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BackgroundDeep hypothermic circulatory arrest (DHCA) at

PURPOSE Our objective was to calculate the positive predictive value (PPV) of the ICD-9 diagnosis code for angioedema when physicians adjudicate the events by electronic health record review. Our secondary objective was to evaluate the inter-rater reliability of physician adjudication. METHODS Patients from the Cardiovascular Research Network previously diagnosed with heart failure who were started on angiotensin-converting enzyme inhibitors (ACEI) during the study period (July 1, 2006 through September 30, 2015) were included. A team of two physicians per participating site adjudicated possible events using electronic health records for all patients coded for angioedema for a total of five sites. The PPV was calculated as the number of physician-adjudicated cases divided by all cases with the diagnosis code of angioedema (ICD-9-CM code 995.1) meeting the inclusion criteria. The inter-rater reliability of physician teams, or kappa statistic, was also calculated. RESULTS There were 38 061 adults with heart failure initiating ACEI in the study (21 489 patient-years). Of 114 coded events that were adjudicated by physicians, 98 angioedema events were confirmed for a PPV of 86% (95% CI: 80%, 92%). The kappa statistic based on physician inter-rater reliability was 0.65 (95% CI: 0.47, 0.82). CONCLUSIONS ICD-9 diagnosis code of 995.1 (angioneurotic edema, not elsewhere classified) is highly predictive of angioedema in adults with heart failure exposed to ACEI.

Cardiac tissue engineering, a fairly new concept in cardiovascular research, could substantially improve our success in both in vitro modeling of cardiac microtissue and in vivo cardiac regenerative medicine. To a large extent, this success was attributed to mechanical as well as electrical properties of cardiac-designated biomaterials which inherit the fundamental characteristics of a native myocardial extracellular matrix. Large efforts have been made toward designation and construction of these scaffolds which paved the way for more natural-like biomaterials. As an important characteristic, electrical conductivity has grabbed special attention, thus opening up a whole new area of research to achieve the best biomaterial. Electroconductive scaffolds have benefitted from both incorporation of conductive particles in polymeric matrix and fabrication of organic conductive polymers which supported cardiac tissue engineering. However, conductive scaffolds have not yet achieved full success and more work is required to obtain the optimal conductivity with highest similarity to the native heart for in vitro cardiac microtissue engineering.

The complexity of cardiovascular diseases (CVDs), which remains the leading cause of death worldwide, makes the current clinical pathway for cardiovascular risk assessment unsatisfactory, as there remains a substantial unexplained residual risk. Simultaneous assessment of a large number of plasma proteins may be a promising tool to further refine risk assessment, and lipoprotein-associated proteins have the potential to fill this gap. Technical advances now allow for high-throughput proteomic analysis in a reproducible and cost-effective manner. Proteomics has great potential to identify and quantify hundreds of candidate marker proteins in a sample and allows the translation from isolated lipoproteins to whole plasma, thus providing an individual multiplexed proteomic fingerprint. This narrative review describes the pathophysiological roles of atherogenic apoB-containing lipoproteins and the recent advances in their mass spectrometry-based proteomic characterization and quantitation for better refinement of CVD risk assessment.

Chlorisondamine (CSD) has been used to assess the neurogenic contribution to blood pressure (BP) and vasomotor sympathetic tone in animal models. It is assumed that the reduction in BP following CSD administration is associated to decreases in cardiac output (CO) and peripheral resistance, reflecting cardiac and vasomotor sympathetic tone, respectively. Surprisingly, this has not been characterized experimentally in mice, despite the extensive use of this animal model in cardiovascular research. We hypothesize that a specific dose of CSD can selectively block the sympathetic vasomotor tone. To test this hypothesis, we evaluated the effects of different doses of CSD (intraperitoneal) on BP and heart rate (HR) using telemetry, and on CO using echocardiography. BP and HR in normotensive C57Bl/6J mice reduced to a similar extent by all CSD doses tested (1–6 mg/kg). CSD at 6 mg/kg also reduced CO without affecting left ventricular stroke volume or fractional shortening. On the other hand, lower doses of CSD (1 and 2 mg/kg) produced significantly larger BP and HR reductions in DOCA‐salt–induced hypertensive mice, indicating a greater neurogenic BP response. In addition, all doses of CSD reduced CO in hypertensive mice. Our data suggest that the BP response to CSD in mice likely reflects reduced CO and vasomotor sympathetic tone. We conclude that CSD can be used to assess the neurogenic contribution to BP in mice but may not be appropriate for specifically estimating vasomotor sympathetic tone., Ganglionic blocker, chlorisondamine, can be used to assess the neurogenic contribution to BP in mice, but may not be appropriate to specifically estimate the vasomotor sympathetic tone.

