Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-6-30
pubmed:abstractText
We compared the effects of heart rate reduction (HRR) by the hyperpolarization-activated pacemaker current (I(f)) channel inhibitor ivabradine (MI+Iva) and the beta(1)-blocker atenolol (MI+Aten) on ventricular remodeling and perfusion after myocardial infarction (MI) in middle-aged (12 mo) Sprague-Dawley rats. Mean HRR was virtually identical in the two treated groups (19%). Four weeks after coronary artery ligation, maximal myocardial perfusion fell in the MI group but was preserved in infarcted rats treated with either Iva or Aten. However, coronary reserve in the remodeled hearts was preserved only with Iva, since Aten treatment elevated baseline perfusion in response to a higher wall stress. The higher maximal perfusion noted in the two treated groups was not due to arteriogenesis or angiogenesis. Plasma levels of angiotensin (ANG) II and myocardial ANG type 1 (AT(1)) receptor and transforming growth factor (TGF)-beta1 were reduced during the first week of treatment by both Iva and Aten. Moreover, treatment also reduced arteriolar perivascular collagen density. Despite these similar effects of Iva and Aten on vascularity and ANG II, Iva, but not Aten, attenuated the decline in ejection fraction and lowered left ventricular (LV) end-diastolic volume (LVEDV)-to-LV mass ratio, determined by echocardiography. In conclusion, 1) Iva has advantages over Aten in postinfarction therapy that are not due to differential effects of the drugs on heart rate, and 2) age limits growth factor upregulation, angiogenesis, and arteriogenesis in the postinfarcted heart.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1522-1539
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
297
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H322-30
pubmed:meshHeading
pubmed-meshheading:19411283-Adrenergic beta-Antagonists, pubmed-meshheading:19411283-Angiotensin II, pubmed-meshheading:19411283-Animals, pubmed-meshheading:19411283-Atenolol, pubmed-meshheading:19411283-Benzazepines, pubmed-meshheading:19411283-Bradykinin, pubmed-meshheading:19411283-Cardiotonic Agents, pubmed-meshheading:19411283-Collagen, pubmed-meshheading:19411283-Coronary Circulation, pubmed-meshheading:19411283-Electrocardiography, pubmed-meshheading:19411283-Heart Rate, pubmed-meshheading:19411283-Immunohistochemistry, pubmed-meshheading:19411283-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:19411283-Male, pubmed-meshheading:19411283-Myocardial Infarction, pubmed-meshheading:19411283-Neovascularization, Physiologic, pubmed-meshheading:19411283-Organ Size, pubmed-meshheading:19411283-Perfusion, pubmed-meshheading:19411283-Rats, pubmed-meshheading:19411283-Rats, Sprague-Dawley, pubmed-meshheading:19411283-Receptor, Angiotensin, Type 1, pubmed-meshheading:19411283-Ventricular Remodeling
pubmed:year
2009
pubmed:articleTitle
Postmyocardial infarction remodeling and coronary reserve: effects of ivabradine and beta blockade therapy.
pubmed:affiliation
Department of Anatomy and Cell Biology, Department of Internal Medicine, and Cardiovascular Center, University of Iowa, Iowa City, IA 52242, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't