218 research outputs found

    When to use stress echocardiography in the evaluation of patients with valvular heart disease

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    Stress testing and stress echocardiography are firmly established diagnostic tests in the evaluation of patients with suspected or known coronary artery disease, but less established in the evaluation of patients with valvular heart disease. However, there is emerging data supporting the incremental benefit of stress testing and stress echocardiography in patients with known valvular heart disease. Particular applications include hemodynamic assessment of valve function and pulmonary response during exercise induced or chemically-induced stress to correlate with the patient’s exertional symptoms. In addition, stress testing affords the opportunity for functional assessment of ventricular systolic function for prognostication and planning for surgery

    Determinants of Pulmonary Hypertension in Left Ventricular Dysfunction

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    AbstractObjectives. This study sought to analyze the determinants of pulmonary hypertension in patients with left ventricular dysfunction.Background. Pulmonary hypertension in patients with left ventricular dysfunction is a predictor of poor outcome. The independent role of cardiac functional abnormalities in the genesis of pulmonary hypertension is unclear.Methods. In 102 consecutive patients with primary left ventricular dysfunction (ejection fraction <50%), systolic pulmonary artery pressure was prospectively measured by Doppler echocardiography (using tricuspid regurgitant velocity), and left ventricular systolic and diastolic function, functional mitral regurgitation, cardiac output and left atrial volume were quantified.Results. Systolic pulmonary artery pressure was elevated in patients with left ventricular dysfunction (51 ± 14 mm Hg [mean ± SD]), but the range was wide (23 to 87 mm Hg). Of the numerous variables correlating significantly with systolic pulmonary artery pressure, the strongest were mitral deceleration time (r = −0.61, p = 0.0001; odds ratio of pulmonary pressure ≥50 mm Hg [95% confidence interval] if <150 ms, 48.8 [14.8 to 161]) and mitral effective regurgitant orifice (r = 0.50, p = 0.0001; odds ratio [95% confidence interval] if ≥20 mm2, 5.9 [2.3 to 15.5]). In multivariate analysis, these two variables were the strongest predictors of systolic pulmonary artery pressure in association with age (p = 0.005). Ejection fraction or end-systolic volume was not an independent predictor of pulmonary artery pressure.Conclusions. Pulmonary hypertension is frequent and highly variable in patients with left ventricular dysfunction. It is not independently related to the degree of left ventricular systolic dysfunction but is strongly associated with diastolic dysfunction (shorter mitral deceleration time) and the degree of functional mitral regurgitation (larger effective regurgitant orifice). These results emphasize the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.(J Am Coll Cardiol 1997;29:153–9)

    Amplitude-weighted mean velocity: Clinical utilization for quantitation of mitral regurgitation

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    AbstractObjectives. The purpose of this study was to determine the clinical usefulness of the amplitude-weighted mean velocity method for quantitation of mitral regurgitation.Background. Amplitude-weighted mean velocity is a nonvolumetric method for calculating the mitral regurgitant fraction. Its previous validation at one center mandated an independent assessment of its usefulness and limitations.Methods. In 56 patients with and 16 patients without mitral regugitation, the regurgitant fraction was measured simultaneously by amplitude-weighted mean velocity, quantitative Doppler study and quantitative two-dimensional echocardiography. In 16 patients, multiple gain settings were used to determine the influence of this variable on amplitude-weighted mean velocity.Results. In ptients without regurgitation, amplitude-weighted mean velocity showed more scattering of regurgitant fraction (−18% to 23%) than Doppler (p = 0.016) or two-dimensional echocardiography (p = 0.022). The absolute value of regurgitant fraction was (mean ± SD) 8 ± 6%, 4 ± 2% and 4 ± 3%, respectively (p = NS). With increasing gain, the amplitudeweighted mean velocity mitral and aortic integrals increased, but the calculated regurgitant fraction remained unchanged. In patients with mitral regurgitation, significant correlation was found between amplitude-weighted mean velocity and Doppler study (r = 0.79, p = 0.0001) and between implitude-weighted mean velocity and two-dimensional echocardiography (r = 0.76, p = 0.0001) for calculated regurgitant fraction, but the standard error of the estimate (12%) was large.Conclusions. The amplitude-weighted mean velocitycalculated regurgitant fraction is gain independent, whereas the aortic and mitral integrals are gain dependent. Compared with Doppler and two-dimensional echocardiography, It shows more scattering of values in patients without regurgitation, but the methods correlate significantly in patients with mitral regurgitation. Amplitude-weighted mean velocity can be used as a simple adjunctive tool for comprehensive, noninvasive quantitation of mitral regurgitation

