bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 5502: Ultrasound-Controlled Therapeutic Gas Delivery Provides Enhanced Neuroprotection Following Hypoxic-Ischemia
Authors: Kim Hyunggun , Britton George L , Holland Christy K , McPherson David D , Huang Shao-Ling 
Published: April 2024

Background: Neurologic damage following ischemic insult is a major problem for stroke survivors. Xenon (Xe) exerts favorable neuroprotective properties with few side effects. This study describes a unique application of ultrasound for controlled release of Xe from liposomes (Xe-ELIP) for targeted therapeutic gas delivery and neuroprotection.
Method: Xe-ELIP were created by a pressurization-freezing method. One-MHz continuous ultrasound wave with pressure amplitudes of 0.16, 0.22 and 0.33 MPa was used to trigger Xe release from Xe-ELIP, and endothelial cell permeability and cell viability were measured. Male Sprague-Dawley rats underwent right middle cerebral artery occlusion for 2 hours (n=28). In the treatment group (n=8), Xe-ELIP were administered through the right common carotid artery. Continuous ultrasound (0.22 MPa) was applied over the common carotid artery during the Xe-ELIP administration for 4 minutes. Infarct size as well as behavioral outcomes were determined 3 days after treatments.
Results: Ultrasound application in the presence of ELIP resulted in a temporary (5 minutes) enhancement of cell permeability. The amount of released Xe depended on the ultrasound pressure amplitude. Xe-ELIP in combination with ultrasound exposure (0.22 MPa) enhanced neuroprotection by decreasing infarct volume by 88% vs the non-ultrasound Xe-ELIP group (64%). Behavioral tests mirrored neurological results.
Conclusions: One MHz continuous ultrasound can be used to release therapeutic gas from encapsulated liposomes. Administration of Xe-ELIP with ultrasound exposure over the carotid artery after a cerebral ischemic insult provides enhanced neuroprotection.

This research has received full or partial funding support from the American Heart Association, Midwest Affiliate (Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, South Dakota & Wisconsin).
Abstract 5511: Natural Regulatory T Cells Control Coronary Arteriolar Endothelial Dysfunction and Hypertension in Mice
Authors: Elmageed Zakaria T Abd , Nair Devika , Gonzalez-Villalobos Romer A , Chentoufi Aziz A , Partyka Megan , Belmadani Souad , Matrougui Khalid 
Published: April 2024

Background and Purpose: Coronary arteriolar endothelial dysfunction and hypertension are the main cause for heart disease, and represent a major health problem. The cellular and molecular mechanisms that trigger this pathology are not well understood. Evidence from experimental and clinical research indicates a central role of immune cells and inflammation in cardiovascular diseases. In this study we determined that CD4+CD25+ regulatory T cells, which actively maintain immunological tolerance to self and nonself antigens, are key element in the control of blood pressure and coronary arteriolar endothelial dysfunction in angiotensin-II-dependent hypertensive mice model.
Methods and Results: Mice infused with angiotensin-II significantly increased blood pressure determined by telemetry, reduced the number of CD4+CD25+ regulatory T cells apoptosis-dependent mechanism as determined by flow cytometry, increased macrophages inflammatory cytokines release (increased local tumor necrosis factor alpha release), and induction of adhesion molecules (I-CAM and V-CAM) expression facilitating the infiltration of macrophages into coronary arterioles and heart; and induced coronary arteriolar endothelial dysfunction assessed with reduced relaxation in response to dose-response of acetylcholine using arteriograph. Interestingly, hypertensive mice injected with purified CD4+CD25+ regulatory T cells (3 times a week for two weeks) or treated with copolymer-I (which enhances the conversion of CD4+CD25− T cells to CD4+CD25+ RegTC through the induction of transcription factor Foxp3 in CD4+ T cells and Known as glatiramer acetate, novel medication for the treatment of human multiple sclerosis) significantly reduced blood pressure and macrophages inflammatory cytokines release, and improved coronary arteriolar endothelial function.
Conclusion: Our novel data strongly indicate that CD4+CD25+ regulatory T cells play a critical role in the regulation of blood pressure and coronary arteriolar endothelial function. These results provide new direction in the investigation of hypertension and coronary arteriolar disease and could lead to new therapeutic approaches that involve immune system modulation using CD4+CD25+ regulatory T cells.
Understanding Ventricular Remodeling after Correction of Mitral Regurgitation: Thinking Volumetrically
Authors: Schaff Hartzell V. 
Published: April 2024

Early after correction of mitral valve (MV) regurgitation, systolic function of the left ventricle (LV) declines, but the underlying mechanisms of this phenomenon are unknown. Most studies in this area have analyzed LV function at one week postoperatively or later. In a retrospective study from our Clinic, Enriquez-Sarano et al. reported a decline in LV ejection fraction (EF) from 62% to 52% (
P
<0.001) in 217 patients with organic mitral regurgitation who were studied within the first year after MV replacement or repair. This decline was due to decreased left ventricular end-diastolic dimension (LVEDD) and minimal change in left ventricular end-systolic dimension (LVESD). Surgical investigators have compared the outcomes for different techniques of MV replacement and studies indicate that decline in EF may be mitigated by chordal preservation.

It has been suggested that early postoperative measurements of cardiac geometry and function are confounded by the effects of global ischemia, reperfusion, and myocardial protection. Indeed, some clinicians have suggested that reduced EF early after MV repair results from myocardial dysfunction that, in turn, is related to poor myocardial protection. In addition, cardiac loading conditions change dramatically early after operation.
We speculated that a postoperative decline in LV systolic indexes (eg, EF, FAC, and FS) may be interpreted as a volumetric adjustment of the heart to the correction of mitral regurgitation rather than as postoperative LV dysfunction due to impaired myocardial contractility, and clinical studies support this hypothesis. Soon after MV repair, the LV remodels gradually. Very early after correction of mitral regurgitation, the LVESD increases, preventing an acute increase in forward stroke volume. Within the next few postoperative days, the LVEDD begins to decrease and the LVESD changes accordingly to maintain a normal forward stroke volume; the remodeling occurs when neurohumoral mechanisms of the body adapt to the new hemodynamic milieu. This progression of remodeling may explain why some investigators have observed unchanged LV systolic and decreased diastolic size on the first postoperative echocardiogram about a week after MV repair.
Abstract 18398: Long-term Surgical Outcome of Mitral Valve Repair for Degenerative Mitral Regurgitation with Chronic Atrial Fibrillation: The Impact of Maze Procedure on Long-term Survival and Cardiac Function
Authors: Murashita Takashi , Okada Yukikatsu , Fukunaga Naoto , Konishi Yasunobu , Koyama Tadaaki 
Published: April 2024

