bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract 69: Evaluation Of Abdominal Blood Flow During Chest Compression In Cardiac Arrest Patients Using Enhanced Computed Tomography (CT)
Authors: Oode Yasumasa , Shimizu Kentarou , Matsushima Asako , Kajino Kentarou , Nakagawa Yuukou , Tasaki Osamu , Shiozaki Tadahiko , Ogura Hiroshi , Kuwagata Yasuyuki , Tanaka Hiroshi , Shimazu Takeshi , Sugimoto Hisashi
Published: July 2021

Background: The mechanism of blood flow during chest compression in cardiac arrest patients remains under investigation. We often experience that cardiac arrest patients suffer severe diarrhea after successful cardiopulmonary resuscitation(CPR), which would be attributable to intestinal ischaemia during cardiac arrest and resuscitation. However, few studies have been made to evaluate abdominal blood flow during chest compression in cardiac arrest patients.

Patients and Methods: The study was made in four patients immediately after termination of cardiopulmonary resuscitation. A 100ml bolus of 300 mgI/ml contrast medium was injected from a short femoral vein catheter, followed by continuous chest compression at a rate 100/min. In order to evaluate the distribution of contrast medium, CT images of the chest and abdomen were taken after 100 and/or 200 chest compressions, respectively.

Results: CT scans showed similar enhance patterns in the patients. After 100 chest compressions, enhancement values were higher at inferior vena cava(IVC) regions compared to ascending aorta and main arteries. After 200 compressions, enhancement values of the arteries were increased by two to four times. However, significant enhancement of hepatic veins and limited enhancement of portal veins suggest impaired perfusion of the liver and the bowel.

Conclusion: One hundred or 200 chest consecutive compressions are not sufficient to enhance abdominal organs including the liver and bowel.

Figures:

Typical MPR(Multiplanar reconstruction) images after 100compressions at two different coronal planes; hepatic vein and IVC(left), portal veins(right) are depicted.
Abstract 73: Rapid Whole Body Cooling in Large Swine: Effects on Heart Rate and Arterial Blood Pressure
Authors: Ohley William , Schock Robert B , Klock Cathy , Schofield Lorraine , Cote Marc , Freedman Robert
Published: July 2021

There have been recent reports of a variety of cooling methods for reducing the body temperature of victims of post resuscitative syndrome. In the work reported here we cooled a series of large (> 60 kg) domestic swine (n=6) using a whole body approach. The animals were anesthetized using propofol and buprinorphine and instrumented with arterial pressure monitoring and ECG, and thermocouple sensors in the pulmonary artery (PA), carotid artery, tympanic membrane and esophagus. With an initial average PA temperature at 37 (± 0.3) °C, the swine underwent a rapid cooling sequence. This was performed with a flexible surround suit system that provided for a thin 0.5 cm layer of circulating ice water in direct skin contact held between 0.5° and 1.5 °C. A pumping system was used to circulate the water volume of 20 liters at a rate of 15 liters per minute. The average PA temperature at the start was 37 (±0.3) °C. Cooling was targeted at 34 °C with an average value of 34.1 (±0.3) °C. Time to fall 3°C was13.0 (±3.0) min. At the same time, heart rate dropped (although not significantly) from 71 ± 7.9 BPM to 59.5 ± 11.4 BPM while mean carotid pressure dropped from 100.3 ± 16 mmHg to 77.3 ± 14.9 mmHg (p<.05). We interpret these changes as beneficial reductions in cardiac work while the subject is kept cool. It is hypothesized that this is due to a reduction in total body metabolic demands. Thus it is possible, in addition to positive neurological effects, that the process of rapid whole body cooling also may be effective in reducing total workload seen by the heart, and thus may aid in salvaging myocardium in such patients.
Abstract 87: Cyclosporin A does not Prevent Myocardial Dysfunction after Resuscitation from Cardiac Arrest in Rats
Authors: Ayoub Iyad M , Radhakrishnan Jeejabai , Gazmuri Raúl J
Published: July 2021

Objective:
We have previously reported in a rat model of VF and closed-chest resuscitation that cytochrome
c
is released into the bloodstream after resuscitation from cardiac arrest attaining plasma levels inversely proportional to survival. Recent evidence indicates that release of cytochrome
c
during ischemia and reperfusion may be a manifestation of prolonged opening of the mitochondrial permeability transition pore (mPTP). In this study, we investigated whether cyclosporin A (CsA, an inhibitor of mPTP opening) can prevent post-resuscitation (PR) myocardial dysfunction and improve survival.

Methods:
VF was electrically induced and left untreated for 10 mins. Resuscitation was attempted by 8 mins of chest compression followed by biphasic waveform defibrillation. Rats were randomized to received a bolus CsA (10 mg/kg) five minutes before inducing VF (n=6), immediately before starting chest compression (n=6), or to receive vehicle control before inducing VF (n=3) or before starting chest compression (n=3). CsA-treated (n=12) and vehicle-treated (n=6) rats were pooled for this analysis after noticing no differences between subgroups. Resuscitated rats were monitored for up to 6 hours.

Results:
All rats were successfully resuscitated. Treatment with CsA did not improve PR myocardial function (Table

). Survival time was comparable between CsA-treated (321±67 mins) and vehicle-treated (331±67 mins) rats.

Conclusions:
In our rat model of VF and resuscitation, CsA failed to prevent PR myocardial dysfunction and improve survival. These data contrast with numerous studies demonstrating a protective effect in isolated heart models of ischemia and reperfusion. Two possible explanations are

the mPTP does not open in this unique setting of cardiac arrest and resuscitation, and

the optimal
in vivo
dose of CsA needs to be determined as the protective effects of CsA are dose dependent.

