Abstract:
BACKGROUND:Studies in patients support a beneficial effect of statin treatment early after acute coronary syndrome and/or prior percutaneous coronary intervention. However, statin effect during total occlusion remains unknown. OBJECTIVES:To investigate whether infusion of activated simvastatin during ischemia and prior reperfusion and oral administration thereafter confers cardioprotection and improves cardiac healing in a preclinical model of myocardial infarction. METHODS:Pigs (n=24) fed a 10 day Western-type diet underwent a 90 min coronary-balloon occlusion (MI) being randomized to a single intravenous infusion of active β-hydroxy acid derivative of simvastatin (β-OH-S; 0.3 mg/kg) 15 min prior to reperfusion or vehicle. Animals were either sacrificed 2.5 h post-reperfusion or kept under the same regime ± simvastatin (p.o., 20 mg/day) for 3 weeks. Jeopardized and remote myocardium was obtained for molecular/histological studies. Echocardiography was assessed. RESULTS:β-OH-S infusion prior to reperfusion reduced coronary and cardiac oxidative DNA-damage, diminished neutrophil infiltration at the site of ischemia, preserved mitochondrial membrane potential and reduced apoptosis in the ischemic myocardium (lower mRNA levels of Fas, casp8, p53, and casp3 and mitochondrial-p-Bcl2; and reduced TUNEL and active caspase-3; p<0.05 vs. vehicle/control). This treatment regime attenuated reperfusion-related arrhythmias and stunning leading to a 40% increased myocardial salvage (p<0.05 vs. vehicle/control). 3 weeks post-MI simvastatin-treated animals showed P-PKCε increase, lower intramyocardial lipotoxicity, TβRII/Smad2/3 signaling restoration and subsequent myofibroblast differentiation and collagen-fibril formation in the evolving scar (p<0.05 vs. control). Simvastatin suppressed cardiac RhoA mobilization and triggered Akt/eNOS signaling. CONCLUSIONS:Acute HMG-CoA-reductase inhibition during total ischemia and prior reperfusion limits reperfusion injury and prolonged oral simvastatin treatment thereafter improves cardiac healing post-MI.
journal_name
Int J Cardioljournal_title
International journal of cardiologyauthors
Vilahur G,Casani L,Peña E,Juan-Babot O,Mendieta G,Crespo J,Badimon Ldoi
10.1016/j.ijcard.2014.06.040subject
Has Abstractpub_date
2014-08-20 00:00:00pages
528-38issue
3eissn
0167-5273issn
1874-1754pii
S0167-5273(14)01107-3journal_volume
175pub_type
杂志文章abstract:PURPOSE:It is thought that the mechanisms responsible for impaired chronotropic response to exercise are related to disturbance of cardiovascular autonomic regulation such as the baroreflex. However, it is still unclear whether the baroreflex mechanisms modulate heart rate (HR) responses to exercise via vagal and/or sy...
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