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ISCHEMIC HEART
DISEASE, (IHD )
(CORONARY ARTERY DISEASE, CAD)
Dr. Alemiga Job
Definition
Is focal narrowing of coronary arteries as result of intimal
proliferation of smooth muscle cells & the deposition of lipids
Basic lesion is plaque( Atheromatous plaque )
Epidemiology
Common cause of cardiovascular morbidity & mortality, more so in western
world
Male: female ratio:
2:1 (all age groups)
8:1 (age<40)
1:1 (age>70)
Disparity due to protective effect of estrogen
Peak incidence of symptomatic IHD is from ages 50 to 60 for men, 60-70 for
women.
Spectrum of IHD ranges anywhere from asymptomatic to sudden death
Risk factors
Non-modifiable risk factors
Age: average - 60 (men) –(70) women
Gender
Family history
Risk factors con’t
Major Modifiable risk factors
• Elevated serum cholesterol levels
• Cigarette smoking
• Hypertension
• Impaired glucose tolerance
• Diabetes mellitus
Risk factors con’t
Other risk factors:
Obesity
Sedentary lifestyle
Stress
Oral contraceptives
Pathogenesis
The RESPONSE TO INJURY THEORY:
Some injurious stimulus (e.g HTN, Hypercholesterolemia)
cause endothelial damage
Release of growth factors leading to smooth cell
proliferation & migration of macrophages into vessel wall
Pathogenesis con’t
The now injured endothelium becomes more permeable, admitting
lipids into the intima
Above changes result into plaque formation, which may
compromise vessel lumen enough to impede blood flow.
If plaque is disrupted, platelets are activated, leading to thrombus
formation & worsening obstruction
Pathophysiology: Ischemia
Supply-demand relationship:
Increase in HR & wall stress (e.g with exercise) increases
myocardial oxygen demand.
If demand exceeds supply, ischemia results
Reduced supply: changes in lumen diameter may reduce blood
flow & thus produce ischemia without increase in demand
Angina Pectoris
Is chest pain or pressure produced by myocardial ischemia
Precipitated by exertion
It may radiate to: left arm, jaw, teeth, right arm
Symptom complex begins at low intensity, increases over 2-3 min &
lasts < 30 min.
Episodes longer than 30 min imply myocardial infarction
Angina Pectoris: Etiology
Decreased myocardial oxygen supply:
Atherosclerotic heart dz (vast majority)
Coronary vasospasm (variant angina)
Severe aortic stenosis/insufficiency
Thromboembolism
Severe anemia
Aortic dissection
Arteritis.
Angina Pectoris: Etiology con’t
Increased myocardial oxygen demand:
Myocardial hypertrophy
Severe tachycardia
Severe hypertyroidism
Angina Pectoris: Types
• 1: Chronic stable angina: is angina that recurs under similar
circumstances & with similar frequency over time
2: Unstable angina: is a term applied to angina when a change in status
occurs, thus;
- rest angina
- angina of increasing severity, duration or frequency
- new-onset angina
Its more serious clinical condition than chronic stable angina
Angina: Diagnosis
History
Classically precordial/ Retrosternal chest pain, tightness or discomfort
radiating to left shlouder/arm/jaw
Predictably precipitated by 3Es: Exercise, Emotion, Eating.
Brief duration < 10-15 min, Relieved by Rest
Note presence of cardiac risk factors (HTN, smoking, DM, Family
history, dyslipidemia)
Angina: Diagnosis
• Examination: May be normal in btn attacks, or anxious, ↑PR, ↑BP, S4 or
MR
Investigations
• Resting ECG: Taken in absence of pain is normal in 50% of cases
• Stress testing: Increases sensitivity & specificity of ECG.
• Other stress tests: Scintigraphy, stress radionuclide ventriculography,
Echocardiography,
• Cardiac catheterization with coronary arteriography
Intravascular ultrasound
Angina: Treatment
• Β-blockers: propranolol, metoprolol, atenolol, nadolol, timolol
• NITRATES: Nitroglycerine, Isosorbide di (mono) nitrate,
• Preparations: Sublingual, oral, dermal, I.V
• CALCIUM CHANNEL BLOCKERS:
• E.G nifedipine, verapamil, dilitiazem, amlodipine, nicardipine
SURGERY.
Removing or reducing the obstructive coronary athersclerotic lesion
can alleviate the angina,Balloon dilatation, stenting,
Manage risk factors
MYOCARDIAL INFARCTION (MI):
Pathogenesis
Atheromatous plaque rapture, attracts platelets, triggering
thrombus formation
Total vascular occlusion occurs
Myocardial death (Infarction) follows:
Extent of infarct governed by:
- Collateral circulation
- Anearobic metabolism
- Workload demands of myocardium
MI: Clinical features
MI: Clinical features
Chest pain
Angina like but more severe ,longer in duration>20 mins,
Not relieved by rest or nitroglycerine
Described as heavy,squeezing,crushing,stabbing
Retrosternal ,Central epigastric,may radiate to arms ,throat
,shoulder, jaw
MI: Clinical features
MI without chest pain- post op ,elderly, DM
Isolated dyspnea, exacerbation of HF,or acute confusion may be the presenting features.
