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Traumatic tricuspid valve insufficiency (TTVI) is a relatively uncommon disease. To summarize the experience in the diagnosis and treatment of TTVI, we have analyzed the clinical data of 3 patients with TTVI who were admitted to the department of cardiac surgery of our hospital between April 1997 to April 2002. Relevant literatures have also been reviewed.
To detect tricuspid incompetence (TI) right ventricular angiography was performed in 167 patients suffering from moderate to severe mitral valve disease. Holosystolic reflux of contrast medium to the right atrium through the central part of the tricuspid valve was thought to represent true TI, whereas a jet of contrast medium following the injection catheter and originating from the region of its valve passage was assumed to reflect arteficial regurgitation. True TI was found in 35% of the total group (30% mild to moderate, 5% severe TI). TI was often accompanied by atrial fibrillation (91%), pulmonary hypertension (74%) and reduced contraction of the tricuspid annulus (55%). Since tricuspid regurgitation in mitral valve disease commonly represents "functional" incompetence surgical intervention may be recommandable only in case of severe TI or concomitant valvular stenosis.
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Tricuspid valve insufficiency following acute myocardial infarction is uncommon. It may be explained by right ventricular papillary muscle dysfunction. We report the case of a patient with acute tricuspid valve incompetence during the acute phase of a left ventricular inferior infarction with right ventricular myocardial involvement. The treatment during the acute phase consisted of volume loading and positive inotropic agents. Seven days later the clinical signs of tricuspid valve insufficiency and concomitant right heart failure had disappeared. To our knowledge transient tricuspid valve insufficiency following acute inferior myocardial infarction has not been reported previously.
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Evaluation of tricuspid regurgitation was attempted by analyzing the blood flow pattern in the hepatic vein using a combined system of a pulsed Doppler technique and two-dimensional echocardiography. The Doppler incident angle to the hepatic vein from the subcostal approach was approximately 0 degrees to 30 degrees, and the Doppler output was easily recognized as a narrow frequency-band pattern on the sound spectrogram. The study population consisted of 60 patients with valvular heart disease and 17 healthy subjects. Inferior vena cava dimension (IVCD), hepatic vein dimension (HVD) and the blood flow pattern in the hepatic vein were compared with the severity (negative, mild, moderate and severe) of tricuspid regurgitation (TR) assessed by right ventriculography and with right atrial and ventricular pressures. The following conclusions were derived from the study: IVCD and HVD in a group of TR severe were significantly larger than those of the other groups. The normal flow pattern of the hepatic vein was biphasic with a systolic flow greater than a diastolic flow. In cases of valvular heart disease with atrial fibrillation, three types of abnormal blood flow patterns were demonstrated; Type 1 had a slower systolic flow than a diastolic flow. Type 2 had no flow signal during systole, and had only a diastolic flow. Type 3 had a reversed systolic flow with several variations. By this hepatic flow patterns, it was possible to differentiate the TR of severe and moderate groups from the TR of mild group, because 81% of the former groups showed a Type 3 of a flow pattern. The Doppler shifts from the base line on the sound spectrogram were well correlated with right atrial pressure and right ventricular end-diastolic pressure (r = -0.72 and -0.64, respectively). The early changes of the hepatic blood flow pattern after operation were due to the improvement of TR by tricuspid annuloplasty, and also seemed to be affected by the postoperative changes of right atrial compliance and contraction.
Alterations of the ductus arteriosus, e.g. occlusion, constriction or aneurysm, can influence the fetal and neonatal circulation. A case of fetal right atrial and ventricular dilatation, severe tricuspid valve insufficiency and transient pulmonary valve regurgitation at 32 weeks of gestation is reported. Structural heart defects and extracardiac diseases (e.g. high output cardiac failure in arteriovenous shunts and anemia) were excluded by Doppler echocardiography and fetal blood sampling. An abnormally S-shaped kinking of the ductus arteriosus with increased systolic and diastolic flow velocities in the distal part was demonstrated. At 35 weeks' gestation, Cesarean section was performed, because of increased tricuspid valve insufficiency, and a healthy boy was born. After birth, right heart dilatation and tricuspid valve insufficiency decreased. The cardiac changes in relation to the anatomical abnormality of the ductus arteriosus are discussed.
We report a case of tricuspid insufficiency in connection with blunt chest trauma. The patient was involved in a car accident. The central venous catheter showed a right ventricular pressure curve, suggestive of a tricuspid valve insufficiency. A transoesophageal echocardiographic examination supported this by revealing a papillary muscle rupture. This kind of injury has been seen more frequently during the last 35 years, partly because of better diagnostic procedures and a better understanding of the pathology. The decelerating force in the right ventricular chamber produces a regurgitation thereby initiating rupture of the papillary muscle and/or the chordae tendinae. In a literature study twelve out of thirteen patients were involved in car accidents. Some of them had a dominant V-wave in the venous pulse curve, but no clinical observation is directly diagnostic. Therefore, cardiac lesions should be kept in mind whenever there is a history of blunt chest trauma. The best diagnostic approach is echocardiography.
