Angina
Angina, syncope and heart failure are the classic triad of symptomatic aortic stenosis, with a slow-rising pulse, narrow pulse pressure and a murmur radiating to the carotids.
What our notes say
- Angina, syncope and heart failure are the classic triad of symptomatic aortic stenosis, with a slow-rising pulse, narrow pulse pressure and a murmur radiating to the carotids. (Cardiology Question Bank: 15 Clinical MCQs)
- Usually, the first symptom is sudden dyspnea, which may be accompanied by angina or unilateral pleuritic chest pain. (Examination of Respiratory system — Past Paper Questions & Answers)
- Angina: they reduce myocardial oxygen demand (lower heart rate, contractility and afterload) and lengthen diastolic filling, so they prevent ischaemia and relieve symptoms. (Clinical Pharmacology I (MBPL 4400) main exam: 25 January 2023)
- A 70-year-old woman has syncope on exertion, angina and breathlessness. (Cardiology Question Bank: 15 Clinical MCQs)
- | Beta-blocker | Bisoprolol | Not first line alone; used for angina, heart failure, arrhythmia; avoid in asthma | (Hypertension)
- Symptoms: tiredness, breathlessness, palpitations, headache, pallor, and angina or heart failure when severe. (Approach to anaemia)
Study material on Angina
- Cardiovascular system examination revised 2012
- Heart Disease: Must Knows
- Heart Disease — Must Knows
- CARDIOVASCULAR PATHOLOGY
- CVS History & Physical Exam: Symptoms, Chest Pain & Syncope
- CVS History, Physical Exam & ECG: Master Clinical Assessment
- 🫀 VALVULAR HEART DISEASE — ULTRA DEEP NOTES
- Heart Disease: Must Knows
- Heart Disease: Must Knows
- Cardiovascular Pathology MCQs: Rheumatic Fever, AAA, HTN, HFpEF
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Practice questions on Angina
Which plaque change is MOST directly responsible for converting stable angina to an acute coronary syndrome?
- Progressive accumulation of lipid in the plaque core
- Plaque rupture or erosion with superimposed thrombosis
- Calcification reducing plaque elasticity
- Smooth muscle cell proliferation narrowing the lumen
- Neovascularization within the plaque
Answer: B. - ACS results from **acute plaque disruption** (rupture/erosion) exposing thrombogenic core material → **superimposed thrombus** → sudden flow-limiting or occlusive event ---
70-year-old, exertional syncope/angina/dyspnea (classic triad), harsh systolic ejection murmur, calcified aortic valve, mean gradient 52 mmHg. Most likely underlying pathology?
- Rheumatic aortic stenosis with commissural fusion
- Congenitally bicuspid aortic valve with early calcification
- Calcific (senile/degenerative) aortic stenosis of a trileaflet valve
- Infective endocarditis with valve destruction
- Syphilitic aortitis with valve ring dilation
Answer: C. - In an elderly patient, the classic mechanism is **age-related "wear-and-tear" calcific degeneration** of a normal trileaflet valve - Bicuspid valve calcification (B) presents earlier, typically 50s–60s rather than 70s+ ---
Which clinical feature would differentiate a heart attack from stable angina?
- Pain relieved by rest
- Sudden, intense crushing chest pain with associated symptoms
- Pain only with exertion
- Mild discomfort lasting seconds
Answer: B. ** Heart attack presents with sudden, intense crushing or squeezing chest pain, often accompanied by sweating, nausea, and shortness of breath, unlike stable angina which is typically relieved by rest. ---
Which of the following pathological changes in a coronary artery plaque is MOST directly responsible for converting stable angina to an acute coronary syndrome?
- Progressive accumulation of lipid in the plaque core
- Plaque rupture or erosion with superimposed thrombosis
- Calcification reducing plaque elasticity
- Smooth muscle cell proliferation narrowing the lumen
- Neovascularization within the plaque
Answer: B. Plaque rupture or erosion with subsequent superimposed thrombosis is the critical event that converts stable angina into an acute coronary syndrome.