tbuckley/cabot-search huggingface dataset:
Abstract 8995: The Munich Triathlon Heart Study: Ventricular Function, Myocardial Velocities and 2-d Strain In Healthy Children Before and After Endurance Stress
Authors: Michael Hauser, Andreas Kuehn, Curt Petzuch, Patrick Schoen, Julia Elmenhorst, Martin Schoenfelder, Renate Oberhoffer, Manfred O Vogt
Journal: Circulation (2012)

Objectives: Intense exercise has been shown to have negative effects on systolic- and diastolic ventricular function in adults. Very little is known about the normal reaction of the growing heart to endurance stress. Design: Longitudinal follow-up study pre- and post age adopted triathlon Setting: Tertiary paediatric cardiac centre Patients: 26 healthy children (18 males, 7.9-16.4 years, mean 12.6 years) took part in an age adapted triathlon circuit. Methods: The athletes were investigated by 2-D-echo/speckle tracking, M-mode, PW-Doppler, colour-Doppler and colour codes tissue Doppler two to four weeks before and immediately after the race. Results: After the competition there was an increase in cardiac output, mediated by an increase in heart rate and not by an elevated preload, according the mechanism of Frank-Starling. 2-D speckle tracking shows a reduced longitudinal strain in the right ventricle and additionally reduced circumferential strain in the left ventricle with attenuation of the systolic function. The late diastolic inflow velocities are increased in both ventricles, indicating reduced diastolic function due to an impairment of myocardial relaxation. Conclusion: Systolic- and diastolic function were attenuated in children and adolescents after participating in an age adopted triathlon which took place in Munich 2009. The sequelae of these alterations are unclear and especially the growing heart might be more susceptible to myocardial damage caused by intense endurance stress.
Abstract 19012: Impact of Beta-Blocker on Angiographic and Clinical Parameters During Intracoronary Acetylcholine Provocation Test
Authors: Sung Il Im, Seung Woon Rha, Byoung Geol Choi, Se Yeon Choi, Sun Won Kim, Jin Oh Na, Seong Woo Han, Cheol Ung Choi, Hong Euy Lim, Jin Won Kim, Eung Ju Kim, Chang Gyu Park, Hong Seog Seo, Dong Joo Oh
Journal: Circulation (2012)

Background: Beta blockers (BB) are widely used to control hypertension. It is well known that BB may lead to significant vasospasm. However, the impact of chronic administration of BB on clinical and angiographic characteristics during acetylcholine (Ach) provocation test is not clarified yet. Methods: A total 3034 consecutive patients (pts) underwent coronary angiography with Ach provocation test from January 2004 to August 2010 were enrolled for this study. Ach was injected in incremental doses of 20, 50, 100μ g into the left coronary artery. Significant coronary artery spasm (CAS) was defined as focal or diffuse severe transient luminal narrowing (&gt;70%) with/without chest pain or ST-T change on ECG. A total 1394 pts (45.9%) showed positive provocation tests. Among the (+) provocation test pts, we compared the clinical and angiographic characteristics of patients with beta-blocker to those without beta-blocker in pts with myocardial infarction. Results: The baseline clinical and procedural characteristics are well balanced between the two groups. There was no difference in the incidence of myocardial bridges, chest pain, ischemic ECG changes and atrioventricular (AV) block on ECG, incidence of baseline spasm, severe vasospasm, multi-vessel involvements during the Ach provocation test were similar in both groups Conclusion: The use of beta blocker in pts with vasospastic angina was not associated with worse clinical and angiographic parameters during the Ach provocation test. BB may be safely used in pts with vasospastic angina.
