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Aortic Valve Stenosis

Aortic Valve Stenosis is a narrowing of the aortic valve, the opening through which blood flows from the heart's main pumping chamber (the left ventricle) into the aorta and out to the body.
This condition can make it difficult for the heart to pump blood effectively, leading to symptoms such as chest pain, shortness of breath, and fatigue.
Timely diagnosis and appropriate treatment, which may include valve replacement surgery, are crucial for managing Aortic Valve Stenosis and preventing serious complications.
Explore this important cardiovascular condition in depth with PubCompare.ai's AI-driven platform, which can help optimize your research protocols, improve reproducibility, and boost accuracy by comparing the latest litreature, preprints, and patents.

Most cited protocols related to «Aortic Valve Stenosis»

We first consider methods in which the contribution of some genetic variants (for example, heterogeneous or outlying variants) to the analysis is downweighted (or penalized). If the causal conclusion from a Mendelian randomization investigation depends only on a single genetic variant (particularly if the estimate from this variant is heterogeneous with those from other variants) then the result may be driven by a pleiotropic effect of that particular variant and not by the causal effect of the risk factor.
The simplest way of performing a penalization method is to omit some of the variants from the analysis. This could be done systematically. For example, with a small number of genetic variants, the causal estimates omitting one variant at a time could be considered. Alternatively, it could be done stochastically. For example, we could consider estimates omitting (say) 30% of the genetic variants at a time by selecting the 30% of variants at random a large number of times, and calculating the causal estimate in each case. This sensitivity analysis has been undertaken for the effect of LDL-c on aortic stenosis see eFigure in ref.49 (link). If the spread of results includes only (say) positive effect estimates, then we can be confident that the overall finding does not depend only on the influence of a few variants. However, even if only a small proportion of the estimates are discordant, these cases should be investigated and the omitted variants leading to the discordant estimates should be carefully investigated for potential violations of the instrumental variable assumptions. The causal estimates for the example of CRP on CAD risk based on the genome-wide significant variants using the inverse-variance weighted method are displayed in Figure 6. Two of the 17 variants are omitted from the analysis in turn in a systematic way, and then the 136 resulting estimates are arranged in order of magnitude. The overall estimate excluding the two strongest variants with negative causal estimates is positive, indicating that the overall negative finding based on all the variants seems to be driven by these two variants, and is not supported by the majority of variants.
A more focused approach to omitting genetic variants is to omit genetic variants from the analysis with heterogeneous instrumental variable estimates. This could be done by calculating the contribution to Cochran’s Q statistic for each genetic variant, and omitting any variant whose contribution to the statistic is greater than the upper 95th percentile of a chi-squared distribution on one degree of freedom (3.84). This approach has been applied for investigating the causal effect of lipid fractions on CAD risk.50 (link) More formal penalization methods have been proposed using L1-penalization to downweight the contribution of outlying variants to the analysis in a continuous way.51 , 52 (link) These methods have desirable theoretical properties, giving consistent estimates of the causal effect even if up to half of the genetic variants are not valid instrumental variables. However, they require individual-level data and a one-sample setting (genetic variants, risk factor and outcome measurements are available for the same individuals).
Publication 2016
Aortic Valve Stenosis Genetic Diversity Genetic Heterogeneity Genome Hypersensitivity Lipids Self Confidence
We first consider methods in which the contribution of some genetic variants (e.g., heterogeneous or outlying variants) to the analysis is downweighted (or penalized). If the causal conclusion from a Mendelian randomization investigation depends only on a single genetic variant (particularly if the estimate from this variant is heterogeneous with those from other variants), then the result may be driven by a pleiotropic effect of that particular variant and not by the causal effect of the risk factor.
The simplest way of performing a penalization method is to omit some of the variants from the analysis. This could be done systematically. For example, with a small number of genetic variants, the causal estimates omitting one variant at a time could be considered. Alternatively, it could be done stochastically. For example, we could consider estimates omitting (say) 30% of the genetic variants at a time by selecting the 30% of variants at random a large number of times, and calculating the causal estimate in each case. This sensitivity analysis has been undertaken for the effect of LDL-c on aortic stenosis. See eFigure in Ref. 49 (link). If the spread of results includes only (say) positive effect estimates, then we can be confident that the overall finding does not depend only on the influence of a few variants. However, even if only a small proportion of the estimates are discordant, these cases should be investigated and the omitted variants leading to the discordant estimates should be carefully investigated for potential violations of the instrumental variable assumptions. The causal estimates for the example of CRP on CAD risk based on the genome-wide significant variants using the inverse-variance weighted method are displayed in Figure 6. Two of the 17 variants are omitted from the analysis in turn in a systematic way, and then the 136 resulting estimates are arranged in order of magnitude. The overall estimate excluding the two strongest variants with negative causal estimates is positive, indicating that the overall negative finding based on all the variants seems to be driven by these two variants, and is not supported by the majority of variants.
