bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 2647: Analysis of the Anatomical and Electrophysiological Characteristics of Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia Accompanied by the Block in the Upper Common Pathway
Authors: Morihisa Kenji , Yamabe Hiroshige , Tanaka Yasuaki , Uemura Takashi , Ogawa Hisao 
Published: July 2021

We examined the anatomical and electrophysiological characteristic of the atrioventricular nodal reentrant tachycardia (AVNRT) accompanied by the ventriculo-atrial block during tachycardia, suggesting the presence of upper common pathway in 8 patients. Tachycardia was induced by the atrial burst and/or extrastimulation followed by the AH jump and the earliest atrial electrogram was observed at the His bundle (HB) site in all patients. The HA block was observed after gradual prolongation of the HA interval in 2 patient and abruptly in 6 patients. After administration of isoproterenol, 1:1 HA conduction was resumed in all patients. The tachycardia cycle length, AeHe interval and HeAe interval were 357±89, 275±55 and 80±44 msec, respectively. Single extrastimulus delivered from the HB site reset the tachycardia as soon as it was delivered during late diastole. However, single extrastimulus delivered from the inferior portion of the coronary sinus ostium (I-CSOS) was unable to reset the tachycardia without capturing the earliest atrial electrogram at the HB site, suggesting that atrium is not involved in the circuit. Thus, the longest coupling interval of single extrastimulus that reset the tachycardia at the HB site was significantly longer than that at I-CSOS (347±89 msec vs. 324±109 msec, p=0.012). The following return cycle after extrastimulation at the HB site did not differ from the tachycardia cycle length (357±89 msec, vs. 357±89 msec, p=NS), however, that at I-CSOS was significantly longer than the tachycardia cycle length (398±85 msec, vs. 357±89 msec, p=0.012). Catheter ablation was performed in a stepwise fashion starting at the inferior CSOS. Although the results of single extrastimulation showed that the atrial myocardium at I-CSOS was out of the reentry circuit, ablation near the I-CSOS, distant from HB site, selectively eliminated slow pathway conduction in all patients without impairment of fast pathway conduction.
Conclusions: The AVNRT with upper common pathway has the characteristic of relatively long HA interval during tachycardia. Sub-atrial tissue, but not the atrium, extending from the HB site to I-CSOS forms the upper common pathway in AVNRT. It was shown that upper common pathway has an anatomical structure of a certain range.
Abstract 2686: Can Real-Time 3D Echocardiography Be Used to Assess Myocardial Perfusion?
Authors: Bhan Amit , Kapetanakis Stamatis , Rana Bushra S , Ho Emily , Wilson Karen , Monaghan Mark J 
Published: July 2021

Introduction: 2D low mechanical index (LMI) contrast specific myocardial perfusion imaging is now an accepted technique. Advancements in technology now allow us to use this technique in combination with real-time 3D echo. We assessed the hypothesis that real time 3D myocardial contrast echo (RT3DMCE) is feasible in a clinical setting.
Methods: 46 consecutive patients (24 male) referred for contrast enhanced echocardiography were imaged using a 3D scanner equipped with novel 3D LMI power modulation software. All patients underwent 2D contrast echo and real-time 3D apical full volume acquisition, during contrast infusion. Datasets were taken in left ventricular opacification (LVO) and LMI perfusion modes. These were then evaluated segmentally for wall motion and myocardial contrast enhancement, relative to the LVO mode.

Results: A total of 736 left ventricular segments were analysed. Wall motion and perfusion could be assessed in 726 (98.6%) and 721(98%) respectively of the 2D segments and 708 (96.2%) and 701(95.2%) of the 3D segments. Although p=<0.05 for these comparisons, they showed good agreement: 97.6% (
kappa
0.52) for wall motion and 97.3% (
kappa
0.61) for perfusion. 661 segments had normal wall motion and thickening in 2D. Of these, normal 3D myocardial opacification was seen in 91.8% of apical, 85% of mid and 77.2% of basal segments. 34 segments were akinetic with no 2D evidence of perfusion and of these RT3DMCE successfully identified a perfusion defect in 31 (91% p=NS).

