Coronary Heart Disease

  • Diana GorogEmail author


Globally, cardiovascular disease (CVD) remains the leading cause of mortality and morbidity, accounting for some 18 million deaths worldwide in 2015, and this is expected to grow to >23.6 million by 2030. The biggest cause of cardiovascular death is ischemic heart disease (IHD), for both men and women. Global CVD rates rose by 12.5% between 2005 and 2015, with deaths attributable to IHD increasing by 16.6% to 8.9 million deaths, whilst age-standardised mortality rates fell by 12.8%, reflecting improved survival. IHD is largely attributable to atherosclerosis, a complex, chronic inflammatory process, determined by both genetic and environmental factors. Advances in the understanding of atherosclerotic plaque morphology, acute alterations in plaque morphology associated with acute coronary thrombotic events, and the complex interplay with a prothrombotic milieu and inflammation, have led to the concept of a “vulnerable patient”, rather than just a vulnerable plaque. There remains an important, ongoing need to further reduce mortality and morbidity from IHD, and an appreciation of the pathophysiology of IHD is essential to enable this.


Atherosclerosis Ischemic heart disease Cardiovascular disease Lipoprotein Endothelium Hypertension Diabetes mellitus Acute coronary syndrome 



  1. GBD 2015 Mortality and Causes of Death Collaborators. Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016;388:1459–544.CrossRefGoogle Scholar


  1. Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004;43(10):1731–7.CrossRefPubMedGoogle Scholar
  2. Arbab-Zadeh A, Fuster V. The myth of “the vulnerable plaque”: transitioning from a focus on individual lesions to atherosclerotic disease burden for coronary artery disease risk assessment. J Am Coll Cardiol. 2015;65(8):846–55.CrossRefPubMedPubMedCentralGoogle Scholar
  3. Boudoulas KD, Triposciadis F, Geleris P, Boudoulas H. Coronary atherosclerosis: pathophysiologic basis for diagnosis and management. Prog Cardiovasc Dis. 2016;58(6):676–92.CrossRefPubMedGoogle Scholar
  4. GW Stone for PROSPECT Investigators. A prospective natural-history study of coronary atherosclerosis. N Engl J Med. 2011;364:226–35.CrossRefGoogle Scholar
  5. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005;352:1685–95.CrossRefPubMedGoogle Scholar
  6. Michel J-B, Martin-Ventura JL, et al. Pathology of human plaque vulnerability: Mechanisms and consequences of intraplaque haemorrhages. Atherosclerosis. 2014;234:311e319.CrossRefGoogle Scholar
  7. Nikpay M, et al. A comprehensive 1000 Genomes–based genome-wide association meta-analysis of coronary artery disease. Nat Genet. 2015;47(10):1121–30.CrossRefPubMedPubMedCentralGoogle Scholar
  8. Yahagi K, et al. Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis. Nat Rev Cardiol. 2016;13:79–98.CrossRefPubMedGoogle Scholar

Ischemia Reperfusion, Preconditioning, Postconditioning

  1. Carden DL, Granger DN. Pathophysiology of ischaemia-reperfusion injury. J Pathol. 2000;190(3):255–66.CrossRefPubMedGoogle Scholar
  2. Kalogeris T, Baines CP, Krenz M, Korthuis RJ. Cell biology of ischemia/reperfusion injury. Int Rev Cell Mol Biol. 2012;298:229–317.CrossRefPubMedPubMedCentralGoogle Scholar
  3. Vinten-Johansen J, Shi W. Perconditioning and postconditioning: current knowledge, knowledge gaps, barriers to adoption, and future directions. J Cardiovasc Pharmacol Ther. 2011;16(3-4):260–6.CrossRefPubMedGoogle Scholar
  4. Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007;357:1121–35.CrossRefPubMedGoogle Scholar

Stunning, Hibernation

  1. Bolli R, Marbán E. Molecular and cellular mechanisms of myocardial stunning. Physiol Rev. 1999;79:609–34.CrossRefPubMedGoogle Scholar
  2. Camici PG, Prasad SK, Rimoldi OE. Stunning, hibernation, and assessment of myocardial viability. Circulation. 2008;117:103–14.CrossRefPubMedGoogle Scholar
  3. Depre C, Vatner SF. Cardioprotection in stunned and hibernating myocardium. Heart Fail Rev. 2007;12(3–4):307–17.CrossRefPubMedGoogle Scholar
  4. Slezak J, Tribulova N, Okruhlicova L, Dhingra R, Bajaj A, Freed D, Singal P. Hibernating myocardium: pathophysiology, diagnosis, and treatment. Can J Physiol Pharmacol. 2009;87(4):252–65.CrossRefPubMedGoogle Scholar

SVG Disease

  1. Yahagi K, Kolodgi FD, Otsuka F, Finn AV, Davis HR, Joner M, Virmani R. Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis. Nat Rev Cardiol. 2016;13(2):79–98.CrossRefPubMedGoogle Scholar


  1. Alfonso F, Byrne RA, Rivero F, Kastrati A. Current treatment of in-stent restenosis. J Am Coll Cardiol. 2014;63:2659–73.CrossRefPubMedGoogle Scholar
  2. Dangas GD, Claessen BE, Caixeta A, Sanidas EA, Mintz GS, Mehran R. In-stent restenosis in the drug-eluting stent era. J Am Coll Cardiol. 2010;56:1897–907.CrossRefPubMedGoogle Scholar

Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.National Heart and Lung Institute, Imperial College LondonLondonUK

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