Introduction: It is unclear whether maze procedure for atrial fibrillation (AF) would positively affect long-term survival, stroke and cardiac function. The aim of this study is to investigate the long-term surgical outcomes of mitral valve repair for degenerative mitral regurgitation with chronic AF and to determine the impact of concomitant maze procedures on long-term survival, cardiac events, stroke and cardiac function, comparing the outcomes of patients who underwent maze procedure and patients who did not undergo maze procedure.
Methods: We retrospectively investigated 159 patients who underwent mitral valve repair for degenerative mitral regurgitation with chronic AF between 1991 and 2010. The mean age was 63.1±10.5 years old. We started Cox-maze IV procedure in 2002. As a result, 65 patients underwent concomitant maze procedure (maze(+) group) and 94 patients did not undergo maze procedure (maze(-) group). Follow-up was completed in 156 patients (98.1%). The median follow-up duration was 7.6 years (max 21 years).
Results: There was one operative death (0.63%). The survival rate was significantly better in the maze(+) group than maze(-) group (5-year survival; 100% vs 85.2±4.0%, p<0.001). The actual freedom from atrial fibrillation in the maze(+) group was 86.4±4.5% at 1 year and 81.1±5.6% at 5 years. The actual freedom from cardiac events (cardiac death, cardiac-related re-admission and re-operation) was not different between the maze(+) group and maze(-) group (5-year freedom rate; 81.6±5.9% vs 88.9±3.5%, p=0.113). The rate of freedom from stroke was better in the maze(+) group than maze (-) group (5-year freedom rate; 92.1±3.9% vs 82.6±4.2%), though the difference of them was not statistically significant (Log-rank p=0.081). The latest NYHA functional class was worse in the patients who did not covert to sinus rhythm (AF group) than who did (SR group)(1.4±0.5 vs 1.1±0.3, p<0.001). The systolic and diastolic diameter of left ventricle gradually enlarged in AF group, which became significant difference during the long-term period.
Conclusions: Maze procedure can improve long-term survival, rate of freedom from stroke and cardiac function in the patients with degenerative mitral regurgitation with chronic atrial fibrillation.
Abstract 18633: Prevalemce and Clinical Outcomes of Stent Fracture and Stent Recoil After Drug-eluting Stent Implantation at the Right Coronary Artery Ostial Site at Mid and Late Term
Authors: Ozaki Masatomo , Kadota Kazushige , Goto Tsuyoshi , Fujii Satoki , Yamamoto Hiroyuki , Kato Harumi , Oka Naoki , Fuku Yasushi , Hirono Akitoshi , Maruo Takeshi , Tanaka Hiroyuki , Tada Takeshi , Habara Seiji , Shigemoto Yoshikazu , Hasegawa Daiji , Tasaka Hiroshi , Okamoto Yoji , Otsuru Suguru , Saito Naoki , Hayakawa Yuki , Ohashi Noriyuki , Miyake Koshi , Eguchi Haruki , Yoshino Mitsuru , Hyodo Yusuke , Kubo Syunsuke , Ichinohe Tahei , Amano Hideo , Izawa Yu , Nakamura Michitaka , Mitsudo Kazuaki 
Published: April 2024

Background: After stent implantation at the right coronary artery (RCA) ostial site, in-stent restenosis (ISR) often occurs and target lesion revascularization (TLR) is required. But at the RCA ostial site, the impact of stent fracture(SF) or stent recoil(SR) on midterm and especially late term restenosis is unknown.
Methods: From March 2004 to June 2010, 129 RCA ostial sites were successfully treated with 3 types of drug-eluting stent: sirolimus-eluting stent (SES), n=74; paclitaxel-eluting stent (PES), 39; everolimus-eluting stent (EES), 16. Mid and late term follow-up coronary angiography(CAG) was performed at 8 months and after 20 months. And SF and SR were assessed. We defined SF as apparent strut separation and SR as axial recoil less than 80% in the stent diameter, both analyzed by coronary angiography.
Results: We found 41 SF lesions (31.8%) and 24 SR lesions (18.6%) at the 8months follow up CAG. Out of the 102 patients without ISR at the 8months CAG, we were able to follow up 86 patients until the late term. The data of ISR and TLR at 8month and ISR at late term are shown in the table.
Conclusion: At the RCA ostial site, SF and SR have an effect on the ISR and TLR at 8month. Furthermore SF and SR have impact on late term ISR consecutively.
Abstract 18696: Feasibility of Transcatheter Closure of Secundum Atrial Septal Defect with Deficient Rims Other than the Antero Superior
Authors: Fraisse Alain , Kammache Issam , Assaidi Anass , Aldebert Philippe , Mancini Julien , Habib Gilbert 
Published: April 2024