Conclusion: Evaluation of myocardial perfusion using RT3DMCE is feasible in most segments. In the future it has the potential to specify accurate location of perfusion defects and quantify volumes.
Abstract 2722: Large Scale Mutation Discovery Screen Identifies Functionally Variant UGDH Alleles in Patients with Atrioventricular Valve Defects
Authors: Bakkers Jeroen , Chocron Sonja , Gouriev Victor , Smith Kelly , Deprez Ronald Lekanne dit , Joziasse Irene C , Doevendans Pieter A , Mulder Barbara J , Simpson Melanie , Barycki Joseph , Cuppen Edwin 
Published: July 2021

Background: Congenital heart defects are the most common birth defects. Although genetic dispositions are believed to cause CHDs, only few genes have been identified that harbour mutations causing such defects. Studies in model organisms have identified many essential genes for cardiac development. UDP-glucose dehydrogenase (UGDH) enzymatic activity is required for the signal transduction of FGF and Wnt ligands and zebrafish jekyll/ugdh mutations lack AV valves.
Methods and Results: From literature candidate genes were selected that are essential for AV canal-, septum-, and valve formation. By large scale sequencing we analysed the coding regions of 36 candidate genes in 192 patients with reported AVSDs. As a result we identified 457 genetic variations of which 207 variants are in flanking non-coding regions, 156 variants are in coding regions but silent and 94 variants are non-synonymous variants that alter the protein sequence. Comparison with the available databases such as HapMap and screening 350 control individuals resulted in the validation of 49 non-synonomous missense mutations in 23 genes only present in the patient group. These included novel GATA4 missense mutations (R285C and M224V) located in the highly conserved DNA binding domains, which by in vitro analysis significantly reduce transcriptional activity of the protein. Three patients with mitral valvar prolapse and mitral regurgitation were identified with novel missense mutations in the UDP-glucose dehydrogenase (UGDH) gene (R141C and E416D). In vitro experiments demonstrated a negative affect on enzyme activity and stability by a change in protein conformation. Furthermore, experiments in zebrafish jekyll/ugdh mutants showed that UGDH R141C and UGDH E416D couldn’t rescue the defects in AV formation demonstrating an inactivating effect of these missense mutations in vivo.
Conclusions: A model organism based candidate gene screen in CHD patients resulted in the identification of novel functional missense mutations in the UGDH gene not previously implicated in congenital heart defects.
Abstract 2837: Delayed Calpain Inhibition Is Neuroprotective After Transient Global Brain Ischemia
Authors: Chen Zhaoming , Frederick James R , Bevers Matthew B , Ingleton Lori P , Ma Marek , Neumar Robert W 
Published: July 2021

Introduction/Hypothesis: The delay in neurodegeneration after transient global brain ischemia offers a potentially broad therapeutic window for inhibiting molecular injury mechanisms. One such mechanism, calpain-mediated proteolysis, peaks between 24 and 72 hours after transient forebrain ischemia (TFI) in rats. This study tests the hypothesis that calpain inhibition is neuroprotective when initiated 22 hours after TFI.
Methods: Male Long Evans rats (400 – 450 g) were anesthetized (halothane), mechanically ventilated, and instrumented for temperature and hemodynamic monitoring. Each underwent 10 minutes of TFI induced by reversible bilateral carotid occlusion and hypovolemic hypotension (MAP 30 mm Hg). Twenty-two hours after TFI, rats were block randomized (n=6/group) to receive either calpain inhibitor (CEP-3453 (Cephalon), 60 mg/kg IV bolus and 30 mg/kg IV infusion for 50 hours) or vehicle (normal saline IV bolus and infusion for 50 hours). Sham operated rats served as controls. Rats were euthanized 72 hours after injury and brains were processed for immunohistochemistry. Hippocampal CA1 sector calpain activity was analyzed by immunofluorescence using primary antibody that specifically detects calpain-cleaved alpha-spectrin (Ab38). Neurodegeneration was quantified by counting normal appearing Hoechst-stained neuronal nuclei in the hippocampal CA1 pyramidal layer. Ab38 immunofluorescence intensity and normal nuclei counts were compared between vehicle and CEP-3453 treatment groups using a two-tailed Student’s t-test (alpha error 0.05).
Results: Baseline and post-injury hemodynamic parameters and temperature were not significantly different between vehicle and CEP-3453 treatment groups. Relative to sham operated controls, mean CA1 sector Ab38 immunofluorescence increased by 263 ± 281% in vehicle treated rats and 68 ± 147% in CEP-3453 treated rats (p=0.17). Normal CA1 pyramidal layer nuclei averaged 10 ± 12% of control in vehicle treated rats and 50 ± 42% of control in CEP-3453 treated rats (p=0.047).
Conclusion: These results suggest a causal role for calpains in delayed post-ischemic neurodegeneration, and demonstrate a broad therapeutic window for calpain inhibition in this model of transient global brain ischemia.
Abstract 2875: Long-Term Outcomes Following Vascular Surgery in Patients With Multivessel Coronary Artery Disease: Analysis of Randomized and Excluded Patients from the Coronary Artery Revascularization Prophylaxis (CARP) Trial
Authors: Garcia Santiago , Ward Herbert B , Moritz Thomas , Littooy Fred , Goldman Steve , Pierpont Gordon , Larsen Greg , Reda Domenic , McFalls Edward O 
Published: July 2021