Hemodynamic and Left Ventricular Function
Abstract 115: Relationship of Body Mass Index (BMI) to Minimum Distance from Skin Surface to Myocardium: Implications for Neuromuscular Incapacitating Devices (NMID)
Authors: Bashian Gregory G , Wagner Gabriel A , Wallick Don W , Tchou Patrick J
Published: July 2021

Introduction

: It is controversial whether NMIDs can induce cardiac arrhythmias in humans. Studies in swine models have shown varying results. Two reported no induced VF, while a third showed 1 case of induced VF during epinephrine infusion. Two studies showed site sensitivity of cardiac capture depending on location of NMID electrodes. Human studies have not shown any induced arrhythmias. However, it is unclear whether electrodes were placed at the most vulnerable regions of the chest. This study sought to assess the thoracic location and range of minimum skin-to-heart distances (mSHD) and its relationship to BMI.

Methods

: Forty-five patients who had undergone cardiac CT scans were randomly selected for evaluation. These scans were analyzed to determine the mSHD and the location of this point on the chest surface relative to anatomic landmarks (horizontal distance from midsternum and vertical distance from sternal insertion of the lowest left rib). Linear regression analysis was performed using BMI and mSHD.

Results

: mSHD ranged from 1.8 cm to 6.4 cm. FIGURE 1

shows the linear regression of mSHD vs. BMI. mSHD was to the left of mid sternum (2.5 ± 2.5 cm) and slightly inferior (0.5 ± 2.0 cm) to the lowest left rib sternal insertion. The area of myocardial contact with the anterior chest wall averaged 51 ± 25 cm
2
, and was unrelated to BMI.

Conclusions

: In this study of adults, the average location of the site of mSHD was slightly to the left of mid sternum and just below the lowest rib insertion. There is a linear relationship between BMI and mSHD. The size of a person and the anatomic relationship of the heart to the anterior chest wall can influence the potential cardiac capture by NMIDs at the site of mSHD.

Figure 1:

mSHD vs. BMI
Abstract 537: Sildenafil Suppresses Cardiac Hypertrophy through Inhibition of Canonical Transient Receptor Potential Cation Channel 6 Expression in Cardiac Myocytes
Authors: Koitabashi Norimichi , Zhang Manling , Takimoto Eiki , Nagayama Takahiro , Kass David A
Published: July 2021

Background:
We have shown that a phosphodiesterase 5A (PDE5A) inhibitor, sildenafil blocks cardiac pathological hypertrophy through inhibition of Gαq mediated signaling and calcineurin (Cn) signaling. However, the precise molecular mechanism is still unknown. Recently canonical transient receptor potential cation channel 6 (TRPC6) and its up-regulation have been shown to play a critical role for Gαq-mediated Cn activation in pathogenesis of cardiac hypertrophy. Therefore, we hypothesized that PDE5A inhibition blocks TRPC6 gene induction in cardiac myocytes and thus prevents cardiac hypertrophy.

Methods and Results:
We examined TRPC6 expression levels using real-time RT-PCR in hypertrophied mouse heart created by transverse aortic constriction (TAC). TRPC6 mRNA expression was significantly increased after TAC. Sildenafil effectively attenuated TAC-induced hypertrophy, Cn protein level and upregulation of TRPC6 mRNA. To investigate role of TRPC6 in sildenafil’s anti-hypertrophic effects, we studied cultured adult mouse cardiac myocytes (AMCM) and neonatal rat cardiac myocytes (NRCM). Stimulation with Endothelin 1 (ET1) or angiotensin II (AngII) increased cell surface area, leucine uptake, Cn protein expression and TRPC6 gene expression. Sildenafil dose-dependently blocked these increases. 8-bromo cGMP also blocked TRPC6 induction by ET1 and AngII. In addition, 8-bromo cGMP stimulation following adenovirus-mediated overexpression of cGMP-dependent protein kinase I-α (PKG) showed a marked decrease in TRPC6 expression. These results suggest that PKG activation regulates TRPC6 gene in cardiac myocytes. Using adenovirus-based expression of artificial PDE5A-gene silencing miRNA, PDE5 protein was effectively knocked down both in NRCM and AMCM. Importantly, PDE5-miRNA completely blocked ET1-mediated increase of Cn and TRPC6 same as sildenafil.

Conclusion:
Sildenafil effectively blocks TRPC6 induction both
in vivo
and
in vitro
. TRPC6 gene regulation is PKG and PDE5A dependent in cardiac myocytes. Given that TRPC6 induction triggers Gαq-mediated maladaptive signaling, especially Cn, these data show that the inhibition of TRPC6 gene expression contributes to the Gαq-coupled anti-hypertrophic mechanism of sildenafil.
Abstract 555: Heme-Oxygenase 1 Upregulation Attenuates Acute Myocardial Reperfusion Injury and Left Ventricular Remodeling in Rats
Authors: Tee Rebecca E
Published: July 2021

Background:
Reperfusion injury occurring after reestablishment of blood flow after MI is thought to be mediated by reactive oxygen species and neutrophilic cellular damage. The Heme-Oxygenase-1 (HO-1) dependent decrease in oxidative stress may attenuate injury in part by inhibiting transcription factor NFκB-mediated inflammation. We tested the hypothesis that exogenous upregulation of HO-1 by hemin administration confers acute and chronic cardioprotection against I/R injury in rats and attenuates LV remodeling post-infarction.

Methods:
Six week-old male Wistar rats were randomly assigned to sham, vehicle, or hemin-treated groups. Vehicle and hemin were administered i.p. once daily for 3 days prior to LAD occlusion, and 48 hours post-operatively once every 3 days. Infarct size was determined by H&E histological analysis and fibrosis was quantified by Masson’s Trichrome staining. We used transthoracic echocardiography to assess LV size, function and wall motion.

Results:
Hemin increased HO-1 expression and decreased infarct size and fibrosis, and attenuated LV wall thinning and chamber dilatation in the short-term (4 days post-infarction). The decrease in infarct size and fibrosis in the hemin group was accompanied by a decrease in NF-κB activity. We observed no significant difference in infarct size and area of fibrosis between hemin and vehicle-treated groups at 3 months (p=0.6681, p=0.6382, respectively). Cavity dilatation did not differ between the two groups at 3 months, however attenuated interventricular septum thinning (p<0.05) was observed in the hemin group compared with the vehicle group.

