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Angina Pectoris


Ranya N. Sweis

, MD, MS, Northwestern University Feinberg School of Medicine;

Arif Jivan

, MD, PhD, Northwestern University Feinberg School of Medicine

Last full review/revision Jul 2020| Content last modified Jul 2020
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Angina pectoris is a clinical syndrome of precordial discomfort or pressure due to transient myocardial ischemia without infarction. It is typically precipitated by exertion or psychologic stress and relieved by rest or sublingual nitroglycerin. Diagnosis is by symptoms, ECG, and myocardial imaging. Treatment may include antiplatelet drugs, nitrates, beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, statins, and coronary angioplasty or coronary artery bypass graft surgery.

Etiology of Angina Pectoris

Angina pectoris occurs when

  • Cardiac workload and resultant myocardial oxygen demand exceed the ability of coronary arteries to supply an adequate amount of oxygenated blood

Such imbalance between supply and demand can occur when the arteries are narrowed. Narrowing usually results from coronary artery atherosclerosis but may result from coronary artery spasm or, rarely, coronary artery embolism. Acute coronary thrombosis can cause angina if obstruction is partial or transient, but it usually causes acute myocardial infarction (MI).

Because myocardial oxygen demand is determined mainly by heart rate, systolic wall tension, and contractility, narrowing of a coronary artery typically results in angina that occurs during exertion and is relieved by rest.

In addition to exertion, cardiac workload can be increased by disorders such as hypertension, aortic stenosis, aortic regurgitation, or hypertrophic cardiomyopathy. In such cases, angina can result whether atherosclerosis is present or not. These disorders can also decrease relative myocardial perfusion because myocardial mass is increased (causing decreased diastolic flow).

A decreased oxygen supply, as in severe anemia or hypoxia, can precipitate or aggravate angina.

Pathophysiology of Angina Pectoris

Angina may be

  • Stable

  • Unstable

In stable angina, the relationship between workload or demand and ischemia is usually relatively predictable.

Unstable angina is clinically worsening angina (eg, angina at rest or with increasing frequency and/or intensity of episodes).

Atherosclerotic arterial narrowing is not entirely fixed; it varies with the normal fluctuations in arterial tone that occur in all people. Thus, more people have angina in the morning, when arterial tone is relatively high. Also, abnormal endothelial function may contribute to variations in arterial tone; eg, in endothelium damaged by atheromas, stress of a catecholamine surge causes vasoconstriction rather than dilation (normal response).

As the myocardium becomes ischemic, coronary sinus blood pH falls, cellular potassium is lost, lactate accumulates, ECG abnormalities appear, and ventricular function (both systolic and diastolic) deteriorates. Left ventricular (LV) diastolic pressure usually increases during angina, sometimes inducing pulmonary congestion and dyspnea. The exact mechanism by which ischemia causes discomfort is unclear but may involve nerve stimulation by hypoxic metabolites.

Symptoms and Signs of Angina Pectoris

Angina may be a vague, barely troublesome ache or may rapidly become a severe, intense precordial crushing sensation. It is rarely described as "pain." Discomfort is most commonly felt beneath the sternum, although location varies. Discomfort may radiate to the left shoulder and down the inside of the left arm, even to the fingers; straight through to the back; into the throat, jaws, and teeth; and, occasionally, down the inside of the right arm. It may also be felt in the upper abdomen. The discomfort of angina is never above the ears or below the umbilicus.

Atypical angina (eg, with bloating, gas, abdominal distress) may occur in some patients. These patients often ascribe symptoms to indigestion; belching may even seem to relieve the symptoms. Other patients have dyspnea due to the sharp, reversible increase in LV filling pressure that often accompanies ischemia. Frequently, the patient’s description is imprecise, and whether the problem is angina, dyspnea, or both may be difficult to determine. Because ischemic symptoms require a minute or more to resolve, brief, fleeting sensations rarely represent angina.

Between and even during attacks of angina, physical findings may be normal. However, during the attack, heart rate may increase modestly, blood pressure (BP) is often elevated, heart sounds become more distant, and the apical impulse is more diffuse. The 2nd heart sound (S2) may become paradoxical because LV ejection is more prolonged during an ischemic attack. A 4th heart sound (S4) is common, and a 3rd heart sound (S3) may develop. A mid or late systolic apical murmur, shrill or blowing—but not especially loud—may occur if ischemia causes localized papillary muscle dysfunction, causing mitral regurgitation.

