bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 59: The Incidence Of Pulmonary Aspiration With Laryngeal Mask Airway Use During Cardiopulmonary Resuscitation And Positive Pressure Ventilation In Swine.
Authors: Suffoletto Brian , Menegazzi James , Logue Eric , Salcido David 
Published: July 2021

Objective: Pulmonary aspiration of gastric contents occurs 20 –30% of the time during cardiopulmonary resuscitation (CPR) of cardiac arrest. This is due to loss of protective airway reflexes, pressure changes generated during CPR, and positive pressure ventilation (PPV). Even though the American Heart Association (AHA) has recommended the laryngeal mask airway (LMA) as an acceptable alternative airway for use by EMS personnel, concerns over the capacity of the device to protect from pulmonary aspiration remain. We sought to determine the incidence of aspiration after LMA placement, CPR and PPV.

Methods: We conducted a prospective study on 16 consecutive post-experimental mixed-breed domestic swine of either sex (mean mass 25.7 ±1.4 kgs). A standard size-4 LMA was modified so that a vacuum catheter could be advanced into and past the LMA diaphragm. The LMA was placed into the hypopharynx and its position confirmed using End-tidal CO
2
and direct visualization of lung expansion. Fifteen milliliters of heparinized blood were instilled into the pharynx. After 5 PPVs with a mechanical ventilator, chest compressions were performed for 60s with asynchronous ventilations continuing at a rate of 12 per minute. After chest compressions, a suction catheter was inserted through the cuff and suction applied for approximately 1 minute. The catheter was removed and inspected for signs of blood. The LMA cuff was deflated and the LMA removed. The intima of the LMA diaphragm was inspected for signs of blood. In a validation cohort of 4 animals, the LMA was reinserted, a cricothyrotomy performed and 5 mL of blood instilled directly into the trachea.

Results: There were 0/16 (95% CI=0 –17%) with a positive tests for the presence of blood in both the vacuum catheter and the intima of the LMA diaphragm. In the validation cohort, all four were positive for blood in both the vacuum catheter and the intima of the LMA diaphragm.
Conclusions: In this simple model of regurgitation of after LMA placement, there was no sign of pulmonary aspiration, and no evidence that blood had passed beyond the seal created by the LMA cuff. Concerns over aspiration with LMA use may be unfounded. Future studies should determine the frequency of pulmonary aspiration after LMA placement in the clinical setting.
Abstract 89: The Prognostic Factor of Patients with Asystole on Arrival
Authors: Shokawa Tomoki , Tanigawa Koich , Yamamoto Hideya 
Published: July 2021

Background: Patients with asystole on arrival (AOA) at hospital have a poor prognosis. However, little is known about the prognostic factor of patients with AOA.
Objective: The purpose of this study was to determine predictors for 24 hours survival in patients with AOA.

Methods and results: Consecutive patients with AOA admitted to the Hiroshima University Hospital (Hiroshima, Japan) from April 2002 to January 2007 were retrospectively analyzed. Patients were divided into two groups according to the outcomes, i.e. non-survivors vs. survivors at 24 hours after admission. Data including blood gas analysis, lactate levels, and levels of minerals on admission were obtained and analyzed. Of 102 (male; 60) patients with AOA, fourteen patients survived for 24 hours. Univariate analysis found that pH, PaO2, PaCO2, base excess, lactate, and serum potassium concentration were associated with survival (p< 0.05) (Table

). Multivariate analysis determined that serum potassium concentration independently affected 24 hours survival.

Conclusions: These results suggested that the serum potassium level on admission is a strong, independent predictor of survival of patients with AOA.

survivors vs. non-survivors
2008 Stroke Council Award and Lecture—Brain and Heart: The Good, the Bad, and the Different
Authors: Hachinski Vladimir 
Published: July 2021