Conclusion:
HO-1 upregulation by hemin confers acute cardioprotection and decreased inflammation, possibly by inhibiting NF-κB activity, although chronic treatment with hemin does not prevent long-term LV remodeling post-MI. Future research should focus on optimal HO-1 upregulation to attenuate long-term LV remodeling due to reperfusion injury.

Left Ventricle Wall and Chamber Dimensions
Proapoptotic Kinase Mst1 Restricts Myocyte Hypertrophy by Managing Unfolded Protein Responses
Authors: Usui Soichiro
Published: July 2021

Abstract 288

Soichiro Usui, Chull Hong, Shumin Gao, Junichi Sasoshima, UMDNJ New Jersey Medical School, Newark, NJ

Soichiro Usui, 2007 Finalist and Presenting Author
A Typology of Heart Failure Self-Care Management
Authors: Dickson Victoria V
Published: July 2021

Abstract 1730

Victoria V Dickson, Janet Deatrick, Barbara Riegel, University of Pennsylvania, Philadelphia, PA

Victoria V Dickson, 2007 Finalist and Presenting Author
Prevalence and Progression of Subclinical Atherosclerosis in Younger Adults with Low 10-Year Risk but High Lifetime Risk for Cardiovascular Disease: Findings from the CARDIA and MESA Studies
Authors: Berry Jarett D
Published: July 2021

Abstract 3482

Jarett D Berry, Kiang Liu, Northwestern University, Chicago, IL; Aaron R Folsom, University of Minnesota, Minneapolis, MN; Joseph F Polak, Tufts University, Boston, MA; Cora E Lewis, University of Alabama at Birmingham, Birmingham, AL; Steven Shea, Columbia University, New York City, NY; Stephen Sidney, Kaiser Permanente, Oakland, CA; J Jeffrey Carr, Wake Forest University, Winston-Salem, NC; Daniel H O’Leary, Tufts University, Boston, MA; Cheeling Chan, Donald M Lloyd-Jones, Northwestern University, Chicago, IL

Jarett D Berry, 2007 Finalist and Presenting Author
Age-Related Differences in Left Ventricular Structure and Function: The Multi-Ethnic Study of Atherosclerosis
Authors: Cheng Susan
Published: July 2021

Abstract 1752

Susan Cheng, Brigham and Women’s Hospital, Boston, MA; Veronica R Fernandes, David A Bluemke, Joao A Lima, Johns Hopkins University, Baltimore, MD

Susan Cheng, 2007 Finalist and Presenting Author
Chest Pain in an 89-Year-Old Man: A Different Kind of Broken Heart
Authors: Smith Charles S
Published: July 2021

Abstract 1760

Charles S Smith, Yerem Yeghiazarians, Nelson B Schiller, UCSF Medical Center, San Francisco, CA

Charles S Smith, 2007 Finalist and Presenting Author
2008 Thomas W. Smith Memorial Lecture—Protein Kinase C α as a Novel Therapeutic Target for Treating Heart Failure
Authors: Molkentin Jeffrey
Published: July 2021

We have shown that protein kinase C (PKC) α functions as a proximal regulator of Ca
2+
handling in cardiac myocytes (Braz et al,
Nat. Med.
10:248, 2004). Deletion of
PKC
α in the mouse resulted in augmented sarcoplasmic reticulum Ca
2+
loading, enhanced Ca
2+
transients, and augmented contractility, whereas overexpression of PKCα in the heart blunted contractility. Mechanistically, PKCα regulates Ca
2+
handling by altering inhibitor-1 phosphorylation, which suppresses protein phosphatase-1 activity, thus modulating phospholamban activity and sarcoplasmic reticulum Ca
2+
AT-Pase 2 (SERCA2). Acute inhibition of PKCα with the pharmacologic agents Ro-32-0432 or Ro-31-8220 significantly augmented cardiac contractility in vivo or in an isolated work performing heart preparation in wild-type mice, but not in
PKC
α-deficient mice. Ro-32-0432 also acutely increased cardiac contractility in two different models of heart failure in vivo. Moreover, acute or chronic treatment with Ro-32-8220 in a mouse model of heart failure, due to deletion of the
muscle lim protein
(MLP) gene, significantly augmented cardiac contractility and restored normal pump function. Adenoviral-mediated gene therapy with a dominant negative PKCα cDNA rescued heart failure in a chronic rat model of postinfarction cardiomyopathy. Moreover, expression of dominant-negative PKCα in cardiac myocytes using a cardiac-specific transgenic system (tetracycline-regulated) also enhanced cardiac contractility and antagonized heart failure due to myocardial infarction injury. Finally, another PKCα/β inhibitor, ruboxistaurin (LY333531), antagonized heart failure after long-term pressure overload in mice. PKCα is the dominant conventional PKC isoform expressed in the adult human heart, providing potential relevance of these findings to human pathophysiology. Indeed, pharmacological inhibition of PKCα may serve as a novel therapeutic strategy for either enhancing cardiac contractility in the setting of severe functional deterioration or as a long-term treatment option to prevent worsening of heart failure in earlier stages.
Differential Effect of Wall Tension on Matrix Metalloproteinase Promoter Activation in the Thoracic Aorta
Authors: Ruddy Jean Marie
Published: July 2021

Abstract 1102

Jean Marie Ruddy, Jeffrey A Jones, Rupak Mukherjee, Francis G Spinale, John S Ikonomidis, MUSC, Charleston, SC

Jean Marie Ruddy, 2008 Finalist and Presenting Author
Increased Red Blood Cell Distribution Width Is Associated With Greater Risk of All-Cause, Cardiovascular and Non-Cardiovascular Mortality in a Large Community-Based Cohort
Authors: Perlstein Todd
Published: July 2021