Angina pectoris is typically triggered by exertion or strong emotion, usually persists no more than a few minutes, and subsides with rest. Response to exertion is usually predictable, but in some patients, exercise that is tolerated one day may precipitate angina the next because of variations in arterial tone. Symptoms are exaggerated when exertion follows a meal or occurs in cold weather; walking into the wind or first contact with cold air after leaving a warm room may precipitate an attack. Symptom severity is often classified by the degree of exertion resulting in angina (see table Canadian Cardiovascular Classification System for Angina Pectoris).


Canadian Cardiovascular Society Classification System for Angina Pectoris


Activities Triggering Chest Pain


Strenuous, rapid, or prolonged exertion

Not usual physical activities (eg, walking, climbing stairs)


Walking rapidly

Walking uphill

Climbing stairs rapidly

Walking or climbing stairs after meals



Emotional stress


Walking, even 1 or 2 blocks at usual pace and on level ground

Climbing stairs, even 1 flight


Any physical activity

Sometimes occurring at rest

Adapted from Braunwald E, Antman EM, Beasley JW, et al: ACC/AHA Guidelines for the management of patients with unstable angina and non-ST segment elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on the management of patients with unstable angina). Journal of American College of Cardiology 36:970–1062, 2000.

Attacks may vary from several a day to symptom-free intervals of weeks, months, or years. Attacks may increase in frequency (called crescendo angina) leading to a MI or death or gradually decrease or disappear if adequate collateral coronary circulation develops, if the ischemic area infarcts, or if heart failure or intermittent claudication supervenes and limits activity.

Nocturnal angina may occur if a dream causes striking changes in respiration, pulse rate, and BP. Nocturnal angina may also be a sign of recurrent LV failure, an equivalent of nocturnal dyspnea. The recumbent position increases venous return, stretching the myocardium and increasing wall stress, which increases oxygen demand.

Angina decubitus is angina that occurs spontaneously during rest. It is usually accompanied by a modestly increased heart rate and a sometimes markedly higher BP, which increase oxygen demand. These increases may be the cause of rest angina or the result of ischemia induced by plaque rupture and thrombus formation. If angina is not relieved, unmet myocardial oxygen demand increases further, making MI more likely.

Unstable angina

Because angina characteristics are usually predictable for a given patient, any changes (ie, rest angina, new-onset angina, increasing angina) should be considered serious, especially when the angina is severe (ie, Canadian Cardiovascular Society class 3 or 4). Such changes are termed unstable angina and require prompt evaluation and treatment.

Silent ischemia

Patients with coronary artery disease (particularly patients with diabetes) may have ischemia without symptoms. Silent ischemia sometimes manifests as transient asymptomatic ST-T abnormalities seen during stress testing or 24-hour Holter monitoring. Radionuclide studies can sometimes document asymptomatic myocardial ischemia during physical or mental stress. Silent ischemia and angina pectoris may coexist, occurring at different times. Prognosis depends on severity of the coronary artery disease.

Diagnosis of Angina Pectoris

  • Typical symptoms

  • ECG

  • Stress testing with ECG or imaging (using echocardiography, radionuclide imaging, or MRI)

  • Coronary angiography for significant symptoms or positive stress test

Diagnosis of angina is suspected if chest discomfort is typical and is precipitated by exertion and relieved by rest. Presence in the history of significant risk factors for coronary artery disease (CAD) adds weight to reported symptoms. Patients whose chest discomfort lasts > 20 minutes or occurs during rest or who have syncope or heart failure are evaluated for an acute coronary syndrome.

Chest discomfort may also be caused by gastrointestinal disorders (eg, gastroesophageal reflux, esophageal spasm, indigestion, cholelithiasis), costochondritis, anxiety, panic attacks, hyperventilation, and other cardiac disorders (eg, aortic dissection, pericarditis, mitral valve prolapse, supraventricular tachycardia, atrial fibrillation), even when coronary blood flow is not compromised.

ECG is always done. More specific tests include stress testing with ECG or with myocardial imaging (eg, echocardiography, radionuclide imaging, MRI) and coronary angiography. Noninvasive tests are considered first.


If typical exertional symptoms are present, ECG is indicated. Because angina resolves quickly with rest, ECG rarely can be done during an attack except during stress testing.

