Skip to main content

Prevention and Treatment of Heart Failure Based on the Control of Inflammation

  • Chapter
  • First Online:
Chronic Inflammation

Abstract

Heart failure is a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. For decades, there have been three different concepts of heart failure and their corresponding treatment strategies: diuretics for volume retention, cardiotonics, vasodilators for abnormal hemodynamic state, neurohormonal antagonists for abnormalities in interorgan communication. These conventional treatments consistently prolongs survival in patients with heart failure but never cure the underlying heart diseases. Various risk factors induce heart injury and aortic damages, eventually leading to a final stage of cardiovascular disease, namely heart failure. It has become widely accepted that pathogenesis of heart injury and aortic damage is considered to be the result of a chronic inflammatory process. Therefore, chronic inflammation can be regarded as a new target that may treat and/or prevent heart failure. This chapter describes the recent advances in understanding of the mechanisms of chronic inflammation of cardiovascular diseases, especially focused on our accomplishments.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 219.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 279.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 279.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  • Anzai A, Anzai T, Nagai S, Maekawa Y, Naito K, Kaneko H et al (2012) Regulatory role of dendritic cells in postinfarction healing and left ventricular remodeling. Circulation 125:1234–1245

    Article  PubMed  Google Scholar 

  • Anzai A, Shimoda M, Endo J, Kohno T, Katsumata Y, Matsuhashi T et al (2015) Adventitial CXCL1/G-CSF expression in response to acute aortic dissection triggers local neutrophil recruitment and activation leading to aortic rupture. Circ Res 116:612–623

    Article  CAS  PubMed  Google Scholar 

  • Arslan F, de Kleijn DP, Pasterkamp G (2011) Innate immune signaling in cardiac ischemia. Nat Rev Cardiol 8:292–300

    Article  CAS  PubMed  Google Scholar 

  • Carlson RG, Lillehei CW, Edwards JE (1970) Cystic medial necrosis of the ascending aorta in relation to age and hypertension. Am J Cardiol 25:411–415

    Article  CAS  PubMed  Google Scholar 

  • Christopher MJ, Link DC (2007) Regulation of neutrophil homeostasis. Curr Opin Hematol 14:3–8

    Article  CAS  PubMed  Google Scholar 

  • Endo J, Sano M, Isobe Y, Fukuda K, Kang JX, Arai H et al (2014) 18-HEPE, an n-3 fatty acid metabolite released by macrophages, prevents pressure overload-induced maladaptive cardiac remodeling. J Exp Med 211:1673–1687

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Frangogiannis NG (2012) Regulation of the inflammatory response in cardiac repair. Circ Res 110:159–173

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Gissi HFI, Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG et al (2008) Effect of n-3 polyunsaturated fatty acids in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial. Lancet 372:1223–1230

    Article  Google Scholar 

  • Kai H, Mori T, Tokuda K, Takayama N, Tahara N, Takemiya K et al (2006) Pressure overload-induced transient oxidative stress mediates perivascular inflammation and cardiac fibrosis through angiotensin II. Hypertens Res 29:711–718

    Article  CAS  PubMed  Google Scholar 

  • Kang JX, Wang J, Wu L, Kang ZB (2004) Transgenic mice: fat-1 mice convert n-6 to n-3 fatty acids. Nature 427:504

    Article  CAS  PubMed  Google Scholar 

  • Koyanagi M, Egashira K, Kitamoto S, Ni W, Shimokawa H, Takeya M et al (2000) Role of monocyte chemoattractant protein-1 in cardiovascular remodeling induced by chronic blockade of nitric oxide synthesis. Circulation 102:2243–2248

    Article  CAS  PubMed  Google Scholar 

  • Krum H, Teerlink JR (2011) Medical therapy for chronic heart failure. Lancet 378:713–721

    Article  CAS  PubMed  Google Scholar 

  • Kurihara T, Shimizu-Hirota R, Shimoda M, Adachi T, Shimizu H, Weiss SJ et al (2012) Neutrophil-derived matrix metalloproteinase 9 triggers acute aortic dissection. Circulation 126:3070–3080

    Article  CAS  PubMed  Google Scholar 

  • Kuwahara F, Kai H, Tokuda K, Takeya M, Takeshita A, Egashira K et al (2004) Hypertensive myocardial fibrosis and diastolic dysfunction: another model of inflammation? Hypertension 43:739–745

    Article  CAS  PubMed  Google Scholar 

  • Leuschner F, Rauch PJ, Ueno T, Gorbatov R, Marinelli B, Lee WW et al (2012) Rapid monocyte kinetics in acute myocardial infarction are sustained by extramedullary monocytopoiesis. J Exp Med 209:123–137

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Lewis EF, Moye LA, Rouleau JL, Sacks FM, Arnold JM, Warnica JW et al (2003) Predictors of late development of heart failure in stable survivors of myocardial infarction: the CARE study. J Am Coll Cardiol 42:1446–1453