Background: The Coronary Artery Revascularization Prophylaxis (CARP) Trial was a multicenter randomized study that showed no long-term survival benefit with revascularization prior to elective vascular surgery in patients with stable coronary artery disease (CAD). To determine whether subsets with high-risk anatomy benefited from preoperative revascularization, survival was determined in randomized and registry patients who underwent coronary angiography within 6 months of vascular surgery.
Methods: Over a 4-year enrollment period, 4,876 patients were screened prior to vascular surgery and 1,048 (21.5%) had preoperative coronary angiography for either multiple cardiac risks or an abnormal preoperative stress test. The cohort included 462 randomized and 586 excluded patients and the probability of survival was determined at 2.5 years following vascular surgery.

Results: Of 1,048 patients with preoperative coronary angiography, non-obstructive disease (< 70%) was present in 192 (18.3%) and 1 vessel disease (VD) was present in 244 (23.3%), with a combined survival of 0.84. Previous bypass surgery (CABG) was present in 225 (21.5%), with a survival of 0.78. High risk coronary anatomy in patients without prior CABG included 2-VD in 204 (19.5%), 3-VD in 130 (12.4%) and an unprotected left main stenosis > 50% in 48 (4.6%) patients. Their long-term survival according to the preoperative revascularization status is shown in the Table

.

Conclusions: The results demonstrate that an unprotected left main stenosis was present in 4.6% of high-risk patients presenting for vascular surgery and was the only anatomical subset that demonstrated a survival benefit with preoperative revascularization prior to vascular surgery. These data may warrant additional strategies to identify patients with unprotected left main disease either prior to or immediately following vascular surgery.

Long-Term Probability of Survival at 2.5 Years Following Vascular Surgery
Abstract 2968: Postmortem Genetic Testing of the GPD1-L-Encoded Glycerol-3-Phosphate Dehydrogenase 1-Like Protein in Sudden Infant Death Syndrome
Authors: Van Norstrand David W , Valdivia Carmen R , Tester David J , Ueda Kazuo , London Barry , Makielski Jonathan C , Ackerman Michael J 
Published: July 2021

Introduction: Approximately 10 – 15% of sudden infant death syndrome (SIDS) may be caused by cardiac channelopathies including Brugada syndrome (BrS). Type 1 BrS (BrS1), due to mutations in the SCN5A-encoded sodium channel, accounts for approximately 20% of BrS. Recently, a novel mutation in glycerol-3-phosphate dehydrogenase 1-like (GPD1-L) disrupted trafficking of SCN5A in a multi-generational family with BrS. We hypothesized that mutations in GPD1-L may be responsible for some cases of SIDS.
Methods: Using DHPLC and direct DNA sequencing, we performed comprehensive open reading frame/splice site mutational analysis of GPD1-L on genomic DNA extracted from necropsy tissue of 228 anonymous cases of SIDS (86 females, 142 males, average age = 3 + 2 months, range 6 hours to 12 months).
Results: Three putative, SIDS-associated GPD1-L missense mutations, E83K, I124V, and R273C, were discovered in a three-month-old white male, a five-week-old white female, and a one-month-old white male, respectively. All mutations occurred in highly conserved residues and were absent in 600 reference alleles. Compared to wild type GPD1-L, GPD1-L mutations co-expressed with SCN5A in heterologous HEK cells produced a 60% reduction in peak sodium current density (p<0.004). Adenovirus-mediated gene transfer of the E83K-GPD1-L mutation into neonatal mouse myocytes markedly attenuated the sodium current as well (p<0.01). These decreases in current density are consistent with sodium channel loss-of-function diseases like BrS.
Conclusion: This study is the first to report mutations in GPD1-L as a pathogenic cause for a small subset (~1%) of SIDS via a secondary loss-of-function mechanism whereby perturbations in GPD1-L precipitate a marked decrease in the peak sodium current and a potentially lethal, BrS-like pro-arrhythmic substrate.
Abstract 3415: Cardiovascular Magnetic Resonance Accurately Detects Myocardial Hemorrhage in Reperfusion Injury
Authors: Kumar Andreas , Green Jordin D , Mitchell Andrea J , Sykes Jane M , Wisenberg Gerald , Friedrich Matthias G 
Published: July 2021