If done during an angina attack, ECG is likely to show reversible ischemic changes:

  • T wave discordant to the QRS vector

  • ST-segment depression (typically)

  • ST-segment elevation

  • Decreased R-wave height

  • Intraventricular or bundle branch conduction disturbances

  • Arrhythmia (usually ventricular extrasystoles)

Between angina attacks, the ECG (and usually LV function) at rest is normal in about 30% of patients with a typical history of angina pectoris, even those with extensive 3-vessel disease. In the remaining 70%, the ECG shows evidence of previous infarction, hypertrophy, or nonspecific ST-segment and T-wave (ST-T) abnormalities. An abnormal resting ECG alone does not establish or refute the diagnosis.

Stress testing

Stress testing is needed to confirm the diagnosis, evaluate disease severity, determine appropriate exercise levels for the patient, and help predict prognosis. If the clinical or working diagnosis is unstable angina, early stress testing is contraindicated.

Exercise stress testing with ECG is done if a patient has a normal resting ECG and can exercise. In men with chest discomfort suggesting angina, stress ECG testing has a specificity of 70%; sensitivity is 90%. Sensitivity is similar in women, but specificity is lower, particularly in women < 55 (< 70%). However, women are more likely than men to have an abnormal resting ECG when CAD is present (32% vs 23%). Although sensitivity is reasonably high, exercise ECG can miss severe CAD (even left main or 3-vessel disease). In patients with atypical symptoms, a negative stress ECG usually rules out angina pectoris and CAD; a positive result may or may not represent coronary ischemia and indicates need for further testing.

Stress testing with myocardial imaging is done when the resting ECG is abnormal because false-positive ST-segment shifts are common on the stress ECG. Exercise or pharmacologic stress (eg, with dobutamine or dipyridamole infusion) may be used. Imaging options include stress echocardiography, myocardial perfusion imaging with single-photon emission CT (SPECT) or PET, and stress MRI. The choice of imaging technique depends on institutional availability and expertise. Imaging tests can help assess LV function and response to stress; identify areas of ischemia, infarction, and viable tissue; and determine the site and extent of myocardium at risk. Stress echocardiography can also detect ischemia-induced mitral regurgitation.


Coronary angiography is the standard for diagnosing coronary artery disease but is not always necessary to confirm the diagnosis. It is indicated primarily to locate and assess severity of coronary artery lesions when revascularization (percutaneous coronary intervention [PCI] or coronary artery bypass grafting [CABG]) is being considered. Angiography may also be indicated when knowledge of coronary anatomy is necessary to advise about work or lifestyle needs (eg, discontinuing job or sports activities). Although angiographic findings do not directly show hemodynamic significance of coronary lesions, obstruction is assumed to be physiologically significant when the luminal diameter is reduced > 70%. This reduction correlates well with the presence of angina pectoris unless spasm or thrombosis is superimposed.

Intravascular ultrasonography provides images of coronary artery structure. An ultrasound probe on the tip of a catheter is inserted in the coronary arteries during angiography. This test can provide more information about coronary anatomy than other tests; it is indicated when the nature of lesions is unclear or when apparent disease severity does not match symptom severity. Used with angioplasty, it can help ensure optimal placement of stents.

Guidewires with pressure or flow sensors can be used to estimate blood flow across stenoses. Blood flow is expressed as fractional flow reserve (FFR), which is the ratio of maximal flow through the stenotic area to normal maximal flow. These flow measurements are most useful when evaluating the need for angioplasty or CABG in patients with lesions of questionable severity (40 to 70% stenosis). An FFR of 1.0 is considered normal, while an FFR < 0.75 to 0.8 is associated with myocardial ischemia. Lesions with an FFR > 0.8 are less likely to benefit from stent placement.


Imaging studies done at rest can evaluate the coronary arteries.

Electron beam CT can detect the amount of calcium present in coronary artery plaque. The calcium score is roughly proportional to the risk of subsequent coronary events. However, because calcium may be present in the absence of significant stenosis, the score does not correlate well with the need for angioplasty or CABG. Thus, the American Heart Association recommends that screening with electron beam CT should be done only for select groups of patients and is most valuable when combined with historical and clinical data to estimate risk of death or nonfatal myocardial infarction (1). These groups may include asymptomatic patients with an intermediate 10-year ASCVD risk estimate (10 to 20%) and symptomatic patients with equivocal stress test results. Electron beam CT is particularly useful in ruling out significant CAD in patients presenting to the emergency department with atypical symptoms, normal troponin levels, and a low probability of hemodynamically significant coronary artery disease. These patients may have noninvasive testing as outpatients.

