1. ISCHEMIC HEART DZ
Definition disease characterized by ischaemia (reduced blood supply) of the heart
muscle, usually due to coronary artery disease (atherosclerosis of the
coronary arteries
- Result from an imbalance b/w supply and demand of the heart for
oxygenated blood
- Inadequate coronary blood flow
Result in reduced nutrient supply
Aetiology o High blood cholestrol
o High blood pressure
o Smoking
o Obesity
o Diabetes
o Lack of physical activity
Clinical
manifestation
- Myocardial infarct
- Angina pectoris
- Chronic congestive heart failure
- Sudden cardiac death
1) Angina pectoris - chest pain due to ischemia of the heart muscle,
generally due to obstruction or spasm of the coronary arteries
#main cause of Angina pectoris is Coronary Artery Disease, due to atherosclerosis
stable angina = paroxysm of pain tht related toexertion and
relieved by rest or vasodilators
= the developing atheroma is protected with
a fibrous cap
variant@prinzmetal’s
angina
= pain at rest that occurs in cycles.
= It is caused by vasospasm, a narrowing of
the coronary arteries caused by contraction
of the smooth muscle tissue rather than
directly by atherosclerosis
unstable angina = prolonged pain—irregular pain occur
unpredictably at rest --
*pathophysiology is the reduction of coronary flow due to transient
platelet aggregation on apparently normal endothelium, coronary artery
spasms or coronary thrombosis
#process starts with atherosclerosis, and when inflamed leads to an active
plaque, which undergoes thrombosis and results in acute ischemia, which
finally results in cell necrosis after calcium entry
# cap (atherosclerotic plaque) may rupture, allowing blood clots to
precipitate and further decrease the lumen of the coronary vessel.
2) Sudden cardiac death
– within an hour after cardiac event @ w/o the onset of
symptom
3) Myocardial infarct - DISCRETE FOCUS OF ISCHEMIC
NECROSIS OF MUSCLE OF HEART
(PATHOGENESIS IN MI NOTES ^^)
-Types of MI .
classified according to :
a) SIZE AND EXTENT OF INFARCTION
b) ANATOMIC LOCATION OF THE INFARCT
a) SIZE N EXTENT OF INFARCTION
SUBENDOCARDIAL
INFARCT
TRANSMURAL INFARCT
o Affect 1/3rd to ½ of
LEFT VENTRICLE
o Involves the innermost
layer and, in some
cases, parts of the
middle layer of the
myocardium but does
not extend to the
epicardium.
o This infarct due to ATH
o Others dz that can lead
to limitation of blood
flow : AORTIC
STENOSIS | H’AGIC
SHOCK
o *does NOT involve
OCCLUSIVE CORONARY
THROMBI
o Affect FULL LEFT
VENTRICULAR WALL
THICKNESS
o Involve OCCLUSION OF
CORONARY ARTERY
o Distribution of ONE OF THREE
MAJOR CORONARY ARTERIES:
o A) RT. CORONARY ARTERY
-Occlusion of proximal portion of
vessel
-Infarct of posterior basal region of
left ventricle and posterior 1/3rd to ½
of interventricular septum
o B)LEFT ANTERIOR
DESCENDING CORONARY
ARTERY
-Occlusion of artery produces infarct
of apical, anterior, and anteroseptal
wall of left ventricle
o C)LEFT CIRCUMFLEX
CORONARY ARTERY
-Occlusion of artery produces infarct
of lateral wall of left ventricle

2. B) ANATOMIC LOCATION OF THE INFARCT
- POSTEROLATERAL INFARCT – occlusion of left circumflex artery
- ANTERIOR INFARCT – occlusion of anterior descending of left coronary artery
- POSTERIOR INFARCT – occlusion of right coronary artery
- GROSS N MICROSCOPY
Time after onset Gross Microscopy
24-48hrs Pale, edematous muscle Edema , PMN, necrosis
3-4dys Yellow rubbery centre w h’agic
border
Obvious necrosis,
inflammation, early
granulation t/s
1-3wks Central pale infarcted Granulation t/s, collagen
fibrosis
3-6wks Silvery scar, tough n white Dense fibrosis
- RISK FACTOR
- LDL increase (plasma protein that carry cholestrol and trygliceride
- Smoking
- Hypertension
- Increased plasma fibrinogen
- Increased plasminogen activator inhibitor
- Increased CRP
- DM
- Obesity
- Male>Female 4:1
- Lack of exercise
- Oral contraceptives
- LAB DIAGNOSIS OF MI
- Depends on the hours following onset of symptom
- Its indicate markers for acute myocardial infarction
a) Creatine Kinase- has 3 isoenzymes : CK MM, CK MB, CK BB
*CK MM – present in both cardiac and skeletal muscle
*CK MB – Very good marker for AMI. Its rises in serum within 2-8 hrs of
onset of AMI
*CK BB – found in brain, bowel, and bladder
b) Troponin – remain elevated longer than CK for TROPONIN I(up to 5-
9dys) TROPONIN T (up to 2 weeks).