Abstract 1253

Todd S Perlstein, Brigham and Women’s Hosp, Boston, MA; Jennifer Weuve, Harvard Sch of Public Health, Boston, MA; Marc A Pfeffer, Joshua A Beckman, Brigham and Women’s Hosp, Boston, MA

Todd Perlstein, 2008 Finalist and Presenting Author
Abstract 5783: Abnormal Regional Right Ventricular Diastolic Mechanics in Hypertrophic Cardiomyopathy Despite Preserved Systolic Mechanics
Authors: Pinheiro Aurelio C , Dimaano Veronica L , Eulitt Patrick , Abraham Jacob , Corretti Mary , Abraham Theodore P
Published: July 2021

BACKGROUND. Hypertrophic cardiomyopathy (HCM) is an inherited cardiomyopathy with left ventricular (LV) hypertrophy and preserved EF. However, there is little if any information on right ventricular (RV) involvement. We used conventional (ECHO) and strain echocardiography (SE) to examine RV morphology and mechanics in 50 consecutive HCM patients compared to 26 controls.

METHODS/RESULTS. HCM patients were normotensive with asymmetric septal hypertrophy (septal/posterior wall thickness ratio >.5) and SAM with no evidence of other infiltrative cardiomyopathies and pulmonary hypertension. Standard ECHO views and narrow sector, high frame rate (~200 fps) SE images of the RV free wall were obtained. All SE analysis was performed at the basal level of the RV free wall. Acceptable quality images were available in all subjects. RV morphology and function by ECHO was similar in both groups except for higher LVEF and thicker RV free wall in HCM. Despite similar regional systolic mechanics, eSR was significantly lower (p = 0.009) and there was a trend towards lower e′ velocity (p=0.06) in HCM compared to controls (Table

+Figure

).

CONCLUSIONS. In an unselected cohort of consecutive HCM patients, we found significantly abnormal regional RV diastolic mechanics with RV hypertrophy. This is a previously unreported functional abnormality in HCM with potential diagnostic and prognostic implications.

Conventional and strain echocardiography parameters in Control and HCM patients.
Abstract 5818: Stress Thallium-201/Rest Tc-99m Sequential Dual Isotope High-Speed Myocardial Perfusion Imaging
Authors: Berman Daniel S , Hayes Sean W , Wolak Arik , Kang Xingping , Thomson Louise E , Kite Faith , Cohen Ishac , Slomka Piotr J , Friedman John D
Published: July 2021

Recent advances in gamma camera technology are providing opportunities for novel high-speed myocardial perfusion imaging (HS-MPI) protocols. We aimed to develop and evaluate a stress thallium-201 (Tl-201) and rest Tc-99m sestamibi or tetrofosmin imaging protocol that could reduce imaging time and radiation burden.

Methods: We studied 410 consecutive patients undergoing exercise or pharmacologic low-dose stress Tl-201 HS-MPI (4 min/acquisition) in the semi-upright and supine positions (D-SPECT, Spectrum-Dynamics) followed by rest Tc-99m sestamibi (n= 139) or tetrofosmin (n= 271) with immediate post-injection rest imaging. Of 330 patients with no known coronary artery disease (CAD), 29 patients also underwent invasive coronary angiography (ICA) or coronary computed tomography angiography (CCTA) within a three month period and 36 had a < 5% pre-test likelihood of CAD (LLk). Despite low injected doses [Tl-201 (2.2± 0.3 mCi) and Tc-99m sestamibi or tetrofosmin (8.9± 2.4 mCi), the 3 acquisition MPI protocol (2 stress/1 rest) was accomplished < 20 minutes. The quality of stress and resting image was good to excellent in >96% of cases; importantly, no or minor extracardiac activity was seen on 99% of stress and 93% of rest images. HS-MPI was nondiagnostic or uninterpretable in only 2/410 patients. In the 29 patients with CCTA or ICA, the sensitivity and specificity for the detection of ≥70% stenosis were 73% and 89%, respectively, and in 15 patients with ICA, the sensitivity was 89%. The normalcy rate in the LLk group was 100%. A fast stress Tl-201/rest Tc-99m HS-MPI protocol offers promise as a time-efficient, low radiation dose method, in which the superior qualities of Tl-201 for stress imaging and of Tc-99m agents for rest imaging can be utilized.
Abstract 5822: Atherosclerotic Plaque Inflammation Synchronize With Inflammatory Activity OF Visceral Fat
Authors: Kim Eung Ju , Seo Hong Seog , Kim Sungeun , Na Jin Oh , Park Jae Hyoung , Choi Cheol Ung , Lim Hong Euy , Kim Jin Won , Rha Seung-Woon , Park Chang Gyu , Oh Dong Joo
Published: July 2021

Background:
Visceral adipose tissue is thought to confer increased cardiovascular risk through leukocyte infiltration and increased adipose macrophage activity. Previous positron emission tomography (PET) studies using fluorodeoxyglucose (FDG) demonstrated that increased FDG uptake could reflect the severity of inflammation in atherosclerotic plaque. We hypothesized that active atherosclerotic change in the major arteries would accompany increased inflammation within visceral fat and it could be detected in humans using combined FDG PET/computed tomography (CT).

Methods:
We observed 44 consecutive subjects with cardiovascular disease. For all of them, an one-hour PET/CT (from brain to foot) was performed after injection of FDG (370–555 MBq). FDG uptake in the aorta or its major branches was evaluated visually and semiquantitatively. Maximal standard uptake values (SUV) of the highest regions of interest were calculated in the subcutaneous fat and visceral fat area, separately.