Other associated symptomes
Diaphoresis, cold clammy skin, apprehension
Shortnesss of breath, nausea, vomiting, dizziness
Syncope due to bradyarrhythmias
MI: Physical signs
Patients appear apprehensive, anxious,cold clammy
Area of chest pain may be indicated by a clenched fist (Levine
sign)
Tachycardia 100-120/min,↑BP due to ↑sympathetic tone (in
>50% pt with ant MI)
Bradycardia <60/min,fall in BP(in2/3 0f inf. MI), hypotension.
MI: Physical findings
MR murmur due to papillary muscle infarction.
Crepitations.
Elevated JVP due to heart failure.
Frequently physical signs may be lacking but suspicion of MI
should be high if history is suggestive.
MI: Diagnosis
Infarct diagnosis based on 2 of 3:
1. History:
- Sudden onset of characteristic chest pain for > 30 minutes duration
- May be accompanied by symptoms of heart failure
2. ECG Changes
MI: Diagnosis
3. Cardiac enzymes:
Creatine kinase (ck-MB), myocardial proteins (Troponin T & I),
Myoglobin
4. Echocardiography
5. Radioisotope imaging
6. MRI
7. Cardiac catherization
MI: Management
Emergency care
Goal:
1. Minimize infarct size
2. Prevent complications
Bed rest
Oxygen via nasal canula
Sublingual Nitroglycerin
Morphine (pain relief, sedation)
Β-blockers
Thrombolysis (rt-PA, streptokinase, urokinase, anistreplase)
Heparin
surgery
MI: Management
LONG TERM CARE
Antiplatelet therapy: aspirin, clopidegrol
Β-blockers: carvedilol, metoprolol, nadolol
ACEIs: captopril, enalpril,
Lipid-lowering therapy
Nitrates
Manage complications
MI: Complications
Arrhythmias:
• Myocardial rupture: LV free wall, papillary muscle (MR),
ventriculo-septal defects
• Shock/CHF/Ventricular aneurysm
• Post-infarct angina
• Recurrent MI
• Pericarditis (Dressler’s syndrome)
MI: Prognosis
20% of patients with acute MI die before reaching hospital
5-15% of those hospitalized will die:
Risk factors for death:
Infarct size (big size, poor prog)
Age (old age poor prognostic factor)
Co-morbidity(DM, Dyslipidemia)
Devt of HF/Hypotension
Thank you for listening

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Ischemic heart disease (CAD).ppt

  • 1. ISCHEMIC HEART DISEASE, (IHD ) (CORONARY ARTERY DISEASE, CAD) Dr. Alemiga Job
  • 2. Definition Is focal narrowing of coronary arteries as result of intimal proliferation of smooth muscle cells & the deposition of lipids Basic lesion is plaque( Atheromatous plaque )
  • 3.
  • 4. Epidemiology Common cause of cardiovascular morbidity & mortality, more so in western world Male: female ratio: 2:1 (all age groups) 8:1 (age<40) 1:1 (age>70) Disparity due to protective effect of estrogen Peak incidence of symptomatic IHD is from ages 50 to 60 for men, 60-70 for women. Spectrum of IHD ranges anywhere from asymptomatic to sudden death
  • 5. Risk factors Non-modifiable risk factors Age: average - 60 (men) –(70) women Gender Family history
  • 6. Risk factors con’t Major Modifiable risk factors • Elevated serum cholesterol levels • Cigarette smoking • Hypertension • Impaired glucose tolerance • Diabetes mellitus
  • 7. Risk factors con’t Other risk factors: Obesity Sedentary lifestyle Stress Oral contraceptives
  • 8. Pathogenesis The RESPONSE TO INJURY THEORY: Some injurious stimulus (e.g HTN, Hypercholesterolemia) cause endothelial damage Release of growth factors leading to smooth cell proliferation & migration of macrophages into vessel wall
  • 9. Pathogenesis con’t The now injured endothelium becomes more permeable, admitting lipids into the intima Above changes result into plaque formation, which may compromise vessel lumen enough to impede blood flow. If plaque is disrupted, platelets are activated, leading to thrombus formation & worsening obstruction
  • 10. Pathophysiology: Ischemia Supply-demand relationship: Increase in HR & wall stress (e.g with exercise) increases myocardial oxygen demand. If demand exceeds supply, ischemia results Reduced supply: changes in lumen diameter may reduce blood flow & thus produce ischemia without increase in demand
  • 11. Angina Pectoris Is chest pain or pressure produced by myocardial ischemia Precipitated by exertion It may radiate to: left arm, jaw, teeth, right arm Symptom complex begins at low intensity, increases over 2-3 min & lasts < 30 min. Episodes longer than 30 min imply myocardial infarction
  • 12. Angina Pectoris: Etiology Decreased myocardial oxygen supply: Atherosclerotic heart dz (vast majority) Coronary vasospasm (variant angina) Severe aortic stenosis/insufficiency Thromboembolism Severe anemia Aortic dissection Arteritis.
