• Angina pectoris (literally heart pain) is characterized by paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort caused by transient myocardial ischemia.
• The three overlapping patterns of angina pectoris : 1. Stable or typical angina 2. Prinzmetal variant angina 3. Unstable or crescendo angina

Stable angina :

• It is the most common form and is also called typical angina pectoris
• Cause : an imbalance in coronary perfusion (due to chronic stenosing coronary atherosclerosis) relative to myocardial demand, such as that produced by physical activity, emotional excitement or any other cause of increased workload.
• Typical angina pectoris is usually relieved by rest or administering nitroglycerin (a vasodilator that increases perfusion)
• Pharmacology – nitroglycerin is the drug of choice, administered sublingually with an initial dose of 0.5 mg, which usually relieves pain in 2-3 minutes.

Prinzmetal variant angina :

• It is an uncommon form of episodic myocardial ischemia
• Cause : coronary artery spasm
• It is unrelated to physical activity, heart rate or blood pressure
• Pharmacology – episodes of coronary vasospasm are treated with nitrates; for prophylaxis, nitrates and calcium channel blockers (Amlodipine, nifedipine and diltiazem) are effective.

Unstable or Crescendo angina :

• It refers to a pattern of increasingly frequent pain of prolonged duratio, that is precipitated by progressively lower levels of physical activity or that even occurs at rest
• Cause : mostly by disruption of an atherosclerotic plaque with superimposed partial thrombosis and possibly embolization or vasospasm (or both)
• Unstable angina thus serves as a warning that an acute MI may be imminent; indeed, this syndrome is sometimes referred to as preinfarction angina.
• Pharmacology – it requires treatment with multiple drugs – antiplatelet drugs, anticoagulants, nitrates, beta blockers, CCBs and statins

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Source : Robbins and Cotran’s book of pathology

CHAMBERS :

1. Increased left atrial cavity size (2-4 cm generally)
2. Decreased left ventricular cavity size (42-59 mm in men and 39-53 in women normally)
3. Sigmoid shaped ventricular septum

VEINS :

1. Aortic valve calcific deposits
2. Mitral valve annular calcific deposits
3. Fibrous thickening of leaflets
4. Buckling of mitral leaflets towards the left atrium
5. Lambl excrescenses (filiform fronds that occur at sites of valvular closure. They originate as small thrombi on endoardial suraces where the valve margins make contact)

EPICARDIAL CORONARY ARTERIES :

1. Tortuosity

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2. Increased cross sectional luminal area

3. Calcific deposits

4. Atherosclerotic plaque

MYOCARDIUM :

1. Increased mass
2. Increased subepicardial fat
3. Brown atrophy (atrophy of the heart muscle described as brown as fibers become pigmented by intracellular deposits of lipofuscin, a type of lipochrome granule)
4. Basophilic degeneration (an accumulation within cardiac myocytes of a gray-blue byproduct of glycogen metabolism)
5. Amyloid deposits

AORTA :

1. Dilated ascending aorta with rightward shift
2. Atherosclerotic plaque
3. Elastic fragmentation and collagen accumulation
4. Elongated (tortuous) thoracic aorta

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Source : Robbins and Cotran’s book of pathology

Reference : Harsh Mohan textbook of pathology

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Reference : Sparsh gupta textbook of pathology

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