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Mr.

Alfrin Antony
Asst Lecturer
Department of pathology
ICHEMIC HEART DIHEART DISEASE +919738289032
DEFINITION:- Ischemic hear disease is defined as acute or chronic form of cardiac
disability arising from the imbalance between myocardial supply and demand for
oxygenated blood.

ETIOPATHOGENISIS
1). Coronary atherosclerosis
2). Super added changes in coronary atherosclerosis
a). Acute changes in chronic atheomatous plaque
b). Coronary artory thrombosis
c). Local plate let aggregation and coronary artory spasam
3). Nonathero sclerotic causes
a). Vasospasam
b). Stenosis of coronary artory
c). Arteritis
d). Embolism
f). Thrombotic disease
g). Trauma
h). Aneurysms
i). Compression

EFFECTS MYOCARDIAL ISCHEMIA


1). Myocardial infarction
2). Non-Infract effect of ischemia
a). Angina pectoris
b). Chronic ischemic heart disease
c). Sudden cardiac death

MYOCARDIAL INFARCTION
DEFINITION:-Myocardial infarction is a life threatening condition characterized by the
formation of necrotic areas with in the myocardium

ETIOPATHOGENISIS
1). MECHANISAM OF MYOCARDIAL ISCHEMIA
It happened by one or of th following mechanisms
a). Diminished coronary blood flow
b). Increased myocardial demand
c). Hypertrophy of the heart without simultaneous ivrease of coronary blood flow
2). ROLE OF PLATELETS:- Rupture of atherosclerotic plaque exposes subendothelial
collagen to platelets which undergo aggregation, activation and release reaction. These
events contribute to the build up of the platelet mass that may give rise emboli or initiate
thrombosis
3). COMPLICATED PLAQUES:-
a). Coronary Thrombosis (50% of acute MI)
b). Intra mural hemorrhage (33%of acute MI)
Hemorrhage and thrombosis may occur in some cases
4). Non atherosclerotic Causees (10%)
5). TRANSMURAL VERSUS SUBENDOCARDIAL INFARCTS.

SL
NO FEATURE TRANSMURAL SUBENDOCARDIAL
INFARCT INFARCT
1 Definition Full thickness, Solid Inner third to half, patchy

2. Frequency Most frequent (95%) Less frequent

3. Distribution Specific area of coronary Circumfeential


supply
4. Pathogenisis >75% coronary stenosis Hypoperfusion of myocardium

5. Coronary Thrombosis Common Rare

6. Epicarditis Common None

TYPES OF INFARCTS
1). According to anatomic region of the left ventricle involved
a).Anterior
b).Posterior
c). Inferior
d).Lateral
e).Septal
f).Circumferential
g).Antroseptal
h).Antrolateral
i).Infrolateral
2).According to the degree of thickness of ventricular Wall involved
a). Full thickness or transmural
b). Subendocardial or laminar
3). According to the age of Infarcts
a). Newly-formed infarcts are called acute, recent or fresh
b). Advanced Infarcts are called old, healed or organized

LOCATION OF INFARCTS
-Left ventricle > Right ventricle (bcz of thin wall, less metabolic requirement, adequately
nourished by thebesian vessels)
-Right atrial infarct accompanying the infarct of the left ventricle. > Left atrium
(protected by oxygenated blood in the myocardium)
The region of infarction depends upon the area of obstructed there are three coronary
arterial trunks.
1). Stenosis of the left anterior descending coronary artery (40-50) :- The region of
infarction is the anterior part of the left ventricle including apex and the anterior 2/3 of
intervetricular septum
2). Stenosis of the right coronary (30-40%):- Posterior part of the left ventricle and the
posterior 1/3 rd interventricular septum
3). Stenosis of the left circumflex coronary artory (15-20%):- Lateral wall of the left
ventricle

TIME GROSS CHANGES LIGHT MICROSCOPY


FIRST WEEK
0-6 hours No changes ,TTC negative in No changes , Stretching and
infracted area waviness of fibres
6-12 hours -do- Coagulative necrosis begins;
neutrophilic inflammation
begins; edema and
hemorrhages present.
24 hrs Cyanotic red-purple area of Coagulative necrosis
hemorrhage progresses; marginal
neutrophilic infiltrate.
48-72 hours Pale, hyperaemic Coagulative necrosis
complete, neutrophilic
infiltrate developed.
4th day Well defined yellow border Prominent neutrophilic
infiltrate, Some undergoing
degeneration.
7th day Bright yellow to yellow-green Beginning of resorption of
necrosed fibers by
macrophages , onset of fibro
vascular response, neutrophils
gradually disappear.
Second week
10th day Red-purple periphery Most of the necrosed muscle
in a small infarct removed ;
fibrovascular reaction more
prominent; pigmented
macrophages, eosinophils,
lymphocytes, plasma cells
present
14th day ---- Necrosed cells mostly
removed; neutrophils
disappear, fibrocolagenic
tissue at the periphery
Third week ---- Necrosed muscle fibes from
larger infracts removed , more
in growth of fibrocollagenic
tissue
Fourth to sixth Thin ,gray-white, hard, shrunken Increased fibrocollagenic
week fibrous scar tissue, decreased vascularity,
fever pigmented macrophages,
lymphocytes and plasma cells

COMPLICATIONS
 Arrhythmias
 Congestive heart failure
 Cardiogenic shock
 Mural thrombosis and thombembolism
 Rupture
 Cardiac aneurysm
 Pericaditis
 Post-myocardial infarction syndrome

ANGINA PECTORIS

(Greek ankhon ("strangling") Latin pectus ("chest") = "a strangling feeling in the chest".)