Introduction. Transcatheter closure of secundum atrial septal defect (ASD) with deficient rims is usually contraindicated except in cases with a deficient antero-superior rim in whom percutaneous closure is well demonstrated. Our goal was to assess the feasibility of transcatheter closure for secundum ASD with deficient rims (<5 mm) other than the antero-superior.
Method. Between January 1st, 2008 and december 31, 2011, 192 patients underwent percutaneous closure of ASD in our institution under transesophageal echocardiography guidance in children and intracardiac echocardiography guidance in adults. Amplatzer devices (Amplatzer Septal Occluder or Cribriform) were used in 191 whereas one case without deficient rim was closed with intrasept ASD occluder. We retrospectively analyzed the outcomes of the 43 patients (22.4%, 26 children) with one or more deficient rim.
Results.The median age and weight was 16(1.1 to 85) years and 56(8.8 to 99)Kg, respectively. Deficiency of the inferior (toward the AV valves, n= 11), inferior- posterior (toward the inferior vena cava, n=15), and the superior -posterior rim (toward the superior vena cava, n= 17) was confirmed by transesophageal echocardiography in all the cases. Transcatheter closure was successfully accomplished in 37 (86%) of the cases with a median device size of 28(10 to 40) mm. A modified method of implantation (sizing balloon technique) was used in 30 patients (70%).In 6 patients (5 children) the ASD could not be closed. Four children experienced device embolization few hours after successful transcatheter closure and underwent surgical ASD closure without further complication. By Fisher’s exact test, deficiency of the inferior-posterior rim was associated with failure or embolization(p = 0.05)and there was a trend for adult age to be associated with a low risk of embolization or failure (p= 0,06).
Conclusion. Transcatheter closure of secundum ASD is feasible in patients with deficient rims. However, this cannot be recommended because of an intolerable rate of embolization. Possibly, transcatheter closure of such secundum ASDs with deficient rims may be more successful in the adult population.
Abstract 19023: Distinct Remodeling of Mitral Valve Leaflets in Severe Myxomatous and Ischemic Mitral Regurgitation
Authors: Absi Tarek S , Galindo Cristi L , Petracek Michael R , Lenihan Daniel J , Leacche Marzia , Sawyer Douglas B , Byrne John G , Su Yan Ru 
Published: April 2024

OBJECTIVES: The mitral valve (MV) leaflets in severe MR undergo structural remodeling associated with multiple degenerative and adaptive changes. We hypothesized that the gene expression profiles of MV leaflets from patients with severe myxomatous MR (MMR) are distinct from those with severe ischemic MR (IMR), reflecting different underlying pathophysiologic processes.
METHODS: MVs were obtained from 11 MMR patients (9 m, 2 f; age= 60.5±11.9 y, LVEF=58.2±4.6%) and 6 IMR patients (3 m, 3 f, age= 66.5±6.7 y, LVEF=33.3±16.3%) undergoing surgery for severe MR. Hemodynamic abnormalities were similar in the two groups. Tissue RNA was extracted and cDNA were hybridized to the Affymetrix Gene Chip 1.1. Normalization and two-way ANOVA analysis were performed by Partek Genomics Suite. Only genes that resulted in >1.5 fold difference and p <0.05 were considered significantly altered.
RESULTS: Of ∼29,000 genes examined, 453 (1.6%) were differentially expressed between the two groups. Hierarchical clustering of the normalized fluorescence signal values for these genes successfully differentiated all the MMR from the IMR samples (Figure 1). Based on functional analysis, the most statistically enriched biological processes were development (MYH11, ACTA2, ECM1, MMP19), cell growth (IGF1, IGFBP3, ADAMTSL2), adhesion (MCAM, PCDH10, COL4A1) and metabolic processes (ACOT7, CYP4A11) as shown in Table 1.
CONCLUSIONS: MV leaflets in severe MMR and IMR exhibit distinct gene expression patterns, suggesting different pathophysiologic mechanisms are involved in the leaflet remodeling processes. Understanding such adaptive mechanisms can potentially provide therapeutic opportunities.
Abstract 19375: Does Pulmonary Vascular Remodeling Reverse after Restrictive Mitral Annuloplasty in Patients with End-Stage Heart Failure?
Authors: Kainuma Satoshi , Taniguchi Kazuhiro , Toda Koichi , Funatsu Toshihiro , Miyagawa Shigeru , Kondoh Haruhiko , Daimon Takashi , Masai Takafumi , Ueno Takayoshi , Kuratani Toru , Sawa Yoshiki 
Published: April 2024

