Stable angina is a clinical syndrome characterized by recurrent episodes of chest pain or discomfort, typically triggered by physical exertion or emotional stress and relieved by rest or administration of nitrates. It is caused by transient myocardial ischemia due to an imbalance between myocardial oxygen demand and supply, mainly determined by fixed atherosclerotic stenoses of the coronary arteries.
The underlying mechanism is a progressive reduction in the caliber of the coronary arteries due to the formation of atherosclerotic plaques, which limit blood flow in conditions of increased myocardial demand. In addition, endothelial dysfunction and increased vascular tone may contribute to reduced myocardial perfusion, worsening the ischemic picture.
Epidemiology and Risk Factors
Stable angina is one of the most common manifestations of chronic ischemic heart disease.
Its prevalence increases with age and with the presence of cardiovascular risk factors such as arterial hypertension, dyslipidemia, diabetes mellitus, cigarette smoking and sedentary lifestyle.
Hypertension promotes the progression of atherosclerosis and increases left ventricular afterload, while dyslipidemia accelerates the formation of atherosclerotic plaques through LDL accumulation and reduction of HDL.
Diabetes mellitus contributes to endothelial dysfunction and microvascular changes, while cigarette smoking amplifies thrombotic risk and promotes a chronic inflammatory state.
Obesity and physical inactivity are also significant risk factors, as they favor the development of metabolic syndrome and insulin resistance.
Classification of Angina according to the Canadian Cardiovascular Society (CCS)
Class I: Angina only with intense and prolonged exertion.
Class II: Angina with moderate activity, such as walking uphill or for long distances.
Class III: Angina with mild activity, such as walking short distances on flat ground.
Class IV: Angina at rest or with minimal effort.
Diagnosis and Diagnostic Workup
Diagnosis is based on history, physical examination, and instrumental tests to confirm the presence of myocardial ischemia.
History is essential to characterize chest pain. In stable angina, the patient reports a retrosternal oppressive or constrictive pain, possibly radiating to the left arm, neck, or jaw. Pain predictably occurs with exertion or emotional stress and resolves within a few minutes with rest or the use of nitrates.
The physical examination is usually normal, but in some cases a fourth heart sound (S4) can be detected, a sign of impaired left ventricular compliance.
Diagnostic confirmation relies on instrumental tests.
The resting ECG may be normal or show T wave changes and ST-segment depression. A stress test is positive in the presence of ≥1 mm ST-segment depression.
The 24-hour Holter ECG may be useful in patients with atypical symptoms, identifying episodes of silent ischemia or ischemic arrhythmias.
Stress echocardiography assesses myocardial contractility during physical or pharmacological stress, detecting areas of hypokinesia, akinesia or dyskinesia suggestive of inducible ischemia. Myocardial scintigraphy distinguishes reversible perfusion defects (ischemia) from fixed defects (prior infarction), while coronary angiography is the gold standard for the evaluation of coronary artery disease.
Stress cardiac MRI uses vasodilator drugs (adenosine, regadenoson, dipyridamole) or inotropes (dobutamine) to simulate physiological stress, allowing identification of myocardial perfusion defects, assessment of ventricular function, and detection of areas of fibrosis using the Late Gadolinium Enhancement (LGE) technique.
Treatment of Stable Angina
Treatment aims to reduce symptoms and prevent cardiovascular events.
Lifestyle modifications play a crucial role in disease management. Smoking cessation significantly reduces the risk of ischemic events, while regular physical activity improves cardiovascular capacity and metabolic control. A balanced diet, based on the Mediterranean model, helps lower cholesterol and maintain an adequate body weight.
Pharmacological therapy includes beta-blockers and calcium channel blockers to reduce myocardial oxygen consumption, antiplatelet agents to prevent thrombotic events, statins to control atherosclerosis, and ACE inhibitors or ARBs in patients with hypertension or left ventricular dysfunction.
Myocardial revascularization can be performed by percutaneous coronary intervention (PCI) in patients with critical stenoses or by coronary artery bypass grafting (CABG) in cases of multivessel disease.
Prognosis and Complications
If properly treated, stable angina has a favorable prognosis. However, if not adequately managed, it may evolve into acute coronary syndrome, ventricular arrhythmias or ischemic heart failure.
References
Fihn SD, et al. 2012 ACCF/AHA guideline for stable ischemic heart disease. J Am Coll Cardiol. 2012;60(24):2564-603.
Montalescot G, et al. 2013 ESC guidelines on stable coronary artery disease. Eur Heart J. 2013;34(38):2949-3003.
Task Force Members. 2019 ESC guidelines for chronic coronary syndromes. Eur Heart J. 2020;41(3):407-477.
Patel MR, et al. Appropriate use criteria for diagnostic coronary angiography. J Am Coll Cardiol. 2012;59(22):1995-2027.
Fox K, et al. Management of stable angina. BMJ. 2011;342:d3317.
Jneid H, et al. Contemporary medical therapy for chronic stable angina. Curr Atheroscler Rep. 2016;18(4):21.
Shah SJ, et al. Microvascular dysfunction and ischemic heart disease. J Am Coll Cardiol. 2020;75(20):2534-48.
O’Donoghue ML, et al. Antiplatelet therapy in stable coronary artery disease. Circ Res. 2020;126(4):492-504.
Shah NR, et al. Advances in non-invasive imaging for stable angina. Heart. 2018;104(3):213-222.
Greenland P, et al. Coronary artery calcium score and risk classification in asymptomatic adults. JAMA. 2018;319(3):286-295.
