Inflammation as a Driver of Adverse Left Ventricular Remodeling after Acute Myocardial Infarction

Peter C. Westman; Michael J. Lipinski; Dror Luger; Ron Waksman; Robert O. Bonow; Edwin Wu; Stephen E. Epstein

doi:10.1016/j.jacc.2016.01.073

Inflammation as a Driver of Adverse Left Ventricular Remodeling after Acute Myocardial Infarction

Peter C. Westman, Michael J. Lipinski, Dror Luger, Ron Waksman, Robert O. Bonow, Edwin Wu, Stephen E. Epstein^*

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

342 Scopus citations

Abstract

Treatment of acute myocardial infarction (AMI) has improved significantly in recent years, but many patients have adverse left ventricular (LV) remodeling, a maladaptive change associated with progressive heart failure. Although this change is usually associated with large infarcts, some patients with relatively small infarcts have adverse remodeling, whereas other patients with larger infarcts (who survive the first several days after AMI) do not. This paper reviews the relevant data supporting the hypothesis that individual differences in the intensity of the post-AMI inflammatory response, involving 1 or more inflammatory-modulating pathways, may contribute to adverse LV remodeling. It concludes by outlining how individual variations in the inflammatory response could provide important novel therapeutic targets and strategies.

Original language	English (US)
Pages (from-to)	2050-2060
Number of pages	11
Journal	Journal of the American College of Cardiology
Volume	67
Issue number	17
DOIs	https://doi.org/10.1016/j.jacc.2016.01.073
State	Published - May 3 2016

Keywords

heart failure
infarct size
left ventricular function
stem cells

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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10.1016/j.jacc.2016.01.073

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title = "Inflammation as a Driver of Adverse Left Ventricular Remodeling after Acute Myocardial Infarction",

abstract = "Treatment of acute myocardial infarction (AMI) has improved significantly in recent years, but many patients have adverse left ventricular (LV) remodeling, a maladaptive change associated with progressive heart failure. Although this change is usually associated with large infarcts, some patients with relatively small infarcts have adverse remodeling, whereas other patients with larger infarcts (who survive the first several days after AMI) do not. This paper reviews the relevant data supporting the hypothesis that individual differences in the intensity of the post-AMI inflammatory response, involving 1 or more inflammatory-modulating pathways, may contribute to adverse LV remodeling. It concludes by outlining how individual variations in the inflammatory response could provide important novel therapeutic targets and strategies.",

keywords = "heart failure, infarct size, left ventricular function, stem cells",

author = "Westman, {Peter C.} and Lipinski, {Michael J.} and Dror Luger and Ron Waksman and Bonow, {Robert O.} and Edwin Wu and Epstein, {Stephen E.}",

note = "Funding Information: Dr. Epstein has received a consultancy stipend and equity interests in CardioCell. Dr. Waksman has received consultancy fees from Biotronik, Medtronic Vascular, Boston Scientific, Abbott Vascular, and Biosensors International; grant support from Biotronik, Boston Scientific, Biosensors International, Edwards LifeSciences, and AstraZeneca; and served as a member of a speakers bureau for AstraZeneca. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Publisher Copyright: {\textcopyright} 2016 American College of Cardiology Foundation.",

year = "2016",

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doi = "10.1016/j.jacc.2016.01.073",

language = "English (US)",

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AU - Westman, Peter C.

AU - Lipinski, Michael J.

AU - Luger, Dror

AU - Waksman, Ron

AU - Bonow, Robert O.

AU - Wu, Edwin

AU - Epstein, Stephen E.

N1 - Funding Information: Dr. Epstein has received a consultancy stipend and equity interests in CardioCell. Dr. Waksman has received consultancy fees from Biotronik, Medtronic Vascular, Boston Scientific, Abbott Vascular, and Biosensors International; grant support from Biotronik, Boston Scientific, Biosensors International, Edwards LifeSciences, and AstraZeneca; and served as a member of a speakers bureau for AstraZeneca. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Publisher Copyright: © 2016 American College of Cardiology Foundation.

PY - 2016/5/3

Y1 - 2016/5/3

N2 - Treatment of acute myocardial infarction (AMI) has improved significantly in recent years, but many patients have adverse left ventricular (LV) remodeling, a maladaptive change associated with progressive heart failure. Although this change is usually associated with large infarcts, some patients with relatively small infarcts have adverse remodeling, whereas other patients with larger infarcts (who survive the first several days after AMI) do not. This paper reviews the relevant data supporting the hypothesis that individual differences in the intensity of the post-AMI inflammatory response, involving 1 or more inflammatory-modulating pathways, may contribute to adverse LV remodeling. It concludes by outlining how individual variations in the inflammatory response could provide important novel therapeutic targets and strategies.

AB - Treatment of acute myocardial infarction (AMI) has improved significantly in recent years, but many patients have adverse left ventricular (LV) remodeling, a maladaptive change associated with progressive heart failure. Although this change is usually associated with large infarcts, some patients with relatively small infarcts have adverse remodeling, whereas other patients with larger infarcts (who survive the first several days after AMI) do not. This paper reviews the relevant data supporting the hypothesis that individual differences in the intensity of the post-AMI inflammatory response, involving 1 or more inflammatory-modulating pathways, may contribute to adverse LV remodeling. It concludes by outlining how individual variations in the inflammatory response could provide important novel therapeutic targets and strategies.

KW - heart failure

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KW - left ventricular function

KW - stem cells

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Inflammation as a Driver of Adverse Left Ventricular Remodeling after Acute Myocardial Infarction

Abstract

Keywords

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