- Ischemic heart disease is caused by a reduced blood supply to the heart muscle due to coronary artery atherosclerosis. The heart requires constant blood flow to function properly but atherosclerotic plaques can block this blood flow. - Symptoms range from stable angina (predictable chest pain) to unstable angina (increasing chest pain) to myocardial infarction (heart attack caused by severe blockage or clot). - Risk factors include high blood pressure, high cholesterol, smoking, obesity, and lack of exercise. Proper management can reduce the risk of further heart problems.

1. Ischemic heart disease
Pre by Lect: ZAHID
REHMAN
IPMS(KMU)

2. Ischemic Heart Disease

3. Heart Anatomy
The average adult heart pumps about 6000-
7500 liters of blood per day through 60,000
miles of blood vessels each minute at rest.
• Structure
– Covered by pericardium
• Parietal
• Visceral (epicardium)
– Outer heart layer: epicardium
– Middle heart layer: myocardium
– Inner layer: endocardium

5. – Four hollow chambers
• Two upper, atria
• Two lower, ventricles
– Divided by septum and valves
• Function
– Right atrium receives
deoxygenated blood
– Right ventricle pumps
blood to lungs

8. Peripheral Vascular System
• Aorta, arteries, arterioles, capillaries
• Venules, veins, superior and inferior vena cava
• Three layers
– Intima
– Media
– Adventitia

10. • Coronary Artery Disease
• Atherosclerotic Plaque/Atheroma
• Angina Pectoris
• Myocardial Infarction
• Sudden Death
• Overall Management

11. CAD: Statistics
• CAD is the largest killer of American males and females
• 13 million Americans have CAD
• 1.1 million MI’s per year
• Every 26 seconds  an American will suffer from a
coronary event
• Every 60 seconds  an American will die because of a
coronary event

12. • " Ischaemia “
Refers to an insufficient amount of blood. The
coronary arteries are the only source of blood for
the heart muscle. If this coronary arteries are
blocked, the blood supply will reduce.

13. • Ischemic heart disease (IHD):
• cardiac myocytes generate energy almost exclusively
• through mitochondrial oxidative phosphorylation, cardiac
• function is strictly dependent upon the continuous flow of
oxygenated blood through the coronary arteries
• caused by coronary atherosclerotic plaque formation
which leads to imbalance between O2 supply & demand
– results in myocardial ischemia
• Chest pain

14. • High blood cholesterol
• High blood pressure
• Smoking
• Obesity
• Lack of physical activity

15. – Remember that the coronary arteries are the
only source of fuel to the heart.The coronary
arteries may become partially/completely
occluded:
– Atherosclerotic Plaques
• In more than 90% of cases, IHD is a
consequence of reduced
• coronary blood flow secondary to obstructive
atherosclerotic vascular disease

16. Atherosclerotic Plaque
• Focal accumulation of smooth muscle cells,
foam cells, cholesterol crystals and lipid under
the endothelium of the artery (within the Tunica
Intima)
• Given time, this plaque can protrude into the
lumen of the vessel reducing blood flow
• Often develops at branch points or curves within
the vasculature  blood is slowed and/or
turbulent

17. • Where does the plaque begin?  within the
Tunica Intima, the innermost wall of the artery.
The plaque is made of Superficial fibrous cap
made of smooth muscle cells, collagen, elastin
and proteins
• Also contains Macrophages, Foam Cells, T
Cells
• Foam cells are one of the first cells found at
the site of the fatty streak, which is the
beginning of atherosclerotic plaque
formation in vessels

18. 18

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21. • As the atheroma within the coronary arteries
enlarges, the blood flow to the heart decreases
and therefore so does the O2 supply
• The heart is not in danger of hypoxia until 50%
of the vessel is occluded
• As the heart senses a decrease in O2, there is
attempted compensation:
– Increase Heart Rate
– Increase Blood Pressure
• When 70% of the artery is occluded, Angina
Pectoris will occur

22. Pathogenesis.....mean maner of disease
• In most cases IHD occurs because of
inadequate coronary perfusion relative to
myocardial demand. This may result from a
combination of pre-existing ("fixed")
atherosclerotic occlusion of coronary arteries
and new superimposed thrombosis and/or
vasospasm .
• Atherosclerotic narrowing can affect any of the
coronary
arteries—left anterior descending (LAD), left
circumflex (LCX), and right coronary artery
(RCA)—singly or in any combination.