In August 2017, the Cardiovascular Developmental Biology Center (CDBC), together with the "Department of Regenerative Medicine and Cell Biology (RMCB) at the Medical University of South Carolina (MUSC), organized their 13th Annual CDBC Symposium. During this special event, which was organized in collaboration with The Anatomical Record, the unique and important contributions of Dr. Roger Markwald (known to all of us as Roger) to the field of cardiovascular research were celebrated. Fifteen leading investigators in the field presented their ideas and reported results of their studies to an audience that included many familiar faces from Roger's past and present. This group consisted of established investigators from around the world as well as young and upcoming scientists from local institutions. In their presentations, the platform speakers emphasized the significance of Roger's scientific contributions and advice to their professional development and career. In this Special Issue of The Anatomical Record, we assembled a collection of invited papers written by several attendees of the symposium. The issue also contains a number of articles written by colleagues who, for one reason or the other, were not able to attend the meeting, but expressed their desire to contribute to this special "festschrift" of The Anatomical Record in honor and recognition of Roger's amazing career. Anat Rec, 302:14-18, 2019. © 2018 Wiley Periodicals, Inc.

This is the second of the two White Papers from the fourth UC Davis Cardiovascular Symposium Systems Approach to Understanding Cardiac Excitation-Contraction Coupling and Arrhythmias (3-4 March 2016), a biennial event that brings together leading experts in different fields of cardiovascular research. The theme of the 2016 symposium was 'K+ channels and regulation', and the objectives of the conference were severalfold: (1) to identify current knowledge gaps; (2) to understand what may go wrong in the diseased heart and why; (3) to identify possible novel therapeutic targets; and (4) to further the development of systems biology approaches to decipher the molecular mechanisms and treatment of cardiac arrhythmias. The sessions of the Symposium focusing on the functional roles of the cardiac K+ channel in health and disease, as well as K+ channels as therapeutic targets, were contributed by Ye Chen-Izu, Gideon Koren, James Weiss, David Paterson, David Christini, Dobromir Dobrev, Jordi Heijman, Thomas O'Hara, Crystal Ripplinger, Zhilin Qu, Jamie Vandenberg, Colleen Clancy, Isabelle Deschenes, Leighton Izu, Tamas Banyasz, Andras Varro, Heike Wulff, Eleonora Grandi, Michael Sanguinetti, Donald Bers, Jeanne Nerbonne and Nipavan Chiamvimonvat as speakers and panel discussants. This article summarizes state-of-the-art knowledge and controversies on the functional roles of cardiac K+ channels in normal and diseased heart. We endeavour to integrate current knowledge at multiple scales, from the single cell to the whole organ levels, and from both experimental and computational studies.

Aim We studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B-type natriuretic peptide (BNP) from Langendorff heart. Methods Rat hearts were isolated and perfused with a physiological Krebs–Henseleit solution at a constant hydrostatic pressure in Langendorff set-up. The basal O2 level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1 over 20 min using N2 gas (n = 7). BNP and O2 level were measured from coronary flow. During control perfusions (n = 5), the O2 concentration was kept at 26.6 ± 0.3 mg L−1. Results A low oxygen concentration in the perfusate was associated with a significant increase in BNP release (F = 40.4, P

Cardiac therapies are commonly tested preclinically in small-animal models of myocardial infarction. Following functional evaluation, post-mortem histological analysis is essential to assess morphological and molecular alterations underlying the effectiveness of treatment. However, non-methodical and inadequate sampling of the left ventricle often leads to misinterpretations and variability, making direct study comparisons unreliable. Protocols are provided for representative sampling of the ischemic mouse heart followed by morphometric analysis of the left ventricle. Extending the use of this sampling to other types of in situ analysis is also illustrated through the assessment of neovascularization and cellular engraftment in a cell-based therapy setting. This is of interest to the general cardiovascular research community as it details methods for standardization and simplification of histo-morphometric evaluation of emergent heart therapies. © 2015 by John Wiley & Sons, Inc.

With >35 000 participants, the European Society of Cardiology (ESC) congress was one of the biggest ESC events ever and basic science activities were well implemented. I here summarize the basic science activities during the congress. This includes a section ‘Basic science activities in a nutshell’ summarizing the most important sessions as well as ‘Emerging science activities in the ESC’ section with special focus on novel research fields such as the characterization of long non-coding RNAs in cardiovascular research.

