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Effects of (−)-Epicatechin on Myocardial Infarct Size and Left Ventricular Remodeling After Permanent Coronary Occlusion
- Source :
-
Journal of the American College of Cardiology (JACC) . Jun2010, Vol. 55 Issue 25, p2869-2876. 8p. - Publication Year :
- 2010
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Abstract
- Objectives: We examined the effects of the flavanol (−)-epicatechin on short- and long-term infarct size and left ventricular (LV) structure and function after permanent coronary occlusion (PCO) and the potential involvement of the protective protein kinase B (AKT)/extracellular signal-related kinase (ERK) signaling pathways. Background: (−)-epicatechin reduces blood pressure in hypertensive patients and limits infarct size in animal models of myocardial ischemia–reperfusion injury. However, nothing is known about its effects on infarction after PCO. Methods: (−)-epicatechin (1 mg/kg daily) treatment was administered via oral gavage to 250 g male rats for 10 days before PCO and was continued afterward. The PCO controls received water. Sham animals underwent thoracotomy and treatment in the absence of PCO. Immunoblots assessed AKT/ERK involvement 2 h after PCO. The LV morphometric features and function were measured 48 h and 3 weeks after PCO. Results: In the 48-h group, treatment reduced infarct size by 52%. There were no differences in hemodynamics among the different groups (heart rate and aortic and LV pressures). Western blots revealed no differences in AKT or ERK phosphorylation levels. At 3 weeks, PCO control animals demonstrated significant increases in LV end-diastolic pressure, heart and body weight, and LV chamber diameter versus sham. The PCO plus (−)-epicatechin group values were comparable with those of the sham plus (−)-epicatechin group. Treatment resulted in a 33% decrease in myocardial infarction size. The LV pressure-volume curves demonstrated a right shift in control PCO animals, whereas the (−)-epicatechin curves were comparable with those of the sham group. The LV scar area strains were significantly improved with (−)-epicatechin. Conclusions: These results demonstrate the unique capacity of (−)-epicatechin to confer cardioprotection in the setting of a severe form of myocardial ischemic injury. Protection is sustained over time and preserves LV structure and function. The cardioprotective mechanism(s) of (−)-epicatechin seem to be unrelated to AKT or ERK activation. (−)-epicatechin warrants further investigation as a cardioprotectant. [Copyright &y& Elsevier]
Details
- Language :
- English
- ISSN :
- 07351097
- Volume :
- 55
- Issue :
- 25
- Database :
- Academic Search Index
- Journal :
- Journal of the American College of Cardiology (JACC)
- Publication Type :
- Academic Journal
- Accession number :
- 51816649
- Full Text :
- https://doi.org/10.1016/j.jacc.2010.01.055