Report of the Joint International Society and Federation of Cardiology/World Health Organization Task Force on Nuclear Cardiology.
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Biomedical subjects
Publications and source records attributed to H N Neufeld.
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Eleven children are reported who had stenosis under a malposed aorta with gradients of 20 to 76 mm Hg between the right ventricle and aorta. The subaortic obstruction was caused by hypertrophy of the foreshortened infundibulum and malalignment of the infundibular septum relative to the remainder of the ventricular septum. Of these 11 patients, nine had a ventricular septal defect and seven had coarctation of the aorta. Rightward deviation of the infundibulum and aorta produced an unusually long left main coronary artery that was compressed by the stent of a bioprosthetic conduit valve in one patient. Serial cardiac catheterization studies in four patients showed progressive stenosis in each. Subaortic stenosis can develop in patients with malposition of the aorta and the frequency may be greater than 5% since milder forms are likely to occur. The obstruction can be progressive. The left coronary artery may be particularly vulnerable to compression after operative repair with an extracardiac conduit.
The effect of intrathoracic pressure variations on the hemodynamics of dogs with cardiac arrest were studied experimentally and simulated on a computer. High intrathoracic pressure (up to 90 mm Hg) was generated by lung inflation with passive and active modes of external fixation. Abdominal binding was found to be essential for the generation of high intrathoracic pressure. Remarkable Doppler flow signals were detected over the femoral artery with each lung inflation. Blood gases measured after 30 minutes of cardiac fibrillation in dogs together with intrathoracic pressure variations showed well oxygenated arterial blood with metabolic acidosis. A computer model was used to explore the effects of intrathoracic pressure variations over a large range of parameters. For intrathoracic pressure of 50/0 mm Hg. the mathematical model predicted maximal flow of 663 ml/min, occurring at a rate of 115 cpm, with a duty cycle of 58%. The heart showed only minor volume changes during the cycle, indicating its main function as a passive conduit during cardiopulmonary resuscitation. The data show that intrathoracic pressure variation with no direct heart compression can cause systemic blood flow of the magnitude occurring in most cardiopulmonary resuscitation techniques.
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Over the 3 year period from 1980 to 1982, mechanical prosthetic valves were implanted in the pulmonary pathway in seven patients. In two the procedure was a pulmonary valve replacement. In two it was an implantation of a pulmonary valve with transannular pericardial patching, and in three, complete pericardial (tube) conduits, which included mechanical valves, were constructed. There were neither perioperative nor late complications. Four patients were recatheterized. In three residual right ventricular hypertension was observed. In one of the three the cause of obstruction was not verified, but in the remaining two it was unrelated to the mechanical valve. No thromboembolic phenomena were observed.
To determine whether tricuspid regurgitation (TR) can be diagnosed by direct imaging of regurgitant flow in the right atrium (RA) using contrast echocardiography, echocardiography was performed in 35 patients using peripheral intravenous injections of 5% dextrose solution. Fifteen patients had TR judged by v-wave synchronous contrast appearance on the inferior vena cava echogram (a previously validated method for diagnosing TR), 5 of whom had clinically obvious TR. Twenty patients had no TR on inferior vena cava contrast echocardiography, 9 of whom were normal volunteers. On subsequent blind review, 13 of the 15 patients with TR were correctly identified on the basis of the regurgitant contrast flow just posterior to the tricuspid valve in the RA. Of the 20 without TR, 19 were correctly identified and there was 1 false-positive result. Using different criteria for the diagnosis (insisting on imaging of flow across the tricuspid valve in systole), another blinded observer correctly diagnosed only 8 of the 15 patients as having TR, but had no false-positive results. To avoid false-positive results, it is important to realize that there are 2 regions where retrograde flow can normally be seen in the RA: (1) briefly at the onset of systole coincident with tricuspid valve closure, and (2) in the posterior RA, as distinct from the anterior RA area just behind the tricuspid valve where TR is diagnosed in this study.(ABSTRACT TRUNCATED AT 250 WORDS)
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Discrete subaortic stenosis has only rarely been reported in association with congenital valvular aortic stenosis. The valvular lesion may obscure the subaortic stenosis or may be obscured by it. Our experience with seven such cases (10% of our 71 patients with discrete subaortic stenosis) is reported and the diagnostic problems are discussed. In six cases the discrete subaortic stenosis was membranous and in one it was a fibromuscular tunnel. Two patients had associated coarctation of the aorta, two had aortic insufficiency, and one had a ventricular septal defect. An important clinical clue to the diagnosis was an ejection systolic click, which was found in four patients. Four patients were accurately diagnosed at cardiac catheterization. Two patients, in whom cross-sectional echocardiography (2DE) was performed, were accurately diagnosed by it.
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Contrast echocardiography was first described in 1968. Since then, many reports have described clinical and experimental uses for the technique. Contrast echocardiography is performed at least occasionally in most echocardiography laboratories, but most physicians use this technique merely to determine the presence of a shunt or, more rarely, for structure identification. Contrast echocardiography can provide much more information. Some different types of information available from contrast echocardiographic records are discussed, including timing of contrast appearance within the cardiac cycle, relative timing of appearance in different cardiac structures, relative intensity of contrast opacification, cyclical changes in contrast opacification, negative contrast effect, slope of contrast trajectories on M-mode contrast echocardiography, and clearance times.
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The severity of aortic stenosis was assessed by echocardiography in 81 consecutive adult patients, 40 of whom underwent cardiac catheterization. The patients' mean age was 54 +/- 16.4 years. A good correlation was found between the severity of aortic stenosis assessed by cross-sectional echocardiography and cardiac catheterization. Aortic valve separation of 7 mm or less occurred only in severe aortic stenosis whereas a separation of 12 mm ruled out any significant aortic stenosis. A separation of 8-11 mm constituted a 'grey' area between mild and severe aortic stenosis. Cross-sectional echocardiography provides a reliable method for crude evaluation of aortic stenosis.
Congestive heart failure has never been described in patients with dysplastic stenotic pulmonary valve without associated shunt lesions. We describe two patients with mild pulmonic stenosis due to valvular dysplasia associated with cardiomyopathy who developed severe congestive heart failure. Since the small pressure gradients across the pulmonary valve cannot cause this complication, we suggest that it resulted from the associated hypertrophic non-obstructive cardiomyopathy. The presence of cardiomyopathy may alter the clinical presentation and prognosis of patients with dysplastic pulmonary valve. In some cases, like our two cases, the cardiomyopathy rather than the valvular lesion should be considered the main disease.