23. • Fixed obstructions that occlude less than
70% of a coronary
vessel lumen typically are asymptomatic,
even with exertion.
In comparison, lesions that occlude more
than 70%
of a vessel lumen—resulting in so-called
critical stenosis,
cause chest pain, and the patient is said to
have stable

24. Classification = mainly 4 types
– Myocardial infarction (MI)
– Sudden cardiac death(Cardiac Arrest)
– Angina pectoris
– Chronic IHD with heart failure

25. Angina Pectoris

27. 1. Stable / Typical
2. Prinzmetal / Variant
3. Unstable / Crescendo
Stable Angina
• Typical or stable angina is predictable episodic chest pain
associated with particular levels of exertion or some other
increased demand (e.g., tachycardia). The pain is
classically described as a crushing or squeezing substernal
sensation, that can radiate down the left arm or to the left
jaw (referred pain). The pain usually is relieved by rest
(reducing demand) or by drugs such as nitroglycerin, a
vasodilator that increases coronary perfusion.

28. Variant Angina
• Prinzmetal or variant angina occurs at rest and
is caused
• by coronary artery spasm. Although such
spasms typically occur on or near existing
atherosclerotic plaques, completely normal
vessel can be affected. Prinzmetal angina
typically responds promptly to vasodilators such
as nitroglycerin and calcium channel blockers.

29. Unstable Angina
• Unstable angina (also called crescendo angina) is
characterized
by increasingly frequent pain, precipitated by
progressively less exertion or even occurring at
rest.
Unstable angina is associated with plaque
disruption
and superimposed thrombosis, distal embolization
of
the thrombus, and/or vasospasm; it is often the
cause of MI, caused by complete vascular
occlusion.

30. Sign and symptom:
Dyspnea, nausea, diaphoresis resolve
quickly after cessation of angina

31. Myocardial infarction
• Myocardial infarction (MI), also commonly
referred to as
“heart attack,” is necrosis of heart muscle
resulting from ischemia.
• Roughly 1.5 million people per year in the
United
States suffer an MI; of these, one third die.

32. Myocardial Infarction
• Partial or total occlusion of one or more of the
coronary arteries due to an atheroma, thrombus or
emboli resulting in cell death (infarction) of the heart
muscle
• When an MI occurs, there is usually involvement of
3 or 4 occluded coronary vessels
• Region of myocardial necrosis due to prolonged
cessation of blood supply
• Results from acute thrombus at side of coronary
atherosclerotic stenosis
• May be first clinical manifestation of ischemic heart
disease or history of Angina Pectoris

33. • The frequency of MIs rises progressively with
increasing age and presence of other risk
factors such as
 hypertension,
 smoking,
 and diabetes.

34. • Approximately 10% of MIs occur in people younger
than 40 years, and 45% occur in people younger
than age 65. Blacks and whites are equally affected.
• Men are at significantly greater risk than women,
although the gap progressively narrows with age.
• In general, women tend to be remarkably protected
against
MI during their reproductive years. However,
menopause—
with declining estrogen production—is associated with
exacerbation of coronary artery disease and IHD is the
most common cause of death in elderly women.

35. Pathogenesis
• Although any form of coronary artery occlusion
can cause acute MI, angiographic studies
demonstrate that most MIs are caused by acute
coronary artery thrombosis.
• In most cases, disruption of an atherosclerotic
plaque results in the formation of thrombus.
Vasospasm and/or platelet aggregation can
contribute but are infrequently the sole cause of
an occlusion.

36. Sometimes, particularly with infarcts limited to the
innermost (subendocardial) myocardium, thrombi
may be absent. In these cases, severe diffuse
coronary atherosclerosis significantly limits
coronary vessel perfusion, and a prolonged period
of increased demand (e.g., due to tachycardia or
hypertension) may be sufficient to cause necrosis
of myocytes most distal to the epicardial vessels.

37. • Location,
• severity,
• rate of development of the coronary occlusion
• Size of the vascular bed perfused by the
obstructed vessels
• Duration of the occlusion
• Metabolic demands of the myocardium (affected,
e.g., by blood pressure and heart rate).
• Extent of collateral supply.

38. Clinical Features
• An MI is usually heralded by severe, crushing
substernal chest pain or discomfort that can
radiate to the neck, jaw, epigastrium, or left arm.
• In contrast to the pain of angina pectoris, the
pain of an MI typically lasts from 20 minutes to
several hours and is not significantly relieved by
or rest. In a substantial minority of patients (10%
to 15%) MIs can be entirely asymptomatic. Such
"silent" infarcts are particularly common in
patients with underlying diabetes mellitus (with
peripheral neuropathies) and in the elderly.

39. • With MIs the pulse is generally rapid and weak, and
patients can be diaphoretic and nauseated
particularly with posterior-wall MIs. Dyspnea is
common and is caused by impaired myocardial
contractility and dysfunction of the mitral valve
apparatus, with resultant pulmonary congestion and
edema.
• Electrocardiographic abnormalities are important
markers of MIs;
• Laboratory evaluation of MI is based on measuring
the blood levels of intracellular macromolecules that
leak out of injured myocardial cells through
damaged cell membranes.

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