Determinants of Pulmonary Hypertension in Left Ventricular Dysfunction

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

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

Strain echocardiography tracks dobutamine-induced decrease in regional myocardial perfusion in nonocclusive coronary stenosis

ObjectivesThis study was designed to determine whether strain echocardiography parameters reflect changes in regional myocardial perfusion during dobutamine stress.BackgroundStrain echocardiography depicts regional myocardial mechanical activity. Ischemia has been shown to reduce systolic strain rate (sSR) and prolong the time to regional lengthening (TRL). In an experimental model, we tested whether sSR and TRLtracked dobutamine-induced changes in regional myocardial perfusion (regional myocardial blood flow [RMBF]), as measured by colored microspheres.MethodsWe used a closed-chest pig model of nonocclusive coronary stenosis (n = 14) created by inflating an angioplasty balloon in the proximal left anterior descending artery. Invasive hemodynamics, RMBF, and strain parameters were measured at baseline and peak dobutamine stimulation before and during the coronary stenosis. We compared segments with reduced RMBF versus those with preserved RMBF at peak dobutamine stimulation.ResultsPeak sSR correlated with RMBF (r = 0.70). In the absence of coronary stenosis, dobutamine stimulation caused a significant increase in RMBF and sSR and a decrease in TRL. This response was blunted during coronary stenosis. Using the “best cutoff” method, the sensitivity and specificity for prediction of reduced RMBF (ischemia) was 81% and 91% for sSR and 65% and 91% for TRL, respectively. These changes occurred in the absence of any change in global systolic and diastolic function (dP/dTmax, dP/dTmin, and tau).ConclusionsNovel strain parameters that depict regional myocardial mechanics are able to predict changes in RMBF during dobutamine stress. Quantitative strain parameters may complement current echocardiographic techniques for ischemia detection and potentially improve the accuracy and reproducibility of stress echocardiography

Pericardial Thickness Measured With Transesophageal Echocardiography: Feasibility and Potential Clinical Usefulness

AbstractObjectives. This study assessed the reliability of transesophageal echocardiographic measurements of pericardial thickness and the potential diagnostic usefulness of this technique.Background. Transthoracic echocardiography cannot reliably detect thickened pericardium. The superior resolution achieved with transesophageal echocardiography should allow better pericardial definition.Methods. Pericardial thickness measured at 26 locations in 11 patients with constrictive pericarditis who underwent intraoperative transesophageal echocardiography was compared with pericardial thickness measured with electron beam computed tomography. Intraobserver and interobserver variabilities were determined. Pericardial thickness was then measured in 21 normal subjects. With these values as a guide, two observers reviewed 37 transesophageal echocardiographic studies to determine whether echocardiographic measurement of pericardial thickness could be used to distinguish diseased from normal pericardium.Results. The correlation between echocardiographic and computed tomographic measurements (r ≥ 0.95, SE ≤ 0.06 mm, p < 0.0001) was excellent. The ±2 SD limits of agreement were ±1.0 mm or less for pericardial thickness <5.5 mm and ±2.0 mm or less for the entire range of thicknesses. Intraobserver and interobserver agreements were good. Mean normal pericardial thickness was 1.2 ± 0.8 mm (±2 SD) and did not exceed 2.5 mm. Pericardial thickness ≥3 mm on transesophageal echocardiography was 95% sensitive and 86% specific for the detection of thickened pericardium.Conclusions. Measurement of pericardial thickness with transesophageal echocardiography is reproducible and should be a valuable adjunct in assessing constrictive pericarditis.(J Am Coll Cardiol 1997;29:1317–23

Intravascular ultrasound imaging: In vitro validation and pathologic correlation

AbstractIntravascuiar ultrasound imaging is a new method in which high resolution images of the arterial wall are obtained with use of a catheter placed within an artery. An in vitro Plexiglas well model was used to validate measurements of the luminal area, and an excellent correlation was obtained. One hundred thirty segments of fresh peripheral arteries underwent ultrasound imaging and the findings were compared with the corresponding histopathologic sections. luminal areas determined with ultrasound imaging correlated well with those calculated from microscopic slides (r = 0.98).Three patterns were identified on the ultrasound images: 1) distinct interface between media and adventitia, 2) indistinct interface between media and adventitia but different echo density layers, and 3) diffuse homogeneous appearance. The types of patterns depended on the relative composition of the and adventitia. Calcification of intimal plaque obscured underlying structures. Atherosclerotic plaque was readily visualized but could not always be differentiated from the underlying media

Medical and surgical outcome of tricuspid regurgitation caused by flail leaflets

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

Feasibility of identifying amyloid and hypertrophic cardiomyopathy with the use of computerized quantitative texture analysis of clinical echocardiographic data

AbstractUltrasound tissue characterization, the evaluation of certain physical properties of a tissue based on its acoustic properties, is an evolving application in echocardiography. The ability to identify acutely and chronically injured tissue has been demonstrated in a number of animal studies, but data in humans are limited. The present study tested the hypothesis that quantitative echocardiographic texture analysis, a method of evaluating the spatial pattern of echoes in echocardiographic images, would differentiate amyloid and hypertrophic cardiomyopathy from normal myocardium. Routine clinical echocardiographic data were obtained on 34 subjects at the Mayo Clinic (10 normal subjects, 10 patients with amyloid heart disease, 8 patients with hypertrophic cardiomyopathy and 6 patients with left ventricular hypertrophy due to hypertension). Standard videotape recordings of these echocardiograms were analyzed at the University of Iowa.Echocardiographic data were digitized with use of a calibrated, 256 gray level digitization system. Quantitative texture analysis was performed on data from the ventricular septum and posterior left ventricular wall in end-diastolic and end-systolic, short-axis and long-axis echocardiographic images. The gray level run length texture variables were able to discriminate hypertrophic cardiomyopathy and amyloid heart disease from normal myocardium and from each other (p < 0.0083 for comparisons of the quantitative texture features of amyloid versus hypertrophic cardiomyopathy versus normal by multivariate analysis of variance). The texture of the myocardium in hypertensive left ventricular hypertrophy not associated with amyloid or hypertrophic cardiomyopathy was in general not significantly different from that of normal myocardium.On the basis of these data, it was concluded that quantitative texture analysis of clinical echocardiographic data has the potential to identify amyloid and hypertrophic cardiomyopathy; false positive results occur rarely in left ventricular hypertrophy due to hypertension. Further prospective studies of this technique are needed to establish its utility in identifying the etiology of clinical cardiomyopathies