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CORONARY ARTERY DISEASE
Definition:
• Coronary artery disease is narrowing or
blockage of the coronary arteries, usually
caused by atherosclerosis.
• Coronary artery disease (CAD) is the
commonest cause of angina and acute
coronary syndrome and the leading cause of
death worldwide.
Epidemiology:
• The prevalence of CAD in Indians is 21.4% for
diabetics and 11% for nondiabetics.
RISK FACTORS:
• MODIFIABLE:
High blood cholesterol or triglycerides level
Tobacco use, Smoking
Laack of exercise
Obesity
Stress
RISK FACTORS:
• NON-MODIFIABLE:
Old age
Hypertension
Diabetes
Family history of heart disease.
CORONARY ATHEROSCLEROSIS
• Epicardial coronary arteries are the major site of
atherosclerotic disease.
• Atherosclerosis is a progressive infammatory
disorder of the arterial wall that is characterised
by focal lipid-rich deposits of atheroma that
remain clinically silent until they become large
enough to impair tissue perfusion, or until
ulceration and disruption of the lesion occurs
resulting in thrombotic occlusion.
• The rupture of atherosclerotic plaque leads to
formation of thrombus.
• A thrombus composed of platelet aggregates
and fibrin strands traps red blood cells and can
reduce coronary blood flow, leading to the
clinical manifestations of myocardial ischemia.
• The location of the obstruction influences the
quantity of myocardium rendered ischemic and
determines the severity of the clinical
manifestations.
• Thus, critical obstructions in vessels, such as the
left main coronary artery and the proximal left
anterior descending(LAD) coronary artery, are
particularly hazardous.
IHD-ISCHEMIC HEART DISEASE
• Ischemic heart disease (IHD) is a condition in
which there is an inadequate supply of blood
and oxygen to a portion of the myocardium; it
typically occurs when there is an imbalance
between myocardial oxygen supply and
demand.
• When ischemia is transient, it may be
associated with angina pectoris; when it is
prolonged, it can lead to myocardial necrosis
and scarring with or without the clinical
picture of acute myocardial infarction.
Angina pectoris
• Angina pectoris is a symptom complex caused
by transient myocardial ischaemia, which
occurs whenever there is an imbalance
between myocardial oxygen supply and
demand.
Three characteristic features of angina
• 1. Constricting discomfort in the centre of the
chest, or in the neck, shoulders, jaw or arms
• 2. Precipitated by physical exertion
• 3. Relieved by rest (or NTG) within 5 minutes
Classification :
• Typical angina: All three features
• Atypical angina: Two features
• Non-anginal chest pain: One or no features
APPROACH
to STABLE
ANGINA
MANAGEMENT
The principles of management involve:
• A careful assessment of the extent and
severity of arterial disease
• Identification and treatment of risk factors
• Advice on smoking cessation
• Introduction of drug treatment for symptom
control
• Identification of high-risk patients for
treatment to improve life expectancy.
• All patients with angina secondary to CAD
should receive antiplatelet therapy. Low-dose
(75 mg) aspirin should be prescribed for all
patients and continued indefinitely since it
reduces the risk of MI.
• Clopidogrel (75 mg daily) is an equally
effective alternative if aspirin causes
dyspepsia or other side effects.
• All patients should be prescribed a statin, even
if cholesterol is normal.
ANTI-ANGINAL therapy:
Nitrates
•Nitrates act directly on vascular smooth muscle to
produce venous and arteriolar dilatation.
•They help angina by lowering preload and
afterload, which reduces myocardial oxygen
demand, and by increasing myocardial oxygen
supply through coronary vasodilatation.
•Sublingual GTN, administered as a tablet (300 or
500 μg), is indicated for acute attacks and will
usually relieve an attack in 2–3 minutes.
Beta-blockers
•These lower myocardial oxygen demand by
reducing heart rate, BP and myocardial contractility,
but they may provoke bronchospasm in patients
with asthma.
•Metoprolol (50–200 mg daily) or bisoprolol (5–15
mg daily) is preferable.
•Beta-blockers should not be withdrawn abruptly, as
rebound effects may precipitate dangerous
arrhythmias, worsening angina or MI.
Calcium channel antagonists:
•These drugs lower myocardial oxygen demand by
reducing BP and myocardial contractility.
•Since dihydropyridine calcium antagonists, such as
nifedipine and amlodipine, may cause a reflex
tachycardia, it is best to use them in combination
with a β-blocker.
• In contrast, verapamil and diltiazem can be used
as monotherapy because they slow SA node firing,
inhibit conduction through the AV node and tend
to cause bradycardia. They are particularly useful
when β-blockers are contraindicated.
Potassium channel activators:
Nicorandil (10–30 mg twice daily orally) is the only
drug in this class that is currently available for
clinical use. It acts as a vasodilator with effects on
the arterial and venous systems, and has the
advantage that it does not exhibit the tolerance
seen with nitrates.
Ranolazine:
This drug inhibits the late inward sodium current in
coronary artery smooth muscle cells, with a
secondary effect on calcium flux and vascular tone,
reducing angina symptoms.
NON PHARMACOLOGICAL TREATMENTS:
•Percutaneous coroary interventon.
•Coronary artery bypass grafting.
THANK YOU

