bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 63: Time to Target Temperature and Neurological Outcome in Survivors of Cardiac Arrest
Authors: Perman Sarah M , Grossestreuer Anne V , Leary Marion , Gaieski David F , Carr Brendan G , Abella Benjamin S 
Published: April 2024

Introduction: Substantial variability exists in time to target temperature for patients who undergo therapeutic hypothermia (TH) after cardiac arrest. How this variability may affect or predict neurologic outcomes is unknown.
Hypothesis: Prolonged pre-induction time, or shorter times to target temperature will be associated with poor neurologic outcomes compared to shorter pre-induction times and a more gradual decline to target temperature.
Methods: We conducted a retrospective chart review of TH patients from three institutions with identical TH protocols (PATH Database). Demographic variables were collected and analyzed using chi square and Student’s t-tests. We examined the association between time from arrest to return of spontaneous circulation (ROSC) (downtime), time from ROSC to initiation of TH (pre-induction) and time from initiation of TH to arrival at target temperature (induction) and Cerebral Performance Category (CPC) using logistic regression.
Results: We enrolled 180 patients with mean age 59.1 ± 15.5 yrs, 56% male, and 26.1% with VF/VT as an initial rhythm. At discharge, 26% (47/180) of the cohort had CPC category 1 or 2 (good neurologic outcome). Mean downtime for survivors with a good outcome was 21.5 ± 13.7 mins vs. 32.6 ± 21.7 mins (p=0.004) for those with poor outcome. Mean pre-induction time for good outcome (CPC 1 or 2) was 144.5 ± 205.4 mins compared to 145.5 ± 171.1 mins for bad outcome (p=ns). Mean induction time for good outcome (CPC 1 or 2) was 270.8 ± 160.8 mins compared to 252.3 ± 151.3 mins for bad outcome (p=ns). In analyses adjusting for gender, initial rhythm, and downtime, there was no association between pre-induction time (OR 1.00, 95% CI 0.99-1.0, p=ns) or induction time (OR 0.99, 95% CI 0.99-1.0, p=ns), and neurologic outcome.
Conclusion: In this cohort of post-arrest TH patients, pre-induction time and induction time do not appear to be associated with poor neurologic outcome. Further analysis is necessary to examine this phenomenon.
Abstract 8: Dynamic ECG Changes in Wearable Cardioverter-Defibrillator Patients Predict Sudden Cardiac Arrest
Authors: Karia Darshak , Bianco Nicole R , Wan Chingping , Glad Jo Ann M , Szymkiewicz Steven J 
Published: April 2024

Purpose:
Sudden cardiac arrest (SCA) prediction continues to be an active area of investigation. The wearable cardioverter defibrillator (WCD) records ECG periodically. The objective of this study was to study the predictive value of dynamic ECG changes occurring between baseline (Base), one week prior to SCA (1WK), and immediately prior to shock (pre-S) for ventricular tachyarrhythmias VT/VF

Methods:
100 sequential patients (pts) who were prescribed a WCD for bridge to ICD or recovery, and who were shocked for VT/VF between November 2009 and June 2011 were retrospectively analyzed. ECG’s were examined for dynamic changes in heart rate (HR), QRSd, QRS amplitude, QTc, PVCs, rhythm, and NSVT to see if they were predictive of impending shock. Individual manual measurements were collected at Base, 1WK, and pre-S. Only pts wearing the WCD ≥1 week were included for analysis.

Results:
Pts (68% male, age 59 ± 16 years, mean LVEF 23±7.5%) had dynamic increases in mean HR and PVC burden from Baseline to 1WK to pre-S (p≤0.0001)(Table 1). Interestingly, changes in traditional measures such as QTc or QRSd or amplitude did not predict shock.