  • 13. Angina Pectoris: Etiology con’t Increased myocardial oxygen demand: Myocardial hypertrophy Severe tachycardia Severe hypertyroidism
  • 14. Angina Pectoris: Types • 1: Chronic stable angina: is angina that recurs under similar circumstances & with similar frequency over time 2: Unstable angina: is a term applied to angina when a change in status occurs, thus; - rest angina - angina of increasing severity, duration or frequency - new-onset angina Its more serious clinical condition than chronic stable angina
  • 15. Angina: Diagnosis History Classically precordial/ Retrosternal chest pain, tightness or discomfort radiating to left shlouder/arm/jaw Predictably precipitated by 3Es: Exercise, Emotion, Eating. Brief duration < 10-15 min, Relieved by Rest Note presence of cardiac risk factors (HTN, smoking, DM, Family history, dyslipidemia)
  • 16. Angina: Diagnosis • Examination: May be normal in btn attacks, or anxious, ↑PR, ↑BP, S4 or MR Investigations • Resting ECG: Taken in absence of pain is normal in 50% of cases • Stress testing: Increases sensitivity & specificity of ECG. • Other stress tests: Scintigraphy, stress radionuclide ventriculography, Echocardiography, • Cardiac catheterization with coronary arteriography Intravascular ultrasound
  • 17. Angina: Treatment • Β-blockers: propranolol, metoprolol, atenolol, nadolol, timolol • NITRATES: Nitroglycerine, Isosorbide di (mono) nitrate, • Preparations: Sublingual, oral, dermal, I.V • CALCIUM CHANNEL BLOCKERS: • E.G nifedipine, verapamil, dilitiazem, amlodipine, nicardipine SURGERY. Removing or reducing the obstructive coronary athersclerotic lesion can alleviate the angina,Balloon dilatation, stenting, Manage risk factors
  • 18. MYOCARDIAL INFARCTION (MI): Pathogenesis Atheromatous plaque rapture, attracts platelets, triggering thrombus formation Total vascular occlusion occurs Myocardial death (Infarction) follows: Extent of infarct governed by: - Collateral circulation - Anearobic metabolism - Workload demands of myocardium
  • 20. MI: Clinical features Chest pain Angina like but more severe ,longer in duration>20 mins, Not relieved by rest or nitroglycerine Described as heavy,squeezing,crushing,stabbing Retrosternal ,Central epigastric,may radiate to arms ,throat ,shoulder, jaw
  • 21. MI: Clinical features MI without chest pain- post op ,elderly, DM Isolated dyspnea, exacerbation of HF,or acute confusion may be the presenting features. Other associated symptomes Diaphoresis, cold clammy skin, apprehension Shortnesss of breath, nausea, vomiting, dizziness Syncope due to bradyarrhythmias
  • 22. MI: Physical signs Patients appear apprehensive, anxious,cold clammy Area of chest pain may be indicated by a clenched fist (Levine sign) Tachycardia 100-120/min,↑BP due to ↑sympathetic tone (in >50% pt with ant MI) Bradycardia <60/min,fall in BP(in2/3 0f inf. MI), hypotension.
  • 23. MI: Physical findings MR murmur due to papillary muscle infarction. Crepitations. Elevated JVP due to heart failure. Frequently physical signs may be lacking but suspicion of MI should be high if history is suggestive.
  • 24. MI: Diagnosis Infarct diagnosis based on 2 of 3: 1. History: - Sudden onset of characteristic chest pain for > 30 minutes duration - May be accompanied by symptoms of heart failure 2. ECG Changes
  • 25. MI: Diagnosis 3. Cardiac enzymes: Creatine kinase (ck-MB), myocardial proteins (Troponin T & I), Myoglobin 4. Echocardiography 5. Radioisotope imaging 6. MRI 7. Cardiac catherization
  • 26. MI: Management Emergency care Goal: 1. Minimize infarct size 2. Prevent complications Bed rest Oxygen via nasal canula Sublingual Nitroglycerin Morphine (pain relief, sedation) Β-blockers Thrombolysis (rt-PA, streptokinase, urokinase, anistreplase) Heparin surgery
  • 27. MI: Management LONG TERM CARE Antiplatelet therapy: aspirin, clopidegrol Β-blockers: carvedilol, metoprolol, nadolol ACEIs: captopril, enalpril, Lipid-lowering therapy Nitrates Manage complications
  • 28. MI: Complications Arrhythmias: • Myocardial rupture: LV free wall, papillary muscle (MR), ventriculo-septal defects • Shock/CHF/Ventricular aneurysm • Post-infarct angina • Recurrent MI • Pericarditis (Dressler’s syndrome)
  • 29. MI: Prognosis 20% of patients with acute MI die before reaching hospital 5-15% of those hospitalized will die: Risk factors for death: Infarct size (big size, poor prog) Age (old age poor prognostic factor) Co-morbidity(DM, Dyslipidemia) Devt of HF/Hypotension
  • 30. Thank you for listening