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Angina/angina pectoris, types of angina pectoris, Sign& symptoms of angina, Diagnostic test for Angina, treatment of angina pectoris

Angina/Angina pectoris|Types of angina |Sign & symptoms of angina | diagnosis of angina|Treatment of Angina pectoris


Angina pectoris
Angina pectoris

Angina pectoris is also known as angina. Angina pectoris is a clinical syndrome of IHD
(ischemic heart diseases) resulting from transient myocardial ischaemia. It is characterised by paroxysmal pain in the substernal or precordial region of the chest which is aggravated by an increase in the demand of the heart and relieved by a decrease in the work of the heart. Often,the pain radiates to the left arm, neck, jaw or right arm. It is more common in men past 5th decade of life.

There are 3 overlapping clinical patterns of angina pectoris with some differences in their pathogenesis:
i) Stable or typical angina 
ii) Prinzmetal’s variant angina 
iii) Unstable or crescendo angina


This is the most common pattern. Stable or typical angina is characterised by attacks of pain following physical exertion or emotional excitement and is relieved by rest. 

The pathogenesis of condition lies in chronic stenosing coronary atherosclerosis that cannot perfuse the myocardium adequately when the workload on the heart increases. During the attacks, there is depression of ST segment in the ECG due to poor perfusion of the subendocardial region of the left ventricle but there is no elevation of enzymes in the blood as there is no irreversible myocardial injury.


This pattern of angina is characterised by pain at rest and has no relationship with physical activity.

 The exact pathogenesis of Prinzmetal’s angina is not known. It may occur due to sudden vasospasm of a coronary trunk induced by coronary atherosclerosis, or may be due to release of humoral vasoconstrictors by mast cells in the coronary adventitia. ECG shows ST segment elevation due to transmural ischaemia. These patients respond well to vasodilators like nitroglycerin.


Also referred to as ‘pre-infarction angina’ or ‘acute coronary insufficiency’, this is the most serious pattern of angina. It is characterised by more frequent onset of pain of prolonged duration and occurring often at rest. It is thus indicative of an impending acute myocardial infarction. 

Distinction between unstable angina and acute MI is made by ST segment changes on ECG— acute MI characterised by ST segment elevation while unstable angina may have non-ST segment elevation MI. 

Multiple factors are involved in the pathogenesis of unstable angina which include: stenosing coronary atherosclerosis, complicated coronary plaques (e.g. superimposed thrombosis, haemorrhage, rupture, ulceration etc), platelet thrombi over atherosclerotic plaques and vasospasm of coronary arteries. More often, the lesions lie in a branch of the major coronary trunk so that collaterals prevent infarction.


Sign & symptoms of angina pectoris

• Many ischemic episodes are asymptomatic (silent ischemia). Patients often have a reproducible pattern of pain or other symptoms that appear after a specific amount of exertion. Increased symptom frequency, severity, or duration, and symptoms at rest suggest an unstable pattern that requires immediate medical evaluation.

• Symptoms may include a sensation of pressure or burning over the sternum or near it, which often radiates to the left jaw,shoulder, and arm. Chest tightness and shortness of breath may also occur. The sensation usually lasts from 30 seconds to 30 minutes.

• Precipitating factors include exercise, cold environment, walking after a meal, emotional upset, fright, anger, and coitus. Relief occurs with rest and within 45 seconds to 5 minutes of taking nitroglycerin.

• Patients with variant (Prinzmetal) angina secondary to coronary spasm are more likely to experience pain at rest and in the early morning hours. Pain is not usually brought on by exertion or emotional stress or relieved by rest; the electrocardiogram(ECG) pattern demonstrates current injury with ST-segment elevation rather than depression.

• Unstable angina is stratified into categories of low, intermediate, or high risk for short-term death or nonfatal MI. Features of high-risk unstable angina include:
(1) accelerating tempo of ischemic symptoms in the preceding 48 hours; (2) pain at rest lasting more than 20 minutes; (3) age older than 75 years; (4) ST-segment changes; and (5) clinical findings of pulmonary edema, mitral regurgitation,hypotension, bradycardia, or tachycardia.

• Episodes of ischemia may also be painless, or “silent,” perhaps due to a higher threshold and tolerance for pain than in patients who have pain more frequently.


