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Survival Following Myectomy for Obstructive Hypertrophic Cardiomyopathy-What Causes Late Mortality?

08:00 EDT 9th April 2019 | BioPortfolio

Summary of "Survival Following Myectomy for Obstructive Hypertrophic Cardiomyopathy-What Causes Late Mortality?"

Survival of patients with obstructive hypertrophic cardiomyopathy who undergo septal myectomy appears to be excellent, and in some series, is similar to that of matched populations. In this study, we investigated causes of late death in a large cohort of surgical patients.

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This article was published in the following journal.

Name: The Annals of thoracic surgery
ISSN: 1552-6259
Pages:

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Septal myectomy with versus without subvalvular apparatus intervention in patients with hypertrophic obstructive cardiomyopathy: a prospective randomized study.

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The purpose of the study is to assess the role of mitral valve apparatus in the development of outflow tract obstruction in patients with hypertrophic cardiomyopathy and to identify the be...

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Medical and Biotech [MESH] Definitions

An autosomal dominant inherited form of HYPERTROPHIC CARDIOMYOPATHY. It results from any of more than 50 mutations involving genes encoding contractile proteins such as VENTRICULAR MYOSINS; cardiac TROPONIN T; ALPHA-TROPOMYOSIN.

A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).

A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).

An autosomal recessively inherited glycogen storage disease caused by GLUCAN 1,4-ALPHA-GLUCOSIDASE deficiency. Large amounts of GLYCOGEN accumulate in the LYSOSOMES of skeletal muscle (MUSCLE, SKELETAL); HEART; LIVER; SPINAL CORD; and BRAIN. Three forms have been described: infantile, childhood, and adult. The infantile form is fatal in infancy and presents with hypotonia and a hypertrophic cardiomyopathy (CARDIOMYOPATHY, HYPERTROPHIC). The childhood form usually presents in the second year of life with proximal weakness and respiratory symptoms. The adult form consists of a slowly progressive proximal myopathy. (From Muscle Nerve 1995;3:S61-9; Menkes, Textbook of Child Neurology, 5th ed, pp73-4)

Isoforms of MYOSIN TYPE II, specifically found in the ventricular muscle of the HEART. Defects in the genes encoding ventricular myosins result in FAMILIAL HYPERTROPHIC CARDIOMYOPATHY.

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