Abstract 8950: Simple and Accurate Electrocardiographic Criteria for Differentiation Among Acute Coronary Syndrome, Acute Pulmonary Embolism, and Takotsubo Cardiomyopathy
Authors: Masami Kosuge, Toshiaki Ebina, Kiyoshi Hibi, Kengo Tsukahara, Noriaki Iwahashi, Nobuhiko Maejima, Mitsuaki Endo, Satoshi Morita, Satoshi Umemura, Kazuo Kimura
Journal: Circulation (2012)

Background: Negative T waves (Neg T) in precordial leads are often seen in acute coronary syndrome (ACS), but also occur in acute pulmonary embolism (APE) and takotsubo cardiomyopathy (TC). Differentiating these 3 diseases is important with regard to selecting the appropriate treatment strategy. Methods: We studied 278 patients (178 patients with ACS, 80 with APE, and 20 with TC) who were admitted within 48 h from symptom onset and had Neg T ≥1.0 mm in ≥2 contiguous precordial leads (V1-4) without ST-segment elevation on admission ECG. In all patients with ACS, the culprit lesion was confirmed to be located in the left anterior descending coronary artery by angiography during hospitalization. Baseline characteristics and ECG findings on admission were analyzed. Results: In patients with ACS, APE, and TC, age was 67±10, 64±14, and 69±12 years (p=0.10); the rates of women were 38%, 69%, and 75% (p&lt;0.01); positive troponin T was 46%, 49%, and 85% (p&lt;0.01); S1Q3T3 pattern was 0%, 25%, 0% (p&lt;0.01); right axis deviation was 0%, 8%, and 0% (p&lt;0.01); ST-segment depression ≥0.5 mm was 40%, 18%, and 25% (p&lt;0.01), and the amplitude of maximal Neg T was 5±3, 3±2, and 7±3 mm (p&lt;0.01). The prevalence of Neg T is shown in Figure, in which the anatomically contiguous Cabrera sequence was used to display limb leads, and it significantly differed in all 12 leads among the 3 groups (p&lt;0.001, respectively). Neg T in both leads III and V1 identified APE with 86% sensitivity, 98% specificity, and 95% predictive accuracy, and Neg T in lead -aVR (ie, positive T wave in lead aVR) combined with no Neg T in lead V1 identified TC with 95% sensitivity, 99% specificity, and 99% predictive accuracy, representing the highest diagnostic accuracies. Conclusions: The distribution of Neg T obviously differed among ACS, APE, and TC, suggesting the differences in underlying electrophysiologic mechanisms. These differences were useful for differential diagnosis of these 3 diseases.
Abstract 77: Tachycardia During Hypothermia as a Marker of Poor Outcomes in Cardiac Arrest Survivors
Authors: Theresa Waters, Yong Ji, Matthew Liakos, Basil Saour, Vikash Khurana, Mikhail Torosoff
Journal: Circulation (2012)

Hypothesis: Therapeutic hypothermia in cardiac arrest survivors is typically associated with bradycardia. We investigated clinical and demographic variables and outcomes associated with tachycardia in patients treated with therapeutic hypothermia. Methods: Demographic and clinical data, and ECGs of 26 consecutive cardiac arrest survivors (9 females, 58+/-18 years old, 5 with history diabetes, and 6 with history of coronary artery disease) on admission, during and after therapeutic hypothermia were reviewed. Analyses of variance, chi-square, and logistic regression were used. The study was approved by the IRB. Results: Tachycardia (heart rate &gt; 100 bpm, 81% sinus, no VT-VFib) was observed in 40% of ECG tracings before or during hypothermia or after re-warming. Tachycardia was more common in females (55 vs. 32%, p=0.044), patients with pulmonary disease (39 vs. 13%, p=0.009), or when pre-resuscitation rhythm was PEA (60 vs. 27%, p=0.003) or asystole (23 vs. 15%, p=0.003). Diabetes, myocardial ischemia, LV systolic dysfunction, acute infection, renal insufficiency, treatment with ACE inhibitors or diuretics were not associated with tachycardia. There were multiple biochemical abnormalities associated with tachycardia, including decreased pH (p&lt;0.0001) and decreased hemoglobin (p=0.028), increased glucose (p&lt;0.001), sodium (p=0.078), potassium (p=0.044), or creatinine (p=0.108). Tachycardia was associated with significantly increased hospital mortality (53% vs. 28%, p=0.029), regardless whether it was observed on admission (63 vs. 38%), during hypothermia (67% vs. 33%), or after the re-warming (67 vs. 33%). In multivariate logistic regression analysis only cardiac arrest rhythm (HR of death with PEA-Asystole 11.1, 95%CI 3.2-38.4, p&lt;0.001), but not demographic or biochemical variables or tachycardia (HR 1.7, 95%CI 0.5-5.8, p=0.391) were predictive of mortality. Conclusion: Tachycardia in cardiac arrest survivors undergoing therapeutic hypothermia is a marker of poor prognosis, likely reflective of severe metabolic abnormalities, especially in patients presenting with pulseless electrical activity or asystole. More studies of this important subject are needed.