Background. Prognostic importance of pulmonary hypertension (PH) in patients with heart failure is well known, but its reversibility after restrictive mitral annuloplasty (RMA) is less well established. We assessed the potential reversibility of pulmonary vascular remodeling in relation to plasma B-type natriuretic peptide (BNP), a biomarker of left ventricular (LV) filling pressure and diastolic dysfunction, over time after RMA.
Methods. We studied 98 patients with moderate to severe PH [systolic pulmonary artery pressure (SPAP) >40 mmHg] who underwent RMA for ischemic cardiomyopathy (ejection fraction <40%) and functional mitral regurgitation, and were followed up at least 12 months (mean, 49±26 months). Cardiac catheterization (baseline, 1month) and serial assessments of Doppler-derived SPAP (d-SPAP) and LV end-systolic dimension (ESD), with blood samples for plasma BNP measurement were performed.
Results. At 1 month after RMA, pulmonary capillary wedge pressure (PCWP) and SPAP decreased from 22±7 to 16±6 mmHg and from 50±13 to 40±11 mmHg (p<0.0001 for both), respectively, while transpulmonary gradient (mean PAP minus PCWP) did not change (11±4 mmHg, p=0.56). Cardiac index increased from 2.5±0.6 to 2.7±0.6 l/min/m2 (p= 0.03), and pulmonary vascular resistance changed from 231±100 to 206±73 dynes sec cm-5 (p=0.03), suggesting partial reversibility of pulmonary vascular remodeling. Serial echocardiography showed that s d-SPAP changed from 55±14 at baseline to 37±11 at 1 month, to 40±14 at 1 year, and to 45±19 mmHg at 2 year (p<0.0001). LVESD decreased from 56±8 to 49±9, 48±10, and 48±10 mm, respectively (p<0.0001). Plasma BNP decreased from 741±372 to 283±234, 223±199, and 237±208 pg/ml, respectively (p<0.0001). The percent change from baseline to 1 month and 1 year in BNP were significantly associated with corresponding changes in the d-SPAP (r=0.314, p=0.009 and r=0.391, p=0.006, respectively).
Conclusion. Following RMA, PA pressures commonly and significantly decreased, with a modest reverse pulmonary vascular remodeling in most patients after 2 years follow-up. Progression of pulmonary vascular abnormality may be a potential therapeutic target to reduce the prevalence of subsequent right ventricular dysfunction after RMA.
Abstract 19631: MicroRNAs Modulation in a Mice Model of Physiological Left Ventricular Hypertrophy
Authors: Martinelli Nidiane C , Cohen Carolina R , Schneider Stefanie , Schneider Stefanie , Dos Santos Katia , Andrades Michael E , Clausell Nadine , Biolo Andreia , Rohde Luis E 
Published: April 2024

