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The midsystolic click-late systolic murmur syndrome is a complex entity with variable manifestations that involves a primary process causing myxomatous degeneration of the mitral valve leaflet(s) and subsequent systolic mitral valve leaflet prolapse. Other cardiac diseases may cause mitral valve prolapse and regurgitation associated with a midsystolic click that mimics this primary syndrome. The prolapsing mitral valve leaflet(s) syndrome occasionally may be familial. Most patients are asymptomatic but some complain of chest pain, palpitation, dyspnea or fatigue. Prolapsing mitral valve leaflet(s) can be distinguished from other causes of systolic clicks and mitral regurgitation murmurs by the characteristic movement of the clikmurmur complex in systole with various hemodynamic interventions. The clinical diagnosis usually can be confirmed by echocardiography, which demonstrates the abnormally prolapsdrome usually is minimal but can be progressive and lead to the need for prosthetic valve replacement. Most symptomatic patients can be managed medically but some require cardiac catheterization to evaluate the possibility of coexistent coronary artery disease, to assess the degree of mitral regurgitation and to evaluate other associated cardiac lesions. All patients with this syndrome should receive antibiotic prophylaxis prior to any surgical or dental procedures. Those patients suspected of having arrhythmias should be evaluated by continuous ambulatory ECG monitoring and dangerous arrhythmias probably should be treated. The prognosis usually is excellent, but sudden death and rapidly progressive mitral regurgitation due to ruptured chordae tendineae have been reported. Although more than a decade has elapsed since the midsystolic click-late systolic murmur syndrome was first recognized, much remains to be learned about this common but complex clinical entity.
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PMID:The systolic click-murmur syndrome: clinical recognition and management. 101 8

From 1969 to 1989, 15 patients with an aneurysm of the sinus of Valsalva underwent operative correction. This represents 0.23% of 6515 cardiac operations with cardiopulmonary bypass during that time. There were 8 males and 7 females ranging in age from 15 to 54 years (mean 35.8 years). Symptoms of congestive heart failure, fatigue and palpitation were common. All patients underwent cardiac catheterization including aortography. Associated lesions included aortic valve regurgitation in 6 patients and a ventricular septal defect in 3 patients. The following connections occurred: right coronary sinus to right ventricle (8 patients), right coronary sinus to both right atrium and right ventricle (1 patient), and noncoronary sinus to right atrium (6 patients). The aneurysm was repaired via aortotomy or through the chamber into which it emptied. The aortic valve was replaced in 2 patients. There were no early or late postoperative deaths. Fourteen patients were in NYHA functional class I at late follow-up (range 0.5 to 20.5 years, mean 8.7 years). There have been no recurrences. Our experience supports the concept that early surgical intervention in patients with ruptured aneurysms of the sinus of Valsalva is justified.
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PMID:Ruptured aneurysms of the sinus of Valsalva. 154 97

Tricuspid valve prolapse is an infrequent echocardiographic finding that is most commonly associated with mitral valve prolapse. When compared with patients exhibiting isolated prolapse of the mitral valve, patients with tricuspid valve prolapse are somewhat older individuals with a slightly higher frequency of neurologic symptoms, fatigue, weakness, supraventricular arrhythmias (especially atrial fibrillation) and skeletal deformities. Tricuspid valve prolapse may serve as a marker of more-diffuse connective tissue abnormalities, and its identification also should prompt an echocardiographic search for evidence of prolapse and regurgitation of the other heart valves.
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PMID:Tricuspid valve prolapse. 353 7

A number of centers have recorded a significant incidence of primary tissue failure with the standard Ionescu-Shiley pericardial valve. In most cases severe regurgitation was caused by leaflet tears adjacent to the edge of the cloth-covered stent. Our early clinical experience (up to 4 years' follow-up) with two new pericardial valves (Ionescu-Shiley low-profile and Hancock pericardial valves) has shown that primary tissue failure also occurs in these new valves. In vitro accelerated fatigue studies on seven of these valves (size 29 mm) showed that in vitro premature leaflet failure was caused by abrasion of the leaflet on the cloth-covering at the edge of the stent. Clinically, endothelialization and host tissue ingrowth on the cloth and the leaflets at the edge of the frame greatly reduced the amount of abrasion and the incidence of tissue failure. In seven of the eight explanted valves studied, leaflet tears occurred at the top of the stent posts where there was less endothelialization and tissue ingrowth, close to the points where sutures pass through the leaflets. It is likely that both abrasion and stress concentration around these sutures contributed to the tissue failures in the clinical valves.
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PMID:Primary tissue failure in pericardial heart valves. 362 99