Cardiovascular disease has become the leading cause of death and constitutes a serious public health issue in China. Faced with the burgeoning epidemic of cardiovascular disease and the huge burden and economic losses it causes, the Chinese government has attached the utmost importance to cardiovascular research, increasing funding to support basic and clinical studies, integrating resources and recruiting outstanding talent from overseas. The continued and growing support from the government has yielded substantial changes in terms of new discoveries, scientific publications and drug research and development within the last decade. In spite of the advances in cardiovascular research, China still faces significant challenges ahead in encouraging innovation, developing the prevention-oriented health policies and strengthening international collaboration.

The zebrafish-based assay is a widely used animal model system for cardiovascular research. In this study, we investigated the cardiac defects caused by terfenadine and tested the pharmacological response of digoxin to zebrafish with cardiac defects. The study suggested that zebrafish could be a suitable model for phenotype-based screening and evaluation of positive inotropic agents. This phenotype-based heart failure zebrafish model system was then utilized in in-house library screen. Some positive inotropic compound was discovered, which could attenuate the cardiac defects by increasing the flow velocity of caudal artery blood.

Extensive technical advances in the past decade have substantially expanded quantitative proteomics in cardiovascular research. This has great promise for elucidating the mechanisms of cardiovascular diseases (CVD) and the discovery of cardiac biomarkers used for diagnosis and treatment evaluation. Global and targeted proteomics are the two major avenues of quantitative proteomics. While global approaches enable unbiased discovery of altered proteins via relative quantification at the proteome level, targeted techniques provide higher sensitivity and accuracy, and are capable of multiplexed absolute quantification in numerous clinical/biological samples. While promising, technical challenges need to be overcome to enable full utilization of these techniques in cardiovascular medicine. Here we discuss recent advances in quantitative proteomics and summarize applications in cardiovascular research with an emphasis on biomarker discovery and elucidating molecular mechanisms of disease. We propose the integration of global and targeted strategies as a high-throughput pipeline for cardiovascular proteomics. Targeted approaches enable rapid, extensive validation of biomarker candidates discovered by global proteomics. These approaches provide a promising alternative to immunoassays and other low-throughput means currently used for limited validation.

The right ventricle has become an increasing focus in cardiovascular research. In this position paper, we give a brief overview of the specific pathophysiological features of the right ventricle, with particular emphasis on functional and molecular modifications as well as therapeutic strategies in chronic overload, highlighting the differences from the left ventricle. Importantly, we put together recommendations on promising topics of research in the field, experimental study design, and functional evaluation of the right ventricle in experimental models, from non-invasive methodologies to haemodynamic evaluation and ex vivo set-ups.

Background In basic cardiovascular research focusing on animal models of myocardial infarction (MI), the measurement of infarct size is performed by planimetry of histological sections of the heart. However, in the setting of chronic MI with ongoing changes in ventricular geometry caused by wall thinning and hypertrophy, the scar area tends to become smaller. Materials and Methods Here, in this study we compared infarct measurements in tissue sections (of rat and porcine hearts) based on three different calculation approaches, that is, infarct area, infarct lengths and infarct angles utilizing the centroid of the left ventricle using a newly developed calculation approach. Results Infarct sizes from all three measurement approaches showed significant correlation with parameters of cardiac function. However, results derived from area measurements were significantly smaller than those obtained using the other two measurement approaches due to scar thinning (infarct size area: 14·81% ± 1·27 SEM, length: 23·94% ± 2·04 SEM, angle: 24·75% ± 2·13 SEM, P

This review mirrors progress in cardiovascular medicine as reflected by scientific contributions published in the Journal of Internal Medicine (from 1989), Acta Medica Scandinavica (from 1919 until 1989) and Nordiskt Medicinskt Arkiv (before 1919). A total of 149 articles were identified within this field since the first, published work in this field 1877-1970. The latter year was set as and end for the review since this was the year the first contribution by the author of this review was published in the journal. To cope with the large number individual publications related to different aspects of cardiovascular medicine were grouped together into fields in which Scandinavian contributions were pioneering or for other reasons of particular interest. These articles were briefly summarized together with some information of the author(s) and the contributions were put into the perspective of subsequent importance and/or scientific and clinical development. Among topics with insightful contributions published in the journal are electrophysiology, diagnostic techniques including standardization, endurance exercise and the heart, electrocardiography, myocardial infarction, atrio-ventricular block and cardiac pacing. Some of these early contributions were indeed, considering the methods available at the time for the investigations impressive and many predictions truly insightful and imaginative. Other contributions may, at least by the present day reader, seem somewhat odd.