A 5-month-old Holstein heifer had clinical signs of tricuspid valve insufficiency and histopathologic evidence of endocardial fibroelastosis. The calf had a 3-week history of weight loss, abdominal distention, dyspnea, and decreased appetite. Physical examination revealed signs of right-sided heart failure, and a systolic murmur (II/VI) was heard best over the right heart base. Results of cardiac catheterization and echocardiography indicated tricuspid valve insufficiency and right-sided heart failure. The calf was euthanatized after not responding to treatment with penicillin, furosemide, and removal of fluid from the thorax and abdomen. Necropsy findings included multifocal areas of thickening and opacification of the endocardium of the left and right ventricles. Excessive elastic fibers, consistent with fibroelastosis, were seen by use of special stains applied to sections of endocardium.
From 1964 through June 1993, thirteen patients with traumatic tricuspid insufficiency were treated surgically; all were male, and the ages ranged from 17 to 64 years (median 39 years). The condition was associated with blunt chest trauma in all patients: motor vehicle accidents in twelve and an explosion of a tank of compressed air in one. The median duration between trauma and operation was 17 years (range 1 month to 37 years). Preoperatively, six patients were in sinus rhythm and seven were in atrial fibrillation. At operation, the right ventricular function appeared moderately to severely depressed in twelve patients. In twelve patients, the anterior leaflet was flail because of chordal rupture (n = 9), rupture of anterior papillary muscle (n = 3), or tear in the anterior leaflet (n = 1). In one patient, the septal leaflet was missing and in another it was retracted and adherent to the ventricular septum. In five patients the tricuspid valve was repaired and in eight it was replaced. In seven patients in the latter group, the chordae, papillary muscles, and/or tricuspid valve leaflet(s) were found to be in a contracted and atrophic state, precluding repair. No early or late deaths occurred. At follow-up extending to 26 years (median 12 years), 12 patients are in New York Heart Association class I and one patient is in class II. Nine patients were in sinus rhythm and four were in atrial fibrillation. Although our experience indicates that good functional results can still be achieved many years after the onset of traumatic tricuspid valve insufficiency, earlier diagnosis and surgical treatment should increase the feasibility of tricuspid valve insufficiency, earlier diagnosis and surgical treatment should increase the feasibility of tricuspid valve repair, prevent progressive deterioration of right ventricular function, and increase the possibility of maintaining late sinus rhythm in a greater number of patients.
To assess the postoperative reversibility of functional tricuspid regurgitation (FTR) and its relation to preoperative pulmonary artery systolic pressure (PASP) 103 patients were studied by Doppler echocardiography (DE) in whom at the time of mitral valve replacement the correction of the FTR was not considered to be necessary by the surgeon. Moderate or severe FTR was found in 36% of patients preoperatively, and it diminished or disappeared early after operation if the preoperative PASP was more than 60 mmHg, while the improvement of FTR was found only in the half of patients with PASP less than 60 mmHg. Persistent FTR was still unchanged in 7 of 10 patients at 1 year follow-up. It is concluded that DE should be performed prior to mitral valve replacement and severe FTR found by DE should be surgically treated even in case of negative surgical findings if the PASP is less than 60 mmHg.
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The diagnosis of tricuspid regurgitation (TR) is difficult to make by simple clinical methods or by invasive techniques. Contrast echocardiography and Doppler echocardiography have improved diagnostic results, but a golden standard is still not available. Radionuclide ventriculography (RNV) is a well-established method for the detection and quantification of a volume load on the left ventricle: the regurgitation fraction can simply be derived from the regurgitant index as the ratio of enddiastolic-endsystolic count-rate differences between the left and right ventricle. In left heart valvular regurgitation a regurgitant index exceeding the upper normal limit can be expected. This study was performed to evaluate the diagnostic accuracy of an abnormally low regurgitant index in detecting TR, which is accompanied by an isolated volume load on the right ventricle. A series of 33 patients with TR on physical examination and cardiac catheterization underwent RNV and was compared with 48 patients with right ventricular enlargement or pressure load on the right ventricle. In addition, the specificity of the method was evaluated in 470 consecutive patients with various forms of heart disease. In 18 out of 20 subjects with isolated TR a regurgitant index below the lower normal limit was found. The remaining 2 cases with minor TR had a regurgitant index within the normal range, which is 0.89 to 1.97 in this laboratory. In patients with additional volume load on the left ventricle, the sensitivity of the method was found to be low, as could be expected from the principle of the method. The time-activity curve over the liver was usually in phase with that recorded over the atria in subjects with TR. Therefore, the additional examination of a region of interest over the liver was particularly useful in these patients with concomitant aortic or mitral valve regurgitation. None of the 48 patients with right ventricular enlargement or pressure load on the right ventricle had a falsely positive result. A total of 17 out of 470 consecutive patients had a regurgitant index below the normal range; left ventricular function was severely impaired in 9 of these patients. The remaining subjects had a regurgitant index slightly below the lower normal limit. In conclusion, RNV has a high sensitivity in the diagnosis of TR in patients without left heart valvular regurgitation and a high specificity in patients without severely impaired left ventricular function and without left-to-right shunt through an atrial septal defect.(ABSTRACT TRUNCATED AT 400 WORDS)