    Contribution of Ventricular Diastolic Dysfunction to Pulmonary Hypertension Complicating Chronic Systolic Heart Failure

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    ObjectivesThe aim of the study is to clarify the clinical role of Doppler-echocardiographic parameters of left ventricular diastolic dysfunction (LVDD) as determinants of pulmonary hypertension in patients experiencing left ventricular systolic dysfunction (LVSD) with and without the presence of functional mitral valve regurgitation (FMR).BackgroundPulmonary hypertension (pulmonary venous or mixed pulmonary venous-arterial hypertension) complicating LVSD is associated with poor outcomes beyond that of LVSD alone. The view of the contribution of LVDD as a determinant of pulmonary hypertension is controversial and not well defined as a tool in clinical practice.MethodsData from patients with LVEF ≤40% undergoing Doppler-echocardiography evaluations during the period from August 2001 to December 2004 were analyzed. Pulmonary systolic pressure (PSP), parameters of diastolic function (mitral valve [MV] transmitral flow velocity [E]/mitral annular diastolic velocity [e′] ratio, MV deceleration time [DT]), quantitated effective regurgitant orifice area (EROA) of FMR, and clinical characteristics were evaluated. Pulmonary hypertension was defined as an estimated PSP ≥45 mm Hg.ResultsCriteria were met in 1,541 patients; one-third (n = 533) demonstrating PSP ≥45 mm Hg (58 ± 10 mm Hg, range 45 to 102 mm Hg). Patients with pulmonary hypertension were older with higher E/e′ ratio, EROA, and lower DT and LVEF. In multivariate analysis, pulmonary hypertension was independently predicted not only by severity of FMR (EROA ≥20 mm2, odds ratio: 3.8, p < 0.001) but also by parameters of LVDD (E/e′ ratio ≥15, odds ratio: 3.31, p < 0.001; DT ≤150 ms, odds ratio: 3.8, p < 0.001). Receiver-operating characteristics curve analysis showed that EROA, E/e′ ratio, and DT provided significant incremental value in predicting pulmonary hypertension (c-statistic 0.830, p < 0.001).ConclusionsPatients with LVSD commonly have secondary pulmonary hypertension, which is largely determined by the severity of LVDD even with adjustment for FMR and low LVEF. Thus, measures of LVDD in routine clinical practice where PSP may not be estimated are important physiologic descriptors of hemodynamic status and are cumulatively linked in the prediction of pulmonary hypertension

    B-type natriuretic peptide clinical activation in aortic stenosis : impact on long-term survival

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    Objectives : This study was conducted to define the association between serum B-type natriuretic peptide (BNP) activation and survival after the diagnosis of aortic stenosis (AS).Background : In AS, the link between BNP levels and clinical outcome is in dispute. Failure to account for the normal shifting of BNP ranges with aging in men and women, not using hard endpoints (survival), and not enrolling large series of patients have contributed to the uncertainty.Methods : A program of prospective measurement of BNP levels with Doppler echocardiographic AS assessment during the same episode of care was conducted. BNP ratio (measured BNP/maximal normal BNP value specific to age and sex) >1 defined BNP clinical activation.Results : In 1,953 consecutive patients with at least moderate AS (aortic valve area 1.03 ± 0.26 cm2; mean gradient 36 ± 19 mm Hg), median BNP level was 252 pg/ml (interquartile range: 98 to 592 pg/ml); BNP ratio 2.46 (interquartile range 1.03 to 5.66); ejection fraction (EF) 57% ± 15%, and symptoms present in 60% of patients. After adjustment for all survival determinants, BNP clinical activation (BNP ratio >1) independently predicted mortality after diagnosis (p 2 (HR: 0.56; 95% CI: 0.47 to 0.66; p < 0.0001).Conclusions : In this large series of patients with AS, BNP clinical activation was associated with excess long-term mortality incrementally and independently of all baseline characteristics. Higher mortality with higher BNP clinical activation, even in asymptomatic patients, emphasizes the importance of appropriate clinical interpretation of BNP levels in managing patients with AS