Xenobiotic particles can be considered in two genres: air pollution particulate matter and engineered nanoparticles. Particle exposures can occur in the greater environment, the workplace, and our homes. The majority of research in this field has, justifiably, focused on pulmonary reactions and outcomes. More recent investigations indicate that cardiovascular effects are capable of correlating with established mortality and morbidity epidemiological data following particle exposures. While the preliminary and general cardiovascular toxicology has been defined, the mechanisms behind these effects, specifically within the microcirculation, are largely unexplored. Therefore, the purpose of this review is several fold: first, a historical background on toxicological aspects of particle research is presented. Second, essential definitions, terminology, and techniques that may be unfamiliar to the microvascular scientist will be discussed. Third, the most current concepts and hypotheses driving cardiovascular research in this field will be reviewed. Lastly, potential future directions for the microvascular scientist will be suggested. Collectively speaking, microvascular research in the particle exposure field represents far more than a “niche”. The immediate demand for basic, translational, and clinical studies is high and diverse. Microvascular scientists at all career stages are strongly encouraged to expand their research interests to include investigations associated with particle exposures.

The objectives of this review are to describe the Extracorporeal Life Support (ECLS) research at the Penn State Pediatric Cardiovascular Research evaluating new pediatric ECLS components and to discuss a proposed continuous quality improvement model after implementation of new technology. Review of current literature pertaining to studies at the Penn State Hershey Children's Hospital (PSHCH) is presented along with a retrospective chart review of ECLS pediatric patients from January 2000 to June 2010. We describe improvements in the newest hollow-fiber oxygenator demonstrating a lower pressure drop (compared with silicone), and in the newest RotaFlow centrifugal pump which allows higher hemodynamic energy delivered to the patient at higher flow rates with less retrograde flow. The miniaturized pediatric circuit implemented is portable and primes quickly for rapid deployment. Our model of continuous quality improvement includes in-depth evaluation of all circuit component performance through on-site in vivo and in vitro testing at the PSHCH. We utilize the same model to provide comprehensive education and hands-on training of the staff. This cycle can be repeated for evaluation and implementation of any new circuit component. Our comprehensive approach to ECLS may provide the ideal means from which to safely introduce new technology.

Objective To determine the magnitude and range of increases in peak aerobic capacity with hybrid–functional electrical stimulation (FES) rowing versus arms-only rowing in persons with spinal cord injury. Design Comparison of graded exercise tests for peak responses during FES rowing and arms-only rowing. Preliminary data on adaptations to FES row training were gathered in a subset of individuals. Setting Outpatient cardiovascular research laboratory. Participants Six male patients with spinal cord injury (T4-T9, American Spinal Injury Association class A). Methods or Intervention Arms-only rowing was compared with FES rowing, in which the person who is exercising synchronizes the voluntarily controlled upper body movement with the FES-controlled leg movement via stimulation to the paralyzed leg muscles. A subgroup (n = 3) completed at least 6 months of a progressive FES row training exercise program with graded exercise tests every 6 months. Main Outcome Measurements Peak oxygen consumption, peak ventilation, peak respiratory exchange ratio, peak heart rate, and peak oxygen pulse. Results Peak oxygen consumption was greater during FES rowing than during arms-only rowing (20.0 ± 1.9 mL/kg/min versus 15.7 ± 1.5 mL/kg/min, P = .01). Peak ventilation was similar, whereas peak respiratory exchange ratio and peak heart rate tended to be lower ( P = .14 and P = .19, respectively). As a result, oxygen pulse was greater by 35% during FES rowing. Two of the three persons who completed at least 6 months of FES row training demonstrated increases in aerobic capacity greater than those previously observed in able-bodied individuals. Conclusions FES rowing may provide a more robust exercise stimulus for persons with spinal cord injury than most options currently available because of the greater aerobic demand.

