Effects of (-)-epicatechin on myocardial infarct size and left ventricular remodeling after permanent coronary occlusion

J Am Coll Cardiol. 2010 Jun 22;55(25):2869-76. doi: 10.1016/j.jacc.2010.01.055.


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.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Analysis of Variance
  • Animals
  • Catechin / pharmacology*
  • Coronary Circulation
  • Coronary Occlusion / diagnostic imaging
  • Coronary Occlusion / drug therapy*
  • Coronary Occlusion / mortality
  • Disease Models, Animal
  • Hemodynamics / physiology*
  • Male
  • Myocardial Infarction / drug therapy*
  • Myocardial Infarction / mortality
  • Myocardial Infarction / pathology
  • Myocardial Infarction / prevention & control*
  • Myocardial Reperfusion Injury / prevention & control
  • Probability
  • Radiography
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Reference Values
  • Survival Rate
  • Treatment Outcome
  • Ventricular Remodeling / drug effects*
  • Ventricular Remodeling / physiology


  • Catechin