best 84.6%), amiodarone (OR 0.39, 95% CI 0.31-0.48) and BBs (OR 0.39, 95% CI 0.31-0.49). For safety, BBs (OR 4.09, 95% CI 2.10-7.96), magnesium (OR 2.51, 95% CI 1.09-5.76) and sotalol (OR 2.07, 95% CI 1.06-4.05) were associated with higher incidence of hypotension. Sotalol (OR 2.80, 95% CI 1.66-4.74) and amiodarone (OR 2.27, 95% CI 1.66-3.10) were associated with higher incidence of bradycardia. For secondary outcomes, no significant effect on all-cause or cardiovascular mortality was observed. Amiodarone was the only intervention that reduced stroke rate (OR 0.57, 95% CI 0.34-0.96). Conclusions: Sotalol appeared to be superior in efficiency compared with others. BBs do not work as well as we expected with the highest incidence of hypotension.Further studies are required to define the better interventions
Abstract 17002: It’s All in the Tissue: A Rare Case of Acute Cardiogenic Shock
Authors: Nikhil Narang, Bow Chung, Ann Nguyen, Teruhiko Imamura, Sara Kalantari, Bryan A Smith, Gene H Kim, Jayant Raikhelkar, Nitasha Sarswat, Tae H Song, Takeyoshi Ota, David Onsager, Valluvan Jeevanandam, Gabriel T Sayer, Nir Uriel
Journal: Circulation (2018)

A 53-year-old female with a history of hypothyroidism presented with a 2-week history of dyspnea and abdominal pain. Exam revealed a heart rate of 120 bpm, blood pressure of 87/69 mmHg, elevated JVP, and a 3/6 holosystolic murmur. EKG showed 2 mm ST-segment elevations in V1-V3 and ST-segment depressions in lateral limb leads. Labs showed transaminitis, elevated troponin-T, lactic acid and leukocytosis. An echocardiogram revealed severely reduced global biventricular dysfunction with a normal chamber size. Differential included acute coronary syndrome and myocarditis, with unknown subtype. Coronary angiogram revealed normal coronaries, while right heart catheterization found elevated biventricular pressures/low flow (RA 19 mmHg, RV 33/15 mmHg, PAP 32/19/25 mmHg, PCWP 25 mmHg, Fick CI 1.5 L/min/m 2 ). Endomyocardial biopsy was performed to assess acute cardiogenic shock. Intra-aortic balloon pump was placed for stabilization, but she developed ventricular arrhythmias and urgently underwent implantation of CentriMag biventricular assist devices. The biopsy revealed a diffuse lymphocytic infiltrate and multinucleated giant cells without granulomas consistent with giant cell myocarditis (GCM) (Fig 1). A combination of high-dose prednisone, Tacrolimus and IVIG was initiated. The patients’ condition improved and 12 days following BiVAD implantation the patient had “turn-down” study of the BiVADs (simultaneous echocardiographic and hemodynamics step wise reduction in speed which showed evidence of myocardial recovery). The devices were explanted and the patient was discharged on oral medical therapy plus immunosuppression. The case discusses the (1) indication for early endomyocardial biopsy in setting of cardiogenic shock with unknown etiology (2) medical therapy for GCM include steroids/Tacrolimus (3) acute mechanical support in the setting of myocarditis complicated by cardiogenic shock and (4) turn down study to assess myocardial recovery.
Abstract 16805: Renal Sympathetic Denervation as an Adjunctive Therapy to Radiofrequency Ablation and Cardiac Sympathetic Denervation for Refractory Ventricular Tachycardia
Authors: Kevin C Liu, Duc H Do, Julie Sorg, Eric Buch, Houman Khakpour, Yuliya Krokhaleva, Marmar Vaseghi, Olujimi Ajijola, Osamu Fujimura, Carlos Macias, Geraldine Pavez, Jean Gima, Shelly Cote, Noel G Boyle, Kalyanam Shivkumar, Jason Bradfield
Journal: Circulation (2018)