Multidetector row CT (MDRCT) coronary angiography can accurately identify coronary stenosis and has a number of advantages. The test is noninvasive, can exclude coronary stenosis with high accuracy, can establish stent or bypass graft patency, can show cardiac and coronary venous anatomy, and can assess calcified and noncalcified plaque burden. However, radiation exposure is significant, and the test is not suitable for patients with a heart rate of > 65 beats/minute, those with irregular heart beats, and pregnant women. Patients must also be able to hold their breath for 15 to 20 seconds, 3 to 4 times during the study.

Evolving indications for MDRCT coronary angiography include

  • Asymptomatic high-risk patients or patients with atypical or typical angina who have inconclusive exercise stress test results, cannot undergo exercise stress testing, or need to undergo major noncardiac surgery

  • Patients in whom invasive coronary angiography was unable to locate a major coronary artery or graft

Cardiac MRI has become invaluable in evaluating many cardiac and great vessel abnormalities. It may be used to evaluate CAD by several techniques, which enable direct visualization of coronary stenosis, assessment of flow in the coronary arteries, evaluation of myocardial perfusion and metabolism, evaluation of wall motion abnormalities during stress, and assessment of infarcted myocardium vs viable myocardium.

Current indications for cardiac MRI include evaluation of cardiac structure and function and assessment of myocardial viability. Cardiac MRI, specifically stress perfusion MRI and quantitative myocardial blood flow analysis, may also be indicated for diagnosis and risk assessment in patients with either known or suspected CAD.

Diagnosis reference

Prognosis for Angina Pectoris

The main adverse outcomes of angina pectoris are unstable angina, myocardial infarction, and sudden death due to arrhythmias. Annual mortality rate is about 1.4% in patients with angina, no history of MI, a normal resting ECG, and normal BP. However, women with CAD tend to have a worse prognosis. Mortality rate is about 7.5% when systolic hypertension is present, 8.4% when the ECG is abnormal, and 12% when both are present. Type 2 diabetes about doubles the mortality rate for each scenario.

Prognosis worsens with increasing age, increasingly severe anginal symptoms, presence of anatomic lesions, and poor ventricular function. Lesions in the left main coronary artery or proximal left anterior descending artery indicate particularly high risk. Although prognosis correlates with number and severity of coronary arteries affected, prognosis is surprisingly good for patients with stable angina, even those with 3-vessel disease, if ventricular function is normal.

Treatment of Angina Pectoris

  • Modification of risk factors (smoking, BP, lipids)

  • Antiplatelet drugs (aspirin and sometimes clopidogrel, prasugrel, or ticagrelor)

  • Beta-blockers

  • Nitroglycerin and calcium channel blockers for symptom control

  • Angiotensin-converting enzyme (ACE) inhibitors and statins

  • Revascularization if symptoms persist despite medical therapy

Reversible risk factors are modified as much as possible. Smokers should stop smoking; 2 years after stopping smoking, risk of MI is reduced to that of people who never smoked. Hypertension (BP > 130/80 for patients with CAD) is treated diligently because even mild hypertension increases cardiac workload. Weight loss alone often reduces the severity of angina. Sometimes treatment of mild LV failure markedly lessens angina. Paradoxically, digitalis occasionally intensifies angina, presumably because increased myocardial contractility increases oxygen demand, arterial tone is increased, or both. Aggressive reduction of total cholesterol and low-density lipoprotein (LDL) cholesterol (via diet plus statins) slows the progression of CAD, may cause some lesions to regress, and improves endothelial function and thus arterial response to stress. An exercise program emphasizing walking often improves the sense of well-being, reduces risk of acute ischemic events, and improves exercise tolerance.

Drugs for angina

The main goals of angina treatment are to

  • Relieve acute symptoms

  • Prevent or reduce ischemia

  • Prevent future ischemic events

To relieve symptoms during an acute attack, sublingual nitroglycerin is the most effective drug.