Introduction Hemorrhage can complicate reperfusion injury in myocardial infarction, but no in vivo imaging method exists. We hypothesized that a T2*-weighted cardiovascular magnetic resonance imaging (CMR) sequence accurately detects myocardial hemorrhage in vivo.
Methods Reperfused myocardial infarcts were generated in 14 dogs by ligation of the LAD for 3– 6 hours. At day 3, a CMR study was performed using established sequences for quantification of function, microvascular obstruction and myocardial infarction in short axis slices covering the entire myocardium. For hemorrhage, a T2*-weighted multi-echo gradient-echo sequence was applied (TE=35msec, TR=1 RR, FOV 380x280mm, matrix 256 x 192). A segmental analysis was performed using 6 segments per slice: T2*-segments were considered hemorrhagic when signal intensity was >2 standard deviations below the mean of remote myocardium. The contrast-to-noise ratio of hemorrhagic segments over normal segments was assessed. Post-mortem TTC staining was performed with infarcted and hemorrhagic areas analyzed with the same segmental approach. In vivo/ ex vivo correlation statistics were performed.

Results In 14 dogs, 378 segments were assessed. Of the T2* CMR segments, 10.2% were excluded due to artifacts; 27 segments yielded a signal drop consistent with hemorrhage (see figure

). The correlation with ex vivo TTC staining was R=0.79 and contrast-to-noise ratio was 9.2±3.4. Sensitivity to detect a hemorrhagic segment was 77%, specificity 99%.

Conclusion T2*-weighted CMR accurately detects reperfusion hemorrhage in vivo. The method may be applied in patients to study hemorrhage as a complication of reperfusion injury.
Abstract 3466: Hypertension Treatment and Control Among Patients Hospitalized with Heart Failure: An Analysis of Get With The Guidelines Heart Failure
Authors: Lackland Daniel T , Cannon Christopher P , Egan Brent M , Fonarow Gregg , Yu Yanglin , Hernandez Adrian F , Robertson Rose Marie , Jones Daniel W 
Published: July 2021

Background: Hypertension is a major factor associated with heart failure (HF).While effective blood pressure (BP) control is recommended in patients with HF, little is known regarding treatment and control rates in these patients.
Methods: The analyses assessed HF patients from 195 hospitals participating in the GWTG-HF quality improvement program from January 2005 through September 2006. Patients with hypertension were assessed for number and type of hypertension treatment as well as BP control rates. Analyses were stratified by race-sex groups with multivariate logistic regression models using the generalized estimating equations methods assessed the factors associated with multiple treatment, type of therapy, and BP control levels.
Results: Of 37,318 HF patients, 62.3% (23,257) had diagnosed hypertension. The majority (67.3%) of these high-risk individuals were treated with 3 or more hypertension drugs, which was significantly varied by race-sex groups. The use of ACEI (64.6%), beta blockers (79.9%), angiotensin receptor blockers (18.5%), diuretics (62.4%), loop diuretic (73.8%), and calcium channel blockers (13.3%) significantly varied by race-sex groups. BP control rates (< 140/90 mm Hg) at discharge significantly varied by race-sex group (total 70.8%; white males (WM) 76.3%; white females (WF) 71.1%; black males (BM) 63.0%; and black females (BF) 62.9%). Significant factors associated with BP control at discharge included age, race-sex (WF vs. BF, WM vs. BF), atrial fibrillation, hyperlipidemia, coronary heart disease, ICD, pacemaker, history of MI, and not having one or more of the following co-morbid conditions: diabetes, peripheral vascular disease, CVA and renal disease. Control rates considering BP < 130/80 mm Hg (52.3%) showed similar significant variation by race-sex group (WM 57.4%; WF 53.7%; BM 42.3%.; and BF 44.4%).
Conclusions: The less than optimal blood pressure control levels and the gender/racial disparities support continued emphasis on hypertension treatment and control among patients with heart failure.
Abstract 3648: Clinical Cardiovascular Disease in Women is Associated With Increased Epicardial, but Not Subcutaneous Fat Thickness
Authors: Oyama Noriko , Gona Philimon , Chuang Michael L , Jhaveri Rahul R , Salton Carol J , Blease Susan J , Levy Daniel , Manning Anya R , O’Donnell Christopher J , Manning Warren J 
Published: July 2021

