Abstract:
:Cardiac rupture after a myocardial infarction is an uncommon event with devastating consequences. Although the clinical features of rupture have been described, the genetic and molecular influences on this outcome in patients are less certain. In mice, at least 17 genetic models have been developed that enhance or suppress the likelihood of rupture postmyocardial infarction. The purpose of this review is to describe these recent advances, recognizing that nearly all of the information has been obtained from mouse models of free wall rupture. Although it is probable that the same genetic determinants apply to septal and papillary muscle rupture, the possibility remains that there are unique modulators of risk for rupture at differing anatomic sites within the heart. It is likely that the candidate genes also influence rupture in humans, although this conclusion must be confirmed. The mouse models will be helpful to direct future proteomic and genomic studies in patients and may already suggest certain fundamental pathways. For example, the essential role of collagen production and stabilization postmyocardial infarction may direct therapies to enhance collagen cross-linking and limit its degradation as a strategy to reduce rates of rupture and enhance myocardial healing.
journal_name
Cardiol Revjournal_title
Cardiology in reviewauthors
Sane DC,Mozingo WS,Becker RCdoi
10.1097/CRD.0b013e3181bf4ab4subject
Has Abstractpub_date
2009-11-01 00:00:00pages
293-9issue
6eissn
1061-5377issn
1538-4683pii
00045415-200911000-00008journal_volume
17pub_type
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