Results:
Significant FDG uptake in the arterial wall was noted in 21 patients (plaque positive; PP group), all of whom have experienced acute cardiovascular events (acute coronary syndrome or ischemic stroke) within a week. The other 23 patients (plaque negative; PN group) had chronic stable angina or asymptomatic carotid stenosis. Visceral fat SUV was significantly higher as compared to subcutaneous fat SUV (0.49± 0.15 vs. 0.15± 0.05, p< 0.001) in PP group, whereas there was no significant difference in PN group (0.18± 0.07 vs. 0.16± 0.03, p= 0.622). When we compared two groups, PP group showed higher visceral fat SUV than PN group (p< 0.001). In terms of subcutaneous fat SUV, the results were similar in two groups (p= 0.773).

Conclusions:
We demonstrated that atherosclerotic plaque inflammation was associated with increased inflammation within visceral fat. Our results need to be confirmed by comparison with histologic or other imaging findings. Further evaluation to determine whether metabolic activity of visceral adipose tissue is a marker or mediator of vascular inflammation is also needed.
Abstract 5836: The Effect of Survivor Bias on Surgical Outcomes in Infective Endocarditis
Authors: Sy Raymond , Kritharides Leonard
Published: July 2021

Introduction
Recent studies have demonstrated conflicting results regarding the benefits of surgery in infective endocarditis (IE). In particular, studies have not accounted for potential survivor bias associated with surgery since patients who survive longer have more opportunities to undergo surgery.

Hypothesis
We explored the effect of survivor bias on surgical outcomes in IE.

Methods
We studied 223 consecutive patients admitted with left-sided IE to two centers between 1996–2006. All-cause mortality at one year was compared between medically-treated patients and those undergoing surgery using a Cox proportional-hazards model with adjustment for a patient’s propensity to surgery. To adjust for survivor bias, analyses were repeated with surgery as a time-dependent covariate.

Results
Compared to medically-treated patients (n= 161), patients undergoing surgery (n= 62) had significantly lower mortality at one year (21.0% vs 38.5%, p= 0.017) with an unadjusted hazard ratio of 0.47 (95%CI 0.26–0.86, p= 0.014). However, patients undergoing surgery were significantly younger (46.9± 15.1 yrs vs 57.9± 19.2 yrs, p< 0.001) and had lower Charlson comorbidity scores (0.7± 1.5 vs 1.4± 1.9, p= 0.007), but were more likely to have severe heart failure (NYHA FC III-IV, 27% vs. 12%, p< 0.001). Baseline differences between groups were taken into account by developing a regression model for surgery and assigning a propensity score for surgery to each patient based on this model. Significant predictors of surgery were NYHA class (p< 0.001), aortic valve involvement (p< 0.001), severe regurgitation (p= 0.016), and lower hemoglobin at baseline (p= 0.012). After adjustment for the propensity score, there remained a significant benefit for surgery (hazard ratio 0.24, 95%CI 0.11–0.52, p< 0.001). However, the benefits of surgery were diminished and no longer significant when it was evaluated as a time-dependent covariate (hazard ratio 0.87, 95%CI 0.43–1.78, p= 0.87), suggesting that the apparent benefits of surgery may be related to survivor bias.

Conclusions
Survivor bias may have a significant effect on the evaluation of outcomes associated with surgery in IE and such bias can be reduced with the use of time-dependent covariate analysis.
Abstract 5852: The Impact of Donor-Recipient Gender Pairing On Survival Following Orthotopic Heart Transplantation - An Analysis Of Over 18,000 Matches
Authors: Weiss Eric S , Patel Nishant D , Russell Stuart D , Baumgartner William A , Shah Ashish S , Conte John V
Published: July 2021

Introduction
: Single institution series have suggested that donor-recipient gender matching may be an important factor influencing survival following orthotopic heart transplantation (OHT). The United Network for Organ Sharing (UNOS) database provides a unique and novel opportunity to address this issue by examining outcomes based on gender pairing for a large cohort of OHT patients.

Methods
: We retrospectively reviewed the UNOS dataset to identify 18,240 patients receiving first time OHT between the years 1998 and 2007. Stratification was by both donor and recipient gender so that 4 separate groups were created (male donor with male recipient, female donor with male recipient, male donor with female recipient, and female donor with female recipient). The primary endpoint of all cause mortality was compared between groups using a Cox proportional hazard regression model. Secondary outcomes (thirty day and one year mortality and rejection during the first year) were examined with multiple logistic regression. Post transplant survival was modeled via the Kaplan Meier method.

Results
: Of 18,240 patients, 12,951 (71%) were matched by gender to their donor (77% for male recipients, n= 10,750 and 51% for female recipients n= 2,201). A total of 4,543 patients died during the study period (25%). Donor-recipient gender matching resulted in a reduction in the risk of adjusted cumulative mortality (Hz ratio 0.86 [0.78–0.95], p= 0.003) and the greatest risk for cumulative mortality occurred when pairing a male donor with a female recipient (Hz ratio 1.2 [1.04–1.37], p= 0.01). Thirty day and one year mortality were also significantly decreased by gender pairing (OR 0.75 [0.61–0.95], p= 0.02 for 30 day mortality, and OR 0.8 [0.68–0.93], p= 0.005 for one year mortality). Gender pairing resulted in a 13% decrease in the risk of graft rejection within the first year (OR 0.87 [0.79–0.98], p= 0.02]. Kaplan Meier survival modeling revealed that the greatest cumulative survival occurred when a male recipient received an organ from a male donor (Figure)

Conclusions
: The UNOS dataset has provided a large sample examining donor recipient gender pairing in OHT. Recipients who receive organs for same sex donors have significantly improved short and long term survival.
Abstract 5865: High-density Lipoproteins (HDL) Are Present In Stenotic Aortic Valves And May Protect Them Against Calcification
Authors: Lommi Jaakko I , Kovanen Petri T , Lee-Rueckert Miriam , Kupari Markku , Helske Satu
Published: July 2021

Purpose: The pathogenesis of aortic valve stenosis (AS) is characterized by accumulation of low-density lipoprotein (LDL) cholesterol and inflammatory cells in aortic valves, as well as by marked calcification and bone formation in the affected leaflets. Hitherto, the factors which inhibit aortic valve calcification have remained obscure. We aimed to determine, whether HDL cholesterol particles enter aortic valve leaflets and whether HDL could protect the valves from cholesterol accumulation and calcification.