The brain and the heart are unique and essential organs, with autoregulated blood supplies and sophisticated electrical systems, functioning with harmonious complementarity in health; however, disease of one organ can threaten the other. Cardiac valvular disease, atrial fibrillation, and acute myocardial infarction carry a risk of stroke, and both ischemic and hemorrhagic strokes can lead to cardiac abnormalities and sudden death.
Heart disease and stroke share most of the same risk factors, but not to the same degree, nor necessarily with the same consequences. For example, hypertension represents the single most powerful risk factor for stroke and can result in a major intracerebral hemorrhage, a condition without equivalent in any other organ. Despite the superficial resemblance between angina and transient ischemic attack, the mechanisms differ. Angina can be brought on by exercise, but no amount of mental exercise will lead to “brain angina.” Most cardiac patients can maintain a reasonable quality of life on half of their cardiac output. No meaningful quality of life is likely with half of brain output. Stroke recovery is complex. The brain is the only organ with which one can communicate directly and whose feelings have to be considered in recovery. Although stroke and heart disease prevention have much in common, puzzling differences remain. In primary prevention, aspirin prevents heart attacks in men but not in women, and strokes in women but not in men.
Given the great commonalities and interrelationships between vascular brain and heart disease, it has been sensible and successful to have one organization encompassing cerebrovascular and cardiovascular health and diseases. To continue to progress at an accelerated pace, we need to become more familiar with the mutual relationship between cerebrovascular and cardiovascular disease, work together where we can, and separately where we must, but with the common aim of vanquishing both.
Abstract 5857: Low Operative Mortality with implantation of a Continuous Flow LVAD and Impact of Concurrent Cardiac Procedures
Authors: Pal Jay D , Klodell Charles T , John Ranjit , Pagani Francis , Rogers Joseph G , Farrar David J , Milano Carmelo A 
Published: July 2021

Objective: Our goal was to determine the operative mortality of isolated implantation of the HeartMate II continuous flow LVAD and the impact of additional concurrent cardiac procedures on patient outcomes.
Methods: In a multicenter trial, 279 patients at 33 clinical sites underwent implantation of the HeartMate II continuous flow LVAD as a bridge to transplantation from March 2005 to March 2007. HeartMate II implantation (HM II) was the only procedure required in 172 patients while 80 patients required concurrent cardiac procedures in conjunction with LVAD implantation (HM II+CCP).
Results: Preoperative characteristics were similar, but central venous pressure (14.5 vs 11.6 mmHg) was greater for patients requiring concurrent cardiac procedures, suggesting worse right heart dysfunction. Mean cardiopulmonary bypass times increased from 97 to 120 minutes when a concurrent cardiac procedure was performed (p<0.001). Length of stay slightly increased from 23 to 26 days (p=0.17). Overall 30- and 180-day mortality was 5.8% and 13.3% for the HM II group, and 11.3% and 20.0% for the HM II+CCP group. Concurrent valvular procedures increased the risk to 8.5% and 19.1%. Patients who underwent an aortic valve replacement with cardioplegic arrest had a 30-day mortality of 25%, higher than for isolated concurrent mitral (0%) or tricuspid repair (3.3%). Other cardiac procedures were associated with a 30-day mortality of 27.8%. Survival at 180 days was 87% for HMII alone and 80% for HMII+CCP.
Conclusion: There is a low 5.8% operative mortality for patients requiring uncomplicated HeartMate II implantation, with no apparent increased risk for concurrent PFO closure, mitral or tricuspid repair. However, concurrent aortic valve and other cardiac procedures are associated with a significantly decreased survival. The increased risk of these procedures must be balanced against the negative impact of uncorrected aortic insufficiency during VAD support.
Abstract 5956: Modulation of Urocortin 2 Contractile EFFects by Endocardial Endothelium
Authors: Bras-Silva Carmen , Fontes-Sousa Ana Patrícia , Almeida Mónica , Mendes Susana , Leite-Moreira Adelino F 
Published: July 2021