Nitroglycerin is a potent smooth-muscle relaxant and vasodilator. Its main sites of action are in the peripheral vascular tree, especially in the venous or capacitance system, and in coronary blood vessels. Even severely atherosclerotic vessels may dilate in areas without atheroma. Nitroglycerin lowers systolic BP and dilates systemic veins, thus reducing myocardial wall tension, a major determinant of myocardial oxygen need. Sublingual nitroglycerin is given for an acute attack or for prevention before exertion. Dramatic relief usually occurs within 1.5 to 3 minutes, is complete by about 5 minutes, and lasts up to 30 minutes. The dose may be repeated every 4 to 5 minutes up to 3 times if relief is incomplete. Patients should always carry nitroglycerin tablets or aerosol spray to use promptly at the onset of an angina attack. Patients should store tablets in a tightly sealed, light-resistant glass container, so that potency is not lost. Because the drug deteriorates quickly, small amounts should be obtained frequently.

To prevent ischemia, several classes of drugs are used:

  • Antiplatelet drugs: All patients diagnosed with coronary artery disease or at high risk of developing CAD

  • Beta-blockers: Most patients, unless contraindicated or not tolerated

  • Long-acting nitrates: If needed

  • Calcium channel blockers: If needed

Antiplatelet drugs inhibit platelet aggregation. Aspirin binds irreversibly to platelets and inhibits cyclooxygenase and platelet aggregation. Other antiplatelet drugs (eg, clopidogrel, prasugrel, and ticagrelor) block adenosine diphosphate–induced platelet aggregation. These drugs can reduce risk of ischemic events (MI, sudden death), but the drugs are most effective when given together. Patients unable to tolerate one should receive the other drug alone.

Beta-blockers limit symptoms and prevent infarction and sudden death better than other drugs. Beta-blockers block sympathetic stimulation of the heart and reduce systolic BP, heart rate, contractility, and cardiac output, thus decreasing myocardial oxygen demand and increasing exercise tolerance. Beta-blockers also increase the threshold for ventricular fibrillation. Most patients tolerate these drugs well. Many beta-blockers are available and effective. Dose is titrated upward as needed until limited by bradycardia or adverse effects. Patients who cannot tolerate beta-blockers are given a calcium channel blocker with negative chronotropic effects (eg, diltiazem, verapamil). Those at risk of beta-blocker intolerance (eg, those with asthma) may be tried on a cardioselective beta-blocker (eg, bisoprolol) perhaps with pulmonary function testing before and after drug administration to detect drug-induced bronchospasm.

Long-acting nitrates (oral or transdermal) are used if symptoms persist after the beta-blocker dose is maximized. If angina occurs at predictable times, a nitrate is given to cover those times. Oral nitrates include isosorbide dinitrate and mononitrate (the active metabolite of the dinitrate). They are effective within 1 to 2 hours; their effect lasts 4 to 6 hours. Sustained-release formulations of isosorbide mononitrate appear to be effective throughout the day. For transdermal use, cutaneous nitroglycerin patches have largely replaced nitroglycerin ointments primarily because ointments are inconvenient and messy. Patches slowly release the drug for a prolonged effect; exercise capacity improves 4 hours after patch application and wanes in 18 to 24 hours. Nitrate tolerance may occur, especially when plasma concentrations are kept constant. Because risk of myocardial infarction is highest in early morning, an afternoon or early evening respite period from nitrates is reasonable unless a patient commonly has angina at that time. For nitroglycerin, an 8- to 10-hour respite period seems sufficient. Isosorbide may require a 12-hour respite period. If given once a day, sustained-release isosorbide mononitrate does not appear to elicit tolerance.

Calcium channel blockers may be used if symptoms persist despite use of nitrates or if nitrates are not tolerated. Calcium channel blockers are particularly useful if hypertension or coronary spasm is also present. Different types of calcium channel blockers have different effects. Dihydropyridines (eg, nifedipine, amlodipine, felodipine) have no chronotropic effects and vary substantially in their negative inotropic effects. Shorter-acting dihydropyridines may cause reflex tachycardia and are associated with increased mortality in patients with CAD; they should not be used alone to treat stable angina. Longer-acting formulations of dihydropyridines have fewer tachycardic effects; they are most commonly used with a beta-blocker. Among longer-acting dihydropyridines, amlodipine has the weakest negative inotropic effects; it may be used in patients with left ventricular systolic dysfunction. Diltiazem and verapamil, other types of calcium channel blockers, have negative chronotropic and inotropic effects. They can be used alone in patients with beta-blocker intolerance or asthma and normal left ventricular systolic function but may increase cardiovascular mortality in patients with left ventricular systolic dysfunction.