Conclusions:
The WCD provides a unique opportunity to monitor ECG patterns in at-risk pts prior to defibrillation. A dynamic increase in HR and ventricular ectopy changes prior to VT/VF could indicate a shift of sympathetic-vagal balance towards sympathetic predominance and reduced vagal modulation.
Abstract 83: Cardiac Arrest and Cardiopulmonary Resuscitation Knowledge at an Academic Research Organization in Durham, North Carolina
Authors: Anderson Monique L , Jollis James G , Peterson Eric D , Lopes Renato D , Blanco Rosalia G , Fraulo Elizabeth , Pathman Joshua , Moore Angel , Short Leatrice , Granger Christopher B 
Published: April 2024

Purpose: Bystander CPR is a critical step in the chain of survival for out of hospital cardiac arrest (OHCA). In North Carolina, survival is estimated to be 12%; 17% of victims receive bystander CPR. Current public knowledge of cardiac arrest and CPR skills are not well described.
Methods: We implemented a CPR awareness/ training program during CPR Awareness Week at the Duke Clinical Research Institute (DCRI), a large academic research organization (ARO) traditionally focused on cardiovascular care, to increase awareness of OHCA and CPR. Prior to implementation, employees completed an online survey to gauge prior CPR training, current confidence with CPR, and knowledge of cardiac arrest and CPR skills. The program included expert lectures on cardiac arrest and CPR, a documentary on a Duke patient’s cardiac arrest, as well as a video demonstration (AHA) of Hands-Only CPR. After the education session, trained volunteer instructors taught and evaluated the practical CPR performance skills of each participant. An online post-program survey concluded the program (data collection ongoing).
Results: A total of 173 (14.5%) employees completed the pre-program survey. 75% (n=134) of participants were not health care professionals. 67% (n=120) had been previously trained in CPR, of which 60% (n=70) were trained ≥ 5 years ago. Only 16% (n=28) of participants were “very sure” they could perform CPR if needed immediately. Only a minority of respondents were aware that cardiac arrest is associated with very high mortality rates (20%) or that most cardiac arrests occur in the home (21%). 66% of respondents knew that calling 911 is a necessary first step after witnessing a cardiac arrest. While 84% (n=145) respondents knew correct hand placement position for CPR, only 27% (n=47) and 29% (n=54) knew correct compression rate and depth for CPR performance, respectively. In the presence of gasping, only 37% (n=60) knew to start or continue performing CPR on OHCA victims.
Conclusion: Cardiac arrest and CPR knowledge are not optimal at our ARO, despite one of our research mission’s to improve emergency cardiovascular care. Community awareness is likely lower than observed at the DCRI. These data highlight opportunities for CPR awareness programs in academic settings and in the community.
Abstract 88: Delayed Administration of Argon Reduces Ischemic Brain Damage and Preserves Functional Recovery After Cardiac Arrest in Rats
Authors: Brücken Anne , Bleilevens Christian , Derwall Matthias , Nolte Kay , Weis Joachim , Rosaint Rolf , Fries Michael 
Published: April 2024

Introduction: Argon is neuroprotective when given 1 hour after cardiac arrest (CA) in rats. Here, we investigated if a delayed administration of argon would also reduce neurologic dysfunction.
Material and Methods: 18 male Sprague-Dawley rats were subjected to 7 mins of CA and 3 mins of cardiopulmonary resuscitation (CPR). Three hours after successful CPR, animals were randomized to ventilation with 70% argon for 1h in comparison to untreated controls receiving 70% nitrogen. A neurologic deficit score (NDS) was calculated on seven days following the experiment before the animals were killed and the brains harvested for histopathological analyses. Neuronal damage was semiquantitatively assessed by determining the proportion of neuronal cells showing shrunken and/or hypereosinophilic cytoplasm (HE staining) in combination with a loss of nuclear NeuN-immunoreactivity.
Results: All animals survived. Untreated controls exhibited severe neurologic dysfunction while animals from the argon group showed significant improvements in the NDS at all points in time (Fig.1). This was paralleled by a significant reduction in the degree of ischemic brain damage in the neocortex, the basal ganglia and the hippocampal CA 3/4 region (Fig.2).
Conclusions: Our study demonstrates that a one hour application of 70% argon, even when treatment was delayed for 3 hours after CA, provided a significant reduction in histopathological damage of the neocortex, basal ganglia and hippocampus which was associated with a marked improvement in functional neurologic recovery.
Abstract 9286: Patterns of Red Blood Cell Transfusion Use in Patients Undergoing Percutaneous Coronary Intervention in Contemporary Clinical Practice
Authors: Sherwood Matthew W , Wang Yongfei , Curtis Jeptha P , Peterson Eric D , Rao Sunil V 
Published: April 2024

