Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Suppl
pubmed:dateCreated
1990-3-13
pubmed:abstractText
The association between pressure overload, left ventricular (LV) hypertrophy and failure, and abnormalities in diastolic function has been described both clinically and experimentally. The mechanisms underlying this association, however, are complex and controversial. Factors that have been implicated include mechanical alterations due to hypertrophy alone, changes in collagen type and content, alterations in beta-adrenergic responsiveness, and chronic myocardial ischemia. Studies in our laboratory have identified limitations in subendocardial flow reserve in compensated LV hypertrophy and near exhaustion in subendocardial reserve in animals with decompensated LV hypertrophy and failure. These abnormalities in coronary reserve are associated with impaired diastolic function, particularly during periods of physiological stress. For example, with pacing-induced stress, impairment in diastolic function was observed in conscious dogs with compensated LV hypertrophy. In conscious dogs with LV hypertrophy and failure, isoproterenol also resulted in altered diastolic function. Thus, in the model of severe pressure-overload hypertrophy, which is characterized by limitations in coronary reserve, the mechanism of subendocardial ischemia might be responsible in part for the impairment in diastolic function observed in response to superimposed stress.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0009-7322
pubmed:author
pubmed:issnType
Print
pubmed:volume
81
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
III8-14
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Reduced subendocardial coronary reserve. A potential mechanism for impaired diastolic function in the hypertrophied and failing heart.
pubmed:affiliation
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, Massachusetts.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.