Ranolazine is a sodium channel blocker that can be used to treat chronic angina. Because ranolazine may also prolong QTc, it is usually reserved for patients in whom symptoms persist despite optimal treatment with other antianginal drugs. Ranolazine may not be as effective in women as in men. Dizziness, headache, constipation, and nausea are the most common adverse effects.

Ivabradine is a sinus node inhibitor that inhibits inward sodium/potassium current in a certain gated channel (funny or "f" channel) in sinus node cells, thus slowing heart rate without decreasing contractility. It can be used for symptomatic treatment of chronic stable angina pectoris in patients with normal sinus rhythm who cannot take beta-blockers or in combination with beta-blockers in patients inadequately controlled by beta-blocker alone and whose heart rate is > 60 beats/minute


Drugs for Coronary Artery Disease*




Angiotensin-converting enzyme (ACE) inhibitors












All patients with CAD, especially those with large infarctions, renal insufficiency, heart failure, hypertension, or diabetes

Contraindications include hypotension, hyperkalemia, bilateral renal artery stenosis, pregnancy, and known allergy

Angiotensin II receptor blockers (ARBs)









An effective alternative for patients who cannot tolerate ACE inhibitors (eg, because of cough); currently, not first-line treatment after MI

Contraindications include hypotension, hyperkalemia, bilateral renal artery stenosis, pregnancy, and known allergy



350 mcg/kg (IV bolus) followed by 25 mcg/kg/minute (IV infusion)

As an alternative to heparin in patients with ACS and a known or suspected history of heparin-induced thrombocytopenia




2.5 mg subcutaneously every 24 hours


5 mg orally twice a day

May be useful long-term in patients with non-valvular atrial fibrillation


150 mg orally twice a day (or 110–150 mg orally twice a day for patients also taking P2Y12 inhibitors)


20 mg orally once a day (or 15 mg orally once a day for patients also taking P2Y12 inhibitors)

Low molecular weight heparins:

  • Dalteparin

  • Enoxaparin

  • Tinzaparin


Patients with unstable angina or NSTEMI

Patients < 75 years receiving tenecteplase

Almost all patients with STEMI as an alternative to unfractionated heparin (unless PCI is indicated and can be done in < 90 minutes); drug continued until PCI or CABG is done or patient is discharged

Unfractionated heparin

60–70 units/kg IV (maximum, 5000 units; bolus), followed by 12–15 units/kg/hour (maximum, 1000 units/hour) for 48 hours or until PCI is complete

Patients with unstable angina or NSTEMI as an alternative to enoxaparin

60 units/kg IV (maximum, 4000 units; bolus) given when alteplase, reteplase, or tenecteplase is started, then followed by 12 units/kg/hour (maximum, 1000 units/hour) for 48 hours or until PCI is complete

Patients who have STEMI and undergo urgent angiography and PCI or patients > 75 years receiving tenecteplase


Oral dose adjusted to maintain INR of 2.5–3.5

Recommended for primary prevention in patients at high risk of systemic emboli (ie, with atrial fibrillation, mechanical heart valves, venous thromboembolism, hypercoagulable disorders, or LV thrombus)

May be useful for primary prevention in patients with STEMI and anterior wall akinesis or dyskinesis if risk of bleeding is low

Reasonable for patients with asymptomatic mural thrombus

Antiplatelet drugs


For stable angina†: 75 or 81 mg orally once a day (enteric-coated)

All patients with CAD or at high risk of developing CAD, unless aspirin is not tolerated or is contraindicated; used long-term

For ACS: 160–325 mg orally chewed (not enteric-coated) on arrival at emergency department and once a day thereafter during hospitalization and 81 mg† orally once a day long-term after discharge


75 mg orally once a day

Used with aspirin or, in patients who cannot tolerate aspirin, alone

For patients undergoing PCI: 300–600 mg orally once, then 75 mg orally once a day for 1–12 months

For elective PCI, maintenance therapy required for at least 1 month for bare-metal stents and for at least 6–12 months for drug-eluting stents