Introduction: The autonomic nervous system plays an important role in initiating and perpetuating ventricular arrhythmias. Neuromodulation procedures aimed at reducing sympathetic outflow to the heart, such as cardiac sympathetic denervation (CSD), can successfully treat many patients with refractory ventricular tachycardia (VT). It is unknown if there is benefit in performing CSD in combination with renal sympathetic denervation (RSD) to treat refractory VT. Hypothesis: When used in combination with CSD and catheter ablation, RSD reduces ICD therapy burden in patients with refractory VT. Methods: We reviewed adult patients who underwent RSD at UCLA Ronald Reagan Medical Center after presenting with refractory VT despite having received ablation(s) and, in all but one case, CSD. We evaluated the ICD therapy burden 1 month pre-RSD to monthly ICD therapies over the 6 month period post-RSD. Results: We performed RSD on 10 patients (mean age=62±10 years,90% male). Nine (90%) had NICM. Mean LVEF was 33±10%. All had prior catheter ablations for VT (median 2 ablations). Of the 9 patients who underwent RSD after CSD, 3 (33%) had both performed during the same hospitalization, of whom 1 died during the hospitalization due to uncontrollable VT. Median follow up was 6.5 months. No further deaths occurred during follow-up. The number of ICD therapies decreased significantly after RSD (total monthly VT episodes pre-RSD was median 11 (IQR 6-23) vs. post-RSD 0.33 (IQR 0-3), p=0.004; monthly ICD shocks pre-RSD was median 5 (IQR 1.5-8) vs. post-RSD 0 (IQR 0-1), p=0.004). Two patients (20%) had complete suppression of VT episodes post-RSD and 6 (60%) had over 75% reduction in VT episodes (Fig. 1). Conclusions: We found that RSD was often performed as an adjunctive treatment for patients presenting with refractory VT after catheter ablation and CSD. As hypothesized, RSD in conjunction with CSD significantly reduced the number of VT episodes and ICD shocks over the 6 months following the procedure.
Abstract 12330: The Degree of Common Carotid Artery Stenosis and the Risk of Cardiovascular Disease Incidence in the Suita Study
Authors: Masayuki Teramoto, Yoshihiro Kokubo, Ahmed Arafa, Haytham Sheerah, Yoko Nakao, Yukie Sakai, Emi Watanabe, Jiaqi Li, Kyoko Honda-Kohmo, Rena Kashima, Hiroharu Kataoka
Journal: Circulation (2021)

Introduction: Little is known about whether common carotid artery (CCA) stenosis is associated with the risk of incident cardiovascular diseases (CVD) in a general population. We aimed to examine the impact of CCA stenosis degree on incident CVD in a general population. Methods: We studied 5,133 Japanese men and women (mean age 59.7 years) without CVD whose CCA was measured by carotid ultrasonography on both sides at baseline (April 1994 to March 2005). We confirmed stenosis by color Doppler and calculated the stenosis degree as a percentage of the stenotic area of the lumen in the cross-section perpendicular to the long axis. The Cox proportional hazard model was used to calculate the multivariable-adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of CVD and its subtypes for people with CCA stenosis ≥50 % and 25-49 % compared to those with CCA stenosis &lt;25 % after adjusting for cardiovascular risk factors. Results: During 63,687 person-years of follow-up, we observed 400 cases of incident CVD (237 strokes and 163 coronary heart diseases [CHDs]). The respective prevalence of 25-49 % and ≥50 % stenosis were 8.2 % and 5.3 % in men and 3.8 % and 1.1 % in women. The CCA stenosis degree was associated with increased risks of incident CVD and CHD, and marginally increased risks of stroke; the multivariable-adjusted HRs for 25-49 % and ≥50 % compared to &lt;25 % stenosis were 1.29 (0.94-1.77) and 1.88 (1.28-2.75) for CVD, 1.88 (1.19-2.97) and 2.37 (1.35-4.13) for CHD, and 0.95 (0.61-1.49) and 1.69 (0.99-2.88) for stroke. The sex-specific HRs of incident CVD for 25-49 % and ≥50 % compared to &lt;25 % stenosis were 1.60 (1.10-2.33) and 1.85 (1.19-2.88) for men, and 0.80 (0.43-1.50) and 2.40 (1.04-5.55) for women. Conclusion: The degree of CCA stenosis was associated with increased risks of incident CVD, CHD, and stroke in the general population. For the first time, CCA stenosis can be used as a predictive tool for the onset of CVD in a general urban population.