Ischemic heart diseases (IHD)

Group (F +E)
Dr . Osman Elsaid
Dr. Osman El-Sayed Consultant interventional cardiologist
Associated professor of cardiology
MBBS - ECFMG(USA)- MRCP(UK London)

MSC - DTH & H(Liverpool)

Diploma - TEE(European )

Diploma- TOE(European)
 Ischemic heart disease:

Group of syndromes characterized by narrowing of the coronary arteries that prevents

adequate blood supply to the myocardium leading to myocardial ischemia.

• So the alternative name is Coronary Artery Disease (CAD).

 Causes:
• Caused mainly by Atherosclerosis of Coronary Artery.

• It includes the following syndromes:

- Angina: Stable , Unstable and variant.

- Myocardial infarction.
- Sudden cardiac death.
- Chronic IHD with congestive HF.
 Epidemiology

• most common cause of cardiovascular morbidity and mortality because:

IHD affects around 126 million individuals (1,655 per 100,000), which is approximately
1.72% of the world's population. Nine million deaths were caused by IHD globally.

• peak incidence of symptomatic IHD is age 50-60 (men) and 60-70 (women) M>F.
 Risk factors
 Risk factors for IHD are similar to those of the atherosclerosis.

 divided to:
I. Modifiable.
II. Non modifiable.
 Modifiable factors Vs Non modifiable risk factors
Family history patients having acute
attack before 40 and no obvious risk
 High blood cholesterol factors
level.
 Family history of CAD.
 Cigarette smoking,
 Increasing age.
tobacco use.
 Hypertension.  Gender(male)

 Diabetes mellitus.  Race(non white

populations)
 Lack of estrogen in
women.
 Physical activity.
 obesity.
 Pathogenesis :
 IHD is a consequence of inadequate coronary perfusion relative to myocardial
demand, usually as a consequence of preexisting atherosclerotic occlusion of the
coronary arteries with or without new superimposed thrombosis and/or
vasospasm.
There is no symptom
 less than 70% occlusion of coronary vessel > asymtomatic because the coronary
artery can dilate up to 7
 More than 70% occlusion > stable angina times at rest
 More than 90% occlusion > unstable angina & NSTEMI
 100% occlusion > STEMI
 Atherosclerotic plaque formation:
1. Chronic endothelial injury due to :
 Hyperlipidaemia
 Hypertension The lipid can deposit in the heart in an early age
 Smoking like in infancy

 Hyperhomocysteinemia
 Hemodynamic factors
 Toxins
This leads to LDL accumulation in intima , which is then oxidized.
2. Endothelial dysfunction (increased permeability) leukocytes adhesion,
monocyte adhesion and migration .
Oxidized LDL is engulfed by macrophages forming foam cells > this formes the
initial lesion fatty streak.
3. Macrophages activation, smooth muscle cells recruitment and accumulation of
lipids in vessel wall.
4. Macrophages and smooth muscle cells engulf lipid.
5. Smooth muscle proliferation, lipid, collagen and other ECM deposition > this
produce the stable atherosclerotic plaque.
 Acute plaque change
 Onset of myocardial ischaemia depends not only on the extent and severity of
fixed atherosclerotic plaque but also on dynamic changes in coronary plaque
morphology.
 More than one mechanism of injury maybe involved : rupture, fissuring or
ulceration of plaques expose highly thrombogenic constituents, leading to rapid
thrombosis.
 In addition haemorrhage into the core of plaque can expand plaque volume.
 Some plaques can embolise (atheroembolism)
 Acute plaque rupture, involves factors that influence plaque susceptibility to
disruption by mechanical stress. These include:

1. intrinsic aspects of plaque composition ( plaques that contain large

atheromatous cores or have thin overlying fibrous cap or clusters of
inflammatory cells are more likely to rupture “vulnerable” ).
2. Extrinsic factors such as blood pressure .
 Angina pectoris:
Is sudden ,crushing chest pain that radiates to the neck ,jaw and the arms .
Due to restricted blood supply to the cardiac muscles .
Patterns of angina :
1)Stable ; classic effort induced or typical
angina .
2) Unstable angina
3) Variant ; vasospastic or rest angina
(1)Stable angina :
Is the most common form of angina .
- atherosclerosis is the most common cause which leads to fixed obstruction of
coronary artery ,and the heart becomes at risk of ischemic attack at increased
demand cases such as :