Background Previous studies have shown marked variation in the use of red blood cell transfusion (RBCT) among patients with acute coronary syndromes. Contemporary post-procedure RBCT patterns in patients undergoing PCI are unclear.
Methods Using the NCDR Cath-PCI database we evaluated frequency of RBCT in 1323965 patients undergoing PCI at 1282 hospitals between 7/2009-9/2011 excluding those who underwent in-hospital CABG. Site-level variation in RBCT use was examined; differences in patient baseline characteristics and in-hospital outcomes were compared between patients who did and did not receive RBCT. Logistic regression was used to determine the adjusted association between RBCT and in-hospital death, MI, or stroke.
Results Of the total sample, 29255(2.2%) patients received RBCT. These patients were older, more often female, and more often had HTN, prior CHF, prior MI, cerebrovascular disease, peripheral arterial disease, diabetes, or be on dialysis. Patients receiving RBCT had lower median pre-procedure Hgb (10.7 g/dl vs 13.7 g/dl, P<0.01) and post-procedure Hgb (8.6 g/dl vs 12.7 g/dl, P<0.01) and more often experienced a post-PCI bleeding event (36% vs 1%, P<0.01). RBCT was more frequent in patients with post-procedure Hgb <10 g/dl, irrespective of PCI indication. With respect to site-level variation, 17% of hospitals gave no RBCT, 76% of hospitals used RBCT in 1-4% of patients, while just 7% of hospitals used RBCT in ≥5% of patients (Figure). After adjustment, the use of RBCT was significantly associated with in-hospital death, MI, or stroke (OR 2.18; 95% CI 2.09-2.26). Similar results were seen after excluding patients who bled.
Conclusions In contemporary PCI practice, there is marked site-level variability in the use of RBCT. After adjustment for potential confounders, RBCT is associated with a higher risk for in-hospital adverse events. These data underscore the importance of understanding the appropriate role of RBCT in patients undergoing PCI.
Abstract 9719: Overexpressed Phoshodiesterase 3A1 Protects the Heart against Angiotensin II-induced Cardiac Injury via Regulating Interaction between β-adrenergic and Angiotensin II Signaling Pathways
Authors: Oikawa Masayoshi , Iwaya Shoji , Yan Chen , Takeishi Yasuchika 
Published: April 2024

BACKGROUND: Angiotensin II (AngII) has critical roles in progression of cardiac hypertrophy and fibrosis, leading to subsequent heart failure. Accumulating evidence suggests that there are direct interactions between β-adrenergic and AngII signaling pathways, and β-blocker treatment protects hearts against AngII-induced cardiac injury. Phosphodiesterase 3A (PDE3A) inhibits β-adrenergic receptor (βAR)/protein kinase A (PKA) axis by metabolizing cAMP. Therefore, we hypothesized that overexpressed PDE3A has cardioprotective effects against AngII-induced cardiac injury by regulating AngII signaling.
METHODS AND RESULTS: To induce cardiac injury, AngII (800 ng/kg/min) was continuously infused using osmotic mini-pump for 10 days in wild-type (WT) mice and transgenic (TG) mice with cardiac-specific expression of exogenous PDE3A1. AngII stimulation increased heart weight/body weight ratio by 32% in WT hearts compared with vehicle hearts (5.6±0.5 mg/g vs. 4.3±0.1 mg/g, P<0.05), whereas by 5% in TG hearts (5.8±0.6 mg/g vs. 5.5±0.8 mg/g, ns). Echocardiography revealed that AngII lead to cardiac hypertrophy in WT hearts compared to vehicle hearts (wall thickness, 12.4±1.5 mm vs. 8.2±0.7 mm, P<0.05), but not in TG hearts (10.4±1.5 mm vs. 9.3±0.3 mm, ns). Moreover, AngII-induced cardiac fibrosis was also inhibited in TG hearts compared to WT hearts (4.2±1.1% vs. 6.9±2.6%, P<0.05). Interestingly, basal expression levels of transforming growth factor-β (TGFβ) as well as phosphorylated-phospholamban were inhibited in TG hearts compared to WT hearts, suggesting that overexpressed PDE3A regulated AngII/TGFβ and βAR/PKA axis.
CONCLUSIONS: We thus conclude that PDE3A inhibits AngII-induced cardiac hypertrophy and fibrosis via regulating the interaction between β-AR/PKA and AngII/TGFβ axis.
Abstract 17984: Protective Role of Dicer in Macrophages During Atherogenesis
Authors: Wei Yuanyuan , Heyll Kathrin , Weber Christian , Schober Andreas 
Published: April 2024