A more focused approach to omitting genetic variants is to omit genetic variants from the analysis with heterogeneous instrumental variable estimates. This could be done by calculating the contribution to Cochran’s Q statistic for each genetic variant, and omitting any variant whose contribution to the statistic is greater than the upper 95th percentile of a chi-squared distribution on one degree of freedom (3.84). This approach has been applied for investigating the causal effect of lipid fractions on CAD risk.50 (link) More formal penalization methods have been proposed using L1-penalization to downweight the contribution of outlying variants to the analysis in a continuous way.51 ,52 These methods have desirable theoretical properties, giving consistent estimates of the causal effect even if up to half of the genetic variants are not valid instrumental variables. However, they require individual-level data and a one-sample setting (genetic variants, risk factor, and outcome measurements are available for the same individuals).
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Publication 2016
Aortic Valve Stenosis Genetic Diversity Genetic Heterogeneity Genome Hypersensitivity Lipids Self Confidence
The investigation conforms to the Guide for the Care and Use of Laboratory Animals (NIH publication No. 85–23, revised 1996). In 12 week old female mice volume overload was induced by the creation of a shunt between aorta and vena cava inferior. Pressure overload was induced by transverse aortic constriction. Female mice were used because of high mortality in male mice. Echocardiography, in-vivo hemodynamic measurements, cardiomyocyte isolation, cardiomyocyte shortening, calcium measurements and patch-clamp experiments were performed with standard protocols.
Publication 2010
Animals, Laboratory Aorta Aortic Valve Stenosis Calcium Echocardiography Females Hemodynamics isolation Males Mice, House Myocytes, Cardiac Pressure Vena Cavas, Inferior
Sm22αCre, Brg1F/F,
Mef2cCre, R26R and
Tnnt2-rtTA;Tre-Cre mice have been described23 (link), 24 (link),
27 (link), 31 (link), 38 (link). Immunostaining, RNA in
situ hybridization, quantitative RT-PCR, and whole embryo culture were performed as
described23 (link), 26 (link). TAC was modified from previous descriptions20 (link). The pressure load caused by TAC was
verified by the pressure gradient across the aortic constriction measured by
echocardiography. Only mice with a pressure gradient > 30 mmHg were analyzed
for cardiac hypertrophy and gene expression. Curve modeling was performed with the
Levenburg-Marquardt non-linear regression method and XLfit software. Detailed
methods can be found in the Supplementary Information.
Publication 2010
Aortic Pressure Aortic Valve Stenosis Cardiac Hypertrophy Embryo Gene Expression In Situ Hybridization Mice, Laboratory Pressure Reverse Transcriptase Polymerase Chain Reaction Stenosis
Detailed methods are provided in the Supplemental Material. The data are available through https://cics.bwh.harvard.edu/multiomics_databases11 .
In total, 25 AVs were used in this study. AV leaflets were obtained from AV replacement surgeries for severe AV stenosis (Brigham and Women’s Hospital (BWH) approved IRB protocol number: 2011P001703). Written informed consent was provided. In brief, human stenotic AVs were segmented into stages of disease progression: (1) non-diseased, (2) fibrotic, and (3) calcific under the guidance of near-infrared molecular imaging. Transition zones were excluded from all analyses. In total, 27 sub-samples were prepared for label-free proteomics and 9 for transcriptomics.
AVs obtained from three additional patients with severe aortic valve stenosis were used for tissue layer tandem mass tagging (TMT) proteomics and AVs from autopsy donors served as controls. Anatomical layer-specificity was facilitated by laser capture microdissection.
Side-specific in vitro layer calcification potential was evaluated through a migration assay on AV leaflets from eight additional patients with severe AV stenosis after inspection by a pathologist to distinguish the fibrosa from the ventricularis side, and calcification was assessed by Alizarin Red staining at day 21. All cells which underwent proteomics were cultured and passaged in vitro prior to protein collection.
AV whole tissue label-free peptide samples were examined with the Q Exactive mass spectrometer. AV tissue layer TMT and in vitro migration label-free peptide samples were analyzed with the LTQ-Orbitrap Elite mass spectrometer.
For pathway analysis, the protein sets corresponding to each layer and stage were tested for enrichment by a hypergeometric test and adjusted for multiple comparisons using the Benjamini-Hochberg method for controlling the false discovery rate (FDR). Pathway networks were constructed based on their gene overlap. Layer- and stage-specific subnetworks were generated from literature-curated physical protein interactions. The closeness of the calcific stage subnetwork to human diseases was evaluated using average shortest network distance.
Publication 2018
Aortic Valve Stenosis Autopsy Calcinosis Cell Migration Assays Cells CIC protein, human Disease Progression Donors Fibrosis Gene Expression Profiling Genes Homo sapiens Laser Capture Microdissection Operative Surgical Procedures Pathologists Patients Peptides Physical Examination Proteins Stenosis Tissues Woman

Most recents protocols related to «Aortic Valve Stenosis»

This was a cross-sectional study as well as a part of the Baduanjin-Eight-Silken-Movement with Self-efficacy Building for Patients with Chronic Heart Failure (BESMILE-HF) trial (NCT03180320, ClinicalTrials.gov, registration date: 08/06/2017) [6 (link)]. Patients with CHF were prospectively recruited between February 2019 and July 2022 if they fulfilled the following inclusion criteria: (1) ≥ 18 years of age; (2) met the diagnostic criteria for CHF [7 (link)]; (3) clinically stable, defined as symptoms/signs that remained generally unchanged for ≥ 1 month; (4) New York Heart Association class II or III; (5) used beta-blockers; and (6) provided informed consent [8 (link)].
The exclusion criteria were as follows: (1) patients with contraindications for exercise testing, namely, early phase after acute coronary syndrome (up to 6 weeks), life-threatening cardiac arrhythmias, acute heart failure (during the initial period of hemodynamic instability), uncontrolled hypertension (systolic blood pressure > 200 mmHg and/or diastolic blood pressure > 110 mmHg), advanced atrioventricular block, acute myocarditis and pericarditis, moderate to severe aortic valve/mitral stenosis, severe aortic valve/mitral regurgitation, severe hypertrophic obstructive cardiomyopathy, acute systemic illness, or intracardiac thrombus; (2) patients with serious acute or chronic diseases affecting major organs or with mental disorders; (3) patients with a history of cardiac surgery, cardiac resynchronization therapy, intracardiac defibrillation, or implantation of a combined device within the previous 3 months; (4) patients with a history of cardiac arrest within 1 year; (5) patients with a history of peripartum cardiomyopathy, hyperthyroid heart disease, or primary pulmonary hypertension; and (6) patients unable to perform a recumbent bicycle stress test (Fig. 1) [6 (link)].

Flow chart of this study

Eligible participants underwent clinical evaluation (including history of cardiac risk factors and medications), height and weight measurements, blood testing, and electrocardiography. They then underwent a cardiopulmonary exercise test (CPET) and transthoracic echocardiography assessment at rest on the same day (Fig. 2A, B). The BESMILE-HF study[6 (link)] was approved by the Ethics Committee of the Guangdong Provincial Hospital of Chinese Medicine (Approval No. B2016-202-01). All of the participants provided written informed consent.

Illustration of speckle-tracking echocardiography examination (A) and cardiopulmonary exercise testing (B). Strain analysis of the left atrium in the locally enlarged apical four-chamber view and the LA strain curve throughout the cardiac cycle (C). The curves of VO2 and VCO2 with time and work rate, respectively (D). LA, left atrial; VO2, oxygen uptake; VCO2, carbon dioxide uptake; VO2max/pre, ratio of maximum to predicted oxygen uptake, WR, work rate