INTRODUCTION: Physiological left ventricular hypertrophy (LVH) has distinct phenotypic adaptations that might me modulated by microRNAs (miRs) which are fine-tune regulators of gene expression. We tested the hypothesis that physiological LVH has differential miRs expression in mice subjected to a voluntary exercise protocol.
METHODS: Balb/c mice were kept in cages with exercising wheels (Exercise group - EXE; n=15 sacrificed on day 7 and n=17 sacrificed 35 days after training) or in cages without wheels (Sedentary group - SED; n=12 in each time point). LVH was evaluated by the left ventricular weight/body weight ratio (LVW/BW). MiRs were extracted with miRNeasy kit (Qiagen, USA). A microRNA microarray based on the miRBase version 16 (LC Sciences, Houston, Texas, EUA) was carried out using a pool of miRs extracted from the LV. After miR extraction, 50 pM of synthetic cel-miR-39 were spiked-in as a standard control. RT-qPCR was performed with microRNA Reverse Transcription Kit® and TaqMan Probes® (Applied Biosystems Inc., USA).
RESULTS: After 7 days of training there was an increase of 7% in LVW/BW ratio on EXE compared to SED group (3.6±0.2 vs. 3.3±0.1, respectively; p=0.004) and this result was sustained at 35 days (12% increase; 3.7±0.2 vs. 3.3±0.1, respectively; p<0.001). 7 DAYS analyses: expression of miR-26b and miR-143 was decreased in the EXE compared to the SED group (0.5-fold, p=0.017 and 0.7-fold, p=0.018, respectively). miR-150 showed an increased expression in the EXE group (3.0-fold, p=0.001). 35 DAYS analyses: expression of miR-27a was down-regulated (0.8-fold, p=0.03), while miR-150 was up-regulated (1.9-fold, p=0.016) in the EXE group. miRs previously described to be involved in cardiovascular diseases (miR-21, miR-195 and miR-499) were similar between groups.
CONCLUSIONS: Our data suggest that physiological LVH was associated to significant modulation of miRs that might regulate affect metabolic adaptations (miR-26b:GSK3B) and apoptosis pathway activation (miR-150:FOXO4). Also miRs could have an effect on cellular growth and hypertrophy (miR-27a:IGF1 and miR-143:MTPN).
Abstract 220: Intralipid Fails to Rescue Bupivacaine-Induced Cardiotoxicity in the Presence of the Opioid Antagonist Naloxone
Authors: Partownavid Parisa , Umar Soban , Rahman Siamak , Sharma Salil , Eghbali Mansoureh 
Published: April 2024

Introduction: Exogenous opioids such as morphine protect the heart against I/R injury. This action is mediated through opioid receptors as Naloxone, an opioid receptor antagonist, inhibits the cardioprotective effect of ischemic preconditioning. Here we explored the involvement of opioid receptors in lipid-mediated rescue of Bupivacaine-induced cardiac toxicity.
Methods: Young male SD rats (300-350 g) were anesthetized with ketamine (80 mg/kg) and xylazine (8 mg/kg) and ventilated with a ventilator. The M-mode echocardiography and Electrocardiograms were acquired throughout the experiment. Asystole was achieved with a single injection of Bupivacaine (10mg/kg over 20 s, intravenously), and resuscitation with Intralipid (5ml/kg bolus, and 0.5ml/kg/min maintenance) along with cardiac massage was started immediately. Some rats were pre-treated with different doses of Naloxone (1 mg/kg, 10 µg/kg, 5 µg/kg and 1 µg/kg) 2 min prior to inducing asystole with Bupivacaine.
Results: Administration of Bupivacaine resulted in asystole and Intralipid therapy improved the heart rate gradually within 10 min: 73.3±3.3 beats/min at 1min (23% recovery), 180±23 beats/min at 5 min (56% recovery), and 243±20 beats/min at 10 min (76% recovery, n=6). The left ventricular systolic function was also fully recovered in all rats within 5 min of lipid treatment as the ejection fraction (EF) and fractional shortening (FS) were similar to their baseline values (EF=70±3%, FS=40±3%, n=6)., Interestingly, Intralipid failed to rescue Bupivacaine overdose in rats pretreated with a high dose of Naloxone (1mg/kg) as there was no recovery of cardiac function within 10 min of lipid therapy (n=5). In rats pretreated with lower doses of Naloxone of 5 µg /kg and 10 µg /kg (n=4/group), the heart rate and cardiac function were partially recovered. Lowering the dose of Naloxone further to 1 µg /kg resulted in 76% recovery of the heart rate at 10 min. Complete recovery of the left ventricular systolic function was observed in this group within 10 min of lipid treatment as EF and FS were similar to their baseline values (EF= 73±3%, FS=43±3, n=4). .
Conclusions: The opioid receptor antagonist Naloxone abolishes lipid rescue of Bupivacaine-induced cardiotoxicity in a dose-dependent manner.