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 pre-infarction 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

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

* Morphologic changes of Myocardial Infarction:

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.