Ischaemic Heart Disease

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• Ischaemic Heart Disease

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Etilogy

• Most ischaemic heart disease is caused by
  atherosclerosis of the coronary artereries.
• Initially there is sudden sever narrowing or
  closure of large coronary arteries and\ or
  narrowing of coronary artery end branches.
• Covering plaques.........

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Risk Factors

• 1- age.
• 2- Gender.
• 3- Serum cholesterol VLDL....LDL...HDL.
• 4- Hypertension endothelial damage.
• 5- Cigarate smoking
• nicotine-----catecholamine-----epinephrine-----en
  dothelial damage----lipolysis.
• 6- Diabetes disturbed lipid metabolism.

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Minor risk factors

• 1- Hypothyrodism.
• 2- obesity.
• 3- Sedentary life.
• 4-Intellectual professional.
• 5- Contraceptive pills.

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Clinical Consequences

• A- Angina Pectoris
• Def.
• Clinical syndrome characterized by attack
  of pain due to ischaemia of the heart muscle,
  generally due to obstruction or spasm of coronary
  arteries.

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Types

• 1- Stable occurs under similar circumstances,
  and with similar frequency over time.
• 2- Un-stable
• Recent onset.
• Increased severity and frequency .
• Angina at rest or with minimal exertion.
• 3- Variant
• - At rest. - Spasm of coronary artery. -Not
  precipitated by increase myocardial 02 demand

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Clinical Picture

• Pain
• Site
• Radiation.
• Character
• burning..suffocation. stop all activities.
• - Precipitation
• Relief.
• Duration.

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• Associated Symptoms
• Dyspnea . Palpitation. Dizzness.
• Fainting.Sweating.

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Clinical Picture

• Sings and symptoms
• Pallor...tachycardia....hypertension.
• Investigation
• ECG normal in 50.
• Stress ECG
• Depression of st segment.
• Ventricular Arrhythmias.
• - Cardiac Catheterization arteriography.
• - Echocardiography regional wall abnor. Ex and
  rest.

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Therapy

• Aiming for
• Decrease myocardial oxygen demand.
• Increase myocardial o2 supply.
• I. Medical Treatment
• Nitrates. Vosodilat.... Myo.02 sup
• overload.... Myo o2
  deman
• Beta bolckers
• Calcium channel blockers
• Antiplatelets reduce incidence of MI

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• II. Surgery
• III. Preventive
• 1- Avoid precipitating factors.
• 2- Control Risk factors.
• N.B . During Attack

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Myocardial Infarction

• Def. It is a medical condition that occurs when
  the blood supply to the heart is interrupted ,
  and the myocardium is deprived of its blood
  supply therefore oxygen for a significant
  amount of time.
• Pathogenesis
• - Formation of occlusive thrombus at the site of
  rupture or erosion of atherosclerotic plaques in
  coronary artery.

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• Clinical Picture
• Symptoms
• Prolonged cardiac pain
• Anxiety
• Nausea . Vomiting
• Breathlessness.
• Syncope
• Silent MI......elder....arrythmias

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• II.Signs
• Signs of sympathatic activities
• pallor, sweating, tachycardia
• Signs of vagal activation
• vomiting...bradycardia.
• Signs of impaired myocardial function
• hypotension.
• Narrow pulse pressure.
• - Signs of tissue damage. fever

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Investigation

• ECG-
• Early
• Late
• Advanced
• 2) Blood test
• Cardiac enzymes
• Cardiospecific isoform of CK CK- MB
• Troponin T and I

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• ESR
• 3) Chest x ray
• Pulmonary oedema.
• Cardiac enlargement

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Therapy

• A- Immediate Therapy
• - High flow oxygen.
• Aspirin 300 mg.
• ECG monitoring.
• B) Acute perfusion therapy
• 1- Thrombolysis
• Help restore coronary potency.
• Preserve ventricular function.
• Improve survival.

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• 2) Primary percutaneous coronary intervension
• C) Adjunctive Therapy
• Beta blockers
• relief pain ------reduce arrythmias.
• - Nitrates Nitroglycerin

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