Methods: Stenotic aortic valves were obtained from 10 AS patients undergoing valve replacement surgery. Non-stenotic control valves (n=10) were collected from cardiac transplantations. The amount and localization of HDL/apolipoprotein (apo) A-I, apoB, apoE, and osteoprotegerin (OPG) were analyzed by immunohistochemistry and computer-assisted morphometry. Myofibroblasts were isolated from aortic valves and their secretion of calcific mediators in response to HDL-stimulation was studied by real-time PCR and ELISA.

Results: Accumulation of HDL/apoA-I was detected in both control and stenotic aortic valves. HDL was detected particularly around calcific deposits in the stenotic valves, in which it was colocalized with apoB and apoE, as well as with OPG. Stimulation of cultured aortic valve myofibroblasts with HDL or apoA-I significantly increased secretion of OPG by these cells (p>0.001), whereas the secretion of RANKL, which counteracts the effects of OPG, remained unchanged.

Conclusions: HDL is present locally in human stenotic aortic valves and induces secretion of OPG in valvular cells in vitro. Since OPG is known to inhibit aortic valve calcification, this mechanism may provide HDL a protective role in AS.
Abstract 5882: Myocardial Contractile Dysfunction in Heart Failure with Preserved Ejection Fraction
Authors: Borlaug Barry A , Lam Carolyn S , Roger Veronique , Rodeheffer Richard J , Redfield Margaret M
Published: July 2021

Background
Patients with heart failure and preserved ejection fraction (HFpEF) have diastolic dysfunction, but are traditionally considered to have normal left ventricular (LV) systolic function. However, ventricular remodeling can result in preservation of EF despite abnormal
myocardial
contractility.

Methods
We performed echo-Doppler characterization of LV chamber and myocardial systolic properties in a population-based study, comparing patients with HFpEF (N=244) to healthy controls (CON, N=617), and hypertensives without HF (HTN, N=719), then examined long term outcome.

Results
All subjects had a normal EF (>50%). However, systolic chamber function, measured by wall stress-corrected endocardial fractional shortening (sc-eFS), was impaired in HFpEF (96±12%) compared to both CON (100±8%, p<0.0001) and HTN (108±11%, p<0.0001). Myocardial contractility, assessed by wall stress-corrected midwall shortening (sc-mFS), was also reduced in HFpEF (91±13%) compared to CON (100±10%, p<0.0001) and HTN (105±12%, p<0.0001). HTN had increased sc-eFS and sc-mFS compared with both HFpEF and CON (p<0.0001). In HFpEF, impaired sc-mFS was associated with increased mortality, independent of age (Figure

), while EF and sc- eFS were not.

Conclusions
Despite preservation of EF, unselected HFpEF patients from the community have significantly impaired systolic chamber function and depressed myocardial contractility. Abnormal myocardial contractility in HFpEF is associated with increased mortality. These data suggest that myocardial systolic dysfunction contributes to the pathophysiology of HFpEF and may represent a potential therapeutic target.
Abstract 5891: Incidence and Prognostic impact of Spontaneous Conversion to Sinus Rhythm in Patients with Permanent Atrial Fibrillation treated with Cardiac Resynchronization Devices
Authors: Gasparini Maurizio , Leclercq Christophe , Arshad Aysha , Regoli François , Rosier Arnaud , Galimberti Paola , Kamath Ganesh , Daubert Claude , Klersy Catherine , Matteo Policlinico S. , Steinberg Jonathan S
Published: July 2021

INTRODUCTION
: Anecdotal reports of spontaneous resumption to stable sinus rhythm (SR) of heart failure (HF) patients with permanent atrial fibrillation (PeAF) after cardiac resynchronization therapy (CRT) have been reported. If this incidence is appreciable, additional interventions may be indicated including placement of an atrial lead.

METHODS:
We retrospectively reviewed patients with PeAF who received CRT devices; standard CRT indications were applied. PeAF was defined as AF present for more than 1 year refractory to any rhythm control efforts. Rhythm was sampled at each follow-up visit, generally every 6 months.

RESULTS:
In total, 345 patients with PeAF were implanted with CRT devices (CRT-D 48%); mean age was 70±9 yrs and mostly male gender (83%). Ischemic HF was present in 154 patients (45%). Mean NYHA class was 3,1±0,5, 6MWT distance 308±113 meters, QRS 156±39 ms, LVEF 28±7%, and LVEDD 65±9 mm. PeAF had been present for 2,1 ± 1.6 years. Over a follow-up of 29 ± 24 months, 34 (9,9%) patients spontaneously reverted to stable (> 3 months) SR. Most SR resumptions occurred within the 1
st
year after CRT (28/34, 82%), but also occured even after 5 years (2/34). Mortality rate was 20,4 for PeAF compared to 2,5 per 100 patients-year for SR resumption (Log Rank p=0.004, see figure

) (HR= 0.13, 95% CI 0.031–0.512, p< 0.0001).

CONCLUSION
: Spontaneous resumption to SR in HF patients with PeAF treated with CRT was observed in roughly 10% of cases, generally within 1 year from implant. SR resumption was associated with a significant 87% reduction of total mortality. Identification of predictors for return of SR may be useful to guide routine atrial lead placement in some patients.
Abstract 5908: Prognostic Significance of Poor Sleep Quality in Patients Referred to a Heart Failure Clinic
Authors: Mathur Gaurav , Goode Kevin , Rigby Alan , Bragadeesh Thanjavur , Cullington Damien , Clark Andrew , Cleland John G
Published: July 2021

PURPOSE
To assess whether poor sleep quality carries prognostic significance for patients with suspected heart failure (HF).