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Coronary artery disease.pptx

  • 2. Definition: • Coronary artery disease is narrowing or blockage of the coronary arteries, usually caused by atherosclerosis. • Coronary artery disease (CAD) is the commonest cause of angina and acute coronary syndrome and the leading cause of death worldwide.
  • 3. Epidemiology: • The prevalence of CAD in Indians is 21.4% for diabetics and 11% for nondiabetics.
  • 4. RISK FACTORS: • MODIFIABLE: High blood cholesterol or triglycerides level Tobacco use, Smoking Laack of exercise Obesity Stress
  • 5. RISK FACTORS: • NON-MODIFIABLE: Old age Hypertension Diabetes Family history of heart disease.
  • 6. CORONARY ATHEROSCLEROSIS • Epicardial coronary arteries are the major site of atherosclerotic disease. • Atherosclerosis is a progressive infammatory disorder of the arterial wall that is characterised by focal lipid-rich deposits of atheroma that remain clinically silent until they become large enough to impair tissue perfusion, or until ulceration and disruption of the lesion occurs resulting in thrombotic occlusion.
  • 7.
  • 8. • The rupture of atherosclerotic plaque leads to formation of thrombus. • A thrombus composed of platelet aggregates and fibrin strands traps red blood cells and can reduce coronary blood flow, leading to the clinical manifestations of myocardial ischemia.
  • 9. • The location of the obstruction influences the quantity of myocardium rendered ischemic and determines the severity of the clinical manifestations. • Thus, critical obstructions in vessels, such as the left main coronary artery and the proximal left anterior descending(LAD) coronary artery, are particularly hazardous.
  • 10. IHD-ISCHEMIC HEART DISEASE • Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium; it typically occurs when there is an imbalance between myocardial oxygen supply and demand. • When ischemia is transient, it may be associated with angina pectoris; when it is prolonged, it can lead to myocardial necrosis and scarring with or without the clinical picture of acute myocardial infarction.
  • 11. Angina pectoris • Angina pectoris is a symptom complex caused by transient myocardial ischaemia, which occurs whenever there is an imbalance between myocardial oxygen supply and demand.
  • 12. Three characteristic features of angina • 1. Constricting discomfort in the centre of the chest, or in the neck, shoulders, jaw or arms • 2. Precipitated by physical exertion • 3. Relieved by rest (or NTG) within 5 minutes Classification : • Typical angina: All three features • Atypical angina: Two features • Non-anginal chest pain: One or no features
  • 14. MANAGEMENT The principles of management involve: • A careful assessment of the extent and severity of arterial disease • Identification and treatment of risk factors • Advice on smoking cessation • Introduction of drug treatment for symptom control • Identification of high-risk patients for treatment to improve life expectancy.
  • 15. • All patients with angina secondary to CAD should receive antiplatelet therapy. Low-dose (75 mg) aspirin should be prescribed for all patients and continued indefinitely since it reduces the risk of MI. • Clopidogrel (75 mg daily) is an equally effective alternative if aspirin causes dyspepsia or other side effects. • All patients should be prescribed a statin, even if cholesterol is normal.
  • 16. ANTI-ANGINAL therapy: Nitrates •Nitrates act directly on vascular smooth muscle to produce venous and arteriolar dilatation. •They help angina by lowering preload and afterload, which reduces myocardial oxygen demand, and by increasing myocardial oxygen supply through coronary vasodilatation. •Sublingual GTN, administered as a tablet (300 or 500 μg), is indicated for acute attacks and will usually relieve an attack in 2–3 minutes.
  • 17. Beta-blockers •These lower myocardial oxygen demand by reducing heart rate, BP and myocardial contractility, but they may provoke bronchospasm in patients with asthma. •Metoprolol (50–200 mg daily) or bisoprolol (5–15 mg daily) is preferable. •Beta-blockers should not be withdrawn abruptly, as rebound effects may precipitate dangerous arrhythmias, worsening angina or MI.
  • 18. Calcium channel antagonists: •These drugs lower myocardial oxygen demand by reducing BP and myocardial contractility. •Since dihydropyridine calcium antagonists, such as nifedipine and amlodipine, may cause a reflex tachycardia, it is best to use them in combination with a β-blocker. • In contrast, verapamil and diltiazem can be used as monotherapy because they slow SA node firing, inhibit conduction through the AV node and tend to cause bradycardia. They are particularly useful when β-blockers are contraindicated.
  • 19. Potassium channel activators: Nicorandil (10–30 mg twice daily orally) is the only drug in this class that is currently available for clinical use. It acts as a vasodilator with effects on the arterial and venous systems, and has the advantage that it does not exhibit the tolerance seen with nitrates.
  • 20. Ranolazine: This drug inhibits the late inward sodium current in coronary artery smooth muscle cells, with a secondary effect on calcium flux and vascular tone, reducing angina symptoms.
  • 21. NON PHARMACOLOGICAL TREATMENTS: •Percutaneous coroary interventon. •Coronary artery bypass grafting.

Editor's Notes

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