Background There are no sufficient data to evaluate the relationship between high-sensitivity C-reactive protein (hs-CRP) and uncovered stent struts on optical coherence tomography (OCT) after drug-eluting stent (DES) implantation. Hypothesis We evaluated the relationship between the preprocedural level of hs-CRP and incomplete neointimal coverage of DES struts on OCT. Methods This study was conducted using 124 eligible patients (132 lesions) treated with sirolimus-eluting stents (SES) or zotarolimus-eluting stents (ZES). The subjects were divided into 2 groups based on the preprocedural hs-CRP level: high-CRP (≥3 mg/L; 58 lesions) and normal-CRP (

It was a tremendous honor to be asked to present the Ian Donald Gold Medal to Charles Kleinman this year, an honor that stems in part from the rarity with which this award is given by non-recipients; I very much appreciated being granted this unique opportunity based on the many years over which Charlie Kleinman and I worked together. It is hard to know where to begin, so I will begin at the beginning. Charlie was born in Queens in New York City. At the age of 20 he graduated from New York University, where he had met his wife Jessica who came with him to Prague for this year’s ISUOG meeting. He then went to New York Medical College, an institution perhaps not quite as well known as some other universities in the US, but that now has the distinction of being the alma mater of two Ian Donald Gold Medal recipients, the other being John Hobbins. He did his residency at Cornell in New York and fellowship partly at Cornell, finishing at the Cardiovascular Research Institute of the University of California, San Francisco. At UCSF Charlie was fortunate to have the opportunity to work with the great Professor Abe Rudolph, as well as Michael Heyman, Norm Silverman and others, giving him the grounding in physiology that shaped his ability to teach physicians as well as patients and their families about fetal and neonatal cardiology. Charlie came to Yale in 1977. Shortly after his arrival, John Hobbins came into his office with a large box full of M-mode recordings from fetuses and said, ‘Charlie, do you think you can do anything with these?’ From that came the first paper in the world to describe in English the clinical use of ultrasound for structural and rhythm diagnosis in the fetal heart1. This ground-breaking publication was followed a couple of years later by another classic paper, in New England Journal of Medicine2. Since most people in ObGyn didn’t read Pediatrics, and this was before the days of online tables of contents, the New England Journal paper was how many of us became aware of the field and the practice of fetal cardiology. For me, it was one of the things that made Yale the place to which I wanted to go for my fellowship in Maternal-Fetal Medicine, because of all that was developing there in ultrasound. As many of you know, over the past 30 years Charlie has had occasional health problems. It has not slowed Charles Kleinman (right) being presented with the 2010 Ian Donald Gold Medal by Joshua Copel

More than a quarter of a million women die each year in the industrialized countries from cardiovascular diseases (CVD), and current projections indicate that this number will continue to rise with our ageing population. Important sex-related differences in the prevalence, presentation, management and outcomes of different CVD have discovered in the last two decades of cardiovascular research. Nevertheless, much evidence supporting contemporary recommendations for testing, prevention and treatment of CVD in women is still extrapolated from studies conducted predominantly in men. The compendium of CVD indicates that current research and strategy development must focus on gender-specific issues to address the societal burden and costs related to these incremental shifts in female gender involvement. Indeed, this significant burden of CVD in women places unique diagnostic, treatment and financial encumbrances on our society that are only further intensified by a lack of public awareness about the disease on the part of patients and clinicians alike. This societal burden of the disease is, in part, related to our poor understanding of gender-specific pathophysiologic differences in the presentation and prognosis of CVD and the paucity of diagnostic and treatment guidelines tailored to phenotypic differences in women. In this, scenario is of outmost importance to know these differences to provide the best care for female patients, because under-recognition of CVD in women may contribute to a worse clinical outcome. This review will provide a synopsis of available evidence on gender-based differences in the initial presentation, pathophysiology and clinical outcomes of women affected by CVD.

The zebrafish heart provides a useful vertebrate cardiovascular model with outstanding advantages, including genetic manipulatability, optical accessibility and rapid development. In addition, an emerging topic in cardiotoxicity assay and drug discovery is its use in phenotype-based chemical screening. Here, we report a technique that allows non-invasive voltage mapping in beating heart using a genetically encoded probe for transmembrane potential. Application of the anti-allergy compound astemizole resulted in aberrant propagation of excitation, which accounted for a lack of ventricular contraction. This optical method will provide new opportunities in broad areas of physiological, developmental and pharmacological cardiovascular research.