Angina pectoris is severe chest pain due to ischemia of the heart muscle, generally due to
obstruction or spasm of the coronary arteries (the heart's blood vessels).

Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac
arteries It is not common to equate severity of angina with risk of fatal cardiac events.
There is a weak relationship between severity of pain and degree of oxygen deprivation
in the heart muscle (i.e. there can be severe pain with little or no risk of a heart attack,
and a heart attack can occur without pain).

TYPES:-

a).STABLE ANGINA

This refers to the more common understanding of angina related to myocardial ischemia.
Typical presentations of stable angina is that of chest discomfort and associated
symptoms precipitated by some activity (running, walking, etc) with minimal or non-
existent symptoms at rest. Symptoms typically abate several minutes following cessation
of precipitating activities and resume when activity resumes. In this way, stable angina
may be thought of as being similar to claudication symptoms.
b).UNSTABLE ANGINA (“CRESCENDO”)

Unstable angina (UA) is defined as angina pectoris that changes or worsens. [1]

It has at least one of these three features:

1. it occurs at rest (or with minimal exertion), usually lasting >10 min;
2. it is severe and of new onset (i.e., within the prior 4-6 weeks); and/or
3. it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or
frequent than previously).

UA may occur unpredictably at rest which may be a serious indicator of an impending


heart attack. What differentiates stable angina from unstable angina (other than
symptoms) is the pathophysiology of the atherosclerosis. In stable angina, the developing
atheroma is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture in
unstable angina, allowing blood clots to precipitate and further decrease the lumen of the
coronary vessel. This explains why an unstable angina appears to be independent of
activity.

c).PRINZMETAL’S ANGINA

A variant form of angina (Prinzmetal's angina) occurs in patients with normal coronary
arteries or insignificant atherosclerosis. It is thought to be caused by spasms of the artery.
It occurs more in younger women.

ETIOPATHOGENISIS:

1. a reduction of blood flow to the heart that can be caused by stenosis, spasm, or
acute occlusion (by an embolus) of the heart's arteries
2. resistance of the blood vessels
3. reduced oxygen-carrying capacity of the blood.

Myocardial fibrosis respesents healing of minute infarcts involving small scattered


groups of myocardial fibers

PATHOLOGIC CHANGES

GROSSLY MICROSCOPICALLY
Normal or hypertrophy of heart, gray white Scattered areas of diffuse myocardial
fibrosis of brown myocardium (left fibrosis, especially around small blood
ventricle), previous scars of MI may be vessels in interstitial tissue of myocardium.
present, valves may be calcified distorted
or calcified, moderate to severe Variation in fiber size and foci of
atherosclerosis (coronary artery) myocytolysis

Areas of brown atrophy myocardium may


present

Coronary arteries show atherosclerotic


plagues and may have complicated lesions
in the form of superimposed thrombosis

CLINICAlL MANIFESTATION

Most patients with angina complain of chest discomfort rather than actual pain: the
discomfort is usually described as a pressure, heaviness, tightness, squeezing, burning, or
choking sensation. Apart from chest discomfort, anginal pains may also be experienced in
the epigastrium (upper central abdomen), back, neck, jaw, or shoulders, following skin
dermatomes. Typical locations for radiation of pain are arms (often inner left arm),
shoulders, and neck into the jaw. Angina is typically precipitated by exertion or emotional
stress. It is exacerbated by having a full stomach and by cold temperatures. Pain may be
accompanied by breathlessness, sweating and nausea in some cases. It usually lasts for
about 3 to 5 minutes, and is relieved by rest or specific anti-angina medication. Chest
pain lasting only a few seconds is normally not angina.

Myocardial ischemia comes about when the myocardia (the heart muscles) receive
insufficient blood and oxygen to function normally either because of increased oxygen
demand by the myocardia or by decreased supply to the myocardia. This inadequate
perfusion of blood and the resulting reduced delivery of oxygen and nutrients is directly
correlated to blocked or narrowed blood vessels.

Some experience "autonomic symptoms" (related to increased activity of the autonomic


nervous system) such as nausea, vomiting and pallor.

SUDDEN CARDIAC DEATH


Sudden cardiac death is defined as sudden death with in 24 hr of onset of cardiac
symptoms.
Causes:
 IHD
 Coronary vasospasm
 Calcific aortic stenosis
 Myocarditis
 Hypetrophic cadiomyopathy
 Mitral valve prolapse
 Endocarditis
 Heriditory and acquired defects of the conduction system

The mechanisam of sudden death by myocardial ischemia is always by fatel arrhythmias,


chiefly ventricular asystole or fibrilation.