Atherosclerosis is a disease characterized by plaque buildup within the arteries that can restrict blood flow. It is caused by risk factors like age, sex, family history, hyperlipidemia, hypertension, smoking, obesity, and diet. Over time, plaque growth can obstruct blood vessels and reduce oxygen supply to organs. This can lead to complications like heart attacks, strokes, and peripheral vascular disease depending on the affected arteries. Diagnosis involves examining physical signs, blood tests, imaging studies, and coronary angiography. Treatment focuses on modifying risk factors and managing complications.

1. ATHEROSCLEROSIS
BY: AJAY KUMAR MANDAL
FROM: NEPAL

2. ATHEROSCLEROSIS
Atherosclerosis is a disease of large and medium-sized muscular arteries and is
characterized by endothelial dysfunction, vascular inflammation, and the buildup of
lipids, cholesterol, calcium, and cellular debris within the intima of the vessel wall. This
buildup results in plaque formation, vascular remodeling, acute and chronic luminal
obstruction, abnormalities of blood flow, and diminished oxygen supply to target
organs.
RISK FACTORS
• Age >50-60 years
• Male sex
• Family history of atherosclerosis
Fixed risks Modifiable risks
• Hyperlipidemia
• Arterial hypertension
• Cigarette smoking
• Obesity
• Diabetus mellitus
• Physical inactivity
• “Western” diet
• hyperhomocystinemia

3. A SCHEMATIC LIFE HISTORY OF AN
ATHEROSCLEROTIC LESION
In westernized societies, and increasingly in developing countries, atherogenesis
begins in early life. Lesion evolution usually occurs slowly over decades, often
progressing in a asymptomatic manner or eventually causing stable symptoms related
to embarrassment of flow, such as angina pectoris or intermittent claudication. For the
first part of the life history of the lesion, growth proceeds abluminally, in an outward
direction preserving the lumen (compensatory enlargement or “positive remodeling”).
A minority of lesions will produce thrombotic complications, leading to clinical
manifestations such as the unstable coronary syndromes, thrombotic stroke, or critical
limb ischemia.

4. Platelet adhesion and aggregation occur at the site of plaque rupture
("white thrombus"). Activated platelets exert procoagulant effects and
the soluble coagulation cascade is activated. Fibrin strands and
erythrocytes predominate within the lumen of the vessel and
downstream in the "body" and "tail" of the thrombus.
DIAGRAM OF ARTERIAL THROMBUS RESPONSIBLE
FOR ACUTE MYOCARDIAL INFARCTION

5. CARDIOVASCULAR DISEASES CAUSED BY
ATHEROSCLEROSIS
Places of affection Complications
Arteries of brain
Carotid arteries
Coronary arteries
Tibial arteries
Renal arteries
Femoral arteries
Iliac arteries
Aorta
Strokes,
transient ischemic attacks,
chronic ischemia of brain
Ischemic heart disease,
myocardial infarction
Peripheral
vascular
disease
Arterial hypertension
Aortic aneurysm

6. PHYSICAL SIGNS OF ATHEROSCLEROSIS
provide objective evidence of extracellular lipid deposition, stenosis or
dilatation of large muscular arteries, or target organ ischemia or
infarction
• Hyperlipidemia - Xanthelasma, tendon xanthomata
• Coronary artery disease - Fourth heart sound, tachycardia, hypotension,
hypertension
• Cerebrovascular disease - Diminished carotid pulses, carotid artery
bruits, focal neurological deficits
• Peripheral vascular disease - Decreased peripheral pulses, peripheral
arterial bruits, pallor, peripheral cyanosis, gangrene, ulceration
• Abdominal aortic aneurysm - Pulsatile abdominal mass, peripheral
embolism, circulatory collapse
• Atheroembolism - Livedo reticularis, gangrene, cyanosis, ulceration
(The presence of pedal pulses in the setting of peripheral ischemia
suggests microvascular disease and includes cholesterol embolization.)

7. ISCHEMIC HEART DISEASE
Disease of myocardium caused by acute or chronic discrepancy between
myocardial oxygen demand and real coronary blood flow that leads to
development of myocardial ischemia, myocardial injury, necrosis or scars
and is accompanied by disturbance of systolic or diastolic function of the
heart.
1. Stenosis of proximal (epicardial) coronary arteries by atherosclerotic
plaque leading to reduction of coronary blood flow and/or its
functional reserve and inability of adequate response to myocardial
oxygen demand (“fixed stenosis”);
2. Coronary spasm (“dynamic stenosis”);
3. Thrombosis of coronary artery;
4. Microvascular dysfunction (Abnormal constriction or deficient
endothelial-dependent relaxation of resistant vessels associated
with diffuse vascular disease ).
Main mechanisms of coronary insufficiency:

8. SCHEMATIC DIAGRAM OF STUNNED
MYOCARDIUM
During coronary occlusion, a wall motion abnormality of the left ventricle is present in
the region supplied by the occluded artery. With relief of ischemia and reestablishment
of coronary blood flow, there is a persistent wall motion abnormality despite
reperfusion and viable myocytes. There is then gradual improvement in function that
requires hours to days for recovery.