Atherosclerotic lesion development is characterized by the subendothelial accumulation of lipid-laden macrophages. It is known that microRNAs (miRs) are generated by the RNase Dicer and play important roles in macrophage function by negatively regulating post-transcriptional gene expression. Previously, we found that macrophage-derived miR-342-5p enhances atherosclerosis by fostering inflammatory macrophage activation. However, the impact of Dicer-dependent miR expression in macrophages during atherosclerosis is unclear.
To study the role of Dicer in macrophages in atherosclerosis, we fed Apoe-/- mice with a myeloid cell-specific deletion of Dicer (LysMCre-Dicerflox) and littermate controls (LysMCre-DicerWT) a high cholesterol diet (HCD) for 3 months. Dicer deletion in myeloid cells was confirmed in bone marrow-derived macrophages isolated from LysMCre-Dicerflox mice by real-time PCR. The lipid deposition in the aortas was increased by 50% in LysMCre-Dicerflox (3.3±0.3%) compared to LysMCre-Dicerwt mice (2.1±0.3%) (p = 0.01, n = 13). The differential blood counts and the serum cholesterol and triglyceride levels were not altered between two groups. We found that 79 miRs, including those highly expressed in macrophages (e.g., miR-146a and miR-223), were down-regulated in LysMCre-Dicerflox aortas compared to controls after 3 months of a HCD (p < 0.05, n = 3) using a miR real-time PCR array. In aortas from LysMCre-Dicerflox mice, 471 genes were up-regulated as determined by whole-genome gene expression profiling using Agilent Mouse Microarrays (p < 0.05, n = 3-4). Genes involved in fatty acid and lipid metabolism were enriched among the up-regulated genes as analyzed by GeneGo MetaCore. Up-regulation of Plg, Ptges2, Eci1, Impa2, Acox2, Thrsp, and the lipid droplet-related genes plin-1, -2, -5 and Cidea was confirmed by real-time PCR. Whereas Plg was predicted to be a target of miR-223 by Targetscan, plin-1, -2, and Ptges2 were identified as potential targets of miR-146a using miRanda.
These data indicate a protective role of Dicer during atherogenesis by inhibiting lipid metabolism in lesional macrophages through miRs. Thus, regulation of the lipid metabolism in macrophages might be a critical step in the development of atherosclerosis.
Abstract 18923: S-Nitroso Human Serum Albumin versus Inhaled Nitric Oxide for the Treatment of Pulmonary Hypertension in a Chronic Right Ventricle Volume Overload Model
Authors: Rungatscher Alessio , Hallström Seth , Linardi Daniele , Milani Elisabetta , Tessari Maddalena , Luciani Giovanni Battista , Mazzucco Alessandro , Faggian Giuseppe 
Published: April 2024

Background:
The study aimed to compare the acute overall hemodynamic and oxidative stress effects of intravenous S-NO-human serum albumin (S-NO-HSA) infusion and inhaled nitric oxide (iNO) in a chronic left-to-right shunt-induced pulmonary arterial hypertension model.

