2,259 research outputs found

    Incidence of Right Ventricular Dysfunction In Patients of LV Dysfunction with Coronary Artery Disease and Short Term Outcome

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    Objective: To determine the incidence of RV dysfunction in patients of LV dysfunction with coronary artery disease and short term outcome. Methodology: This prospective study was carried out on 168 patients of LV dysfunction with coronary artery disease in the Echocardiography Unit of the departments of Cardiology, Liaquat University Hospital, Hyderabad from 1st October 2017 to 31st October 2018 and followed for three months. All patients with documented CAD were included. RV evaluation was performed on echocardiography through visual evaluation of RV function, RV region measured in four-chamber perspective and RV duration in a lengthy parasternal perspective. RV dysfunction was characterized as TAPSE of less than 1.2 cm. (RV ejection fraction < 35%). All the data was calculated on SPSS version 16.0. Results:  A total of 168 patients were included in this study based on inclusion criteria, out of the 92(54.7%) were male and 76 (45.3%) were female. The mean ± SD (range) was 52.36 ± 10.44 (30 to 60 years). The mean ± SD of RV ejection fraction was 40.73  ± 8.23% (range 25 to 52). The incidence of RV dysfunction was present in 30(17.8%) patients. Conclusion: In patients with LV dysfunction with coronary disease, in our pateints. It is an independent predictor of death and the development of HF in patients with LV dysfunctio

    Hybrid Imaging of the Autonomic Cardiac Nervous System

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    Cardiac autonomic innervation is an integrative part of the physiology of the heart. This chapter reveals an overview of SPECT and PET application in cardiac sympathetic nervous system imaging in various cardiovascular diseases, including acquisition techniques and data analysis.</p

    Sensors for Rate Responsive Pacing

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    Advances in pacemaker technology in the 1980s have generated a wide variety of complex multiprogrammable pacemakers and pacing modes. The aim of the present review is to address the different rate responsive pacing modalities presently available in respect to physiological situations and pathological conditions. Rate adaptive pacing has been shown to improve exercise capacity in patients with chronotropic incompetence. A number of activity and metabolic sensors have been proposed and used for rate control. However, all sensors used to optimize pacing rate metabolic demands show typical limitations. To overcome these weaknesses the use of two sensors has been proposed. Indeed an unspecific but fast reacting sensor is combined with a more specific but slower metabolic one. Clinical studies have demonstrated that this methodology is suitable to reproduce normal sinus behavior during different types and loads of exercise. Sensor combinations require adequate sensor blending and cross checking possibly controlled by automatic algorithms for sensors optimization and simplicity of programming. Assessment and possibly deactivation of some automatic functions should be also possible to maximize benefits from the dual sensor system in particular conditions. This is of special relevance in patient whose myocardial contractility is limited such as in subjects with implantable defibrillators and biventricular pacemakers. The concept of closed loop pacing, implementing a negative feedback relating pacing rate and the control signal, will provide new opportunities to optimize dual-sensors system and deserves further investigation. The integration of rate adaptive pacing into defibrillators is the natural consequence of technical evolution

    Allogenic adipose-derived stem cell therapy overcomes ischemia-induced microvessel rarefaction in the myocardium : systems biology study

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    Altres ajuts: This work was supported by the Spanish Cardiovascular Network of Cell Therapy (Red TerCel RD16/0011/018) and Ciber CV(CB16/11/00411) from the Instituto Salud Carlos III (to LB). Additional funding was received from Plan Nacional de Salud (PNS SAF2016-76819-R to LB, 2015-71653-R to GV) from the Spanish Ministry of Science and Innovation and FEDER funds; from Instituto de Salud Carlos III (CPII13/00012 to GA); and support from a grant from the Muy Ilustrísima Administración from the Hospital de la Santa Creu I Sant Pau (to MG). The authors thank Fundacion Jesus Serra, Barcelona for continuous support.Myocardial microvascular loss after myocardial infarction (MI) remains a therapeutic challenge. Autologous stem cell therapy was considered as an alternative; however, it has shown modest benefits due to the impairing effects of cardiovascular risk factors on stem cells. Allogenic adipose-derived stem cells (ASCs) may overcome such limitations, and because of their low immunogenicity and paracrine potential may be good candidates for cell therapy. In the present study we investigated the effects of allogenic ASCs and their released products on cardiac rarefaction post MI. Pig subcutaneous adipose tissue ASCs were isolated, expanded and GFP-labeled. ASC angiogenic function was assessed by the in-vivo chick chorioallantoic membrane (CAM) model. Pigs underwent MI induction and 7 days after were randomized to receive: allogenic ASCs (intracoronary infusion); conditioned media (CM; intravenous infusion); ASCs + CM; or PBS/placebo (control). Cardiac damage and function were monitored by 3-T cardiac magnetic resonance imaging upon infusion (baseline CMR) and 1 and 3 weeks thereafter. We assessed in the myocardium: microvessel density; angiogenic markers (CD105, CD31, TF, VEGFR2, VEGFR1, vWF, eNOS, CD62); collagen deposition; and reparative fibrosis (TGFβ/TβRII/collagen). Differential proteomics of ASCs and CM was performed to characterize the ASC protein signature. CAM indicated a significant ASC proangiogenic capacity. In pigs after MI, only PBS/placebo animals displayed an impaired cardiac function 3 weeks after infusion (p < 0.05 vs baseline). Administration of ASCs + CM significantly enhanced neovessel formation and favored cardiac repair post MI (p < 0.05 vs the other groups). Molecular markers of angiogenesis were significantly upregulated both at transcriptional and protein levels (p < 0.05). The in-silico bioinformatics analysis of the ASC and CM proteome (interactome) indicated activation of a coordinated protein network involved in the formation of microvessels and the resolution of rarefaction. Coadministration of allogenic ASCs and their CM synergistically contribute to the neovascularization of the infarcted myocardium through a coordinated upregulation of the proangiogenic protein interactome. The online version of this article (doi:10.1186/s13287-017-0509-2) contains supplementary material, which is available to authorized users