Abstract 19255: A Role for Mitochondria in Triggered Activity from Cardiomyocytes with Reduced Sarcoplasmic Reticulum Calcium Release
Authors: An Xie, Nidhi Kapoor, Hong Liu, Dan Bare, Lianzhi Gu, Kenneth R Boheler, Kathrin Banach, Samuel C Dudley
Journal: Circulation (2012)

Introduction: A prominent feature of systolic heart failure is the reduction of Ca2+ induced Ca2+ release from sacroplasimic reticulum (SR). Moreover, patients with heart failure are at high risk of arrhythmic sudden cardiac death. Hypothesis: The basis for increased arrhythmic risk with reduced SR Ca2+ release was investigated using embryonic stem cell derived ventricular-like cardiomyocytes (CMs) deficient for the expression of the ryanodine receptor (RYR-/-). Methods: Action potentials (APs) and L-type Ca2+ currents were recorded in the perforated current-clamp and whole cell voltage-clamp respectively. Changes in [Ca2+]i were determined by confocal imaging of Fluo-4/AM ESCs. APs were recorded from CMs differentiated for 19 days. Results: Compared with wild type CMs, L-type Ca2+ channels showed less current density and slightly slower activation/inactivation kinetics in RyR-/- CMs. AP and Ca2+ transient frequency were decreased. Ca2+ transient amplitudes were smaller in RyR-/- CMs and had prolonged transient duration at 50% amplitude. Ca2+ transients are comparable to those of WT cells after SR depletion by caffeine, indicating that the SR in RyR-/- CMs did not contribute significantly to Ca2+ release or removal. Despite a shorter AP duration at 90% repolarization (APD90: 187.7 ± 13.8 ms vs. 274.3 ± 36.3 ms), RyR-/- ventricular-like CMs displayed more delayed after-depolarizations (DADs, 75% vs. 0%, p&lt;0.05) than WT CMs. Arrhythmia-inducing Ca2+ leak in RyR-/- CMs can come from IP3R mediated Ca2+ release or from mitochondrial Ca2+. In the presence of the IP3R blocker 2-APB, AP frequency decreased (from 1.3±0.1 to 0.3±0.1 Hz) supporting its role in pacemaker activity, but DADs remained. In the absence of [Ca2+]o, an increase in SR load after a caffeine-induced depletion of the SR indicated Ca2+ transfer from the mitochondria to the SR. Application of the mitochondrial NCX blocker (CGP) suppressed this transfer in WT CMs. Block of the mitochondrial Ca2+ uptake (Ru360) prevented DADs in RyR-/- CMs. Conversely application of PPT, an activator of the mitochondrial Ca2+ uniporter, enhanced DADs in RyR-/- ESCs. Conclusions: DADs may occur in the presence of reduced SR Ca2+ release. DADs in RyR-/- CMs depends on mitochondrial Ca2+ flux.
