Cardiac Path Online

Pathology of Angina Pectoris 

Dr Sampurna Roy MD





Angina pectoris is the name for a clinical syndrome rather than a disease.

It is characterized by paroxysmal substernal or precordial pain or discomfort resulting from ischemia without frank infarction.

Assessment of Ischaemic Myocardial Damage

Clinical presentation:  

The typical patient with angina is a 50 to 60 year old man who seeks medical help for troublesome chest discomfort, usually described as heaviness, pressure, squeezing, smothering or choking and only rarely frank pain.

This symptom  usually lasts from 15 seconds to  15 minutes.

There are three distinct patterns of angina clinically based on provocation and severity of pain:

1. Stable (typical) ; 2. Prinzmetalís variety : 3. Unstable (crescendo) 

Cause of angina pectoris : 

Coronary atheroma is the commonest cause.

Factors which increase myocardial oxygen requirement include any which add to the ventricular preload such as exercise, anaemia or hyperthyroidism and those which increase afterload such as hypertension, aortic stenosis or   cardiomyopathy .

Increased tension of the ventricular wall  as occurs in dilatation or hypertrophy may also reduce coronary flow.

Tachycardia increases cardiac work and often brings on pain. 

Other factors causing angina include fixed stenosing plaques, disrupted plaques, vasospasm, thrombosis, platelet aggregation and embolization.

1.Stable or typical angina : Most common form of angina. Ischemia is most intense in the poorly perfused subendocardial region of the left ventricular myocardium.

Pathogenesis:  Reduction of coronary perfusion to a critical level by chronic stenosing coronary atherosclerosis (greater than 75% stenoses in major coronary arteries).

Pain is relieved by rest (decrease demand) or by coronary dilator - nitroglycerine (increasing supply).

2. Prinzmetalís variant angina : Pattern of episodic angina that occurs at rest.

Pathogenesis: It is caused due to coronary artery spasm. Patients with this form of angina may have coronary atherosclerosis, but the attacks are usually unrelated to physical activity, heart rate or blood pressure.

Patients respond  prompty to vasodilator-nitroglycerine and calcium channel blockers.

3. Unstable or crescendo angina :  Pattern is characterized by an increased frequency of anginal pain.

It is precipitated with progressively less effort, often occurs at rest and tends to be of prolonged duration ;

Pathogenesis: It is induced by fissuring, ulceration, or rupture of an atherosclerotic plaque with superimposed partial (mural) thrombosis and possibly embolization or vasospasm (or both).

This pattern forewarns of the possibility of subsequent Acute Myocardial Infarction  and is also referred to as preinfarction angina or acute coronary insufficiency.

Further reading:

Monocyte subsets and monocyte-platelet aggregates in patients with unstableangina.

Chronic stable angina is associated with lower health-related quality of life: evidence from chinese patients.

Stable angina pectoris.

Comparison of Outcomes After Percutaneous Coronary Intervention Among Different Coronary Subsets (Stable and Unstable Angina Pectoris and ST-Segment and Non-ST-Segment Myocardial Infarction).

Young adulthood obesity and risk of acute coronary syndromes, stable angina pectoris, and congestive heart failure: a 36-year cohort study.

Diagnostic potential of plasmatic MicroRNA signatures in stable and unstableangina.

Association of increased serum glycated albumin levels with low coronary collateralization in type 2 diabetic patients with stable angina and chronic total occlusion.

Relationship between the red cell distribution width and the one-year outcomes in Chinese patients with stable angina pectoris.

Combined effects of fibrinogen genetic variability on atherosclerosis in patients with or without stable angina pectoris: focus on the coagulation cascade and endothelial function.




Dr Sampurna Roy  MD

Consultant  Histopathologist (Kolkata - India)







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