Walther Stoeckenius received a MD degree at the University of Hamburg, Germany in 1950. After 18 months of clinical work as an intern, he began postdoctoral work on the development of pox viruses at the Institute for Tropical Medicine in Hamburg using mainly electron microscopy techniques. After two years he moved as Assistant Professor to the Department of Pathology at the University of Hamburg and became Docent for Pathology in 1958. In addition to teaching and routine pathology work, he continued to use electron microscopy to explore the fine structure of cells and developed an interpretation of the triple-layered appearance of membranes in electron micrographs in terms of molecular structure and the chemistry of osmium tetroxide fixation. In 1959 he obtained a position as Research Associate in Keith Porter's laboratory at Rockefeller University. This was changed after a few months to Assistant Professor and he stayed there, later as Associate Professor, for eight years. The work on membrane structure continued, and a model was developed that described the membrane as a lipid bilayer with embedded protein domains. In efforts to isolate such domains, the purple membrane and bacteriorhodopsin were discovered. In 1966, the lure of California became irresistible and Dr. Stoeckenius accepted a professorship at the University of California at San Francisco. The work on bacteriorhodopsin continued there with the emphasis changing from electron microscopy to spectroscopy and biochemical techniques. He is now Professor Emeritus there in the Department of Biochemistry and Biophysics and the Cardiovascular Research Institute.

The mouse is the animal model principally used to study biological processes in mammals. The mutation, overexpression or knockout of one or several genes can provide insight into human disease. In cardiovascular research, evaluation of autonomic nervous function is an essential tool for a better understanding of the pathophysiological conditions in which cardiomyopathy arises and develops. Analysis of heart rate variability is the least invasive method to evaluate the sympathovagal balance on the sino-atrial level. The need to perform this technique on freely moving mice emerged in the 1990s, but despite previous studies it has been difficult to set up and standardize a common protocol. The multitudes of techniques used, plus subtle differences in methodology, impede the comparison and clear interpretation of results. This article aims to make a survey of heart rate variability analysis and to establish a standardized protocol for the assessment of the autonomic neural regulation of heart rate in mice.

[Background] Local fluid dynamics and exposed atherosclerotic lesions regulate thrombus formation. Activated cells in the attached thrombi release microparticles to the circulation (circulating microparticles [cMPs]); however, their phenotype is unknown. [Objectives] To investigate the specific phenotype of the cMPs released by growing thrombi. [Methods/patients] cMPs released by thrombi growing in different well-characterized thrombogenic conditions were investigated. cMP contents just before and immediately after perfusion of the thrombogenic surfaces were analyzed by triple-labeling flow cytometry. cMPs were tested for their thrombin-generating capacity. The cMPs identified in the ex vivo perfusion experiments were validated in blood of ST-elevation myocardial infarction (STEMI) patients undergoing thrombectomy and percutaneous coronary intervention. Culprit coronary blood (STEMI-CCB) and peripheral artery blood (STEMI-PAB) were simultaneously analyzed and compared with peripheral artery blood from age-matched controls (C-PAB) and peripheral artery blood from patients who had recovered from acute coronary syndrome (ACS) (pSTEMI-PAB). [Results] The levels of annexin V+ cMPs significantly increased in blood collected after perfusion of the exposed thrombogenic surfaces. cMP release was directly related to the formed thrombus mass and the plasma procoagulant activity. Post-thrombus blood showed higher thrombin generation potential and contained higher levels of cMPs carrying glycophorin-A (CD235a+; erythrocyte-derived microparticles [ErMPs]) than preperfusion blood (P < 0.05), whereas the levels of cMPs carrying activated and adhesion platelet markers were decreased. STEMI-CCB and STEMI-PAB had significantly higher ErMP levels than control blood (P < 0.005). ErMP levels were also significantly higher in STEMI-PAB than in pSTEMI-PAB, validating the experimental mechanistic studies and suggesting that ErMPs are markers of ongoing coronary thrombosis (C-statistics: 0.950; 95% confidence interval 0.889–1.000; P < 0.001). [Conclusion] Glycophorin-A-rich microparticles are released from evolving growing thrombi into the distal perfusing blood, and can be measured in peripheral blood. CD235a+ cMPs may constitute a novel systemic biomarker of ongoing thrombosis., This work was supported by Spanish Ministry of Science Plan Estatal I+D+I 2013-2016 (SAF2013-42962-R) cofunded by Fondo Europeo de Desarrollo Regional (FEDER-‘Una manera de hacer Europa’), Agència de Gestió d'Ajuts Universitaris i de Recerca (AGAUR-2014SGR1303), Red de Terapia Celular (RD/12/0019/0026) and Red Investigación Cardiovascular (RD/12/00420027) from Instituto Salud Carlos III (ISCIII), Associació Esportiva Jordi Pitarque Ceprià and Fundación Investigación Cardiovascular Jesús Serra to the Cardiovascular Research Chair-UAB to L. Badimon, Spanish Ministry of Science Plan Nacional I+D+I (SAF2012-40208) cofunded by FEDER to G. Vilahur, and Spanish Ministry of Health (FIS-PI13/02850) from ISCIII to T. Padró. G. Vilahur has a contract from the Spanish Ministry of Science and Innovation (RyC-2009-5495; MICINN).

