657-662, 1984. A NUMBER of noninvasive methods for assessing right ventricular pressure have been developed based on physical examination results and the use of electrocardiograms, phonocardiograms, chest x-rays, and echocardiograms. ' '°While these methods can discriminate mild from severe right ventricular pressure elevation, they lack sufficient sensitivity to be useful in evaluating the effects of short-term therapeutic interventions or in monitoring the clinical course of outpatients.Recently The purpose of this study was to test the accuracy of the tricuspid gradient method in prospectively estimating right ventricular systolic pressures in a group of patients with Doppler-detected tricuspid regurgitation who underwent catheterization within 24 hr of their Doppler study. Material and methodsThe study group consisted of 62 patients in whom elevation of right-sided pressures was suspected on the basis of results of physical examination (loud pulmonic closure sound, right ventricular lift), chest x-ray (right ventricular enlargement, prominent pulmonary vasculature), and/or two-dimensional echocardiography (right ventricular chamber enlargement, "'D"-shaped left ventricle'0). Fifteen of the 62 patients were diagnosed as having clinical tricuspid regurgitation on the basis of results of physical examination by the primary ward physician. Criteria used for the clinical diagnosis of tricuspid regurgitation included systolic murmur with positive Carvallo's sign, prominent jugular venous "c-v" and hepatic pulsations, and right-sided S3. Specific criteria applied in a given case were not always stated in the medical record so we did not collate the incidence of such signs. The
In an effort to determine what clinically useful information regarding left ventricular diastolic function can be inferred noninvasively with pulsed wave Doppler echocardiography, mitral flow velocity patterns and measured variables were correlated with hemodynamic findings in 70 patients: 30 with coronary artery disease, 20 with idiopathic congestive cardiomyopathy, 14 with a restrictive myocardial process and 6 without significant cardiac disease. The effect of sudden changes in hemodynamics on the mitral flow velocity pattern was also investigated in a subgroup of patients who had simultaneous recording of mitral flow velocity and left ventricular pressure before and after left ventriculography. Mitral flow velocity recordings from 30 healthy adults served as a reference group. This analysis suggests that 1) the majority of patients with these cardiac disorders demonstrate abnormal mitral flow velocity patterns or variables; 2) markedly different flow velocity patterns can be seen in patients with impaired left ventricular relaxation; 3) the different mitral patterns appear to relate more to myocardial function and hemodynamic status than to the type of disease process present; 4) certain mitral patterns suggest different filling pressures and rates of early diastolic left ventricular filling; 5) an increase in left atrial pressure can "normalize" an abnormal mitral flow velocity pattern and "mask" a left ventricular relaxation abnormality; and 6) the different patterns appear to represent a dynamic continuum with the potential to change from one to another as a result of disease progression, medical therapy or sudden changes in hemodynamics. It is concluded that, despite the indirect method of estimation and certain limitations, mitral flow velocity recordings have clinical potential in assessing left ventricular diastolic function that merits further investigation.
Most adolescents and young adults who had bronchopulmonary dysplasia in infancy have some degree of pulmonary dysfunction, consisting of airway obstruction, airway hyperreactivity, and hyperinflation. The clinical consequences of this dysfunction are not known.
Doppler ultrasound recordings of mitral, tricuspid, aortic, and pulmonary flow velocities, and their variation with respiration, were recorded in 12 patients with a restrictive cardiomyopathy and seven patients with constrictive pericarditis. Twenty healthy adults served as controls. The patients with constrictive pericarditis showed marked changes in left ventricular isovolumic relaxation time and in early mitral and tricuspid flow velocities at the onset of inspiration and expiration. These changes disappeared after pericardiectomy and were not seen in patients with restrictive cardiomyopathy or in normal subjects. The deceleration time of early mitral and tricuspid flow velocity was shorter than normal in both groups, indicating an early cessation of ventricular filling, but only patients with restrictive cardiomyopathy showed a further shortening of the tricuspid deceleration time with inspiration. Diastolic mitral and tricuspid regurgitation was also more common in the patients with restrictive cardiomyopathy. These results suggest that patients with constrictive pericarditis and restrictive cardiomyopathy can be differentiated by comparing respiratory changes in transvalvular flow velocities. In addition, although baseline hemodynamics in the two groups were similar, characteristic changes were seen with respiration that suggest differentiation of these disease states may also be possible from hemodynamic data. (Circulation 1989;79:357-370) T he differentiation between constrictive pericarditis and restrictive cardiomyopathy is often difficult by clinical examination as well as with hemodynamic studies. Although elevated and "equalized" diastolic pressures that demonstrate a "dip and plateau" pattern at catheterization suggest a constrictive process, restrictive cardiomyopathy may show similar findings. Furthermore, diastolic pressures may not be equalized in patients who have constriction when additional cardiac pathology is present.1-4 In a patient with constrictive pericarditis, we noted a striking respiratory variation in early mitral and tricuspid flow velocities recorded by Doppler ultrasound. To assess the possible diagnostic value of this finding, transvalvular flow velocities were recorded with respiration in patients with constrictive pericarditis, stud-
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