Methods and Results:
Male Wistar rats underwent surgical creation of aorto-caval fistula (Qp/Qs> 2.0). After 10 weeks they were randomly treated with human serum albumin (HSA) (controls; n. 25), S-NO-HSA (0.5 μmol/kg/h; n. 30) or iNO (20 ppm; n. 35) for 60 minutes.

Right ventricular contractility, right ventricular-vascular coupling and ventricular interdependence were assessed in vivo at different preloads by biventricular conductance catheters prior and after 60 minutes treatment. Heart and lung biopsies were obtained to determine oxidative stress by oxidized to reduced glutathione (GSSG/GSH) ratio and high-energy phosphates content.
Both S-NO-HSA and iNO led to a significant reduction in right ventricular afterload expressed by effective pulmonary arterial elastance (Ea) (from 1.3 ±0.2 to 0.5 ±0.3 and 0.4 ±0.2 respectively; P< 0.001). Only S-NO-HSA significantly improved right ventricle diastolic function (slope of end-diastolic pressure-volume relation) and contractility indicated by end-systolic elastance (Ees). Therefore a significant increase in the efficiency of ventricular-vascular coupling (Ees/Ea) occurred after S-NO-HSA but not iNO treatment (from 0.33 ±0.15 to 0.98 ±0.21; P< 0.005 and from 0.35 ±0.16 to 0.45 ±0.18; P< 0.1 respectively) with significant increase in left ventricular stroke volume (58 ±7 vs 18 ± 9 %; P< 0.003).
S-NO-HSA compared to iNO improved right ventricle phosphocreatine content (27.08 ±11.35 vs. 8.41 ±1.80 nmol/mg protein; P<0.001) and myocardial energy charge (0.85 ±0.03 vs. 0.78 ±0.03; P<0.01). Both S-NO-HSA and iNO decreased lung and right ventricular GSSG/GSH ratio (P<0.001).

CONCLUSIONS:
S-NO-HSA is more effective than iNO in treating pulmonary hypertension, improving right ventricle diastolic function and right ventricular-arterial coupling with a positive effect on ventricular interdependence. This results in superior energetic reserve of the heart, despite similar reduction of lung and right ventricular oxidative stress.
Abstract 18971: Changes in HDL Quality Rather Than Macrophage Function Mediate the Atheroprotective Phenotype in Usf1 Knockout Mice
Authors: Soronen Jarkko , Laurila Pirkka-Pekka P , Kaiharju Essi , Van Eck Miranda , Kovanen Petri , Jauhiainen Matti 
Published: April 2024

We previously demonstrated that allelic variants of Usf1 are associated with myriad metabolic phenotypes in human populations and the knockout of Usf1 in mice leads to a favorable metabolic phenotype. Here, we have studied the role of macrophages and HDL particles in the development of atherosclerosis in the Usf1 -/- mice.
A mouse strain of double knockout of Usf1 and Ldlr (Usf1 -/- Ldlr -/-) was generated, and mice along with their Usf1 +/+ Ldlr -/- littermates were fed with a high fat diet diet for 20 weeks. The double knockouts displayed a three-fold reduction in their atherosclerotic lesion area as demonstrated by the aortic longitudinal section based en face technique.
To study the potential mechanisms behind the attenuated lesion development in the Usf1 -/- mice, we knocked down USF1 by constitutive expression of shRNA from human monocyte cell line (THP1). We differentiated monocytes into macrophages and loaded them with acetylated LDL for 48 hours. We observed no change in cholesterol efflux from USF1 knockdown macrophages to wild type mouse serum or HDL when compared to efflux from control cells expressing non-targeting shRNA. Furthermore, we performed bone marrow transplantation of Usf1 -/- and wild type bone marrow to Ldlr -/- mouse background. After 12 weeks of western diet we saw no change in atherosclerotic lesion development in the aortic root area in the mice with Usf1 -/- bone marrow compared to the mice with wild type bone marrow, indicating a macrophage independent mechanism for the atheroprotection in Usf1 -/- mice.
The Usf1 -/- mice displayed both elevated cholesterol (p<0.001) and phospholipids (p<0.001) in their serum both on western and regular chow diet. Interestingly, cholesterol efflux from wild type THP1 macrophages to Usf1 -/- serum and HDL was significantly increased (p<0.05 and p<0.001, respectively) compared to serum and HDL from the wild type mice indicating that not only increased serum HDL concentration but also changes in HDL particle quality in the Usf1 -/- mice have properties increasing cholesterol efflux.
Our study establishes the atheroprotective role for Usf1 deficiency that could be in part due to the favorable changes HDL particle quality rather than macrophage specific effects in the Usf1 -/- mice.
Abstract 19229: Effect of Blood Pressure Control on Mortality in Patients With Hypertension - Using the VA National Database
Authors: Fletcher Ross D , Kheirbek Raya , Amdur Richard L. Amdur L , Jones Ronald E , Faselis Charles , Papademetrious Vasalios 
Published: April 2024