9. PATHOGENESIS OF A CORONARY THROMBUS
Most coronary thrombi (about three fourths) are initiated by plaque rupture, exposing thrombogenic material to
the flowing blood; the atheromatous gruel appears to be highly thrombogenic. The thrombus is platelet-rich and
usually gray-white at the rupture site; severe stenosis, if present, promotes thrombosis via shear-induced
platelet activation. Fibrin soon enmeshes the platelets, stabilizing the thrombus. Thrombus formation is
dynamic: recurrent thrombosis, thrombolysis, and peripheral embolization occur simultaneously, with or without
concomitant vasospasm, causing intermittent flow obstruction. Nonoccluding thrombi may extend post-
stenotically, and if the platelet-rich thrombus occludes the vessel, the blood proximal and distal to the occlusion
may stagnate and coagulate, giving rise to upstream and/or downstream propagation of a red, fibrin-dependent,
venous-like thrombus. Upstream thrombus propagation does not occlude major side branches.

10. SEVERAL POTENTIAL OUTCOMES OF REVERSIBLE AND
IRREVERSIBLE ISCHEMIC INJURY TO THE MYOCARDIUM

11. CLASSIFICATION OF IHD
2.1. Stable angina pectoris (grades from I to IV)
2.2. Unstable angina
2.3. Variant angina pectoris (Prinzmetal's angina)
1. Sudden cardiac arrest
2. Angina pectoris
3. Silent myocardial ischemia
4. Microvascular angina pectoris (syndrome X)
5. Acute myocardial infarction
6. Postinfarction cardiosclerosis
7. Congestive heart failure
8. Disorders of cardiac rhythm and conduction (specifying the clinical form)
5.1. Q-wave myocardial infarction
5.2. Non-Q-wave myocardial infarction

12. ANGINA PECTORIS
Typical description of chest pain in angina pectoris
• As a rule, the pain is described as a pressure, heaviness
or squeezing, burning and choking sensation behind the
sternum
• it radiates to the left arm, shoulder, left side of the neck
• angina is precipitated by exertion, eating, exposure to
cold, or emotional stress
• anginal pain is relieved by rest or nitroglycerin
• it lasts for approximately 1-5 minutes (not more than 15
minutes).
The most informative method of examination for
angina pectoris to be diagnosed is inquire.

13. PHYSICAL SIGNS OF ANGINA PECTORIS
• For most patients with stable angina, physical examination findings are
normal. Diagnosing secondary causes of angina, such as aortic stenosis,
is important.
• A positive Levine sign (characterized by the patient's fist clenched over
the sternum when describing the discomfort) is suggestive of angina
pectoris.
• Look for physical signs of abnormal lipid metabolism (e.g., xanthelasma,
xanthoma) or of diffuse atherosclerosis (e.g., absence or diminished
peripheral pulses, increased light reflexes or arteriovenous nicking upon
ophthalmic examination, carotid bruit).
• Examination of patients during the angina attack may be more helpful.
Useful physical findings include third and/or fourth heart sounds due to
LV systolic and/or diastolic dysfunction and mitral regurgitation secondary
to papillary muscle dysfunction.

14. ADDED METHODS OF EXAMINATION IN
ANGINA PECTORIS
• Routine blood tests (CBC count, chemistry panel, thyroid
function tests)
• Fasting lipid profile (total cholesterol level, LDL-C level, HDL-C
level, triglyceride level)
• 12-lead ECG
• Treadmill ECG stress test
• Holter monitoring for silent ischemia
• Chest radiograph
• Nuclear imaging studies (myocardial perfusion imaging)
• Magnetic resonance angiography
• Selective coronary angiography
• Echocardiography

15. PATIENT EXERCISING ON TREADMILL
Baseline Maximal 10 min. rest

16. CORONARY ARTERY THROMBUS IN A
PATIENT WITH UNSTABLE ANGINA
Coronary angiography shows an irregular hazy filling defect in the left anterior
descending artery at the level of the second diagonal branch (arrow). Contrast
medium surrounds the globular thrombus, which extends into the diagonal branch .

