Linked Life Data

3673882

Source:http://linkedlifedata.com/resource/pubmed/id/3673882

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SubjectPredicateObjectContext
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pubmed-article:3673882pubmed:dateCreated1987-11-30lld:pubmed
pubmed-article:3673882pubmed:abstractTextThree patients with midventricular obstruction resulting from three different pathophysiologic mechanisms and differing anatomic bases for the development of obstruction are presented. In the first patient, a membrane-like structure appeared to cause some fixed obstruction, but a superimposed dynamic component to the obstruction was also evident. Papillary muscle hypertrophy with approximation of the papillary muscles during systole was the mechanism in the second patient. In the third patient, apical infarction with hyperdynamic contraction of the mid- and basal portions of the myocardium appeared to be the pathophysiologic mechanism. Color flow Doppler echocardiography was particularly useful in localizing the site of obstruction and allowed further evaluations by pulsed and continuous-wave Doppler techniques to precisely determine pressure gradients.lld:pubmed
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pubmed-article:3673882pubmed:authorpubmed-author:KotlerM NMNlld:pubmed
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pubmed-article:3673882pubmed:authorpubmed-author:WertheimerJJlld:pubmed
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pubmed-article:3673882pubmed:volume114lld:pubmed
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pubmed-article:3673882pubmed:pagination1162-8lld:pubmed
pubmed-article:3673882pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:3673882pubmed:year1987lld:pubmed
pubmed-article:3673882pubmed:articleTitleNoninvasive evaluation of mid-left ventricular obstruction by two-dimensional and Doppler echocardiography and color flow Doppler echocardiography.lld:pubmed
pubmed-article:3673882pubmed:affiliationDepartment of Medicine, Albert Einstein Medical Center, Temple University School of Medicine, Philadelphia, PA 19141.lld:pubmed
pubmed-article:3673882pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3673882pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:3673882pubmed:publicationTypeCase Reportslld:pubmed
pubmed-article:3673882pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed