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dc.contributor.authorParker, Matthew
dc.contributor.authorAurigemma, Gerard P.
dc.date2022-08-11T08:08:03.000
dc.date.accessioned2022-08-23T15:40:30Z
dc.date.available2022-08-23T15:40:30Z
dc.date.issued2016-05-24
dc.date.submitted2018-05-02
dc.identifier.citation<p>J Am Coll Cardiol. 2016 May 24;67(20):2330-2333. doi: 10.1016/j.jacc.2016.03.549. <a href="https://doi.org/10.1016/j.jacc.2016.03.549">Link to article on publisher's site</a></p>
dc.identifier.issn0735-1097 (Linking)
dc.identifier.doi10.1016/j.jacc.2016.03.549
dc.identifier.pmid27199055
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26415
dc.description.abstractAortic stenosis (AS) is the prototypical pressure overload lesion. The Gunther-Grossman paradigm of the 1970s dictates that as afterload increases, concentric hypertrophy—increases in left ventricular (LV) mass index and relative wall thickness—normalize systolic load and allow for normal ejection fraction despite markedly increased intraventricular systolic pressure. In some individuals, this compensatory process appears to be excessive and can be associated with poor outcome even with aortic valve replacement (AVR). Increasingly, attention has been focused on the malefic consequences for diastolic function of such ‘compensatory’ hypertrophy.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27199055&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/j.jacc.2016.03.549
dc.subjectadverse events
dc.subjectaortic regurgitation
dc.subjectaortic stenosis
dc.subjectmixed aortic valve disease
dc.subjectCardiology
dc.subjectCardiovascular Diseases
dc.titleThe Simple Arithmetic of Mixed Aortic Valve Disease: LVH + Volume Load = Trouble
dc.typeEditorial
dc.source.journaltitleJournal of the American College of Cardiology
dc.source.volume67
dc.source.issue20
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cardio_pp/98
dc.identifier.contextkey12057203
html.description.abstract<p>Aortic stenosis (AS) is the prototypical pressure overload lesion. The Gunther-Grossman paradigm of the 1970s dictates that as afterload increases, concentric hypertrophy—increases in left ventricular (LV) mass index and relative wall thickness—normalize systolic load and allow for normal ejection fraction despite markedly increased intraventricular systolic pressure. In some individuals, this compensatory process appears to be excessive and can be associated with poor outcome even with aortic valve replacement (AVR). Increasingly, attention has been focused on the malefic consequences for diastolic function of such ‘compensatory’ hypertrophy.</p>
dc.identifier.submissionpathcardio_pp/98
dc.contributor.departmentDivision of Cardiovascular Medicine, Department of Medicine
dc.source.pages2330-2333


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