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Publication 2023
Acute Coronary Syndrome Adrenergic beta-Antagonists Aortic Valve Insufficiency Aortic Valve Stenosis Atrioventricular Block Atrium, Left Carbon dioxide Cardiac Arrest Cardiac Arrhythmia Cardiac Resynchronization Therapy Cardiomyopathies Chinese Diagnosis Disease, Chronic Echocardiography Electric Countershock Electrocardiography Ethics Committees, Clinical Exercise Tests Heart Heart Diseases Heart Failure Hemodynamics High Blood Pressures Hyperthyroidism Hypertrophic Obstructive Cardiomyopathy Idiopathic Pulmonary Arterial Hypertension Medical Devices Mental Disorders Movement Myocarditis Ovum Implantation Oxygen Patients Pericarditis Pharmaceutical Preparations Pressure, Diastolic Signs and Symptoms Silk Strains Surgical Procedure, Cardiac Systolic Pressure Thrombus
Data from clinical examination, 12-lead ECG and transthoracic echocardiography (TTE) performed in our institution by experienced cardiologists within 3 months prior to surgery and at 6 months FU were available in all patients. Transthoracic echocardiograms were performed within routine clinical practice using standard methods (21 (link), 22 (link)). LV and LA diameters and volumes were recorded in the long axis parasternal and apical views, and the left ventricular ejection fraction (LVEF) was estimated visually using the Simpson biplane method. The diagnosis of MVP was made as recommended (1 (link)), and the diagnosis of flail leaflet was based on failure of leaflet coaptation with rapid systolic movement of the flail segment into the LA (23 (link), 24 (link)). MR severity was assessed following an integrative approach as recommended (22 (link)). Original data were used that were unaltered from the original prospective echocardiographic data collection by means of electronic transfer. The LV outflow tract (LVOT) diameter was measured in the parasternal long axis view, and LVOTTVI was recorded as recommended (22 (link)) by pulse wave Doppler in the apical 5-chamber view. Three cardiac cycles at least in sinus rhythm and 10 in atrial fibrillation were averaged. Stroke volume (SV) was calculated as the product of LVOT area by LVOTTVI and was indexed to body surface area (BSA) and referred to as SVi. A threshold of <35 ml/m2 was considered as a priori abnormal by reference to aortic stenosis (25 (link)). Forward LVEF was calculated as the ratio of LVOT stroke volume to LV end-diastolic volume (LVEDV), and a value <50% was considered abnormal (26 (link)).
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Publication 2023
Aortic Valve Stenosis Atrial Fibrillation Body Surface Area Cardiologists Diagnosis Diastole Echocardiography Electrocardiography, 12-Lead Electron Transport Epistropheus Movement Operative Surgical Procedures Patients Physical Examination Pulse Rate Sinus, Coronary Stroke Volume Systole Ventricular Ejection Fraction
A total of 165 hospitalized patients with T2DM categorized by World Health Organization criteria [11 (link)] at the Department of Endocrinology of Xijing Hospital of Air Force Medical University during the period of June 2021 to December 2021 were enrolled. The exclusion criteria were as follows: (1) LVEF < 50%; (2) moderate-to-severe aortic/mitral valve stenosis or insufficiency; (3) a coronary artery disease history or other heart disease; (4) arrhythmia such as left bundle-branch block, frequent ventricular premature complexes or atrial fibrillation; and (5) too poor speck tracking image quality for analysis. According to the exclusion criteria, 15 participants were excluded. Ultimately, 150 patients with T2DM were included in the present study.
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Publication 2023
Aortic Valve Stenosis Atrial Fibrillation Cardiac Arrhythmia Coronary Artery Disease Heart Diseases Left Bundle-Branch Block Patients System, Endocrine Ventricular Contractions, Premature
Cardiotoxicity will be assessed at the hospital to have a more exhaustive control and safety of the participants and at the end of the program. On the one hand, ç hemograms will be carried out to assess of High-Sensitivity Cardiac Troponin, Troponin I, N-terminal portion of B-type natriuretic pro-peptide (NT-proBNP), Troponin T due to their predictive values of cardiac damage in patients under the effects of chemotherapy [54 (link), 55 (link)]. Although these variables were primarily planned in the trial registration, the hospital will be only able to assess High-Sensitive Cardiac Troponin and NT-proBNP.
In addition, an echocardiogram will be performed to measure the left ventricular ejection fraction and GLS due to its modification caused by cardiotoxicity [56 (link)–58 (link)] together with mean and maximum aortic valve gradient, ventricles’ diameters and thicknesses and valve velocities because their possible aortic stenosis risk [59 (link)]. Moreover, a resting electrocardiogram will also be performed on each patient to obtain values for heart rate, heart rhythm, heart rate variability, I-axis and aVF, Q-T interval, QRS complex, S-T segment and T-wave [60 (link)].
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Publication 2023
Aortic Valve Stenosis Cardiotoxicity Echocardiography Electrocardiography Epistropheus Heart Heart Ventricle Hypersensitivity Patients Pharmacotherapy pro-brain natriuretic peptide (1-76) Rate, Heart Safety Troponin Troponin I Troponin T Valves, Aortic Ventricular Ejection Fraction
The primary aim of the evaluation study was to investigate the precision and reliability of the contactlessly measured vital parameters compared to vital parameters measured in the usual manner. To do this, synchronous evaluation measurements were taken in the study patients using a tablet camera and reference measuring devices. Measured with standard measuring devices were pulse and blood pressure (oscillometric blood pressure device), oxygen saturation (Spo2 finger and ear clip) and respiratory rate (portable Philips IntelliVue X3 monitor).
The evaluation study was conducted in close collaboration between the Institute for Biomedical Engineering at the Technische Universität Dresden (development of the measuring station and analysis of the measurements) and the Department of General Practice at the Technische Universität Dresden (recruitment and taking evaluation measurements).
From January 2020 to July 2021, nineteen of the initially planned 20 study patients were included in the evaluation study and 250 evaluation measurements (an average of 13.16 per study patient) were taken in the homes of the study patients by study nurses. Unfortunately, the inclusion of the 20 planned study patients could not be fully achieved despite intensive efforts because the corona pandemic occurred during the recruitment period and made it very difficult to recruit the corresponding patient group. Inclusion criteria was, in addition to a minimum age of 18 years, the presence of one of the following diagnoses: chronic heart failure (at least NYHA stage 2), coronary artery disease, hypertensive heart disease, chronic obstructive pulmonary disease (COPD, at least gold stage 3) or aortic valve stenosis (at least moderate). For a complete list of inclusion and exclusion criteria, see S4 Table. Since the evaluation study was similar in character to a pilot study, case number planning was based on pragmatic reasoning.
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Publication 2023
Aortic Valve Stenosis Blood Pressure Character Chronic Obstructive Airway Disease Clip Congestive Heart Failure Coronary Artery Disease Diagnosis Fingers Gold Heart Heart Diseases High Blood Pressures Medical Devices Nurses Oscillometry Oxygen Saturation Pandemics Patients Pulse Rate Respiratory Rate Saturation of Peripheral Oxygen Sphygmomanometers Tablet