Cardiovascular disease has severe consequences for both individual betterment and organizational health. Yet, organization-based cardiovascular research remains quite limited. This commentary addresses this void by integrating research dating from the famous Hawthorne experiments with current medical science. It then suggests future organizational research on cardiovascular health and recommends use of specific composite cardiovascular measures to advance our understanding of the organizational implications of cardiovascular disease. Copyright © 2006 John Wiley & Sons, Ltd.

The 11th Annual Weinstein Cardiovascular Development Conference was held May 19-22, 2005 at the Westward Look Resort and Conference Center in Tucson, Arizona. The Westward Look was the site of the 6th Weinstein Meeting in 1999, and this year, 330 basic research scientists and research clinicians returned to Tucson for 3 days of meetings, Mariachis, and margaritas. The meeting was hosted by the cardiovascular research group at the University of Arizona and offered flavors of the desert southwest that included record temperatures, the Skopopelli conference logo modified from the Kokopelli of Native American mythology (Fig. 1), and liberal use of a cattle prod to encourage speaker timeliness.

Glenn P. Kelley, M.D.,∗ Frederick R. Helmcke, M.D.,∗ and Edmund Kenneth Kerut, M.D.∗†‡§ ∗Department of Medicine, Section of Cardiology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, †Heart Clinic of Louisiana, Marrero, Louisiana, ‡Cardiovascular Research Laboratory, LSU Health Sciences Center, New Orleans, Louisiana, §Division of Cardiology, Tulane University School of Medicine, New Orleans, Louisiana

Cardiac MRI continues to develop and advance. MRI accurately depicts cardiac structure, function, perfusion, and myocardial viability with an overall capacity unmatched by any other single imaging modality. MRI is an accepted and widely utilized tool for cardiovascular research. Its clinical use has been limited, but is increasing because of its proven clinical efficacy, the proliferation of cardiac-capable MRI systems, and the development of improved pulse sequences. The following article reviews the landmark developments in this field, with an emphasis on recent progress in the evaluation of ischemic or acquired heart disease.

Understanding the mechanisms of natural compounds in modulating disease has moved to the forefront of cardiovascular research. Thymoquinone (TQ), a constituent of the volatile oil derived from Nige...

Jaume Padilla, Nathan T. Jenkins, Pamela K. Thorne, Jeffrey S. Martin, R. Scott Rector, J. Wade Davis, and M. Harold Laughlin Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri; Department of Child Health, University of Missouri, Columbia, Missouri; Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri; Department of Kinesiology, University of Georgia, Athens, Georgia; Department of Biomedical Sciences, University of Missouri, Columbia, Missouri; Department of Biomedical Sciences, Quinnipiac University, Hamden, Connecticut; Research Service, Harry S Truman Memorial Department of Veterans Affairs Medical Center, Columbia, Missouri; Division of Gastroenterology and Hepatology, Department of Internal Medicine, University of Missouri, Columbia, Missouri; Department of Health Management and Informatics, University of Missouri, Columbia, Missouri; Department of Statistics, University of Missouri, Columbia, Missouri; MU Informatics Institute, University of Missouri, Columbia, Missouri; and Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, Missouri