    Medical and surgical outcome of tricuspid regurgitation caused by flail leaflets

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    AbstractObjectiveWe sought to evaluate the medical and surgical outcome of tricuspid regurgitation caused by flail leaflets.MethodsWe analyzed the cause, clinical presentation, outcome, and natural history of 60 patients with tricuspid regurgitation caused by flail leaflets, a cause of mostly severe and organic tricuspid regurgitation, diagnosed by means of echocardiography between 1980 and 2000.ResultsThe main cause was traumatic (62%). Clinical presentation was often severe: 57% were symptomatic, 33% had a history of congestive heart failure, and 40% had a history of atrial fibrillation. Compared with expected survival of the US matched population, excess mortality (39% ± 10% at 10 years or 4.5% yearly, P < .01) was observed. Even patients asymptomatic at presentation experienced high tricuspid-related event rates (at 10 years, 75% ± 15% had symptoms or heart failure, atrial fibrillation, surgical intervention, or death). In those patients severe enlargement of right-sided chambers was predictive of poor outcome (at 5 years: 86% ± 9% vs 39% ± 11%, P < .01) independent of cause (P = .31). The poor medical outcome was further confirmed by high event rates (69% ± 9% at 15 years) in the natural history beginning from the flail's occurrence. Tricuspid operations were performed in 33 patients (55% ± 7% at 5 years), with valve repair in 82%, low mortality (3%), and, despite frequently refractory atrial fibrillation, symptomatic improvement in 88%.ConclusionTricuspid regurgitation caused by flail leaflets is a serious disease associated with excess mortality and high morbidity. Tricuspid valve repair can often be performed with low risk, allowing symptomatic improvement. These results suggest that surgical intervention should be considered early in the course of the disease before the occurrence of irreversible consequences

    Arrhythmias in Patients With Valvular Heart Disease: Gaps in Knowledge and the Way Forward.

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    peer reviewedThe prevalence of both organic valvular heart disease (VHD) and cardiac arrhythmias is high in the general population, and their coexistence is common. Both VHD and arrhythmias in the elderly lead to an elevated risk of hospitalization and use of health services. However, the relationships of the two conditions is not fully understood and our understanding of their coexistence in terms of contemporary management and prognosis is still limited. VHD-induced left ventricular dysfunction/hypertrophy and left atrial dilation lead to both atrial and ventricular arrhythmias. On the other hand, arrhythmias can be considered as an independent condition resulting from a coexisting ischemic or non-ischemic substrate or idiopathic ectopy. Both atrial and ventricular VHD-induced arrhythmias may contribute to clinical worsening and be a turning point in the natural history of VHD. Symptoms developed in patients with VHD are not specific and may be attributable to hemodynamical consequences of valve disease but also to other cardiac conditions including arrhythmias which are notably prevalent in this population. The issue how to distinguish symptoms related to VHD from those related to atrial fibrillation (AF) during decision making process remains challenging. Moreover, AF is a traditional limit of echocardiography and an important source of errors in assessment of the severity of VHD. Despite recent progress in understanding the pathophysiology and prognosis of postoperative AF, many questions remain regarding its prevention and management. Furthermore, life-threatening ventricular arrhythmias can predispose patients with VHD to sudden cardiac death. Evidence for a putative link between arrhythmias and outcome in VHD is growing but available data on targeted therapies for VHD-related arrhythmias, including monitoring and catheter ablation, is scarce. Despite growing evidences, more research focused on the prognosis and optimal management of VHD-related arrhythmias is still required. We aimed to review the current evidence and identify gaps in knowledge about the prevalence, prognostic considerations, and treatment of atrial and ventricular arrhythmias in common subtypes of organic VHD
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