    Article  PubMed  Google Scholar 

  • Martin C, Burdon PC, Bridger G, Gutierrez-Ramos JC, Williams TJ, Rankin SM (2003) Chemokines acting via CXCR2 and CXCR4 control the release of neutrophils from the bone marrow and their return following senescence. Immunity 19:583–593

    Article  CAS  PubMed  Google Scholar 

  • Morrison DF, Foss DL, Murtaugh MP (2000) Interleukin-10 gene therapy-mediated amelioration of bacterial pneumonia. Infect Immun 68:4752–4758

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Mozaffarian D, Wu JH (2011) Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events. J Am Coll Cardiol 58:2047–2067

    Article  CAS  PubMed  Google Scholar 

  • Nahrendorf M, Swirski FK, Aikawa E, Stangenberg L, Wurdinger T, Figueiredo JL et al (2007) The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions. J Exp Med 204:3037–3047

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Nahrendorf M, Pittet MJ, Swirski FK (2010) Monocytes: protagonists of infarct inflammation and repair after myocardial infarction. Circulation 121:2437–2445

    Article  PubMed  PubMed Central  Google Scholar 

  • Nicoletti A, Heudes D, Mandet C, Hinglais N, Bariety J, Michel JB (1996) Inflammatory cells and myocardial fibrosis: spatial and temporal distribution in renovascular hypertensive rats. Cardiovasc Res 32:1096–1107

    Article  CAS  PubMed  Google Scholar 

  • Nodari S, Triggiani M, Campia U, Manerba A, Milesi G, Cesana BM et al (2011) Effects of n-3 polyunsaturated fatty acids on left ventricular function and functional capacity in patients with dilated cardiomyopathy. J Am Coll Cardiol 57:870–879

    Article  CAS  PubMed  Google Scholar 

  • Sadik CD, Kim ND, Luster AD (2011) Neutrophils cascading their way to inflammation. Trends Immunol 32:452–460

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Schlatmann TJ, Becker AE (1977) Histologic changes in the normal aging aorta: implications for dissecting aortic aneurysm. Am J Cardiol 39:13–20

    Article  CAS  PubMed  Google Scholar 

  • Shi FD, Ljunggren HG, La Cava A, Van Kaer L (2011) Organ-specific features of natural killer cells. Nat Rev Immunol 11:658–671

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Sobirin MA, Kinugawa S, Takahashi M, Fukushima A, Homma T, Ono T et al (2012) Activation of natural killer T cells ameliorates postinfarct cardiac remodeling and failure in mice. Circ Res 111:1037–1047

    Article  CAS  PubMed  Google Scholar 

  • Summers C, Rankin SM, Condliffe AM, Singh N, Peters AM, Chilvers ER (2010) Neutrophil kinetics in health and disease. Trends Immunol 31:318–324

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  • Vivier E, Tomasello E, Baratin M, Walzer T, Ugolini S (2008) Functions of natural killer cells. Nat Immunol 9:503–510

    Article  CAS  PubMed  Google Scholar 

  • Weirather J, Hofmann UD, Beyersdorf N, Ramos GC, Vogel B, Frey A et al (2014) Foxp3+ CD4+ T cells improve healing after myocardial infarction by modulating monocyte/macrophage differentiation. Circ Res 115:55–67

    Article  CAS  PubMed  Google Scholar 

  • Yan X, Shichita T, Katsumata Y, Matsuhashi T, Ito H, Ito K et al (2012) Deleterious effect of the IL-23/IL-17A axis and gammadeltaT cells on left ventricular remodeling after myocardial infarction. J Am Heart Assoc 1:e004408

    PubMed  PubMed Central  Google Scholar 

  • Yan X, Anzai A, Katsumata Y, Matsuhashi T, Ito K, Endo J et al (2013) Temporal dynamics of cardiac immune cell accumulation following acute myocardial infarction. J Mol Cell Cardiol 62:24–35

    Article  CAS  PubMed  Google Scholar 

  • Yan X, Hegab AE, Endo J, Anzai A, Matsuhashi T, Katsumata Y et al (2014) Lung natural killer cells play a major counter-regulatory role in pulmonary vascular hyperpermeability after myocardial infarction. Circ Res 114:637–649

    Article  CAS  PubMed  Google Scholar 

  • Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH et al (2013) 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 62:e147–e239

    Article  PubMed  Google Scholar 

  • Yokoyama M, Origasa H, Matsuzaki M, Matsuzawa Y, Saito Y, Ishikawa Y et al (2007) Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis. Lancet 369:1090–1098

    Article  CAS  PubMed  Google Scholar 

  • Yoshidome H, Kato A, Edwards MJ, Lentsch AB (1999) Interleukin-10 inhibits pulmonary NF-kappaB activation and lung injury induced by hepatic ischemia-reperfusion. Am J Physiol 277:L919–L923

    CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Motoaki Sano .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2016 Springer Japan

About this chapter

Cite this chapter

Sano, M. (2016). Prevention and Treatment of Heart Failure Based on the Control of Inflammation. In: Miyasaka, M., Takatsu, K. (eds) Chronic Inflammation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-56068-5_52

Download citation

Publish with us

Policies and ethics