A) Physical activity B) emotional stress or excitement

C) Other causes of increased heart work load .
 Symptoms of stable angina :
1)Short lasting burning ,or squeezing feeling in the chest .
2) fatigue
 3) Dyspnea and diaphoresis
 4) Nausea
 Treatment :
 Stable angina relieved by rest or nitroglycerin
 (2) Unstable angina
 It’s characterized by new onset or rapidly worsening angina (crescendo angina) , angina at minimal
exertion or angina at rest in the absence of myocardial infarction or necrosis.
 Caused by atherosclerotic plaque rupture or ulceration leading to thrombosis with partial occlusion
of vessel , and this leads to subendocardial ischemia .
 It has the same pathogenesis & clinical features of NSTEMI except that in unstable angina there is no
damage to myocardial tissue and cardiac biomarkers aren’t elevated .
 Clinical features:
o squeezing central chest pain radiating to jaw, epigastrium , neck & arm
o Nausea & vomiting
o Diaphoresis
o Dyspnea
o Tachycardia and palpitations
o Hypotension
 Diagnosis is based on patient history & ECG changes .
 Treatment is the same as NSTEMI.
 (3)Variant(prinzmetals) angina

 This type occurs secondary to epicardial coronary artery

spasm as result of exposure to cold weather or stress or
without any provocation or known cause .
 It occurs more frequently in women

Symptoms:
- Chest pain at rest often in early morning and at night and
rarely occur with exertion .
-Sweating and Palpitation.
-Lightheadedness and Dyspnea.
Diagnosis:
 ECG : show ST segment elevation during attack , between attacks ECG may be
normal
 Confirmation is by provocative testing with ergonovine or acetylcholine ; which
may precipitate coronary artery spasm

Treatment:
 Sublingual nitroglycerin
 Calcium channel blockers
Complications:
Life threating arrhythmia
Heart attack.

Note:
Non selective Beta-Blockers (propranolol) may
exacerbate spasm by allowing unopposed alpha –
adrenergic vasoconstriction , SO don’t use it
 Myocardial Infraction

Definition:
MI or Heart Attack is a condition caused by irreversible damage of
myocardial tissue or myocardial necrosis due to reduced blood
supply to the myocardium leading to prolonged ischemia &
hypoxia .

The difference between acute MI and unstable angina

Why when there is severe MI there is a hypotension because there is a scar in the
myocardial muscles lead to decrease the output.
 Epidemiology:

 MI account for 10-25% of all deaths in industrial countries.

 Incidence is higher in elderly , it’s approximately 8 times lower in
patients of 18-45 years than in older patients.
 Males have higher risk than females during reproductive age.
 MI under the age of 40 account for around 3-10% of cases of
coronary artery disease.
 Pathogenesis:

 Myocardial infarction generally occurs when there is an abrupt

increase in coronary blood flow following a thrombotic occlusion of a
coronary artery that is previously narrowed by atherosclerosis.
 Plaque rupture is the major trigger of coronary thrombosis.This
then leads to platelet activation , endothelial induced
vasoconstriction, coronary thrombosis & occlusion.
 Pathogenesis:

 Non atherosclerotic causes of MI:

i. Coronary artery embolization.
ii. Coronary artery occlusion secondary to vasculitis.
iii. Primary coronary vasospasm(variant angina).
iv. Congenital abnormalities of coronary artery.
v. Cocaine use .
The heart can form a clot due to stenosis or due to dilatation eg ventricular clot
caused by aortic stenosis and dilated cardiomyopathy and this thrombus can
travel to the coronary and causes angina . Also it can be caused by dissection
after in those who are cocaine abuser ,also it can occur in pregnancy .
 Types:
 According to the findings in ECG , MI is classified into:
i. NSTEMI
ii. STEMI
 According to anatomical region of left ventricle involved into:
i. Anterior MI
ii. Lateral MI
iii. Posterior MI
iv. Inferior MI
v. Septal MI
vi. Combination
 NSTEMI:
 Associated with sub-endocardial ischemia .
 Due to subtotal occlusion of the artery.
 There is elevated cardiac bio markers.
 ECG changes : ST depression , T wave inversion.