For ACS, dual antiplatelet therapy (typically with aspirin) is recommended for at least 12 months (for any type of stent)


60 mg orally once before PCI, followed by 10 mg orally once a day for 1–12 months

Only for patients with ACS undergoing PCI

Not used in combination with fibrinolytic therapy


For patients undergoing PCI: 180 mg orally once before the procedure, followed by 90 mg orally twice a day for 1–12 months


250 mg orally twice a day for 1–12 months

Rarely used routinely because neutropenia is a risk and white blood cell count must be monitored regularly

Glycoprotein IIb/IIIa inhibitors



Some patients with ACS, particularly those who are having PCI with stent placement and high-risk patients with unstable angina or NSTEMI and large thrombus burden

Therapy started during PCI and continued for 6–24 hours thereafter







50 mg orally every 12 hours acutely; 50–100 mg orally twice a day long-term

All patients with ACS, unless a beta-blocker is not tolerated or is contraindicated, especially high-risk patients; used long-term

Intravenous beta-blockers may be used in patients with ongoing chest pain despite usual measures, or persistent tachycardia, or hypertension in patients with unstable angina and myocardial infarction. Caution is necessary in patients with hypotension or other evidence of hemodynamic instability.


2.5–5 mg orally once a day, increasing to 10–15 mg once a day depending on heart rate and BP response


25 mg orally twice a day (in patients with heart failure or other hemodynamic instability, the starting dose should be as low as 1.625–3.125 mg twice a day and increased very slowly as tolerated)


25–50 mg orally every 6 hours continued for 48 hours; then 100 mg twice a day or 200 mg once a day given long term

Calcium channel blockers


5–10 mg orally once a day

Patients with stable angina if symptoms persist despite nitrates use or if nitrates are not tolerated

Diltiazem (extended-release)

180–360 orally once a day


2.5–10 mg orally once a day

Nifedipine (extended-release)

30–90 mg orally once a day

Verapamil (extended-release)

120–360 mg orally once a day

Nitrates: Short acting

Sublingual nitroglycerin (tablet or spray)

0.3–0.6 mg every 4–5 minutes up to 3 doses

All patients for immediate relief of chest pain; used as needed

Nitroglycerin as continuous IV drip

Started at 5 mcg/minute and increased 2.5–5.0 mcg every few minutes until required response occurs

Selected patients with ACS:

During the first 24 to 48 hours, those with heart failure (unless hypotension is present), large anterior myocardial infarction, persistent angina, or hypertension (BP is reduced by 10–20 mm Hg but not to < 80–90 mm Hg systolic)

For longer use, those with recurrent angina or persistent pulmonary congestion

Nitrates: Long acting

Isosorbide dinitrate

10–20 mg orally 3 times a day; can be increased to 40 mg 3 times a day

Patients who have unstable angina or persistent severe angina and continue to have anginal symptoms after the beta-blocker dose is maximized

A nitrate-free period of about 8–10 hours (typically at night) recommended to avoid tolerance (specific drugs recommend different durations of nitrate-free period)

Isosorbide dinitrate (sustained-release)

40–80 mg orally twice a day (typically given at 8 AM and 2 PM)

Isosorbide mononitrate

20 mg orally twice a day, with 7 hours between 1st and 2nd doses

Isosorbide mononitrate (sustained-release)

30 or 60 mg orally once a day, increased to 120 mg or, rarely, 240 mg

Nitroglycerin patches

0.2–0.8 mg/hour applied between 6:00 and 9:00 AM and removed 12–14 hours later to avoid tolerance

Nitroglycerin ointment 2% preparation (15 mg/2.5 cm)

1.25 cm spread evenly over upper torso or arms every 6 to 8 hours and covered with plastic, increased to 7.5 cm as tolerated, and removed for 8–12 hours each day to avoid tolerance



2–4 mg IV, repeated as needed

Morphine should be used judiciously (eg, if nitroglycerin is contraindicated or if patient has symptoms despite maximal doses of nitroglycerin) given a possible increase in mortality as well as attenuation of P2Y12 receptor inhibitor activity

PCSK-9 inhibitors


Initial dose: 75 mg subcutaneously, once every 2 weeks or 300 mg subcutaneously once every 4 weeks

For patients not at target LDL-C levels, used alone or in combination with other lipid-lowering therapies (eg, statins, ezetimibe) for the treatment of adults with primary hyperlipidemia (including familial hypercholesterolemia)