Diagnosis for angina pectoris

• Obtain medical history to identify the nature or quality of chest pain, precipitating factors, duration, pain radiation, and response to nitroglycerin or rest. Ischemic chest pain may resemble pain from noncardiac sources, and diagnosis of anginal pain may be difficult based on history alone.

• Ask the patient about personal risk factors for coronary heart disease (CHD), includ￾ing smoking, hypertension, and diabetes mellitus.

• Obtain family history that includes information about premature CHD, hypertension,lipid disorders, and diabetes mellitus.

• Findings on cardiac examination may include abnormal precordial systolic bulge, decreased intensity of S1, paradoxical splitting of S2, presence of S3 or S4, apical systolic murmur, and diastolic murmur.

• Laboratory tests: hemoglobin, fasting glucose (to exclude diabetes), and fasting lipid panel. High-sensitivity C-reactive protein (hsCRP); homocysteine level; evidence of Chlamydia infection; and elevations in lipoprotein (a), fibrinogen, and plasminogen activator inhibitor may be helpful. Cardiac enzymes are normal in stable angina.Troponin T or I, myoglobin, and creatinine kinase myocardial band (CK-MB) may be elevated in unstable angina.

• Resting ECG is normal in about half of patients with angina who are not experiencing acute ischemia. Typical ST–T-wave changes include depression, T-wave inversion, and ST-segment elevation. Variant angina is associated with ST-segment elevation, whereas silent ischemia may produce elevation or depression. Significant ischemia is associated with ST-segment depression greater than 2 mm, exertional hypotension, and reduced exercise tolerance.

• Exercise tolerance (stress) testing (ETT), thallium myocardial perfusion scintigraphy, radionuclide angiocardiography, ultrarapid computed tomography, and coronary angiography may be performed in certain circumstances. Obtain a chest radiograph if the patient has HF (heart failure) symptoms.


The sign & symptoms of angina can be reduce by giving non-pharmacological therapy and pharmacological therapy.


Risk factors modification

a. Smoking cessation cuts coronary heart disease (CHD) risk in half by 1 year after quitting.

b. HTN—vigorous BP control reduces the risk of CHD, especially in diabetic patients.

c. Hyperlipidemia—reduction in serum cholesterol with lifestyle modifications and HMG-CoA reductase inhibitors (statins) reduce CHD risk.

d. DM—type II diabetes is considered to be a cardiovascular heart disease equivalent, and strict glycemic control should be strongly emphasized.

e. Obesity—weight loss modifies other risk factors (diabetes, HTN, and hyperlipidemia) and provides other health benefits.

f. Exercise is critical; it minimizes emotional stress, promotes weight loss, and helps reduce other risk factors.

g. Diet: Reduce intake of saturated fat (<7% total calories) and cholesterol (<200 mg/day).


a. May be preferred for high-risk patients, although there is some controversy whether revascularization is superior to medical management for a patient with stable angina and stenosis >70%.
b. Two methods—PCI(Percutaneous Coronary Intervention) and CABG(Coronary Artery Bypass Grafting).
c. Revascularization does not reduce incidence of MI, but does result in significant improvement in symptoms


a. Aspirin
• Indicated in all patients with angina pectoris
• Decreases morbidity—reduces risk of MI, aspirin acts as anti platelets aggregants in low dose, prevent the blood clot.

b. β-Blockers—block sympathetic stimulation of heart. First-line choices include atenolol and metoprolol.
• Reduce HR, BP, and contractility, thereby decreasing cardiac work (i.e., β-blockers lower myocardial oxygen demands).
• Beta blockers have been shown to reduce the frequency of coronary events.

c. Nitrates—cause generalized vasodilation
• Relieve angina; reduce preload myocardial oxygen demand.
• May prevent angina when taken before exertion. Nitroglycerin sublingually given in 0.5 mg dose.
• Effect on prognosis is unknown; main benefit is symptomatic relief.
• Can be administered orally, sublingually, transdermally, intravenously, or in paste form. For chronic angina, oral or transdermal patches are used. For acute coronary syndromes , either sublingual, paste, or IV forms are used.

d. Calcium channel blockers
• Cause coronary vasodilation and afterload reduction, in addition to reducing contractility.
• Now considered a secondary treatment when β-blockers and/or nitrates are not fully effective. Do not routinely use these drugs in CAD.
e. If congestive heart failure (CHF) is also present, treatment with ACE inhibitors and/or diuretics may be indicated as well.