PMID- 20864196
OWN - NLM
STAT- MEDLINE
DCOM- 20120820
LR  - 20181201
IS  - 1874-1754 (Electronic)
IS  - 0167-5273 (Linking)
VI  - 153
IP  - 3
DP  - 2011 Dec 15
TI  - Carvedilol administration in acute myocardial infarction results in stronger 
      inhibition of early markers of left ventricular remodeling than metoprolol.
PG  - 256-61
LID - 10.1016/j.ijcard.2010.08.018 [doi]
AB  - BACKGROUND: The structural secuelae of acute myocardial infarction (AMI) is 
      mostly dictated by left ventricular (LV) remodelling, leading to heart failure. 
      Monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinases (MMPs) and 
      their tissue inhibitors (TIMPs) play a critical role in LV remodelling. 
      beta-blockers are first line therapy for AMI and heart failure; however, the 
      mechanisms responsible for their benefits remain poorly understood. Different 
      beta-blocker agents have been shown to exert beneficial activities both in AMI and 
      heart failure, however, their role in early remodelling after 
      ischemia/reperfusion is to be fully elucidated. We sought to compare the effect 
      of 2 of the most prescribed beta-blocker agents in early markers of LV remodelling 
      after AMI. METHODS: A reperfused AMI was induced in Yorshire pigs, being 
      randomized to early intravenous carvedilol, metoprolol or placebo. Twenty-four 
      hours after reperfusion markers of early remodelling were addressed in the LV. 
      RESULTS: The early administration of both beta-blockers is able to significantly 
      reduce macrophage infiltration as well as the expression and activity of MCP-1 
      and MMP-2 compared to placebo. The effects of carvedilol were much stronger than 
      those of metoprolol. Conversely, carvedilol upregulated the expression TIMP-2 to 
      a greater extent than metoprolol. CONCLUSIONS: In an AMI model closely mimicking 
      human pathophysiology, the early administration of carvedilol reduced the 
      expression of markers associated with early LV remodelling to greater extent than 
      metoprolol. These findings may explain the superior clinical benefits exerted by 
      carvedilol in heart failure.
CI  - Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
FAU - Cimmino, Giovanni
AU  - Cimmino G
AD  - Atherothrombosis Research Unit, Cardiovascular Institute, Mount Sinai School of 
      Medicine, New York, NY 10029, USA.
FAU - Ibanez, Borja
AU  - Ibanez B
FAU - Giannarelli, Chiara
AU  - Giannarelli C
FAU - Prat-Gonzalez, Susanna
AU  - Prat-Gonzalez S
FAU - Hutter, Randolph
AU  - Hutter R
FAU - Garcia, Mario
AU  - Garcia M
FAU - Sanz, Javier
AU  - Sanz J
FAU - Fuster, Valentin
AU  - Fuster V
FAU - Badimon, Juan J
AU  - Badimon JJ
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100922
PL  - Netherlands
TA  - Int J Cardiol
JT  - International journal of cardiology
JID - 8200291
RN  - 0 (Biomarkers)
RN  - 0 (Carbazoles)
RN  - 0 (Propanolamines)
RN  - 0K47UL67F2 (Carvedilol)
RN  - GEB06NHM23 (Metoprolol)
SB  - IM
MH  - Animals
MH  - Biomarkers/metabolism
MH  - Carbazoles/pharmacology/*therapeutic use
MH  - Carvedilol
MH  - Down-Regulation/*drug effects
MH  - Metoprolol/pharmacology/*therapeutic use
MH  - Myocardial Infarction/*drug therapy/metabolism/pathology
MH  - Propanolamines/pharmacology/*therapeutic use
MH  - Random Allocation
MH  - Swine
MH  - Ventricular Remodeling/*drug effects/physiology
EDAT- 2010/09/25 06:00
MHDA- 2012/08/21 06:00
CRDT- 2010/09/25 06:00
PHST- 2010/01/12 00:00 [received]
PHST- 2010/07/20 00:00 [revised]
PHST- 2010/08/08 00:00 [accepted]
PHST- 2010/09/25 06:00 [entrez]
PHST- 2010/09/25 06:00 [pubmed]
PHST- 2012/08/21 06:00 [medline]
AID - S0167-5273(10)00608-X [pii]
AID - 10.1016/j.ijcard.2010.08.018 [doi]
PST - ppublish
SO  - Int J Cardiol. 2011 Dec 15;153(3):256-61. doi: 10.1016/j.ijcard.2010.08.018. Epub 
      2010 Sep 22.