Purpose: The urocortin (Ucn) peptides Ucn1, Ucn2, and Ucn3 are recently isolated members of the corticotropin-releasing factor family. Ucn2 promotes positive inotropic and lusitropic effects and both endothelium-dependent and -independent vasodilatation. In the current study, we investigated the modulation of Ucn2 contractile effects by endocardial endothelium (EE).
Methods: The effects of increasing concentrations of Ucn2 (10 –10 to 10 – 6M) were evaluated in isolated right papillary muscles (Krebs-Ringer: 1.8mM CaCl2, 35°C) with intact EE (n=11) and after damaging EE (0.5% Triton X-100, n=12). Reported parameters include: active tension (AT; mN/mm2) and maximum velocities of tension rise and tension decline (dT/dtmax and dT/dtmin, respectively; mN/mm2/s). Only significant results (mean±SEM, p<0.05) are given, expressed as % change from baseline.
Results: Ucn2 induced concentration-dependent positive inotropic and lusitropic effects in muscles with intact EE (at 10 – 6M it increased 65.6±5.2% AT, 196.9±16.7 dT/dtmax and 145.0±13.5% dT/dtmin). These effects were potentiated in papillary muscles with damaged EE. In this condition, the higher concentration of Ucn2 increased 169.1±39.2% AT, 412.5±43.9% dT/dtmax and 296.7±56.7%dT/dtmin.
Conclusions: This study shows that the positive inotropic and lusitropic effects induced by Ucn2 are enhanced in the presence of endocardial endothelial dysfunction. These findings reinforce the importance of Ucn2 in the regulation of myocardial function and provide new elements for the comprehension of the pathophysiology of HF, a condition where Ucn2 levels are increased and endothelial dysfunction might be present.
Abstract 5998: Final Results of the HEALING 2B Trial to Evaluate a Bioengineered CD34 Antibody Coated Stent (Genous
™
Stent) Designed to Promote Vascular Healing by Capture of Circulating Endothelial Progenitor Cells in CAD Patients
Authors: Duckers H , Onuma Yoshinobu , Benit Edouard , de Winter Robert J , Wijns William , Grisold Manfred , Verheye Stephan , Silber Sigmund , Teiger Emmanuel , Hill Jonathan , Serruys Patrick W 
Published: July 2021

Background: In contrast to a cytotoxic or cytostatic pharmacotherapy, promoting the vascular healing response by capturing and sequestering circulating endothelial progenitor cells (EPC) to the stent surface by a CD34 antibody coating (Genous
™
stent) may accelerate stent reendo-thelialization and prevent restenosis formation, as well as stent thrombosis (ST)

Methods: The HEALING IIB study was a multi-center, prospective trial designed to assess the safety and efficacy of the Genous
™
bio-engineered stent in conjunction with HmG CoA reductase inhibitors (statins) to stimulate EPC recruitment, in the treatment of patients with de novo coronary artery lesions (n=100 pts). The primary safety endpoint was major adverse cardiac events (MACE) at 30 days, whereas the primary efficacy endpoint was late luminal loss by QCA at 6 months follow-up.

Results: At interim analysis of the first 45 patients that completed the 6-month angiographic follow-up, the composite MACE rate was 11.1%, whereas 6.6% clinically justified target lesion revascularizations were observed. 2 Patients died within the first 30 days after stent implantation due to angiographically verified stent thrombosis. Low circulating EPC titers were previously associated with a poor response to the EPC capture stent with TLR events and high late loss. Therefore, patients were pre-treated with Atorvastatin 80 mg qd prior to the PCI in order to augment EPC levels. Statin therapy stimulated the levels of committed EPCs by +294%, but failed to increase the titer of CD34+cells (+25%). Although statin pretreatment stimulated EPC levels, the angiographic outcome of the EPC capture stent was not improved in these patients: in-stent late luminal loss was 0.77±0.46 mm. We anticipate to complete analysis of the 6 month angiographic follow-up of all 100 patients by the time of the AHA2008.
Conclusions: The HEALING-IIB study suggests that the EPC capture coronary stent in combination with statin therapy does not sufficiently impede stent restenosis formation for the treatment of de novo coronary artery disease. Although concomitant statin therapy was able to stimulate EPC recruitment, it failed to stimulate CD34+ stem cell levels and did not improve the angiographic outcome of the bioengineered EPC capture stent.
Abstract P108: Orexin-A Improves Arousal and Electroencephalographic Entropy in Rats after Cardiac Arrest
Authors: Koenig Matthew A , Jia Xiaofeng , Kang Xiaxu , Velasquez Adrian , Thakor Nitish V , Geocadin Romergryko G 
Published: July 2021

