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Query: UMLS:C0232605 (regurgitation)
 8,217 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The percentage of shortening of the echocardiographic left ventricular dimension (% delta D) was prospectively evaluated in 42 patients without detectable asynergy during diagnostic cardiac catheterization and was found to correlate well with angiographic ejection fraction (r = 0.90). Ejection fraction was calculated as the product of % delta D X 1.7 or as % delta (D2), both formulae having similar degrees of accuracy and a better correlation with the angiographic determination than conventional formulae. Ejection fractions (angiographic and echocardiographic) of 51 percent or greater were always associated with a % delta D of 30 percent or more. In five patients the echocardiographically derived ejection fractions were normal (greater than or equal to 51 percent), while the angiographic ejection fractions were reduced; four of these patients had valvular regurgitation. End-diastolic volumes were calculated from end-diastolic echocardiographic dimensions utilizing a linear regression equation derived from correlating the end-diastolic echocardiographic dimension with the end-diastolic volume in 27 patients without valvular regurgitation (end-diastolic echocardiographic dimension ranged from 3.7 to 8.2 cm). The value for stroke volume determined as the product of calculated end-diastolic volume times ejection fraction correlated with the angiographically determined stroke volume (r = 0.88; standard error of estimate, +/- 11 ml) better than the value for stroke volume derived from conventional echocardiographic formulae.
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PMID:Percentage of shortening of the echocardiographic left ventricular dimension. Its use in determining ejection fraction and stroke volume. 66 37

In 38 children with typical tetralogy of Fallot recatheterization was performed 15 days to 410/12 years after correction. Their age ranged from 47/12 to 181/12 years and their weigh? 14;8 TO 54.4 KG. The biplane angiocardiograms were especially evaluated with respect to thcy to decrease from intraoperative to postoperative values. We did not find a parameter, determined during the operation, which can predict with certainty the operative result, found at the time of recatheterization. The peak pressure ration PRV/PLV seems to be most suitable but in an individual case one cannot rely on it. A diastolic murmur was heart postoperatively in 25 children, 9 of whom had a regurgitation index greater than 10%. In all 38 patients an infundibulectomy was performed, which in every case resulted in a disturbance of the contraction pattern (asynergy) of the right ventricular outflow tract. In the area of the ostium infundibuli small aneurysms were demonstrated in 50% of the cases. They were divided according to their angiographic appearance, the type of asynergy and their visibility on the two standard x-ray projections. In 11 children we observed incompletely resected muscle bundles of the infundibulum. Hemodynamically they were insignificant. Residual muscular infundibular stenoses, causing a pressure gradient, were observed in 8 cases. Aortal indentations of varying degree at the site of cannulation for the extracorporal circulation were present in 91%. In 13 patients an outflow tract reconstruction was necessary. In 8 children the patch was clearly identifiable as such. The necessity of recatheterization after correction of tetralogy of Fallot is discussed.
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PMID:[Videodensitometric, angiocardiographic and hemodynamic examinations in corrected tetralogy of fallot]. 114 72

Doppler echocardiography has become a very useful and widely employed imaging technique for evaluating valvular regurgitation, and has thus lead to the discovery of regurgitation in unexpected subjects. In this study, we examined left-sided valvular regurgitation in 31 healthy subjects, 35 patients with hypertension and 43 patients with old myocardial infarction by Doppler echocardiography. Aortic regurgitation was found in 3% of healthy subjects, 8% of hypertensive patients and 5% of patients with myocardial infarction. Mitral regurgitation was found in 35% of healthy subjects, 69% of hypertensive patients and 84% of patients with myocardial infarction. The pathogenesis of mitral regurgitation in hypertension is considered to be the impairment of the mitral leaflets, since neither anatomical nor functional abnormalities were found in the subvalvular mitral apparatus. Left ventricular dilatation and asynergy near the papillary muscles were related to the pathogenesis of mitral regurgitation in myocardial infarction. Mitral regurgitation in healthy subjects and hypertensive patients was mild and resistant to afterload stress, suggesting that it was less pathological. On the other hand, mitral regurgitation in myocardial infarction was easily worsened by afterload stress. Doppler echocardiography has thus provided us with new insights into valvular regurgitation in healthy subjects and patients without rheumatic valvular disease.
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PMID:Evaluation of left-sided valvular regurgitation in healthy, hypertensive and myocardial infarction subjects by Doppler echocardiography. 236 14

The aim of the present study was to elucidate the mechanisms of mitral regurgitation accompanying myocardial infarction. Severity and site of mitral regurgitation was evaluated by the real-time two-dimensional Doppler flow imaging technique in 81 patients with old myocardial infarction. The incidence of mitral regurgitation did not depend on the region of infarction. There was, however, a close relationship between the site of regurgitation and the region of infarction. In patients with mitral regurgitation spurting from the posteromedial area of the valve, the inferior wall was involved in infarction without exception and in some of these patients, the posteromedial papillary muscle was also found to be affected by myocardial infarction; in those with regurgitation spurting from the anterolateral area, the anterior wall showed asynergy. On the other hand in patients with mitral regurgitation spurting from the central area, the region of infarction varied. In these patients, however, the larger the diameter of the mitral anulus, the more severe the grade of regurgitation. The extent of asynergy was another factor related to the severity of mitral regurgitation. Both longitudinally and transversely, broad infarction leads to the enlargement of the mitral anulus. However, even if the mitral anulus is not so dilated, severe involvement of either commissural area results in severe mitral regurgitation from the same commissural side. Thus, there are two major causative factors of mitral regurgitation: (1) asynergy of the papillary muscle or the ventricle that results in mitral regurgitation located in the commissural area of the same side as asynergy, and (2) enlargement of mitral anulus, which results in regurgitation from the central area of the orifice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of mitral regurgitation in patients with myocardial infarction: a study using real-time two-dimensional Doppler flow imaging and echocardiography. 365 21

In order to evaluate the effect of handgrip on left ventricular dynamics, cineventriculography was performed in 16 patients with heart disease and 5 normal subjects at 30% of maximal voluntary contraction. No patient had ventriculographic evidence of asynergy or valve regurgitation. During exercise, left-ventricular end-diastolic volume (LVEDV) insignificantly increased, left ventricular end-systolic volume (LVESV) decreased, and hence stroke volume (SV) and ejection fraction (EF) rose in the normal group, while in the patient group a similar change in LVEDV was associated with increased LVESV, resulting in unchanged SV and decreased EF. It is notable that during exercise LVEDV increased in both groups, despite a shortened diastolic filling period. Mean velocity of fiber shortening (mean VCF) increased in the normal group and remained unchanged in the patient group. The changes in mean VCF during exercise were correlated with the alterations in SV and EF (r=0.46, p less than 0.05 and r=0.90, p less than 0.001), respectively). These data signify that an increased afterload induced by handgrip leads to an enhanced left ventricular myocardial contraction in addition to an increase in preload in the normal group, while the Frank-Starling mechanism is mainly utilized in the patient group.
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PMID:Cineventriculographic analysis of left ventricular dynamics during sustained handgrip exercise. 736 7