- Good for the recent past MI better than lactate dehydrogenase
c) Myoglobin – not specific for cardiac muscle
d) Lactate dehydrogenase – begins to rise in 12-24 hrs following MI
- Peaks in 2-3 dys
- COMPLICATION OF MI
- Arrythmia
- Extension of infarction
- Congestive heart failure
- Pericarditis
- Papillary muscle ruptured with possible valvular insufficiency
- Ventricular aneurysm
- Myocardial wall ruptured with possible tamponade
HYPERTENSIVE HEART DZ
Definition Refers to HEART PROBLEM due to HIGH BLOOD PRESSURE
-HEART PROBLEM such as Coronary Artery Disease due to ATH
Causes Main causes * high level of Blood pressure – pressure inside blood vessel
is high so when heart pump against this pressure must work harder, cause
the heart muscle to be thicken
Classification
based on
Aetiology
Hypertension
Primary / essential Secondary
Causes :
- Idiopathic
- Genetic susceptibility
- Excessive sympathetic
nervous activity
- High salt intake
- Abnormality of Na/K
membrane transport
Abnormality in RAAS
Causes :
- Renal disease (AGN/CRF)
- Endocrine tumor
(Pheomochromocytoma)
- Cushing syndrome
- Coarctation
aorta(narrowing of aorta)
- Drugs :steroid, oral
contraceptives
Classification
based on
anatomical
position
i) Systemic hypertension :
a) Pressure in aorta increased
b) So left ventricular need to pump harder
c) So left ventricular hypertrophy
ii) Pulmonary hypertension :
a) Long term of elevated BP in pumonary artery n Rt.
Ventricle
Cause Cor-Pulmonale
Pathogenesis of
hypertension
Blood pressure = CO x Peripheral Resistance
HTN is caused by increased COor Peripheral Resistance
- INCREASED CO due to
: increased preload (increased ECF due to salt retention)
: increase heart contractility / increased heart rate due to sympathetic activity
- INCREASED PERIPHERAL RESISTANCE – due to arteriolar
vasoconstriction /remodelling
For primary HT such as Obesity:

3. Obesity
When Increased BP lead to change in heart Structure n Function
Change in structure Changes in function
o LV hypertrophy : patterns
(CRESCENTRIC)—
compensatory response to
increased afterload
o Left Atrial abnormality:
increased LA size n thickness
due to increased afterload
*absence of valvular heart dz
n systolic dysfx *predispose
to atrial fibrillation
i) Diastolic dysfx
ii) Systolic dysfx
iii) decompensated
Benign (essential) hypertension
: Mild – diastolic BP b/w 95-104 mmHg
: Moderate – 105-114mmHg
: Severe – above 115mmHg
Malignant Hypertension
: raised BP :130-140mmHg
Progressive renal failure
Gross n
microscopic
Gross : LV hypertrophy (crescentric)
a) compensated stage
- hypertrophy w/o dilatation
- symmetrical thickening if LV >2 cm wall
- increase weight of heart disproportionately to increase in
size >500gm
b) decompensated stage ( LV fails to compensated by
increased CO and LV begin to dilate to maintain CO)
- LV dilatation
- Wall thinning
- Enlargement of external dimension
Microscopic : Benign : thickening of smooth muscle layers of small
blood vessel
(Hyaline arteriolosclerosis) seen in renal arteriole
: Malignant : Thickening of wall of small blood vessel with features
of Onion Skinning due to Hyperplasia of smooth muscle cells
(Hyperplastic arteiolosclerosis)
Complication i) Benign
: spontaneous intracerebral h’age
: dissecting aneurysm
: subarachnoid h’age due tu ruptured berry aneurysm
: hypertensive heart failure (LVF)
ii) Malignant
: LVH n LVF
: Retinal H’age (blurred vision)
: Haematuria n renal Failure due to fibrinoid necrosis of glomeruli
: severe headache n cerebral h’age