Initial dose for primary hyperlipidemia: 140 mg subcutaneously every 2 weeks or 420 mg subcutaneously once monthly

For patients not at target LDL-C levels, used alone or in combination with other lipid-lowering therapies (eg, statins, ezetimibe) for the treatment of adults with primary hyperlipidemia (including familial hypercholesterolemia)









Patients with CAD should be given maximally tolerated statin dose

Other drugs


5 mg orally twice a day, increased to 7.5 mg orally twice a day if needed

Inhibits sinus node

For symptomatic treatment of chronic stable angina pectoris in patients with normal sinus rhythm who cannot take beta-blockers

In combination with beta-blockers in patients inadequately controlled by beta-blocker alone and whose heart rate > 60 beats/minute


500 mg orally twice a day, increased to 1000 mg orally twice a day as needed

Patients in whom anginal symptoms continue despite treatment with other antianginal drugs

* Clinicians may use different combinations of drugs depending on the type of coronary artery disease that is present.

† Higher doses of aspirin do not provide greater protection and increase risk of adverse effects.

‡ Of low molecular weight heparins (LMWHs), enoxaparin is preferred.

ACS = acute coronary syndromes; BP = blood pressure; CABG = coronary artery bypass grafting; CAD = coronary artery disease; INR = international normalized ratio; LV = left ventricular; MI = myocardial infarction; NSTEMI = non–ST-segment elevation MI; PCI = percutaneous intervention; STEMI = ST-segment elevation MI.


Revascularization, either with PCI (eg, angioplasty, stenting) or CABG, should be considered if angina persists despite drug therapy and worsens quality of life or if anatomic lesions (noted during angiography) put a patient at high risk of mortality. The choice between PCI and CABG depends on extent and location of anatomic lesions, the experience of the surgeon and medical center, and, to some extent, patient preference.

PCI is usually preferred for 1- or 2-vessel disease with suitable anatomic lesions and is increasingly being used for 3-vessel disease. Lesions that are long or near bifurcation points are often not amenable to PCI. However, as stent technology improves, PCI is being used for more complicated cases.

CABG is very effective in selected patients with angina. CABG is superior to PCI in patients with diabetes and in patients with multivessel disease amenable to grafting. The ideal candidate has severe angina pectoris and localized disease, or diabetes mellitus. About 85% of patients have complete or dramatic symptom relief. Exercise stress testing shows positive correlation between graft patency and improved exercise tolerance, but exercise tolerance sometimes remains improved despite graft closure.

CABG improves survival for patients with left main disease, those with 3-vessel disease and poor left ventricular function, and some patients with 2-vessel disease. However, for patients with mild or moderate angina (CCS class 1 or 2) or 3-vessel disease and good ventricular function, CABG appears to only marginally improve survival. PCI is increasingly being used for unprotected left main stenosis (ie, no left anterior descending or circumflex graft present), with outcomes at one year that are similar to CABG. For patients with 1-vessel disease, outcomes with drug therapy, PCI, and CABG are similar; exceptions are left main disease and proximal left anterior descending disease, for which revascularization appears advantageous.

Key Points

  • Angina pectoris occurs when cardiac workload exceeds the ability of coronary arteries to supply an adequate amount of oxygenated blood.

  • Symptoms of stable angina pectoris range from a vague, barely troublesome ache to a severe, intense precordial crushing sensation; they are typically precipitated by exertion, last no more than a few minutes, and subside with rest.

  • Do stress testing with ECG for patients with normal resting ECG or with myocardial imaging (eg, echocardiography, radionuclide imaging, MRI) for patients with abnormal resting ECG.

  • Do coronary angiography when revascularization (percutaneous intervention or coronary artery bypass grafting) is being considered.

  • Give nitroglycerin for immediate relief of angina.

  • Maintain patients on an antiplatelet drug, a beta-blocker, and a statin, and add a calcium channel blocker for further symptom prevention if needed.

  • Consider revascularization if significant angina persists despite drug therapy or if lesions noted during angiography indicate high risk of mortality.

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Cardiac Catherization
Cardiac catheterization of the left or the right heart can be used to do various tests, and it also can be used to determine appropriate therapeutic interventions. Right heart catheterization is most commonly used to assess which of the following? 
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