Coronary artery disease: risk factors, symptoms, diagnosis and treatment


Ischemic heart disease (IHD), also known as coronary artery disease (CAD) is caused primarily by coronary atherosclerosis. IHD may present as an acute coronary syndrome (ACS), which includes unstable angina, non ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI), and myocardial infarction (MI).

Coronary heart disease pathological definition:

The narrowing or blockage of the coronary arteries by atheroma, leading to angina, coronary thrombosis or heart attack, heart failure and/or sudden death

Coronary heart disease epidemiological definition:

Fatal or non-fatal myocardial infarction or incident angina.
Cardiovascular disease include:

  • Coronary heart disease plus stroke,
  • peripheral vascular disease and
  • heart failure.

Acute myocardial infarction

Acute myocardial infarction (AMI) is a common cause of death. Most of the deaths are due to ventricular fibrillation occurring soon after the onset of ischaemia. AMI is defined as death or necrosis of myocardial cells and commonly referred to as heart attack. It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes. Conditions associated with increased myocardial metabolic demand include: • extremes of physical exertion • severe hypertension • severe aortic valve stenosis.

Risk factors

Six primary risk factors have been identified with the development of atherosclerotic coronary artery disease and myocardial infarction:

  • hyperlipidemia
  • diabetes mellitus
  • hypertension
  • smoking
  • male gender
  • family history of atherosclerotic arterial disease.

Signs and symptoms

Chest pain: three quarters of patients present with characteristic central or epigastric chest pain radiating to the arms, shoulders, neck, or jaw.
Shortness of breath: may be the patient’s anginal equivalent or a symptom of heart failure.
Atypical presentations are common (especially in women, older men, people with diabetes,) e.g. abdominal discomfort or jaw pain; elderly patients may present with altered mental state.
An MI may occur at any time of the day, but most appear to be clustered around the early hours of the morning, are associated with demanding physical activity, or both. Approximately 50 % of patients have some warning symptoms (angina pectoris or an anginal equivalent) before the infarct.


The first test is electrocardiography, which may demonstrate that a myocardial infarction is in progress or has already occurred.
Blood Tests
Living heart cells contain enzymes and proteins (e.g., creatine phosphokinase, troponin, myoglobin) When a heart muscle dies, cellular membranes lose integrity and intracellular enzymes and proteins slowly leak into the bloodstream.
An echocardiogram may be performed to compare areas of the left ventricle that are contracting normally with those that are not.

Treatment goal

Early treatment aims to reduce the extent of myocardial damage & infarct size can be reduced in two ways:

  1. Dissolution of the thrombus to restore coronary blood flow
  2. Decreasing myocardial oxygen consumption


All patients with a suspected myocardial infarction should be given aspirin. It is a powerful antiplatelet drug, with a rapid effect, which reduces mortality by 20%. Aspirin, 150-300 mg, should be swallowed as early as possible.
Pain and anxiety relief should be treated with intravenous morphine titrated slowly, starting at 2.5 mg.
Oxygen (90 %) therapy is thought to be beneficial, although there have been no trials to confirm this.
Restoration of blood flow
This has become the main aim of treatment as it reduces the mortality significantly. Blood flow is normally restored using drug therapy – fibrinolytic agents (e.g. streptokinase, tissue plasminogen activator), antiplatelet agents (e.g. aspirin) and antithrombins (e.g. heparin). Recently, coronary angioplasty (PTCA) has been used to restore flow mechanically. The speed at which the flow is restored is important. For every hour of delay, the effect of therapy diminishes and mortality increases.

Indications of fibrinolytic therapy

  1. Within 12 hours of onset of chest pain lasting for at least 30 minutes
  2. ECG changes of ST elevation of at least 1 mm in two or more contiguous leads, or left bundle branch block

Contraindications of fibrinolytic therapy

  1. Cerebral event within 6 months
  2. major trauma including surgery within 1 month
  3. bleeding peptic ulcer within 2 months
  4. uncontrolled hypertension
  5. Non-compressible vascular puncture.

Drugs used to restore blood flow


  • This produces generalized systemic fibrinolysis
  • Reduces mortality by 25 %.
  • An intravenous infusion of 1.5 million units is given over 30-60 minutes
  • Streptokinase should be used only once per patient because of potential risk of anaphylactic reaction.

Tissue plasminogen activator (tPA)

  • This binds to thrombus, and produces local fibrinolysis
  • It does not have the same systemic effects as streptokinase.
  • tPA is given as 15 mg bolus and a maintenance dose of 0.75 mg/kg over 30 minutes without exceeding 50 mg, then 0.5 mg/kg over 60 minutes.
  • Clot dissolution occurs more promptly with tPA than streptokinase restoring patency at 90 minutes in 55% of patients.
  • Compared with streptokinase, tPA appears to cause more bleeding and, in particular, produces a higher incidence of cerebral bleeding and stroke.


  • Heparin is an antithrombin agent.
  • It has been utilised with both fibrinolytic drugs and given subcutaneously and intravenously.
  • Intravenous heparin is given as a 5000 unit bolus followed by 1000 units per hour intravenously, adjusted after 24 hours according to the activated partial thromboplastin time (APTT); (APTT measurements are of little use in the first 24 hours as streptokinase also raises the APTT.)

Heparin and streptokinase

  • Routine use is contentious

Heparin and tPA

  • Currently, it is believed that heparin should be given with tPA.
  • The standard regimen is an initial bolus of 5000 units, followed by an infusion of 1000 units per hour adjusted after 6 hours for APTT.

Decreasing myocardial oxygen consumption

The benefit of therapy aimed at decreasing myocardial oxygen consumption is considerably less than the benefit of restoration of flow. Decreased oxygen consumption is achieved by lowering heart rate, blood pressure and cardiac filling pressures. Beta blockers, glyceryl trinitrate and possibly ACE inhibitors work in this way.

Preventive measures

  1. Health screening and intervention initiatives have typically focused on:
  2. Education
  3. Lipid management
  4. Blood pressure monitoring, and Control
  5. Antiplatelet therapy (low dose aspirin),
  6. Smoking cessation.

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