METHODS
Data from patients referred to a HF clinic between July 2001 and October 2006 was analysed in a Cox Regression model to assess the prognostic significance of sleep quality. Patient responses for 3 questions addressing sleep quality (difficulty going to sleep, waking up in the night, and lack of refreshing sleep) were used to generate a sleep quality score (SQS) of 1 (none or minimal sleep impairment, N= 1054); 2 (mild to moderate sleep impairment, N= 908); or 3 (severe sleep impairment, N= 644).

RESULTS
Of 2606 patients, 59% were male. Median age was 72 yrs (Interquartile range (IQR) 65–78). There were 549 deaths during a median follow up of 37.5 months (IQR 26–46.4). Kaplan Meier survival curves showed that SQS 3 was associated with significantly worse prognosis (Figure 1

), and this association persisted despite correction for age, sex, NYHA class, severity of LV systolic dysfunction, BMI, pulse pressure, lab parameters (sodium, creatinine, haemoglobin, NTproBNP, CRP and cholesterol), medication use (loop diuretics, ACE inhibitors, beta-blockers, statins and aldosterone antagonists) and comorbidities (diabetes, hypertension, AF, IHD, COPD and CVA)(Table 1

).

CONCLUSION
Poor sleep quality is an independent prognostic marker in patients referred to a HF clinic.

Cox Regression Analysis: Significant prognostic indicators
Abstract 5921: Medicare Beneficiaries with Mild to Severe Heart Failure See 15–23 Different Providers Annually
Authors: Page Robert L , Hogan Christopher , Strongin Kara , Mills Roger , Lindenfeld JoAnn
Published: July 2021

In fiscal year 2003, Medicare beneficiaries with heart failure (HF) accounted for 37% of all Medicare spending and nearly 50% of all hospital inpatient costs. On average, each beneficiary had 10.3 outpatient and 2 inpatient visits specifically for HF. Despite significant improvements in medical care for HF, mortality and hospital admissions remain high. No data exist regarding the number of providers ordering and providing care for this population. An analysis of fiscal year 2005 Medicare claims was conducted, using a 5% sample standard analytic and denominator file, limited data set version to extrapolate the 34,150,200 Medicare beneficiaries. Three cohorts were defined according to mild, moderate, severe HF employing the Centers for Medicare and Medicaid Services Hierarchical Condition Categories Model and Chronic Care Improvement Program definitions. HMO enrollees, persons without Part A and Part B coverage, and those outside the United States were excluded. We identified physicians by using the unique physician identification number of performing physicians. Based on inclusion criteria, 173,863 beneficiaries were identified. The average number of providers
providing care
in all sites were 15.9, 18.6, 23.1 for beneficiaries with mild, moderate, and severe HF, respectively; and 10.1, 11.5, and 12.1 in the outpatient setting, respectively. The average number of providers
ordering care
in all sites consisted of 8.3, 9.6, and 11.2 for beneficiaries with mild, moderate, and severe HF, respectively; and 6.5,7.3, and 7.8 in the outpatient setting, respectively. For beneficiaries with mild disease, only 10% of all office visits were specifically for HF, while those with moderate or severe disease, only 20% were specifically for HF. Medicare beneficiaries with HF, even those with mild disease, have a large number of providers ordering and providing care. These data highlight the importance for developing systems and processes of coordinated care for this population.
Abstract 5935: Influence of Recent Advances in the Management of Heart Failure and Ventricular Arrhythmias on Survival in Patients with Cardiac Sarcoidosis
Authors: Yazaki Yoshikazu , Horigome Mitsuaki , Aizawa Kazunori , Tomita Takeshi , Kasai Hiroki , Izawa Atsushi , Hongo Minoru , Ikeda Uichi , Sekiguchi Morie
Published: July 2021

Background
: We previously described severity of heart failure and ventricular tachycardia (VT) as independent predictors of mortality in patients with cardiac sarcoidosis (CS). Medical treatment for chronic heart failure has been established over the last few decades. Prophylactic use of implantable cardioverter defibrillator (ICD) and cardiac resynchronization therapy (CRT or CRT-D) have been introduced in patients with severe heart failure. We therefore hypothesized that the prognosis of CS improves due to such advances in the management of heart failure and VT.

Methods
: To confirm our hypothesis, we analyzed 43 CS patients diagnosed between 1988 and 2006 and treated with corticosteroids. We classified two sequential referral patients diagnosed between 1988 and 1997 (n=19) and between 1998 and 2006 (n=24), and compared treatment and prognosis between the two cohorts.

Results
: Left ventricular ejection fraction (LVEF) and dimensions were similar between the two cohorts. Although age in the 1988–1997 referral cohort was significantly younger than that in the 1998–2006 referral cohort (54±14years versus 62±10years, p<0.05), survival in the earlier cohort was significantly worse (log-rank=4.41, p<0.05). The 1- and 5-year mortality rates were 88% and 71% in the 1988–1997 referral cohort, and 96% and 92% in the 1998–2006 referral cohort, respectively. The 1998–2006 referral cohort showed significantly higher incidence of ICD or CRT-D implantation (29% versus 6%, p<0.05), β-blocker use (46% versus 6%, p<0.01) and addition of methotrexate (21% versus 0%, p<0.05), and increased maintenance dose (7.0±1.9mg/day versus 5.0±0.9mg/day, p<0.01) compared to the 1988–1997 referral cohort. Multivariate analysis including age, LVEF, and sustained ventricular tachycardia (sVT) identified diagnosis between 1988 and 1997 (hazard ratio [HR]: 19.8, p<0.01) and LVEF (HR: 0.83/1% increase, p<0.01) as independent predictors of mortality.

