Ischaemic heart disease

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The underlying pathology is arterioscleroses with the formation of fatty plaques which can reduce flow in the coronary vessels leading to angina or the plaques can rupture releasing thrombogenic material leading to vessel occlusion and myocardial infarction or unstable angina. Myocardial Ischaemia upsets the cardiovascular electronics leading to the formation of cardiac arrhythmias. These can just reduce cardiac efficiency such as atrial fibrillation or cause syncope and even sudden cardiac death with ventricular tachycardia and fibrillation.

This data (USA 1980-2000[1]) has been shown to illustrate how important primary prevention of inactivity and gain in mean population BMI is likely to be in Western Countries trying to achieve further reductions in IHD burden once population smoking, hypertension and cholesterol burdens are addressed in primary prevention

Epidemiology

It may not be appreciated that while well known to be a major cause of mortality, this is a primary care disease, with about 60% of all ischaemic heart disease deaths out of hospital, and of these 60% are in people not previously hospitalized for ischaemic heart disease[2]. In many Western countries there has been a marked reduction in mortality rates from ischaemic heart disease over the last 20 to 30 years. For example, in England and Wales, between 1981 and 2000, mortality rates fell by 54% from this cause[3]. Primary prevention achieved a fourfold larger reduction in these deaths than secondary prevention with most attributable gain being due to:

  1. Smoking reduction (35% decreased prevalence)
  2. Cholesterol (population total cholesterol concentrations fell by 4.2%)
  3. Blood pressure (population mean BP fell by 7.7%)

This can be seen in this linked figure for England & Wales. Different populations had different attributable risk reduction and this is illustrated by the graph for USA population.

Effect of Therapy

This graph (data USA 1980-2000[4])demonstrates the low gains from some evidenced based technologies such as clopidogrel and angioplasty compared to other therapies such as statins (used in secondary and primary prevention) or even CPR and cardiac rehabilitation
Studies adjusting for case-mix have suggested how relatively minor changes in secondary prevention medication uptake could explain mortality differences between hospitals. In this case, at 2 years of 5-year follow up there was a 8.5% difference in mortality, partially explained by worse statin and β-blocker prescribing at discharge at the highest mortality hospital.[5]

This has been one of the most successful demonstrations of medical technology since vaccination or interventions against bacterial infectious disease such as public water and sewage infrastructure or antibiotics. Please see the graph for the attributable decrease in mortality from a number of proven medical therapies. The range of attribution depends on assumptions with respect to patient compliance and that study responses are generalised. Similar data exists for a wide range of populations using similar assumptions including:


References

  1. Ford ES, Ajani UA, Croft JB, Critchley JA, Labarthe DR, Kottke TE, et al. Explaining the decrease in U.S. deaths from coronary disease, 1980-2000. The New England journal of medicine 2007;356(23):2388-98. (Direct link – subscription may be required.)
  2. Grey C, Jackson R, Schmidt M, Ezzati M, Asaria P, Exeter DJ, Kerr AJ. One in four major ischaemic heart disease events are fatal and 60% are pre-hospital deaths: a national data-linkage study (ANZACS-QI 8) DOI: http://dx.doi.org/10.1093/eurheartj/ehv524 European Heart Journal, October 2015
  3. Unal B, Critchley JA, Capewell S. Modelling the decline in coronary heart disease deaths in England and Wales, 1981-2000: comparing contributions from primary prevention and secondary prevention. BMJ (Clinical research ed.) 2005;331(7517):614. (Direct link – subscription may be required.)
  4. Ford ES, Ajani UA, Croft JB, Critchley JA, Labarthe DR, Kottke TE, et al. Explaining the decrease in U.S. deaths from coronary disease, 1980-2000. The New England journal of medicine 2007;356(23):2388-98. (Direct link – subscription may be required.)
  5. Wong C,Tang EW, Herbison P. Survival over 5 years in the initial hospital survivors with acute coronary syndrome: a comparison between a community hospital and a tertiary hospital in New Zealand. NZMJ 2007;120(1261)
  6. Ford ES, Ajani UA, Croft JB, Critchley JA, Labarthe DR, Kottke TE, et al. Explaining the decrease in U.S. deaths from coronary disease, 1980-2000. The New England journal of medicine 2007;356(23):2388-98. (Direct link – subscription may be required.)
  7. Unal B, Critchley JA, Capewell S. Modelling the decline in coronary heart disease deaths in England and Wales, 1981-2000: comparing contributions from primary prevention and secondary prevention. BMJ (Clinical research ed.) 2005;331(7517):614. (Direct link – subscription may be required.)
  8. Capewell S, Morrison CE, McMurray JJ. Contribution of modern cardiovascular treatment and risk factor changes to the decline in coronary heart disease mortality in Scotland between 1975 and 1994. Heart (British Cardiac Society) 1999;81(4):380-6.
  9. Bennett K, Kabir Z, Unal B, Shelley E, Critchley J, Perry I, et al. Explaining the recent decrease in coronary heart disease mortality rates in Ireland, 1985-2000. Journal of epidemiology and community health 2006;60(4):322-7. (Direct link – subscription may be required.)
  10. Laatikainen T, Critchley J, Vartiainen E, Salomaa V, Ketonen M, Capewell S. Explaining the decline in coronary heart disease mortality in Finland between 1982 and 1997. American journal of epidemiology 2005;162(8):764-73. (Direct link – subscription may be required.)
  11. Capewell S, Beaglehole R, Seddon M, McMurray J. Explanation for the decline in coronary heart disease mortality rates in Auckland, New Zealand, between 1982 and 1993. Circulation 2000;102(13):1511-6.
  12. Critchley J, Liu J, Zhao D, Wei W, Capewell S. Explaining the increase in coronary heart disease mortality in Beijing between 1984 and 1999. Circulation 2004;110(10):1236-44. (Direct link – subscription may be required.)