INTRODUCTION: Visceral adipose tissue, such as epicardial fat, is metabolically active, and may portend increased risk for cardiovascular disease (CVD) compared to subcutaneous fat. Cardiovascular magnetic resonance (CMR) can accurately delineate fat, but data are sparse regarding the relationship of epicardial and subcutaneous fat burden to CVD in community-living adult women.
METHODS: 957 women (aged 64± 8 years) in the Framingham Heart Study Offspring cohort, followed by serial examinations since 1974, underwent CMR on a 1.5-T Philips system using an ECG-gated cine SSFP sequence. Epicardial fat thickness (EFT) over the midlevel right ventricle was measured from a 4-chamber view. Suprasternal subcutaneous fat thickness (SFT) was measured at the main pulmonary artery level. We compared EFT and SFT between women with clinical CVD, documented by a physician endpoint committee (+CVD), vs. those without (noCVD) based on Cycle 7 (1998 –2002) clinical data. Differences were assessed by two-sample T-test; ANOVA was used to adjust for age, diabetes, hypertension and menopausal status.

RESULTS: The +CVD group comprised 74 (8%) women who were older and more likely to be postmenopausal, diabetic and hypertensive than noCVD women (Table

). EFT was greater in +CVD (10.5 ± 5.1mm) vs. noCVD (8.6 ± 5.2mm) groups, p<0.003. This difference remained significant after adjusting for age, diabetes, hypertension and menopausal status (Table

). No difference in SFT or body mass index was observed between groups (p=NS).

CONCLUSIONS: Women with history of clinical CVD have greater EFT than women without CVD, and this difference persists after adjustment for common cardiovascular risk factors. However, subcutaneous fat, as assessed by chest wall adiposity, did not differ between groups. EFT may be a useful marker for cardiovascular risk, and prospective investigation of the relationship between EFT and future risk for CVD is warranted.
Abstract 39: Atropine for Patients with Out-Of-Hospital Cardiac Arrest
Authors: Nagao Ken , Sakamoto Tetsuya , Igarashi Masaki , Ishimatsu Shinichi , Sato Akira , Hori Shingo , Kanesaka Shigeru , Hamabe Yuichi , Kikushima Kimio 
Published: July 2021

BACKGROUND AHA guidelines for cardiopulmonary resuscitation (CPR) have recommended that administration of atropine can be considered for asystole or pulseless electrical activity (PEA), because atropine has improved survival to hospital admission in a retrospective review (Ann Emerg Med, 1984), and is inexpensive, easy to administer, and has few side effects. However, there are insufficient data in humans.
METHODS We assessed the effects of atropine in 7,443 adults patients with asystole or PEA arrest from the SOS-KANTO study: a prospective, multicenter, observational trial. The medications for asystole or PEA arrest were managed according to the advanced cardiovascular life support algorithm of the CPR guidelines (i.e. a 1-mg dose of epinephrine was administered intravenously every 3 to 5 minutes and a1-mg dose of atropine was administered intravenously every 3 to 5 minutes; maximum total of 3 doses). The primary endpoint was a favorable neurological outcome 30 days after cardiac arrest.
RESULTS Of the 7,443 adult patients who had out-of-hospital cardiac arrest with asystole or PEA, I,708(23%) were treated with epinephrine and atropine and 5,735(77%) were treated with epinephrine. At baseline, the epinephrine and atropine group had significantly higher proportions of cardiac cause, witnessed arrest, and bystander CPR attempt than the epinephrine group. However, the two groups had a similar frequency of the favorable neurological outcome (0.3% in each group, p=0.805). Multiple logistic-regression analysis showed that the adjusted odds ratio for the favorable neurological outcome was 0.6 (95% CI 0.2–1.7, p=0.37) after epinephrine and atropine (compared with epinephrine). On the other hand, the epinephrine and atropine group had significantly higher rate of return of spontaneous circulation (ROSC) than the epinephrine group (35% vs. 23%, p<0.0001), and the adjusted odds ratio for ROSC was 1.6 (95% CI 1.4 –1.7, p<0.0001) after epinephrine and atropine (compared with epinephrine).
CONCLUSIONS We demonstrated that administration of atropine during management of asystole or PEA arrest did not increase the frequency of favorable neurological outcome, although the atropine favored initial ROSC.