J Heart Valve Dis
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The Center for Devices and Radiological Health, Food and Drug Administration, has recently revised its "Replacement Heart Valve Guidance". That document lists the data FDA deems necessary to support the approval of new prosthetic heart valves of all designs, and which should be contained in Premarket Approval Applications for these devices. The Guidance covers detailed data requirements for in vitro, animal, and clinical data. This paper is intended to briefly summarize FDA's requirements for in vitro data, and, for those cases where it may not be obvious, to provide an overview of the significance of these data and how FDA interprets them in the approval decision process.
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Randomized Controlled Trial Clinical Trial
Comparison of the causes of late death following aortic and mitral valve replacement. VA Co-operative Study on Valvular Heart Disease.
This report examines and compares the causes of late non-surgical death in 146 of 690 (21%) patients undergoing isolated aortic valve replacement (AVR) and in 79 of 273 (29%) patients undergoing mitral valve replacement (MVR) over a five year follow up period. The distribution of valve related, cardiac but not valve-related and non-cardiac deaths was 43%, 23% and 34% respectively for AVR and 65%, 29% and 6% respectively for MVR; the difference between these distributions was statistically significant. The specific causes of valve related deaths included bleeding (11% vs. 5% for MVR vs. ⋯ Non-cardiac causes accounted for only 6% of MVR deaths but 34% of AVR deaths (p < 0.001). There was no significant difference in the late mortality between mechanical and bioprosthetic valves in the aortic position (24% vs. 22%), but the cumulative rate of late deaths was higher in patients with the Björk-Shiley than with the Hancock valve in the mitral position (41% vs. 25%, p < 0.02). In conclusion, about one quarter of patients surviving either aortic or mitral valve replacement died within five years.(ABSTRACT TRUNCATED AT 250 WORDS)
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Case Reports
Mitral regurgitation from papillary muscle rupture: role of transesophageal echocardiography.
A case of a 61 year old male with lateral myocardial infarction, congestive heart failure and fever of days is presented. The exact etiology of this patient's heart failure was established with the application of transesophageal echocardiography. The transthoracic two-dimensional and Doppler echo showed a mobile echogenic density attached to the tip of the anterior mitral leaflet accompanied by moderate mitral regurgitation. ⋯ Cardiac catheterization confirmed the severe mitral regurgitation and uncovered significant stenotic lesions of the coronary arteries. The resultant surgical treatment for the replacement of the mitral valve and coronary artery by-pass confirmed the rupture of the head of the anterolateral papillary muscle. It is suggested that transesophageal echocardiography is particularly capable of providing a definitive and prompt diagnosis of papillary muscle rupture.
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Patients with mitral valve prolapse may present with chest pain and dyspnea. Left ventricular hemodynamics as a cause for these symptoms have not been completely evaluated in these patients. The present study was undertaken to investigate left ventricular hemodynamics in symptomatic patients with mitral valve prolapse. ⋯ Left ventricular end diastolic pressures before (chest pain 9.3 +/- 3.7 mmHg; dyspnea 8.2 +/- 4.2 mmHg; chest pain plus dyspnea 9.3 +/- 4.1 mmHg) and after left ventriculography (chest pain 11.6 +/- 5.5 mmHg; dyspnea 10.2 +/- 2.3 mmHg; chest pain plus dyspnea 11.7 +/- 5.6 mmHg) were normal in the majority of patients and similar in all three groups. Likewise, the left ventricular end diastolic volume index (chest pain 72.0 +/- 16 cm3, dyspnea 69.1 +/- 20 cm3, chest pain plus dyspnea 70.0 +/- 16 cm3) and ejection fraction (chest pain 64.0 +/- 8.4%, dyspnea 64.1 +/- 6.1%, chest pain plus dyspnea 64.3 +/- 6.1%) were normal in the majority of patients and similar in the three groups. Symptomatic patients with mitral valve prolapse without significant mitral regurgitation had normal left ventricular hemodynamics, and their symptoms cannot be explained on the basis of hemodynamic abnormalities alone.