Eight asymptomatic patients (mean age 19 years, range 7 to 32) with congenitally corrected transposition of the great arteries (CCTGA) underwent equilibrium gated radionuclide angiocardiography at rest and during supine bicycle exercise to assess systemic (morphologic right) and pulmonary (morphologic left) ventricular function. Five patients had normal intracardiac hemodynamic values, 2 had trivial atrioventricular valve regurgitation and 1 patient had trivial pulmonary ventricular outflow tract obstruction. Average exercise duration was 11 +/- 1 minute, with limitation due only to fatigue. At peak exercise, heart rate increased 225% and systolic blood pressure 152% over the rest value. Pulmonary ventricular ejection fraction at rest was 51 +/- 3% (mean +/- standard error of the mean); it did not change significantly at peak stress, 53 +/- 2%. Systemic ventricular ejection fraction was 48 +/- 4% at rest and increased to 64 +/- 4% at peak exercise (p less than 0.01). Count-based volume changes for the pulmonary chamber showed no significant change in end-diastolic or systolic counts at peak exercise (109 +/- 8% and 106 +/- 9% of rest value, respectively). However, end-diastolic counts decreased 13% (87 +/- 3% of rest value) and end-systolic counts 34% (62 +/- 7% of rest value) at peak exercise in the systemic ventricle. These data suggest normal systemic and impaired pulmonary ventricular function in patients with congenitally corrected transposition of the great arteries unaccompanied by significant associated lesions. These findings have important clinical implications in the setting of complex congenital heart disease in patients in whom a morphologic right ventricle functions as the systemic pumping chamber. Despite the pulmonary ventricular dysfunction, symptoms were not apparent at rest or during exercise.
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PMID:Radionuclide angiographic evaluation of ventricular function in isolated congenitally corrected transposition of the great arteries. 373 22

The aortic root as a functional unit includes the sinuses of valsalva, valve ring, the leaflets and the commissures. This unit is impaired by the insertion of a bioprosthetic three-leaflet valve. Moreover, bioprostheses fail because of fatigue and flexion stresses. Consequently a program was started for free-handed orthotopic transplantation of allogeneous aortic valves at the Department of Cardiovascular Surgery, University Kiel. A series of 16 consecutive antibiotic, sterilized aortic valve allografts were transplanted in the last 12 months without death. There were 4 females and 12 males between 18 and 63 years old (mean 47.9). The dominant lesion was aortic regurgitation (in 9), stenosis (in 3) and mixed (in 4). Out of the 13 patients who maintained their allografts, 10 (77%) were in class III and 3 (23%) in class IV of the NYHA functional classification. Four patients improved from class III to class I, and 9 from class III and IV to class II of the NYHA functional classification after surgery. All patients except one had postoperative recatheterization including videodensitometry to quantitate the regurgitation, expressed as a regurgitant fraction ( RGF ) in percent of the total stroke volume of the left ventricle, and pressure measurements to determine systolic gradients across the aortic valve allograft, 3 to 6 days and 9 months after surgery. Eleven (68.75%) patients had no regurgitation, 2 (12.5%) patients had trivial aortic regurgitation with RGF of 7% and 10%, respectively. Three (18.75%) patients had severe aortic valve regurgitation with RGF between 40% and 60% due to technical errors and their allografts had to be replaced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Orthotopic transplantation of aortic valve allografts. Early hemodynamic results. 620 16

The mitral apparatus is a complex structure composed of several components, each of which can be affected by a variety of diseases, resulting in mitral regurgitation. The physiologic consequences of mitral regurgitation include reduced forward stroke volume; increased left atrial volume and pressure; and reduced resistance to left ventricular ejection. The latter explains why indices of systolic left ventricular function (ejection fraction) are often increased early in the course of mitral regurgitation. With the insidious development of mitral regurgitation, the left atrium dilates to accommodate the increase in volume, thereby reducing the atrial pressure. However, with the acute development of mitral regurgitation into a nondilated left atrium, pressure rises rapidly, producing pulmonary edema. The predominant clinical symptoms in chronic mitral regurgitation of dyspnea and fatigue result from pulmonary venous hypertension and low cardiac output. The cardinal physical finding is a mitral systolic murmur. Since the murmur can assume various configurations, the most reliable way to establish its correct origin is by bedside physiologic maneuvers. Typically, in the beat following a premature contraction or after a long pause during atrial fibrillation, the murmur of mitral regurgitation is unchanged in intensity, but murmurs due to left ventricular outflow obstruction increase. Also, isometric handgrip exercise increases the intensity of the murmur and a Valsalva maneuver decreases it during the strain phase. Echocardiography is the most useful noninvasive technique for evaluating patients with mitral regurgitation. Visualization of the mitral apparatus may establish the etiology of regurgitation, and measurement of left atrial size and left ventricular size and performance is useful for assessing the functional significance of the lesion. Doppler echocardiography can establish the diagnosis of mitral regurgitation in difficult cases with multi valve disease and can estimate the severity of the regurgitation. Cardiac catheterization and angiography are usually reserved for the patient being considered for valvular surgery. The natural history of chronic mitral regurgitation is characterized by slowly progressive symptoms, and often the onset of disabling symptoms is the result of irreversible left ventricular dysfunction. Medical therapy consists of digitalis, diuretics, and vasodilators for symptomatic patients. When symptoms occur despite this therapy, valvular surgery should be considered before left ventricular function becomes abnormal.
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PMID:Mitral valve regurgitation. 637 82