Abstract 9368: Plasma Membrane Calcium ATPase Isoform 1 Protects the Heart from Cardiomyopathy, Arrhythmias and Hypertension
Authors: Mohamed A Shaheen, Tamer M Mohamed, Sukhpal Prehar, Min Zi, Nicholas P Stafford, Samantha Roberts, Hannah Garnett, Yanwen Wang, Ming Lei, Clare E Austin, Ludwig Neyses, Elizabeth J Cartwright
Journal: Circulation (2011)

With 1 in 3 people in the USA dying as a result of cardiovascular disease, and the incidence of these diseases rapidly increasing in the developing world, it is essential that we continue to provide mechanistic insights into their development and progression. Several recent human genome wide association studies have identified single nucleotide polymorphisms in the plasma membrane calcium ATPase isoform 1 (PMCA1) gene as the strongest association with hypertension and blood pressure variance; hypertension along with cardiomyopathy and arrhythmias are central features of heart failure. In this study we provide evidence that PMCA1, which is a transmembrane calcium transporter known to eject calcium from the cell, is involved in all of these key features of heart failure. To elucidate the role of PMCA1 in cardiac function we generated mice carrying a cardiomyocyte-specific gene deletion of PMCA1 (PMCA1 cko ). In response to pressure overload hypertrophic stress induced by transverse aortic constriction (TAC) PMCA1 cko mice displayed accelerated cardiac dysfunction shown by significantly reduced fractional shortening compared to controls (FS; PMCA1 cko /TAC: 21±2%, PMCA1 f/f /TAC 32±3%, PMCA1 cko /Sham and [alpha]-MHC-Cre/TAC 35±2%, p &lt;0.05, n=6). This was accompanied by increased lung weight/body weight in PMCA1 cko /TAC (11.5±1 vs 7.8±0.8 mg/g in PMCA1 f/f /TAC, p &lt;0.05, n=6), greater cardiomyocyte cross-sectional area and significantly elevated interstitial fibrosis. Our data shows that in the myocardium PMCA1 has an additional role in stabilising cardiac rhythm. At 3 months of age PMCA1 cko displayed episodes of spontaneous ventricular tachycardia whilst exhibiting an 80% downregulation in the expression of the voltage gated sodium channel Na v 1.5 and a significant reduction in the corresponding current. To investigate the relationship between PMCA1 and blood pressure we generated PMCA1 heterozygous knockout mice (PMCA1 Ht ) in which both systolic and diastolic carotid pressure was significantly increased in PMCA1 Ht in comparison to wild type littermates. In conclusion, this data addresses the mechanistic basis for the association of PMCA1 with hypertension, cardiomyopathy and arrhythmias which are key contributors to heart failure.
Abstract 8693: Knockout of p47 <sup>phox</sup> Attenuates Angiotensin II-induced Endothelial Dysfunction and Vessel Damage in Vivo
Authors: Junjie Du, Jian-Mei Li
Journal: Circulation (2011)

Increased bioavailability and activity of angiotensin II (AngII) have been found to be associated with vascular oxidative stress derived from a Nox2 enzyme. The Nox2 has several regulatory subunits i.e. p40 phox , p47 phox , p67 phox and rac1. However, it is unclear about the role of p47 phox (a key regulatory subunit of Nox2 activation) in mediating AngII-induced vessel dysfunction. In this study, we examined the effect of p47 phox knockout (KO) on AngII-induced hypertension and aortic dissection using littermates of C57BL/6 wild-type (WT) and p47 phox KO mice (n=7) at the age of 10~12 months. In WT mice, AngII infusion (1.15mg/kg/day delivered by osmotic mini-pump for 14 days) increased significantly the systolic blood pressure (SBP) from 127 + 13 to 172 + 11 mmHg, and this was accompanied with significant indication of cardiac hypertrophy (heart/body weight ratio increased ~17.9 + 0.1%) as compared to vehicle infused controls (P &lt; 0.05), and 3 out of 7 AngII-infused WT mice developed aortic dissection. However, in p47 phox KO mice, AngII infusion caused a mild increase in SBP (from 119 + 9 to 149 + 10 mmHg, P&lt;0.05) without significant increase in heart/body weight ratio, and there was no aortic dissection in AngII-infused KO mice. Aorta organ bath showed that AngII-infusion reduced significantly the endothelium-dependent vessel relaxation to acetylcholine in WT mice (Emax from 82.10 + 8.73% to 54.37 + 6.91%, P &lt; 0.05), which can be returned to the control level by adding a superoxide scavenger, tiron. However, AngII had no significant effect on endothelium-dependent vessel relaxation to acetylcholine in the p47 phox KO mice (Emax from 73.08 + 1.15% to 65.73 + 5.35%). In conclusion, p47 phox plays a critical role in mediating AngII-induced endothelial dysfunction, hypertension and aortic dissection. Knockout or inhibiting p47 phox may protect vessels from these AngII-induced vascular disorders.
