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Published on: June 6, 2011
Cardiogenic shock: the role of inflammation
1Cardiology Department, Moscow State University of Medicine and Dentistry, Moscow, Russia. moscowcardio_23@yahoo.com
Insights
Cardiogenic shock (CS) following myocardial infarction (MI) involves elevated inflammatory cytokines. Future treatments may target specific nitric oxide synthase (NOS) isoforms or explore corticosteroids and hemofiltration.
Area of Science:
- Cardiology
- Immunology
- Critical Care Medicine
Background:
- Cardiogenic shock (CS) is a primary cause of mortality in acute myocardial infarction (MI).
- Elevated inflammatory cytokines (e.g., IL-1β, IL-6, TNF-α) and markers like C-reactive protein (CRP) are observed in acute MI with CS.
- Pro-inflammatory cytokine levels at baseline can predict CS development and patient mortality.
Purpose of the Study:
- To review the role of inflammatory cytokines in acute myocardial infarction complicated by cardiogenic shock.
- To discuss the ineffectiveness of non-selective nitric oxide synthase (NOS) inhibition in CS treatment.
- To propose future therapeutic strategies for CS.
Main Methods:
- Review of existing literature on inflammatory cytokines in acute MI and CS.
- Analysis of findings from the multicenter randomized TRIUMPH study regarding NOS inhibition.
- Consideration of therapeutic approaches used in septic shock.
Main Results:
- Non-selective NOS inhibition proved ineffective in treating cardiogenic shock, as shown by the TRIUMPH study.
- Elevated pro-inflammatory cytokines are linked to CS development and mortality in acute MI patients.
Conclusions:
- Future research should focus on specific inhibitors of the inducible isoform of nitric oxide synthase (iNOS) for CS treatment.
- Investigating the effects of low-dose corticosteroids and hemofiltration in CS patients with systemic inflammatory response syndrome (SIRS) is warranted.
Abstract:
Cardiogenic shock (CS) is the leading cause of death in patients with acute myocardial infarction (MI) and we badly need new approaches in its treatment. It has been demonstrated that a number of inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α, CRP, soluble adhesion molecules, complement system etc) are elevated in acute MI complicated by CS. Baseline levels of pro- inflammatory cytokines have predictive value for the development of CS and subsequent mortality. The deleterious effects of pro- inflammatory cytokines may be due to excessive nitric oxide production by enzyme named NOS. However in multicenter randomized TRIUMPH study non-selective NOS inhibition was ineffective in the treatment of cardiogenic shock. A challenging subject of future studies will be treatment of CS with specific inhibitors of inducible isoform of NOS. Considering the results of treatment of patients with septic shock it would be reasonable to study the effects of small doses of corticosteroids and hemofiltration in patients with CS and signs of SIRS.
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