Medical centers are being presented with an increasing number of hypertensives, and controlling Blood Pressure (BP) has become a healthcare imperative. The outcome of this control can be measured by analysis of mortality. The VA has used an Electronic Health Record with reminders since 1998 to detect and manage hypertension. Vital signs from the entire VA database were analyzed between 2001 and August 2011. Of 8,868,500 patients, 4,353,382 had elevations >140 systolic or >90 on three separate days. BP control was divided into patients who were controlled >66%, 66 to 33%, and <33% of the time.
Mortality improvement varied with age. The mortality decreased in patients with 66% control compared to those with 33% control. This decreased mortality was 10.4% points for those under 70 years old, 13.4% points for 70 - 90 years old, and only .8% for those over 90. The % died was compared between patients with hypertension and those without hypertension in different age groups. The age groups were ≤ 50, 50 - <60, 60 - <70, 70 - <80, 80 - <90 and ≥90. The % point difference between groups and % increase in mortality for patients with hypertension in the ages ≤ 50 was 6.5 - 175%, 50 - <60 was 4.2 - 28%, 60 - <70 was 5.1 - 24%, 70 - <80 was 1.7 - 3.5%, 80 - <90 was .3 - .4%, and for those ≥90 minus .3 - minus .5%. Thus difference in mortality in hypertensive and normotensive groups decreases in higher age groups to the point where a slightly higher percent die in patients without hypertension than with hypertension in patients over 90.
Control of BP over time is associated with decreased mortality in all age groups less than 90. After 90 control of BP has very little effect on mortality. Mortality in hypertensive patients is more than in normotensive patients until 90. When mortality is higher for patients with hypertension than those without, control of hypertension decreases mortality.
Research Priorities for In-Hospital Cardiac Arrest: An Agenda for the Next Decade
Authors: Chan Paul 
Published: April 2024

There are an estimated 200,000 to 300,000 cardiac arrests which occur annually in U.S. hospitals, with relatively low survival rates. In-hospital cardiac arrest (IHCA) remains a ‘silent epidemic’, and as many patients die of IHCA each year in the U.S. as lung cancer. Until recently, however, little was known about the epidemiology, processes of care, and outcomes of IHCA.

In the past decade, a number of key studies have provided important insights. We now know that certain process of care factors, such as defibrillation time and duration of resuscitations, are tightly linked to patient survival and neurological outcomes. Several studies have also demonstrated substantial

hospital variation

in processes of care and survival, suggesting that some hospitals are able to excel in the treatment of IHCA. In fact, survival after IHCA has improved markedly over the past decade (14% in 2000 to 22% in 2009), but these gains have been uneven across sites. Nonetheless, the factors which distinguish top-performer hospitals in IHCA survival from other hospitals have yet to be defined.

In this lecture, Dr. Chan will review the seminal epidemiological and outcomes studies on IHCA over the past decade. He will then propose a research agenda for IHCA for the next decade, as well as promote a paradigm shift in the conceptual model of IHCA, investigator collaborations, and research methodologies.