Objective: Cardiac arrest (CA) survivors progress through electroencephalographic (EEG) burst-suppression prior to arousal. Orexin-A, an excitatory neuropeptide, elicits arousal EEG patterns during anesthetic-induced burst-suppression. We hypothesized that intraventricular injection of orexin-A would improve arousal and burst-suppression after CA in rats.
Methods: Eighteen Wistar rats were subjected to 7-minute asphyxial CA and resuscitation by external cardiac massage. Rats were divided into treatment (n=9) and control (n=9) groups. Twenty minutes after resuscitation, the treatment group received 0.1 mL of 1nM orexin-A intraven-tricularly, while controls received saline. EEG was continuously monitored and quantified using Information Quantity (IQ), a measure of entropy validated for detection of burst-suppression and arousal patterns. IQ was normalized to baseline prior to CA (range 0 –1.0). Arousal was quantified using the neurological deficit scale (NDS). Stereologic microscopy was used to determine the ischemic neuronal fraction of hippocampus CA1 and cortex.
Results: Baseline and post-resuscitation characteristics were similar between the 2 groups. Burst frequency by visual inspection was similar after administration of orexin-A or saline. Rats in the orexin-A group demonstrated higher IQ values (mean±SD) compared to controls beginning 10 minutes after drug injection (0.564±0.098 vs. 0.429±0.116, p=0.024). IQ values remained significantly higher in the orexin-A group for the first 60 minutes after drug injection and subsequently converged. The NDS score (mean±SD) at 4 hours was higher in the orexin-A group compared to controls (57.3±5.8 vs. 40.7±5.9, p<0.02), but scores were similar at 72 hours. The ischemic neuronal fraction was similar between groups in cortex (p=0.54) and hippocampus CA1 (p=0.14).
Conclusions: In rats resuscitated from CA, orexin-A hastened improvement of EEG entropy and arousal measures without increasing ischemic neuronal injury. The role of orexin-A in hastening arousal after CA deserves further investigation.
Abstract P111: Applying the Principles of Functional Stimulation to Electrical CPR
Authors: Gilman Byron L , Brewer James , Kroll Mark W , Ristagno Giuseppe , Li Yongqin , Wang Hao , Sun Shijie , Weil Max Harry , Tang Wanchun 
Published: July 2021

Background: We have previously reported on a specialized electrical stimulus that produces coronary and carotid blood flow during VF. The values selected for the Current (C), Pulse Width (PW), Pulse Period (PP), Train Width (TW) and Train Rate (TR) are critical to obtaining effective blood flow. An initial experiment in which these parameters were systematically studied in order to identify the optimal parameters has been previously reported. In this study we utilized some of the principles established in the field of NeuroMuscular Electrical Stimulation (NMES) of the extremities to further optimize ECPR. A primary principle of interest is that the force produced is proportional to charge delivered (Coulombs or amp-seconds.) Consequently, higher C, longer PW, shorter PP and longer TW would be predicted to produce greater force.
Hypothsis: We hypothesized that for ECPR as in NMES that: CPP over time would be proportional to the total charge delivered per constriction.
Methods: We applied 118 episodes of ECPR in 7 porcine subjects as previously described. VF was electrically induced and untreated for 10 seconds. ECPR was then applied for 60 seconds or until CPP dropped below 15 mm Hg. The specific ECPR intervention applied was determined according to a factorial design of experiment in which two levels each of C, PW, PP and TW were evaluated. The CPP was recorded at 10-second intervals during ECPR until it was terminated.
Results: PP and PW showed significant differences in their ability to maintain CPP > 15 mm Hg (T15) for prolonged periods of time (PP=25 ms: 49±15 s to T15 vs PP=50 ms: 41±17 s to T15, p=0.004) (PW=0.2 ms: 42±17 s to T15 vs PW=0.8 ms: 48±16 s to T15, p=0.05). Regression analysis further showed that an increase in PW and a decrease in PP worked independently and without interaction to increase T15 for CPP. These two parameters relate directly to total charge delivered with the result that, for each additional unit of total charge delivered, there was an almost 8 times increase in the T15 time period (coefficient = 7.7, 95% CI=(6.5,8.9))
Conclusions: The increases in charge provided by longer PP and shorter PW produced significantly longer time of CPP > 15 mm Hg within the limits of this test. Further study is required in order to further extend the duration of action ECPR.
Abstract P134: Total Liquid Ventilation Induced Ultrafast Cardioprotective Hypothermia during Prolonged Myocardial Ischemia in Rabbits
Authors: Tissier Renaud , Lidouren Fanny , Chenoune Mourad , Couvreur Nicolas , Ghaleh Bijan , Bizé Alain , Dubois-Randé Jean-Luc , Berdeaux Alain 
Published: July 2021