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CoreValve is a medical device designed for the treatment of severe aortic stenosis. It is a prosthetic heart valve that is implanted via a minimally invasive procedure to replace the patient's diseased aortic valve.
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The Evolut R is a self-expanding transcatheter aortic valve replacement (TAVR) system designed for the treatment of severe aortic stenosis. It features a dynamic sealing skirt and a recapturable, repositionable design to allow for optimal valve placement.
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More about "Aortic Valve Stenosis"

Aortic Valve Stenosis, also known as Aortic Stenosis (AS), is a condition characterized by the narrowing or obstruction of the aortic valve, the gateway through which blood flows from the heart's left ventricle into the aorta and throughout the body.
This condition can make it challenging for the heart to efficiently pump blood, leading to symptoms such as chest pain, shortness of breath, and fatigue.
Timely diagnosis and appropriate treatment are crucial for managing Aortic Valve Stenosis and preventing serious complications.
Treatment options may include valve replacement surgery, such as procedures using the CoreValve, Evolut R, or Sapien XT and Sapien 3 devices.
Accurate diagnostic imaging is essential for assessing the severity of Aortic Valve Stenosis.
Techniques like echocardiography, using systems like the Vevo 2100 or Vivid E9 and Vivid 7, can provide valuable insights into the structure and function of the aortic valve.
Additionally, the use of Pentobarbital sodium, a sedative-hypnotic drug, may be employed during imaging procedures to facilitate better visualization and evaluation.
Exploring Aortic Valve Stenosis in depth with the AI-driven platform of PubCompare.ai can help optimize research protocols, improve reproducibility, and boost accuracy by comparing the latest literature, preprints, and patents.
This approach can empower researchers and clinicians to make more informed decisions and deliver better outcomes for patients suffering from this cardiovascular condition.