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Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
Published on: December 2, 2014
Selective beta1-blockade attenuates post-infarct remodelling without improvement in myocardial energy metabolism and
E Omerovic1, E Bollano, B Soussi
1Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska Academy at Gothenburg University, 413 45 Gothenburg, Sweden. elmir@wlab.gu.se
Insights
Long-term beta1-blocker treatment in rats with heart failure reduced cardiac remodeling but did not improve energy metabolism or function. This suggests anti-remodeling effects occur independently of metabolic improvements in chronic heart failure.
Area of Science:
- Cardiology
- Pharmacology
- Biochemistry
Background:
- Congestive heart failure (CHF) following myocardial infarction (MI) involves complex cardiac remodeling and metabolic changes.
- Beta-blockers are standard therapy for CHF, but their precise effects on cardiac energy metabolism and remodeling post-MI require further elucidation.
Purpose of the Study:
- To investigate the in vivo effects of long-term selective beta1-blockade on cardiac energy metabolism, remodeling, function, and plasma cytokines in a rat model of post-infarct CHF.
Main Methods:
- Male rats underwent MI and were treated with metoprolol or saline for 6 weeks.
- Left ventricular (LV) energy metabolism, morphology, and function were assessed using 31P magnetic resonance spectroscopy and echocardiography.
- Plasma cytokine levels (IL-1beta, IL-6) and beta-adrenergic receptor density were analyzed.
Main Results:
- Metoprolol treatment attenuated the increase in LV dimensions and volumes post-MI.
- No significant improvements in phosphocreatine/adenosine triphosphate (PCr/ATP) ratio or LV function were observed with metoprolol.
- Plasma IL-1beta levels increased, while IL-6 levels decreased in the metoprolol group; beta-adrenergic receptor density remained similar across groups.
Conclusions:
- Selective beta1-blockade in rats with chronic CHF attenuates post-infarct structural remodeling.
- Improvements in myocardial energy metabolism and function are not prerequisites for the anti-remodeling effects of beta1-blockade in chronic CHF.
Objective:
To investigate in vivo effects of long-term selective beta1-blockade on cardiac energy metabolism, remodelling, function and plasma cytokines in a rat model of post-infarct congestive heart failure (CHF).
Methods:
Myocardial infarction (MI) was induced in male rats by ligation of the left coronary artery. Three different groups of rats were studied, MI rats treated with metoprolol (n=17), MI rats treated with saline (n=14) and sham-operated rats (n=12). The treatment with metoprolol 1 mg/kg/h was initiated in the third week post-infarct for a period of 6 weeks. All rats were investigated non-invasively with volume-selective 31P magnetic resonance spectroscopy and echocardiography for evaluation of left ventricular (LV) energy metabolism, morphology and function. Plasma concentration of IL-1beta and IL-6 and density of beta-adrenergic receptors were analyzed.
Results:
Metoprolol attenuated the increase in LV dimensions and volumes. Treatment with metoprolol had no effect on PCr/ATP and LV function. Plasma level of IL-1beta was higher and IL-6 was lower in the metoprolol group. Density of beta-adrenergic receptors was similar in all three groups.
Conclusion:
Selective beta1-blockade in rats with chronic CHF attenuates post-infarct structural remodelling, without concomitant improvement in myocardial energy metabolism and function. Improvements in myocardial energy metabolism and function do not precede and are not a prerequisite for an anti-remodelling effect of beta1-blockade in the setting of chronic CHF.
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