17. MYOCARDIAL INFARCTION
infarction of an area of the heart muscle, usually as a result of occlusion
of a coronary artery
• transmural MI and large-focal
MI (Q-wave MI)
• intramural MI (non-Q-wave MI)
According to the size
and depth of location
• primary (initial) MI
• repeated MI
• recurrent MI
CLASSIFICATION OF MI
According to the course
of disease

18. • the acutest phase (30 min – 2 h)
formation of ischemia and injury
• acute phase (up to 14-18 days)
formation of necrosis, myomalacia
• subacute period (to the end of 4-8
weeks)
reparation, replacement by granulation tissue
• cicatricial period (2-6 months)
formation of scar
adaptation of the heart to new conditions
• anginal MI
• abdominal MI
• asthmatic MI
• cerebrovascular MI
• arrhythmic MI
• asymptomatic MI
According to the stage of
MI
According to the clinical
variants of MI
CLASSIFICATION OF MI

19. Necrosis begins in a small zone
of the myocardium beneath the
endocardial surface in the
center of the ischemic zone.
This entire region of
myocardium (dashed outline)
depends on the occluded
vessel for perfusion and is the
area at risk. Note that a very
narrow zone of myocardium
immediately beneath the
endocardium is spared from
necrosis because it can be
oxygenated by diffusion from
the ventricle.
SCHEMATIC REPRESENTATION OF THE
PROGRESSION OF MYOCARDIAL NECROSIS AFTER
CORONARY ARTERY OCCLUSION

20. COMPLAINTS IN MI
• Chest pain
• Shortness of breath
• Abdominal pain
• Palpitation
• Intermissions in heart beat
• Dizziness
• syncope.
PHYSICAL FINDINGS IN MI
Physical examination findings can vary enormously
• Low-grade fever may be present.
• Hypotension or hypertension can be observed depending on the extent of the MI.
• Fourth heart sound (S4) may be heard in patients with ischemia. Diastolic dysfunction
is the first physiologically measurable effect of ischemia and can cause a stiff ventricle
and an audible S4.
• Dyskinetic cardiac bulge (in anterior wall MI) occasionally can be palpated.
• Systolic murmur can be heard if mitral regurgitation develops.
• Other findings include cool, clammy skin and diaphoresis.
• Signs of congestive heart failure (CHF) may be found (including third heart sound (S3)
gallop, pulmonary rales, lower extremity edema, elevated jugular venous pressure).

21. MYOCARDIAL INFARCTION
Typical description of chest pain in myocardial infarction
• Substernal pressure sensation that also may be
described as squeezing, aching, burning, or even sharp
pain of severe intensity
• radiation to the left side of body (left arm, left side of the
neck, jaw, head) is common
• prolonged chest discomfort that lasts longer than 30
minutes
• it is not necessarily precipitated by exertion, persists at
rest and is not relieved by taking nitroglycerin
• chest pain may be associated with nausea, vomiting,
diaphoresis, dyspnea, fatigue or palpitations.

22. COMPLICATIONS OF MI
• acute left-ventricular failure (pulmonary oedema)
• cardiogenic shock
• ventricular and supraventricular arrhythmias
• conduction abnormalities
• acute aneurism of LV
• myocardial ruptures
• pericarditis
• mural trombi

23. FEATURES OF RESORPTIVE-NECROTIC
SYNDROME IN ACUTE MI
Marker Range of times
to initial elevation
Mean time to
peak elevations
Time to return to
normal range
Elevated body
temperature (fever)
1-2 days 2-3 days 7-10 days
Leucocytosis 2 hr 2-4 day 7 days
ESR 2-3 day 8-10 day 2-3 weeks
AST 4-12 hr 24-36 hr 4-7 days
LDH 8-10 hr 48-72 hr 8-14 day
LDH 1 8-10 hr 24-84 hr 10-12 day
CK 6-12 hr 24 hr 3-4 day
CK-MB 4-6 hr 12-18 hr 48-72 hr
Myoglobin 1-4 hr 4-8 hr 24-48 hr
cTnI 2-6 hr 24-48 hr 7-14 day
cTnT 2-6 hr 24-48 hr 7-14 day

24. PLOT OF THE APPEARANCE OF CARDIAC MARKERS IN
BLOOD VERSUS TIME AFTER ONSET OF SYMPTOMS
Peak A, early release of myoglobin or CK-MB isoforms after AMI; peak B, cardiac
troponin after AMI; peak C, CK-MB after AMI; peak D, cardiac troponin after
unstable angina. Data are plotted on a relative scale, where 1.0 is set at the AMI
cutoff concentration.