Section I: Biology and Husbandry. Chapter 1 Taxonomy, History, and Use. (James G. Fox). Chapter 2 Anatomy of the Ferret. (Howard E. Evans and Nguyen Quoc An). Chapter 3 Neuroanatomy of the Ferret Brain. (I. Nigel C. Lawes and Paul L. R. Andrews). Chapter 4 Physiology of the Ferret. (Mark T. Whary and Paul L.R. Andrews). Chapter 5 Nutrition. (James G. Fox and Daniel E. McLain). Chapter 6 Housing and Management. (James G. Fox). Chapter 7 Normal Clinical and Biologic Parameters. (James G. Fox). Chapter 8 Growth, Reproduction, and Breeding. (James G. Fox and Judi A. Bell). Section II: Diseases and Clinical Applications. Chapter 9 Hematopoietic Diseases. (Susan E. Erdman, Xiantang Li, and James G. Fox). Chapter 10 Diseases of the Genitourinary System. (James G. Fox, Renee C. Pearson, and Jusi A. Bell). Chapter 11 Diseases of the Gastrointestinal System. (James G. Fox). Chapter 12 Diseases of the Endocrine System. (James G. Fox and Robert P. Marini). Chapter 13 Other Systemic Diseases. (James G. Fox). Chapter 14 Bacterial and Mycoplasmal Disease. (James G. Fox). Chapter 15 Viral Diseases. (James G. Fox, Renee C. Pearson, and John R. Gorham). Chapter 16 Parasitic Diseases. (James G. Fox). Chapter 17 Mycotic Diseases. (James G. Fox). Chapter 18 Neoplastic Diseases. (Xiantang Li and James G. Fox). Chapter 19 Anesthesia, Surgery, and Biomethodology. (Robert P. Marini and James G. Fox). Section III: Research and Applications. Chapter 20 Viral Disease Models. (Renne C. Pearson and John R. Gorham). Chapter 21 Use of the Ferret in Cardiovascular Research. (James P. Morgan and Kerry E. Travers). Chapter 22 use of the Ferret in Behavioral Research. (Michael J. Baum). Chapter 23 Use of the Ferret in Reproductive Neuroendocrinology. (Michael J. Baum). Chapter 24 use f the Ferret in Parasitologic Research. (Mark L. Eberhard). Index.

Despite minimal model characterisation Langendorff perfused murine hearts are increasingly employed in cardiovascular research, and particularly in studies of myocardial ischaemia and reperfusion. Reported contractility remains poor and ischaemic recoveries variable. We characterised function in C57/BL6 mouse hearts using a ventricular balloon or apicobasal displacement and assessed responses to 10-30 min global ischaemia. We examined the functional effects of pacing, ventricular balloon design, perfusate filtration, [Ca(2+)] and temperature. Contractility was high in isovolumically functioning mouse hearts (measured as the change in pressure with time (+dP/dt), 6000-7000 mmHg s(-1)) and was optimal at a heart rate of approximately 420 beats min(-1), with the vasculature sub-maximally dilated, and the cellular energy state high. Post-ischaemic recovery (after 40 min reperfusion) was related to the ischaemic duration: developed pressure recovered by 82 +/- 5 %, 73 +/- 4 %, 68 +/- 3 %, 57 +/- 2 % and 41 +/- 5 % after 10, 15, 20, 25 and 30 min ischaemia, respectively. Ventricular compliance and elastance were both reduced post-ischaemia. Post-ischaemic recoveries were lower in the apicobasal model (80 +/- 4 %, 58 +/- 7 %, 40 +/- 3 %, 32 +/- 7 % and 25 +/- 5 %) despite greater reflow and lower metabolic rate (pre-ischaemic myocardial O(2) consumption (V(O2,myo)) 127 +/- 15 vs. 198 +/- 17 microl O(2) min(-1) g(-1)), contracture, enzyme and purine efflux. Electrical pacing slowed recovery in both models, small ventricular balloons (unpressurised volumes50-60 microl) artificially depressed ventricular function and recovery from ischaemia, and failure to filter the perfusion fluid to0.45 microm depressed pre- and post-ischaemic function. With attention to these various experimental factors, the buffer perfused isovolumically contracting mouse heart is shown to be stable and highly energized, and to possess a high level of contractility. The isovolumic model is more reliable in assessing ischaemic responses than the commonly employed apicobasal model.

1. It has long been held that the microvessels are passive pipes through which the formed elements of blood and plasma course and from which exchange occurs. Physiological and structural data from vascular cells in culture to whole organs strongly support the notion that microvessels, whether in their arrangement as networks, in their microvascular phenotypic subtypes or with regard to their permeability properties, are anything but static. 2. Examples from different models, organs and species are presented to illustrate the spatial and dynamic nature of the microvasculature. 3. Given that the ultimate goal of this cardiovascular research is to apply what is learned from component parts of the microvasculature to understand integrated tissue function, examples of the danger of generalizing results from limited studies are presented. 4. Finally, accurate interpretation of most of the research in this area is predicated on the assumption that probe molecules, rendered visible by the binding of dyes, are biologically inert. 5. We present data demonstrating that some dyes used widely in microvascular studies can alter the barrier under study and/or alter the physicochemical characteristics of the molecule to which they were bound.