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Ventricle

About: Ventricle is a research topic. Over the lifetime, 21456 publications have been published within this topic receiving 507177 citations.


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Journal ArticleDOI
TL;DR: The aim of this paper was to detail the recommended approach to the echocardiographic evaluation of valve stenosis, including recommendations for specific measures of stenosis severity, details of data acquisition and measurement, and grading of severity.
Abstract: AR = aortic regurgitation AS = aortic stenosis AVA = aortic valve area CSA = cross sectional area CWD = continuous wave Doppler D = diameter HOCM = hypertrophic obstructive cardiomyopathy LV = left ventricle LVOT = left ventricular outflow tract MR = mitral regurgitation MS = mitral stenosis MVA = mitral valve area ΔP = pressure gradient RV = right ventricle RVOT = right ventricular outflow tract SV = stroke volume TEE = transesophageal echocardiography T 1/2 = pressure half-time TR = tricuspid regurgitation TS = tricuspid stenosis V = velocity VSD = ventricular septal defect VTI =velocity time integral Valve stenosis is a common heart disorder and an important cause of cardiovascular morbidity and mortality. Echocardiography has become the key tool for the diagnosis and evaluation of valve disease, and is the primary non-invasive imaging method for valve stenosis assessment. Clinical decision-making is based on echocardiographic assessment of the severity of valve stenosis, so it is essential that standards be adopted to maintain accuracy and consistency across echocardiographic laboratories when assessing and reporting valve stenosis. The aim of this paper was to detail the recommended approach to the echocardiographic evaluation of valve stenosis, including recommendations for specific measures of stenosis severity, details of data acquisition and measurement, and grading of severity. These recommendations are based on the scientific literature and on the consensus of a panel of experts. This document discusses a number of proposed methods for evaluation of stenosis severity. On the basis of a comprehensive literature review and expert consensus, these methods were categorized for clinical practice as:

846 citations

Journal ArticleDOI
TL;DR: Left ventricular chamber stiffness, which fell as infarct size increased in untreated rats, was normalized by chronic captopril therapy, which attenuated the left ventricular remodeling and deterioration in performance that were observed in rats with chronic myocardial infarction.
Abstract: To determine whether the relationship between infarct size and ventricular performance, volume, and compliance could be altered favorably, captopril was administered to rats for 3 months following coronary artery ligation. Baseline left and right ventricular and systemic arterial pressures and aortic blood flow, and maximal stroke volume and cardiac indices attained during a volume loading, were measured. Passive pressure-volume relations of the left ventricle were determined, and the slopes of segments of this relation were analyzed to characterize ventricular chamber stiffness. In untreated rats, left ventricular end-diastolic pressure progressively rose (from 5-28 mm Hg) as a function of infarct size, whereas, in captopril-treated rats, filling pressure remained within normal limits (5 +/- 1 mm Hg) in all but those with extensive infarcts. Chronic captopril therapy reduced baseline mean arterial pressure and total peripheral resistance, yet maintained cardiac and stroke outputs in rats both with and without infarcts. In untreated rats, maximal pumping ability progressively declined with increasing infarct size, whereas, in captopril-treated rats, peak stroke volume index remained within normal limits in all but those with extensive infarcts. The in vitro left ventricular volumes of captopril-treated rats were significantly less than those of untreated rats. The maintenance of forward output from a lesser dilated left ventricle yielded an index of ejection fraction for treated rats with moderate and large infarcts that was significantly elevated compared with that of untreated rats with infarcts of comparable size. Left ventricular chamber stiffness, which fell as infarct size increased in untreated rats, was normalized by chronic captopril therapy. Thus, captopril attenuated the left ventricular remodeling (dilation) and deterioration in performance that were observed in rats with chronic myocardial infarction.

839 citations

Journal ArticleDOI
TL;DR: In this article, the authors discuss potential novel therapies for these disorders, including: sildenafil, an unexpected option for anti-transition therapy; surgery for increased sphericity caused by chronic volume overload of mitral regurgitation; an antifibrotic peptide to inhibit the fibrogenic effects of transforming growth factor β; mechanical intervention in advanced heart failure; and stem-cell therapy.

801 citations

Journal ArticleDOI
TL;DR: Findings suggest that plasma BNP is superior to ANP as a predictor of high LVEDP in patients with symptomatic left ventricular dysfunction.

792 citations

Journal ArticleDOI
TL;DR: The extent of hypertrophy is believed to be the principal determinant of the impaired left ventricular relaxation and increased chambers stiffness that characterize diastole in hypertrophic cardiomyopathy.

772 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20231,794
20223,888
2021648
2020599
2019574
2018582