Conclusions
: Survival in the recent CS patients is significantly better than previously described. Recent advances in the device therapies and medical treatments including modified immunosuppression alter the clinical outcome in patients with CS.
Abstract 5939: Inhomogenous Regulation Of Matrix Metalloproteinases And Their Endogenous Inhibitors Intensifies Cardiac Fibrosis In Zucker Diabetic Fatty Rats
Authors: Graf Tobias , Hanke Karoline , Sager Hendrik , Fredersdorf Sabine , Burgdorf Christof , Schunkert Heribert , Weil Joachim
Published: July 2021

AIM: Experimental and clinical studies have demonstrated that matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) are upregulated in dilated failing hearts and involved in the development and progression of myocardial remodelling. However, changes in MMP and TIMP protein levels or activity in the diabetic heart has not yet been described.

METHODS: Untreated male Zucker diabetic fatty (ZDF) and Zucker lean (ZL) rats were sacrificed at the age of 6 (prediabetic), 22 (diabetic) and 42 (late diabetes) weeks (wks) and body weight, total heart weight and plasma glucose were measured (n=7, each group). MMP-2, MMP-9 and TIMP-1 were quantified by Western blot analysis of total protein isolated from left ventricular tissue. Expression of MMP/TIMP mRNA was determined by quantitative PCR (Taqman
®
). Additionally paraffin sections of the left ventricular myocardium were stained with Sirius Red to quantify cardiac fibrosis in percent of visual field.

RESULTS: (see table1

) In summary, expression of myocardial MMP-2 and MMP-9 increased, whereas TIMP-1 decreased throughout life in diabetic and non-diabetic animals. However, expression of MMP-2 and MMP-9 was significantly diminished in ZDF compared to ZL rats during various stages of diabetes. TIMP-1 expression was lower in diabetic animals only in the prediabetic stage. Similar results were found in quantitative RT-PCR. The relative amount of fibrosis in left ventricular myocardium was markedly enhanced in late stage of diabetes (ZDF 41% fibrosis/visual field vs. ZL 18%).

CONCLUSION: The observed results may play a distinctive role in the remodelling processes in late stages of disease. The regulation of expression of MMPs may, therefore, be a useful therapeutic strategy to manage diabetic cardiomyopathy. Table 1

)
Abstract 5954: Does Sirolimus-Eluting Stent Implantation Lead to an Increased Risk of Stent Fracture?
Authors: Umeda Hisashi , Gochi Tomoko , Iwase Mitsuhiro , Izawa Hideo , Yokota Mitsuhiro , Murohara Toyoaki
Published: July 2021

Stent fracture (SF) of sirolimus-eluting stents (SES) has emerged recently in literature and shown to be associated with an increased risk of restenosis. We sought to assess whether the use of SES increases the frequency of SF compared with bare-metal stents (BMS). A consecutive series of 499 lesions of 434 patients undergoing SES implantation (total stent length: 10 to 40 mm) followed by coronary angiography at 6 to 9 months were compared with 137 consecutive patients (147 lesions) treated with BMS (total stent length: 10 to 40 mm) which consists of stent platform of SES. SF was defined as single or multiple stent strut fracture as well as complete separation of stent segments. There were no significant differences in total stent length and the angulation of the lesion between the 2 groups. At follow up, SF occurred in 21 lesions (4.2%) in the SES group and 2 lesions (1.4%) in the BMS group (P=0.129). In-stent restenosis rates were 34.8% (SES; 33.3%, BMS; 50.0%) in lesions with SF and 7.7% (SES; 3.8%, BMS; 20.7%) in lesions without SF (P<0.001). As a result, cumulative rate of major adverse cardiac events at 1 year (death, myocardial infarction, or target lesion revascularization) was higher in patients with SF than in patients without SF (27.3% vs. 12.0%, P=0.035, SES; 25.0% vs. 8.2%, P=0.035, BMS; 50.0% vs. 23.7%, P=0.425). Figure

summarizes multivariable predictors of SF. In this model, SES use was not associated with a significantly increased risk of SF at 6 to 9 months. The implantation of stents in tortuous lesion and/or longer lesions covered with longer stents rather than the use of SES may increase the likelihood of SF in this population subset.
Abstract 5794: Geometric Changes of Mitral Annulus Assessed by Real-Time 3-Dimensional Transesophageal Echocardiography
Authors: Matsumura Yoshiki , Toyono Manatomo , Greenberg Neil L , Yamano Tetsuhiro , Takasaki Kunitsugu , Saraiva Roberto M , Shiota Takahiro
Published: July 2021

Background:

The mitral annular (MA) geometric changes have been reported in patients with various cardiac diseases such as atrial fibrillation (Af), mitral regurgitation (MR) and dilated cardiomyopathy (DCM). The advances of real-time 3D transesophageal echocardiography (TEE) enable us to analyze the MA geometry more accurately and reliably than 3D transthoracic echocardiography (TTE). We sought to determine the independent predictors for MA geometric changes in patients with Af, significant MR, and DCM by 3D TEE.

Methods:

We examined 32 subjects by 3D TEE and 2D TTE; 6 with lone Af, 9 with mitral valve prolapse (MVP), 3 with organic MR, 6 with DCM, and 8 normal subjects. Left ventricular (LV) end-diastolic and end-systolic volume indices (EDVI and ESVI), ejection fraction (EF), left atrial volume index (LAVI), and MR severity were assessed by 2D TTE. We measured MA area index, commissural length, and MA height (Figure 1

). For the index of the saddle-shaped MA geometry, MA shape index was calculated as the (MA height)/(commissural length).

Results:

Patients with MVP and those with DCM had larger MA area index and lower MA shape index than normal subjects (all,
P
<0.05). MA area index was associated with LAVI, MR severity, and LV EDVI (all,
P
<0.05) (Figure 2

). MA shape index was associated with LV EF, ESVI, and the presence of Af (all,
P
<0.05) (Figure 3

). In multivariate analysis, LAVI, MR severity, and LV EDVI independently predicted for MA area index, and LV EF was independent predictor for MA shape index (all,
P
<0.05).

Conclusion:

MA dilatation was independently associated with larger LA and LV volumes and severer MR, not LV EF, while the saddle-shaped MA geometry was associated with LV EF.

Figure 1

Figure 2

Figure 3