Abstract 27: Novel Use of Wireless 12-Lead Electrocardiogram Transmission in a Prehospital Setting
Authors: Go Nishikawa, Hiroshi Nonogi, Noriko Mori, Yoko Matsuo, Shiro Shimizu, Toshiko Oda, Osamu Doi, Hirofumi Kambara
Journal: Circulation (2012)

Introduction The AHA/ACC guidelines recommend pre-hospital 12-lead electrocardiogram (ECG) transmission to a percutaneous coronary intervention (PCI) hospital to facilitate the care of patients with acute coronary syndrome. We created a handheld wireless 12-lead ECG transmission system called Fujiyama involving Cardiospy® Mobile, a handheld 12-lead ECG recording device. Fujiyama functions by transmitting the ECG from Cardiospy® Mobile to a smartphone through Bluetooth wireless technology, converting the ECG to MFER(Medical Waveform Format Encoding Rule)/JPEG, and sending it to a designated email address using ubiquitous and standard network. Hypothesis We predicted that our smaller device will be equally efficacious in transmitting accurate data as the current portable ECG recording device used in the healthcare industry. Methods We recorded and transmitted 12-lead ECGs using our device from a moving vehicle (simulating an ambulance), and investigated the influences of road turbulence, body movements, fast driving, as well as transmission time and accuracy by comparing ECGs recorded in a hospital setting. Furthermore, after approval from the institutional review board, the device was tested on 24 actual patients (4 emergency room, 5 clinic, 4 home hemodialysis, 11 visiting nurse care) transmitting ECGs to the attending cardiologist of a PCI hospital. Results There were no significant ECG differences found between sent and received ECGs, and vehicle speed did not affect the baseline ECG. Body movement, blood pressure measurement and cardiac compression caused the baseline to wander to some extent, but did not affect ECG interpretation. The transmission time of a 250-350 KB file was 7-95 s (median 23 s), short enough for emergency settings. Transmission rate of the 24 ECGs was 100 %, and only one had significant interference from appliances and peripheral equipment. Conclusions As far as we know, this system is the first wireless 12-lead ECG recording and transfer device in this weight (150 g, including batteries) and size category (70 × 38 × 125 mm). In conclusion, successful implementation of this system may improve the communication and care of patients with acute coronary syndrome in various settings, including emergency pre-hospital care.
