Download Cardiovascular System

Ischemic heart diseases
Dr. Gehan mohamed
Dr. Abdelaty shawky
Ischemic Heart Disease (IHD)
* Causes: Usually caused by decreased coronary
artery blood flow (“coronary artery disease”) as in:
1. Coronary artery atherosclerosis.
2. Vasospasm and vasculitis.
Ischemic Heart Disease
(Coronary Heart Disease)
* There are Four syndromes:
1. Angina pectoris (chest pain).
2. Myocardial infarction.
3. Chronic ischemic heart disease with
congestive heart failure.
4. Sudden cardiac death.
* Epidemiology of Ischemic Heart Disease:
 Peak incidence: 60y for males and 70y for females.
 Gender: Men are more affected than women.
 Risk factors: are that of atherosclerosis:
◦ Hypertension.
◦ Diabetes mellitus.
◦ Smoking.
◦ High levels of LDL.
◦ Genetic factors (direct or indirect).
◦ Lack of exercise.
* Pathogenesis Ischemic Heart Disease(IHD) :
• Four different factors play a role in the
pathogenesis of IHD which include :
1. Role of critical stenosis or obstruction:
(>75% of the lumen of one or more coronary
arteries by atherosclerotic plaque).
Natural history of atherosclerosis
2. Role of acute Plaque Changes:
a. Rupture of the plaque.
b. Ulceration of the plaque.
- These expose the thrombogenic subendothelial
basement membrane to blood followed by
thrombosis .
c. Hemorrhage into the plaque expanding its
volume and aggravating the stenosis.
3. Role of coronary thrombosis:
Thrombosis on partially stenotic plaque
converts it to a total occlusion. this can lead to
acute transmural myocardial infarction.
When the extent of luminal obstruction by
thrombosis is incomplete it usually leads to
unstable angina, acute subendocardial
infarction.
4. Role of vasoconstriction:
• Vasoconstriction reduces lumen size and can
therefore potentiate plaque disruption.
Ischemic Heart Disease: Pathogenesis
A. Plaque rupture without superimposed thrombus in a patient who
died suddenly.
B. Acute coronary thrombosis superimposed on an atherosclerotic
plaque with focal disruption of the fibrous cap, triggering fatal
myocardial infarction.
C. Massive plaque rupture with superimposed thrombus, also
triggering a fatal myocardial infarction (special stain highlighting
fibrin in red). In both
Angina pectoris
* Definition:
paroxysmal and usually recurrent attacks of substernal
chest discomfort (variously described as constricting,
crushing, squeezing, choking, or knifelike). May radiate
down the left arm or to the left jaw (referred pain) .
* Cause:
Transient inadequate myocardial perfusion (lasting for
15 seconds to 15 minutes)i.e. duration and severity is
not sufficient for infarction.
There are three overlapping patterns of
angina pectoris:
1. Stable or typical angina.
2. Unstable or crescendo angina.
3. Prinzmetal or variant angina.
1. Stable/ typical angina pectoris
* Definition: Episodic chest pain associated with
exertion or some other forms of stress. Usually
relieved by rest or sublingual nitroglycerin (a strong
vasodilator).

The most common form of angina, caused by
atherosclerotic disease.
2. Unstable or crescendo angina
 Definition: Pain occurs with progressively increasing
frequency, is precipitated by less exertion, even at
rest, and tends to be of more prolonged duration.
 Cause: disruption or rupture of an atherosclerotic
plaque with superimposed partial thrombosis.
 Unstable angina is often the precursor of
subsequent acute MI. Thus this referred to as preinfarction angina.
3. Prinzmetal variant angina
* Definition: uncommon pattern that occurs at
rest and is due to coronary artery spasm and not
related to atherosclerotic disease.
Myocardial Infarction
* Definition: coagulative necrosis of the
myocardium due to acute coronary ischaemia.
* Causes: The most common cause is thrombosis
on a preexisting disrupted atherosclerotic plaque
e.g. hemorrhage, ulceration and rupture…
* Sites of MI:
I. Left ventricle (the commonest):
• a. Anterior infarct (anterior wall of the Lt .ventricle + apex
+ anterior part of IV septum): due to occlusion of the
anterior descending branch of the left coronary artery.
• b. Lateral infarct (lateral wall of the Lt. ventricle): due to
occlusion of circumflex branch of the left coronary.
• c. Posterior infarct (posterior wall of the Lt. ventricle): due
to occlusion of a branch of the Rt. coronary artery that
supplies that part of the left ventricle.
II. Right ventricle (rare): due to occlusion of the right
coronary artery.
Pathogenesis of MI
* Types of MI:
• Transmural
– Full thickness.
• Subendocardial
– Inner 1/3 of myocardium
* Morphologic changes of Myocardial
Infarction:
Time
Gross changes
Microscopic changes
0-4h
None
None
4-12h
Pale and firm
Coagulation necrosis
12-24h Pale and soft
More coagulation necrosis;
neutrophils come in
1-7 d
Yellow infarct center
Neutrophils die, macrophages
come to eat dead cells
1-2 w
Yellow center, red borders
Granulation tissue
2-8 w
Scar
Collagen
Acute Myocardial Infarction
MI: day 1,
day 3,
day 7
* Clinical Features of MI:
1. Pain:
◦ Severe crushing substernal chest pain, which may radiate to the
neck, jaw, epigastrum, shoulder or left arm.
◦ Pain lasts for hours to days and is not relieved by nitroglycerin.
◦ Absent in 20-30% of patients (diabetics, hypertensive, elderly).
2. Pulse is rapid and weak.
3. Dyspnea.
4. Cardiogenic shock in massive MI(>40%of lt. ventricle).
5. ECG shows typical findings of ischemia.
* Laboratory evaluation of MI:
1. Troponins:
• The most specific test for MI.
• Become detectable within 2 to 4 hours, reach the peak at 48
hours. Their levels remain elevated for 7 to 10 days.
2. Creatine kinase (CK-MB):
- Is the second best marker, however, it increases in the blood
also when there skeletal muscle damage.
- It begins to rise within 2 to 4 hours of MI, peaks at 48 hours
and returns to normal within approximately 72 hours.
3. Lactate dehydrogenase (LD1).
– Rise 24 hrs, peaks 72 hrs, persists 72 hrs.
– Non-specific because it aslo increases in cases of cancer,
encephalitis, meningitis…
* Complications of MI:
- Occurs in more than 90% of cases.
1. Cardiac arrhythmia:
- Sudden death can occur due to ventricular arrhythmia.
2. Left ventricular failure.
3. Cardiogenic shock.
4. Myocardial rupture and hemopericardium.
5. Thromboembolism: The combination of a local
myocardial abnormality in contractility (causing stasis)
with endocardial damage (causing a thrombogenic
surface) can foster mural thrombosis and, potentially,
thromboembolism .
6. Pericarditis
7. Ventricular aneurysm.
8. Chronic heart failure.
Thanks
References:
Robbins and Cotran’s: Pathologic Basis of Disease. Seventh edition.