A fifty-six-year-old woman was admitted to Osaka Rosai hospital because of dyspnea, chills, and fatigue. The patient was diagnosed by transthoracic echocardiography as having congestive heart failure due to severe biatrioventricular valve regurgitation, and cardiac surgery was proposed. Preoperative transesophageal echocardiography (TEE) revealed a dilatation of the coronary sinus (CS), a right-sided hemiazygos vein (R-AZ), and another great vessel lying between the CS and the R-AZ. Magnetic resonance imaging (MRI) was also performed, and this showed a persistent right superior vena cava (PRSVC) entering the left atrium via the dilatated CS. However, the site of connection between the R-AZ and the PRSVC could not be detected by MRI because of inadequate slice acquisition. Each method has its limitations, particularly with regard to visualizing the extracardiac vascular system. Therefore, the authors demonstrated that the combination of TEE and MRI might be more useful than each alone, and the combination is as a valuable method as digital subtraction angiography for the diagnosis of extracardiac venous anomalies.
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PMID:Transesophageal echocardiography combined with magnetic resonance imaging for detecting venous anomalies in dextrocardia. A case report. 778 97

Clinical, echocardiographic and haemodynamic features in 14 patients (8 male and 6 females) with primary pulmonary hypertension, diagnosed by strict clinical and haemodynamic criteria are described. Age of the patients at diagnosis ranged from 11 years to 40 years with a mean of 23 years. The mean interval from onset of symptoms to diagnosis was 2.6 years. Common symptoms included dyspnoea on exertion (86%), fatigue (78%) and palpitation (78%). Raynaud's phenomenon was not encountered but one patient had signs and symptoms of left recurrent laryngeal nerve palsy. Pulmonary function studies showed mild restrictive ventilatory impairment (mean forced vital capacity 80% of predicted) with hypoxaemia and hypocapnea. The M-mode tracing of the pulmonary valve showed flat or negative E-F slope, a small or absent 'a' wave, and midsystolic notching in all the patients. Two-dimensional echocardiographic images showed a thickened right ventricular wall in 12(86%) patients; a normal to small left ventricular end-diastolic internal dimension in all the patients and right ventricular and right atrial enlargement in 78% of patients. Significant tricuspid regurgitation and pulmonary regurgitation was documented by Doppler interogation in 87% and 62% of patients examined respectively. Haemodynamic findings consisted of a marked rise of pulmonary artery pressure and pulmonary vascular resistance, low cardiac index and normal pulmonary artery wedge pressure. At cardiac catheterisation the mean right atrial pressure (mean +/- SD) was 9.8 +/- 4.8 mmHg; mean pulmonary artery pressure, 63.2 +/- 14.3 mmHg; cardiac index, 2.2 +/- 0.9 L/min. m2; and pulmonary vascular resistance index, 22.3 +/- 10.6 mmHg/L/min. m2; in these patients. No, death nor any sustained morbid events occurred during the diagnostic evaluation of the patients.
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PMID:Primary pulmonary hypertension: clinical, echocardiographic and haemodynamic features in 14 patients. 803 Dec 85

Symptoms tend to develop late in the course of both chronic mitral and chronic aortic regurgitation, and when the regurgitation is stable patients may enjoy many years of full activity free from disability. In the absence of complicating atrial fibrillation or coronary artery disease the onset of dyspnoe and fatigue usually indicate myocardial failure and possibly a lost opportunity for a low risk operation and long term benefit. Valve replacement for aortic regurgitation is a good operation which reduces left ventricular work. However, mitral valve replacement is unphysiologic and not surprisingly, the operative mortality and long term results are worse with an excess of deaths caused by left ventricular failure. While the need for operation is obvious when patients already have symptoms or when valvar regurgitation is increasing, timing is far more difficult for patients with severe, chronic, stable regurgitation who still enjoy a high quality of life. It is even more difficult in mitral regurgitation because the stakes are higher with a higher operative risk, but suitability for mitral valve reconstruction justifies earlier operation and therefore makes it mandatory for cardiologists to identify such patients.
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PMID:Optimal timing of surgery for chronic mitral or aortic regurgitation. 826 Nov 61


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