    Advances in Electrocardiograms

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    Electrocardiograms have become one of the most important, and widely used medical tools for diagnosing diseases such as cardiac arrhythmias, conduction disorders, electrolyte imbalances, hypertension, coronary artery disease and myocardial infarction. This book reviews recent advancements in electrocardiography. The four sections of this volume, Cardiac Arrhythmias, Myocardial Infarction, Autonomic Dysregulation and Cardiotoxicology, provide comprehensive reviews of advancements in the clinical applications of electrocardiograms. This book is replete with diagrams, recordings, flow diagrams and algorithms which demonstrate the possible future direction for applying electrocardiography to evaluating the development and progression of cardiac diseases. The chapters in this book describe a number of unique features of electrocardiograms in adult and pediatric patient populations with predilections for cardiac arrhythmias and other electrical abnormalities associated with hypertension, coronary artery disease, myocardial infarction, sleep apnea syndromes, pericarditides, cardiomyopathies and cardiotoxicities, as well as innovative interpretations of electrocardiograms during exercise testing and electrical pacing

    Innate immune receptors, key actors in cardiovascular diseases

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    Cardiovascular diseases (CVDs) are the leading cause of death in the industrialized world. Most CVDs are associated with increased inflammation that arises mainly from innate immune system activation related to cardiac damage. Sustained activation of the innate immune system frequently results in maladaptive inflammatory responses that promote cardiovascular dysfunction and remodeling. Much research has focused on determining whether some mediators of the innate immune system are potential targets for CVD therapy. The innate immune system has specific receptors—termed pattern recognition receptors (PRRs)—that not only recognize pathogen-associated molecular patterns, but also sense danger-associated molecular signals. Activation of PRRs triggers the inflammatory response in different physiological systems, including the cardiovascular system. The classic PRRs, toll-like receptors (TLRs), and the more recently discovered nucleotide-binding oligomerization domain-like receptors (NLRs), have been recently proposed as key partners in the progression of several CVDs (e.g., atherosclerosis and heart failure). The present review discusses the key findings related to the involvement of TLRs and NLRs in the progression of several vascular and cardiac diseases, with a focus on whether some NLR subtypes (nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing receptor 3 and nucleotide-binding oligomerization domain-containing protein 1) can be candidates for the development of new therapeutic strategies for several CVDs

    The Heart Is at Risk: Understanding Stroke-Heart-Brain Interactions with Focus on Neurogenic Stress Cardiomyopathy-A Review.

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    In recent years, it has been convincingly demonstrated that acute brain injury may cause severe cardiac complications-such as neurogenic stress cardiomyopathy (NSC), a specific form of takotsubo cardiomyopathy. The pathophysiology of these brain-heart interactions is complex and involves sympathetic hyperactivity, activation of the hypothalamic-pituitary-adrenal axis, as well as immune and inflammatory pathways. There have been great strides in our understanding of the axis from the brain to the heart in patients with isolated acute brain injury and more specifically in patients with stroke. On the other hand, in patients with NSC, research has mainly focused on hemodynamic dysfunction due to arrhythmias, regional wall motion abnormality, or left ventricular hypokinesia that leads to impaired cerebral perfusion pressure. Comparatively little is known about the underlying secondary and delayed cerebral complications. The aim of the present review is to describe the stroke-heart-brain axis and highlight the main pathophysiological mechanisms leading to secondary and delayed cerebral injury in patients with concurrent hemorrhagic or ischemic stroke and NSC as well as to identify further areas of research that could potentially improve outcomes in this specific patient population

    Intracoronary electrocardiogram as a direct measure of myocardial ischemia

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    The electrocardiogram is a valuable diagnostic method providing insight into pathologies of the heart, especially rhythm disorders or insufficient myocardial blood supply (myocardial ischemia). The commonly used surface ECG is, however, limited in detecting short-lasting myocardial ischemia, in particular in the territory of the left circumflex coronary artery supplying the postero-lateral wall of the left ventricle. Conversely, an ECG recorded in close vicinity to the myocardium, i.e., within a coronary artery (intracoronary ECG, icECG) has been thought to overcome these limitations. Since its first implementation during cardiac catheterization in 1985, icECG has shown ample evidence for its diagnostic value given the higher sensitivity for myocardial ischemia detection when compared to the surface ECG. In addition, icECG has been demonstrated to be a direct measure of myocardial ischemia in real-time, thus, providing valuable information during percutaneous coronary diagnostics and interventions. However, a lack of analysing systems to obtain and quantify icECG in real-time discourages routine use. The goals of this MD-PhD thesis are two-fold: First, to determine the diagnostic accuracy of icECG ST-segment shift during pharmacologic inotropic stress in comparison to established indices for coronary lesion severity assessment using quantitative angiographic percent diameter stenosis as reference (Project I). Second, to determine the optimal icECG parameter for myocardial ischemia detection and quantification (Project II and III). In essence, this thesis demonstrates that the icECG is an easy available diagnostic method providing highly accurate information on the amount of myocardial ischemia in real-time. Quantitative assessment of acute, transmural myocardial ischemia by icECG is most accurately performed by measuring ST-segment shift at the J-point, while the quantitative assessment during physical exercise, respectively its pharmacologic simulation, is most accurately performed by measuring ST-segment shift 60ms after the J-point

    Autonomic function after myocardial infarction

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