angina pectoris
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Angina Pectoris
Definition
Angina pectoris is intermittent chest discomfort or pain caused by transient, reversible myocardial ischemia that is insufficient to cause myocyte necrosis. It results from the ischemia-induced release of adenosine, bradykinin, and other molecules that stimulate autonomic afferent nerves. — Robbins & Kumar Basic Pathology
Epidemiology
Nearly 10 million Americans have angina pectoris. Males constitute ~70% of all patients, and an even greater proportion of those aged <50 years. Among adults aged 60–79, ~25% of men and 16% of women have coronary heart disease. Angina is the most frequent clinical expression of myocardial ischemia. — Harrison's Principles of Internal Medicine 22E; Goldman-Cecil Medicine
Pathophysiology
Ischemia rapidly develops when a mismatch arises between myocardial oxygen demand and myocardial oxygen supply. The most common underlying cause is obstructive coronary atherosclerosis. Alternative mechanisms include:
- Microvascular dysfunction (angina with no obstructive CAD)
- Vasoconstriction at the site of a dynamic stenosis
- Mural thrombosis
- Noncardiac conditions that increase demand or reduce supply (severe anemia, aortic stenosis, hypertrophic cardiomyopathy)
— Goldman-Cecil Medicine
Types
1. Stable (Typical) Angina
Predictable, episodic chest discomfort associated with exertion or increased demand (tachycardia). The discomfort is described as a crushing or squeezing substernal sensation, radiating down the left arm or to the jaw. Relieved by rest or nitroglycerin within minutes. — Robbins
2. Prinzmetal (Variant) Angina
Occurs at rest, caused by coronary artery spasm. Can affect atherosclerotic or even otherwise healthy vessels. Responds promptly to vasodilators (nitroglycerin, calcium channel blockers). — Robbins
3. Unstable Angina
Increasingly frequent pain precipitated by progressively less exertion or occurring at rest. Associated with plaque disruption, superimposed thrombosis, distal embolization, and/or vasospasm. Majority of cases show evidence of myocyte injury — treated aggressively to limit irreversible damage. — Robbins
Clinical Presentation (History)
The typical patient is a man >50 years or a woman >60 years. Key features:
- Quality: Heaviness, pressure, squeezing, smothering, or choking — rarely described as frank "pain"
- Location: Central, substernal; patient often places a clenched fist over the sternum (Levine's sign)
- Radiation: Shoulders, both arms (especially ulnar aspects), back, interscapular region, neck, jaw, teeth, epigastrium
- Duration: Typically 2–5 minutes, crescendo-decrescendo pattern
- Precipitants: Exertion, emotional stress, cold exposure, heavy meals, sexual activity
- Relief: Rest, nitroglycerin
- Angina decubitus: Can occur at rest or when recumbent — may reflect nocturnal tachycardia or increased intrathoracic blood volume during sleep
Myocardial ischemic discomfort does NOT radiate to the trapezius muscles — that pattern is more typical of pericarditis. Angina is rarely localized below the umbilicus or above the mandible.
— Harrison's Principles of Internal Medicine 22E
Grading — Canadian Cardiovascular Society (CCS) Scale
| Class | Description |
|---|---|
| I | Angina only with strenuous or prolonged exertion |
| II | Slight limitation of ordinary activity |
| III | Marked limitation of ordinary activity |
| IV | Inability to perform any activity without angina, or angina at rest |
Classes I–II = stable; Classes III–IV = severe/unstable. — Goldman-Cecil Medicine
Investigations
- Resting ECG: May show ST-segment depression, T-wave changes, or evidence of prior MI
- Stress testing (exercise ECG, nuclear imaging, stress echo): To provoke and detect ischemia
- Coronary CT angiography / coronary artery calcium (CAC) score: Adjunctive evidence of atherosclerosis
- Lab work: CBC, fasting lipid profile, fasting glucose/HbA1c, thyroid function, renal function
- Coronary angiography: Gold standard for defining anatomy; guides revascularization decisions
- Echocardiography: Assesses LV function and wall motion
Management
General Approach
- Explain the condition and reassure the patient
- Identify and treat aggravating conditions (anemia, hypertension, hyperthyroidism, obesity, aortic stenosis)
- Adapt activity — reduce speed/intensity, understand diurnal variation in ischemic threshold
- Address cardiovascular risk factors (smoking, dyslipidemia, diabetes, hypertension)
- Drug therapy
- Consider revascularization (PCI or CABG)
Pharmacotherapy
| Drug Class | Examples | Mechanism | Role |
|---|---|---|---|
| Nitrates | Nitroglycerin, isosorbide dinitrate/mononitrate | Release NO → ↑cGMP → vasodilation; ↓venous return, ↓cardiac work | SL NTG for acute episodes; oral/transdermal for prophylaxis |
| Beta-blockers | Propranolol, metoprolol, atenolol | Block β-adrenoceptors → ↓HR, ↓CO, ↓BP → ↓O₂ demand | First-line prophylaxis |
| Calcium channel blockers | Verapamil, diltiazem (non-DHP); nifedipine, amlodipine (DHP) | Block L-type Ca²⁺ channels → ↓vascular resistance and/or ↓cardiac work | Variant angina (especially); stable angina when beta-blockers are contraindicated |
| Antiplatelet | Aspirin, clopidogrel | Inhibit platelet aggregation | Reduce thrombotic events |
| Statins | Atorvastatin, rosuvastatin | ↓LDL cholesterol, plaque stabilization | Reduce CV events, mandatory in IHD |
| Ranolazine | Ranolazine | Inhibits late sodium current → ↓intracellular Ca²⁺ overload | Refractory angina, adjunctive therapy |
Key interaction: Nitrates + phosphodiesterase type-5 inhibitors (sildenafil, tadalafil) → synergistic severe hypotension — combination is contraindicated. — Katzung's Basic and Clinical Pharmacology 16E
Revascularization
- Percutaneous coronary intervention (PCI): For focal lesions, especially in single- or two-vessel disease
- Coronary artery bypass grafting (CABG): Preferred in left main disease, three-vessel disease, or with LV dysfunction
Prognosis
Prognosis is influenced by:
- Severity of LV dysfunction (ejection fraction)
- Number of coronary vessels with significant obstruction
- Extent of viable but jeopardized myocardium
- Presence of risk factors (age >75, hypertension, diabetes, dyslipidemia, obesity, peripheral vascular disease, prior MI)
- Elevated CRP, extensive coronary calcification on CT, carotid intimal thickening — all indicate higher risk
— Harrison's Principles of Internal Medicine 22E
Sources: Robbins & Kumar Basic Pathology | Harrison's Principles of Internal Medicine 22E | Goldman-Cecil Medicine | Katzung's Basic and Clinical Pharmacology 16E
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