25. WHO DEFINITION OF MI
 Typical symptoms of chest pain > 30 minutes
 Characteristic rise and fall of serum enzyme levels
 Typical ECG changes with development of ST elevation
or Q waves
Presence any two criteria from three ones:

26. ECG IN DIAGNOSIS OF ISCHEMIC HEART DISEASE
 myocardial ischemia – changes T wave (and
ST depression)
 myocardial injury – development of ST
elevation (or depression)
 myocardial necrosis – appearance of
pathological Q wave

27. MYOCARDIAL ISCHEMIA
T
Subendocardial ischemia
Subepicardial ischemia
The Т wave is deep and symmetrically inverted
T
The Т wave is tall and hyperacute

28. T WAVE CHANGES ASSOCIATED WITH ISCHEMIA
Suggested criteria for size of T wave
• 1/8 size of the R wave
• <2/3 size of the R wave
• Height <10 mm
T wave inversion
• T wave inversion can be normal
• It occurs in leads III, aVR, and V1 in
association with a predominantly
negative QRS complex (and in V2,
but only in association with T wave
inversion in lead V1)

29. ST CHANGES WITH ISCHEMIA
Normal wave form (A); flattening of ST segment (B), making T wave more
obvious; horizontal (planar) ST segment depression (C); and downsloping ST
segment depression (D)

30. MYOCARDIAL INJURY
With predominant subendocardial ischemia (A), the resultant ST vector is directed
toward the inner layer of the affected ventricle and the ventricular cavity. Overlying
leads therefore record ST depression. With ischemia involving the outer ventricular
layer (B) (transmural or epicardial injury), the ST vector is directed outward.
Overlying leads record ST elevation. Reciprocal ST depression can appear in
contralateral leads.

31. MYOCARDIAL INJURY
Subendocardial injury
Subepicardial injury
R
ST
Q
P
ECG shows ST segment elevation with a curve
which is convex upwards in the leads facing the
subepicardial myocardial injury.
It begins with the top or the descending part of R
wave and joins Т wave, i.e. “monophase curve”
(“tombstone”) is recorded.

32. MYOCARDIAL NECROSIS
ECG records the following patterns in the leads overlying the necrotic zone:
persistent abnormal (pathological) Q wave (it exceeds ¼ amplitude of next R wave
and its length exceeds 0.03 sec).
The more extensive necrosis is, the deeper Q wave is and the less height of R wave
is. QS wave is registered in transmural myocardial infarction.
ST
R
Q
P
T

33. SEQUENCE OF CHANGES SEEN DURING
EVOLUTION OF ACUTE STAGE OF MI
Phase of injury
(several hr – 1-3 d)
Phase of necrosis
Phase of ischemia
(up to 30 min)

34. SUBACUTE STAGE OF MI
Stabilization of the ECG picture means the ending of subacute stage of MI :
absence of any changes of the Т wave and the QRS complex in marginal zones of
myocardial infarction on three ECGs which have been recorded with the interval of
3-4 days.
As the infarct evolves, the ST segment elevation diminishes and the ST
segment returns to the isoelectric line, the T waves begin to invert in
anatomically contiguous leads (It means ending of acute phase of MI).
ST
R
Q
P
T

35. DYNAMIC OF ECG CHANGES IN MI
normal ischemia injury necrosis scargranulations
minutes-hours days-weeks weeks-months

36. LOCALISATION OF SITE OF INFARCTION
Anatomical relationship of leads
Inferior wall: leads III, aVF and II
Anterior wall: leads V1 to V4
Lateral wall: leads I, aVL, V5 and V6

37. PATTERNS OF MYOCARDIAL INFARCTION
Anterior MI with gross ST segment
elevation (showing "tombstone" R
waves)
An inferolateral MI with reciprocal
changes in leads I, avL, V1, and V2

38. ACUTE ANTERIOR LEFT VENTRICULAR INFARCTION
After the first 24 h. Note that the ST segments are less elevated; also note the development of
significant Q waves and the loss of R waves in leads I, aVL, V4
, and V6
.
Tracing obtained within a few hours of the onset of illness. Note the striking hyperacute ST segment
elevation in leads I, aVL, V4
, and V6
, and the reciprocal depression in the other leads.
Several days later. Significant Q waves and the loss of R wave voltage persist. ST segments are
now essentially isoelectric. The ECG will probably change only slowly over the next several months.

39. ACUTE INFERIOR DIAPHRAGMATIC LEFT VENTRICULAR
INFARCTION
Tracing obtained within a few hours of the onset of illness. Note the hyperacute ST segment
elevation in leads II, III, and aVF, and the reciprocal depression in the other leads.
After the first 24 h. Note the development of significant Q waves in leads II, III, and aVF, and the
decreasing ST segment elevation in the same leads.
Several days later. ST segments are now isoelectric. There are abnormal Q waves in leads II, III,
and aVF, indicating that myocardial scars persist.

40. THANK YOU……..