What is Heart Attack (Myocardial Infarction)?

A heart attack, also known as a myocardial infarction or MI, occurs when an area of heart muscle dies or is permanently damaged because of an inadequate supply of oxygen to that area.

Statistics

Coronary artery disease is the most common cause of death in the Western world, and most of these deaths are due to myocardial infarction (heart attack). In Australia, approximately 21% of all deaths are due to coronary heart disease, and there are 605 coronary events per 100,000 people aged 40-90 years.
Myocardial infarction is a common condition. There are thousands of new cases every year. It is a serious and life-threatening condition.  Around one quarter of patients die from the acute event, half of these before the hospital is reached. Survivors have a higher risk of recurrent heart attacks or cardiac death, and a further 10% die within two years. Only 50% of initial survivors are alive at 10 years.

Men

Men have a higher risk of heart attacks and other acute coronary events, and males are more likely to be affected at a younger age. Around three quarters of heart attacks are in male patients. Males and females older than 70 years of age are equally affected.

Women

Women before menopause have lower rates of heart attack, which may be due to the effects of oestrogen (oestrogen reduces the build up of plaques in blood vessels). However, the incidence of heart attacks increases dramatically in women aged 60-70 years to match that of men.
Women have higher mortality and hospitalisation rates from heart attacks, perhaps partly because women receive less aggressive in-hospital therapy for acute myocardial infarction than men. The reasons for this are not clear, but may be due to poor diagnosis and lack of knowledge about the benefits of treatment in women.

Risk Factors

Coronary atherosclerosis is the main process causing myocardial ischaemia (restriction in blood supply to heart muscles) and infarction (death of heart muscle tissue). Fatty plaques (cholesterol is a kind of fat) develop on the inside of the coronary arteries. The diameter of the arteries is reduced, inhibiting blood flow to the heart muscle. Eventually the plaques rupture. When this happens, blood starts to clot around the ruptured plaque. Eventually either a piece of clot or a piece of plaque breaks off and blocks a smaller downstream artery, causing a heart attack.

 
There are many risk factors for coronary artery disease:

  • Hypercholesterolaemia (elevated levels of cholesterol in the blood) plays a central role in the development of plaques.
  • Increased age and male gender.
  • Family history of coronary artery disease.
  • Smoking: Risk is directly related to the number of cigarettes smoked.
  • Diabetes mellitus: Abnormal blood sugar levels promote vascular damage and the development of plaques.
  • Hypertension: High blood pressure promotes artery damage, which may initiate or exacerbate atherosclerosis, causing plaque rupture.

Other, less important risk factors (so-called soft factors) include:

Progression

Coronary atherosclerosis leads to narrowing of the arteries and impairment of blood supply to the heart muscle. Early in the disease process, this causes angina pectoris, or chest pain experienced when the heart muscle’s demand for blood is increased (e.g. during exercise). Later in the disease process, the artery may become completely blocked, usually due to a piece of plaque breaking off, moving downstream and obstructing a smaller artery. This causes myocardial infarction and results in permanent damage to the heart muscle. Even if blood flow to the heart muscle is not physically impaired, ischaemia can still occur when, for example, the blood’s ability to carry oxygen is impaired (e.g. anaemia) or when the heart’s requirements are significantly increased (e.g. during exercise and ventricular hypertrophy).

How is it Diagnosed

Prognosis

Myocardial infarctions (heart attacks) are a serious event: approximately 25% of patients die from the initial event – that is, they may die before reaching hospital, or in the first day or so. Of the rest, 25% will die within the next two years, usually due to recurrent MI or complications. About 50% of the initial survivors are alive after 10 years. The prognosis is better for younger patients with less concurrent medical problems.

Treatment

  1. Management is on a coronary care unit.
  2. Aspirin 300mg is given.
  3. High flow oxygen.
  4. Pain management with morphine.
  5. Heart rate is controlled using a beta-blocker (if no signs of heart failure or heart block).
  6. If within 12 hours and no contraindications (stroke or active bleeding in the last two months) thrombolytic therapy or angiography with angioplasty may be considered.
  7. Management of common complications of MI such as heart failure, pericarditis and arrhythmias.

Long term management is similar to that for angina (if not already instigated). This includes aspirin therapy, beta-blockers, and cholesterol lowering if required. Maintaining a healthy diet, quitting smoking, exercise and weight reduction (if overweight) are important aspects of long-term treatment to reduce the risk of recurrent heart attack.

References

  1. Clarke K, Gray D, Keating N, Hampton J. Do women with acute myocardial infarction receive the same treatment as men? BMJ 1994; 309: 563-6.
  2. Fenton D, Stahmer S. Myocardial Infarction, eMedicine, Web MD, 2006. Available from URL: http://www.emedicine.com/emerg/topic327.htm.
  3. Gan S, Beaver S, Houck P, MacLehose R, Lawson H, Chan L. Treatment of acute myocardial infarction and 30-day mortality among women and men. NEJM 2000; 343(1): 8-15.
  4. Garas S, Zafari A, Myocardial Infarction, eMedicine, Web MD, 2006. Available from URL: http://www.emedicine.com/med/topic1567.htm.
  5. Hurst’s The Heart 8th Edition, McGraw Hill, 1994.
  6. Kumar and Clark. Clinical Medicine 4th Edition, W.B Saunders, 1998.
  7. Martur S, Epidemic of coronary heart disease and its treatment in Australia, AIHW 2002, cat. no. CVD 21.
  8. Mehta S, Eagle K. Secondary prevention in acute myocardial infarction. BMJ 1998; 316: 838-42.

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