STEMI:
 Associated with transmural ischemia .
 Due to complete occlusion of the artery 100%.
 There is elevated cardiac biomarkers.
 ECG changes: ST elevation
Clinical features :
 Symptoms:
I. Squeezing or tightness like Central chest pain that
radiates to the jaw , arm , epigastrium.
II. Nausea & vomiting.
III. Breathlessness or dyspnea
IV. Collapse/syncope.
 Clinical features:
 Physical signs:
I. Sweating & pallor
II. Tachycardia & palpitations
III. Hypotension & cold peripheries
IV. Narrow pulse pressure
V. Raised jugular venous pressure
VI. Lung corporations
 Investigations:
• ECG:
Earliest change is ST segment deviation
• Cardiac bio-marks :
 Troponin T and I are the most sensitive and specific markers
Rise 3-6 hrs. after infarction
 CK MB
 AST & LDH
• Radiography.
• Echocardiography.
• Coronary angiography .
Normal CXR MI with pulmonary edema
 Complications:
 Arrhythmias:
Most common arrhythmias are VF (the most common cause of death in the first hour of MI) , AF , sinus
bradycardia & AV block.
 Acute Heart failure
 Ventricular septum rupture > cause VSD with loud pansystolic murmur.
 Papillary muscle rupture > lead to sudden onset of sever mitral regurgitation.
 Ventricular rupture > this leads to fatal cardiac tamponade.
 Pericarditis > in the 2nd or 3rd day of MI

 Dressler's syndrome > occurs weeks or months after MI

Due to autoimmune etiology.
 Recurrent angina
 Embolism
 Ventricular remodeling
 Ventricular aneurysm
 Treatment and Management
STEMI
• Analgesia
 Reperfusion Therapy with PCI
Is the treatment of choice for those presenting within 12 hours of symptom
onset
• Thrombolytic therapy
If PCI cannot be achieved at a timely manner
• Antithrombotic agents (Aspirin)
The first tablet given within first 12 hrs and therapy continued indefinitely if
there's no side effects
• lipid lowering agents (statin) can protect the patient in 12 ways other than lowering the
lipid , like affecting the platelet pathway …etc
 Treatment and Management
 Anti anginal therapy
Sublingual glicyeral trinitrate is a valuable the first aid
measure to unstable angina or threatened infarction
Avoided if theres heart failure (pulmonary oedema),
hypotension or bradycardia
 ACEIs
 Treatment and Management

• Antianginal therapy :
Nitrates , B blockers , CCB
• Antiplatelet
• Anticoagulants
• ACE
• lipid lowering agents
• PCI Percutaneous coronary intervention & CABG coronary artery
bypass grafting in case medical therapy didn’t work

Spironolactone prolong life and prevent fibrosis , may cause diabetes

Latex used for symptom relief , may cause lower limb edema .
morphine, oxygen, nitroglycerin, and aspirin,
 Late Management of MI
• Lifestyle Modification :
Diet (weight control), smoke cessation, regular exercise
• Secondary prevention drug therapy:
Antiplatelet therapy(aspirin), B-blockers, ACE inhibitors/ARB, Statin,
additional therapy for control of diabetes and hypertension,
Mineralocorticoid receptor antagonist

• Rehabilitation.
• Device implantation :
• Implantable cardiac defibrillator (High risk
patients)
 Sudden cardiac death(SCD):

(SCD): is defined as an unexpected death caused by loss of

heart function (sudden cardiac arrest) within 6 hours of onset of
symptoms.
Pathogenesis of SCD:
The pathogenesis of SCD is multifactorial and incompletely
clear but in summary when the electrical system of the heart
malfunctions and suddenly becomes very irregular-
tachyarrhythmia or bradycardia, The ventricles flutter
(ventricular fibrillation/V fib),low perfusion to the brain leads to
loss of consciousness and death.