Abstract 224: Amplitude Spectrum Area Based Defibrillation Decision Greatly Improves Shock Success Rate and Accuracy During Prehospital Cardiopulmonary Resuscitation
Authors: Giuseppe Ristagno, Weilun Quan, Gary Freeman
Journal: Circulation (2012)

Background. We retrospectively evaluated the capability of “amplitude spectrum area” (AMSA) to predict the likelihood that a defibrillation (DF) would restore a perfusing rhythm during CPR in human victims of out-of-hospital cardiac arrest. We hypothesized that threshold values of AMSA could be identified and would increase DF success rate and accuracy. Methods. ECG data, including 1410 DFs, were obtained from 748 cardiac arrest patients from multiple areas in the US. A 4.1 secs ECG window ending at 0.5 sec before DF was analyzed and AMSA calculated prior to first DF and subsequent DFs delivered in cases of DF-resistant VF. Successful DF was defined as return of an organized rhythm within 60 sec. For first and subsequent DFs, AMSA threshold values were analyzed with regard to their ability to discriminate among successful and not successful DFs. Sensitivity, specificity, accuracy, and positive predictive value (DF success rate) of an AMSA based decision algorithm were calculated. The DF performance was then compared between two DF decision algorithms with and without AMSA threshold, respectively. Results. A total of 1221 qualified DF events from 607 patients, with 578 first DF attempts and 543 subsequent ones for DF-resistant VF, were included in the analyses. For the DF decision algorithm without AMSA, the DF success rate and accuracy were 27%/27% for the first DFs, 9%/9% for the subsequent DFs, respectively. An optimized AMSA threshold was found to be 14 mV-Hz for first DFs and 12 mV-Hz for subsequent ones. Incorporation of these AMSA thresholds into a DF decision algorithm increased both DF success rate and accuracy. The first DF achieved a DF success rate of 54% and an accuracy of 75% while subsequent DF attempts achieved 42% in DF success rate and 89% in accuracy. These results translated into an increase of DF success rate and accuracy by 100% and 180% for the first DFs, and 360% and 880% for the subsequent DFs. Conclusions. In this population, a defibrillation decision algorithm incorporating an AMSA threshold was confirmed to be capable to predict DF success with high accuracy. Different optimized AMSA thresholds can be selected for first and subsequent DF attempts to predict DF success with high accuracy may be selected in the case of first and subsequent DFs.
Abstract 19057: Functional Tricuspid Regurgitation is an Independent Predictor of Mortality and Morbidity in Patients with Aortic Stenosis Undergoing Valve Replacement
Authors: Timothy C Tan, Aidan W Flynn, Luis M Rincon, Maria P Nunes, Praveen Mehrotra, Arvind K Agnihotri, David M Shahian, Michael H Picard, Jonathan Afilalo
Journal: Circulation (2012)

Background: In patients with severe aortic stenosis (AS), pulmonary hypertension (PHT) and right ventricular (RV) dysfunction are predictors of adverse events. PHT and RV dysfunction can lead to progressive functional tricuspid regurgitation (FTR), which has an under-appreciated yet potentially devastating course. We describe the impact of FTR in patients with severe AS undergoing aortic valve replacement (AVR). Methods: We identified consecutive patients with severe AS who underwent AVR in 2009 and 2010. We excluded those with concomitant mitral or tricuspid valve replacement, organic tricuspid valve pathology, and those without an available echocardiogram (echo) within 3 months of surgery. A panel of quantitative echo parameters was measured according to American Society of Echocardiography guidelines. Clinical variables were extracted from the Society of Thoracic Surgeons (STS) database. The outcomes of interest were postoperative STS-composite mortality or major morbidity, and all-cause mortality over a mean follow-up of 1.8 years. Results: Of 207 patients studied, 21 (10.1%) had moderate-to-severe FTR. Moderate-to-severe FTR was associated with higher pulmonary artery systolic pressure (58 vs. 38 mmHg, P&lt;0.001), worse RV myocardial performance index (0.57 vs. 0.42, P=0.003), lower RV fractional area change (38% vs. 47%, P=0.004), lower LVEF (48% vs. 58%, P=0.002), and higher left atrial volume index (56 vs. 42 cm2/m2, P&lt;0.001), but not with aortic valve area (0.71 vs. 0.71 cm 2 , P=0.82) or peak aortic velocity (4.3 vs. 4.4 m/s, P=0.62). Patients with FTR were more likely to suffer postoperative in-hospital mortality or major morbidity (48% vs. 23%, P=0.02) and long-term mortality (17% vs. 9%, P=0.004). When echo parameters were entered in a multivariable model, optimal predictors of all-cause mortality were: FTR (HR 3.46, 95% CI 1.26, 9.49) and restrictive diastolic filling (HR 3.07, 95% CI 1.16, 8.11). Results were similar when adjusted for clinical covariates including chronic lung disease. Conclusion: In the setting of AVR, moderate-to-severe FTR is an independent predictor of postoperative mortality and major morbidity. FTR is prevalent in AS patients with PHT and poor right or left ventricular function.