Introduction: Total liquid ventilation with temperature-controlled perfluorocarbons induces an ultra-fast cardioprotective cooling when instituted during a 30-min coronary artery occlusion (CAO) in rabbits.
Hypothesis: We hypothesized that ultra-fast hypothermia instituted with a short total liquid ventilation episode would be still beneficial after a prolonged CAO as compared to conventional low rate surface cooling.
Methods: Anesthetized rabbits underwent a 60-min CAO followed by 4 hours of reperfusion before infarct size and no reflow evaluations. Rabbits randomly underwent either a normothermic CAO (Control group, n=7) or cooling from 5th min of CAO to the end of CAO (target left atrial temperature: 32°C). Cooling procedures were either low rate surface cooling (LRC) using ice-filled cold blankets (LRC group, n=7) or ultra-fast cooling (UFC) initiated by 20 min of hypothermic total liquid ventilation and maintained if necessary by cold blankets (UFC group, n=6). An additional group underwent a similar ultra-fast cooling protocol started at the 20th min of CAO (UFC-delayed group, n=6). After reperfusion, all hypothermic animals were rewarmed.

Results: Left atrial temperature was similar in all groups at baseline (Table

). Hypothermia was modest in LRC vs UFC and UFC-delayed groups at 30-min CAO but reached similar level at the end of ischemia (i.e., 60-min CAO). Interestingly, no reflow and infarct sizes were only significantly reduced in UFC and UFC-delayed but not in LRC groups as compared to Control. Infarct size reduction was significantly better predicted by the integrated decrease in left atrial temperature throughout ischemia than by the temperature at the end of ischemia.

Conclusion: Ultra-fast cooling induced by total liquid ventilation afforded cardioprotection against prolonged ischemia in rabbits, even when instituted later than a low rate surface cooling.

Left atrial temperature (LAT) at different times of the protocol and infarct and no reflow sizes
Abstract 359: Disordered Chemokine Expression in Diabetes Following Experimental Myocardial Infarction: Potential Role in Impaired Progenitor Cell Recruitment
Authors: Desjardins Jean-Francois , Connelly Kim A , Thai Kerri , Johnson Cory A , Parker Thomas G , Gilbert Richard E 
Published: July 2021

BACKGROUND: Impaired collateral vessel formation is thought to contribute to the excessive morbidity in diabetic subjects with ischaemic heart disease where following myocardial infarction (MI) patients with diabetes are twice more likely to develop heart failure than non-diabetic subjects. Since the trafficking of bone marrow derived endothelial progenitor cells is thought to contribute to new vessel formation in ischemia, we postulated that altered chemokine expression may contribute to the impaired angiogenic response in diabetes.
METHODS: Six week old F344 rats were randomized to vehicle or streptozotocin (35mg/kg i.p.) in order to induce diabetes. Once diabetes was confirmed (plasma glucose >15 mM), a total of 40 animals then underwent sham procedure or LAD ligation (MI) at age 10 weeks, and sacrificed at day 0 (sham) and days 1, 2, 4 and 7 post-MI (4 per group). Infarct size was determined by echocardiography 24 hours after ligation. RT q PCR was used to assess mRNA expression levels of SDF-1 and its receptor CXCR4 at each time point, from tissue obtained from the peri-MI zone.
RESULTS: There was no difference in mortality or infarct size between the groups. In control rats an increase in SDF-1 gene expression was apparent at Day 2 post-MI, persisting through Day 7 (p<0.05). In contrast, diabetic rats showed high basal expression (6-fold vs. control, p<0.01) that fell abruptly after MI and remained persistently low throughout the 7-day time course. Diabetes was also associated with increased basal gene expression of CXCR4 (2-fold vs. control, p<0.05). Post-MI, CXCR4 gene expression increased in control rats at each time point, with fold differences up to maximally 3 times at Day 2 (p<0.05 vs. Day 0). In diabetic rats, the level of expression remained high at Day 1, significantly decreased at Day 2 (3-fold vs. non-diabetic, p<0.01) and was comparable to that of non-diabetic rats at days 4 and 7.
CONCLUSIONS: Diabetes was associated with paradoxical alterations in gene expression of both SDF-1 and its receptor CXCR4 with high baseline expression and diminution following an ischemic insult. These findings suggest that disordered chemokine expression may reduce the diabetic heart’s ability to recruit endothelial progenitor cells to sites of ischemic injury.