 Difference between heart attack and SCD is that heart attack is

cardiac tissue death due to low perfusion to the heart leading to
damage. while SCD is death due to electrical malfunctioning
causing low perfusion to the body.
Causes & risk factors:
All causes of arrhythmia(V fib) lead to SCD,
although causes are multiple and different :
 coronary artery disease is the most common.
 Congenital heart defects (in younger patients)
 cardiomyopathies .
 and valvular diseases.
 A history of previous heart attack is a risk factor to SCD.
 Management of SCD:

 immediate cardiopulmonary resuscitation

(CPR).
 Implantable cardioverter defibrillator.
 Antiarrhythmic drugs.
 Congestive Heart Failure

 Insufficient cardiac output to meet the metabolic demand of the

body's tissues and organs.
 Final common pathway for many cardiac diseases.
 Increasing incidence in the U. S.
 COMPLICATIONS:
 Forward failure : decreased organ perfusion.
 Backward failure : passive congestion of organs.
 Right-and Left - sided heart failure often occur together.
 left heart failure :
Etiology:
1. Ischemic heart disease.
2. Hypertenion .
3. Myocardial disease .
4. Aortic or mitral valve disease .
Gross:
1.Increase heart weight .
2. Left ventricular hypertrophy and dilatation .
3. Heavy, edematous lungs.
Presentation:
Dyspnea, Orthopnea, paroxysmal nocturnal dyspnea, rales and S3
gallop .

Micro:
1.Cardiac myocyte hypertrophy.
2.Pulmonary capillary congestion and alveolar edema.
3. Intra alveolar hemosidrein laden macrophages.
Complication:

Passive Pulmonary congestion and edema.

Activation of renin system leading to 2ry hyperaldosteronism.
Cardiogenic shock.
 Right side heart failure :
Etiology :
Most commonly caused by left sided heart failure.
Pulmonary or tricuspid valve disease.

Cor pulmonale:
Presentation:
Jugular venous distention, hepatosplenomegaly, dependent edema, ascites, weight
gain, pleural and pericardial effusion.
Gross:
RVH and dilatation.
Complications :
1.Chronic passive congestion of the liver.
2. Cardiac sclerosis /cirrhosis. (long standing congestion
 Chronic ischemic heart diseases ( repeated
ischemic attack in the left ventricle ):
 Chronic ischemic heart disease present with congestive cardiac failure especially left
ventricular failure
 There is multiple vessels with multiple plaque pathology
 Such patient may have history of : angina or Myocardial infraction
 Or suffering from silent ischemia
 Due to this repeated ischemic attack myocardium is replaced by lots of fibrous tissue
so it’s sick myocardium it’s known as ischemic cardiomyopathy ,due to fibrosis it
starts to dilate leads to pulmonary edema, hypertension ,right ventricular
hypertrophy and generalized edema = congestive heart failure
 Nowadays 50% of patients with transplanted heart have chronic ischemic
cardiomyopathy
Investigations :
 Chest X-rays: help estimate the size of the heart and the great vessels, as
well as the condition of the lungs.
 Electrocardiogram: also reveal any scar tissue from previous infarctions
or the presence of an arrhythmia
 Cardiac catheterization
Management :
 Lifestyle changes:
 • Quit smoking.
 • Eat healthy foods.
 • Exercise regularly.
 • Lose excess weight.
 • Reduce stress.
 Medications :

1. Cholesterol-modifying medications
2. Aspirin
3. Beta blockers
4. Calcium channel blockers.
5. Angiotensin-converting enzyme (ACE) inhibitors
6. Procedures to restore and improve blood flow :
7. Angioplasty
8. Coronary artery bypass surgery