Coronary artery disease

Coronary artery disease (CAD) is a condition that is most commonly caused by atherosclerosis and the subsequent reduction in blood supply to the myocardium, resulting in a mismatch between myocardial oxygen supply and demand. Acute retrosternal chest pain (angina) is the cardinal symptom of CAD. Other symptoms include dyspnea, dizziness, anxiety, and nausea. Patients with stable CAD may have stable angina or be asymptomatic, while severe ischemia may lead to acute coronary syndrome, including myocardial infarction (MI). Stable CAD can be diagnosed using cardiac stress testing, nonstress cardiac imaging, and/or coronary catheterization. The management of stable CAD involves management of atherosclerotic cardiovascular disease (e.g., smoking cessation, and treatment of diabetes mellitus, hypertension, and dyslipidemia), antiplatelet agents, antianginal medication (e.g., beta blockers), and, in severe cases, revascularization (e.g., percutaneous transluminal coronary angioplasty).

For the diagnostics and management of acute chest pain, see “Acute coronary syndrome” and “Chest pain.” See also “Atherosclerotic cardiovascular disease” and “Myocardial infarction.”

Coronary artery disease

• Coronary artery disease (CAD): ischemic heart disease due to narrowing or blockage of coronary arteries, most commonly due to atherosclerosis, resulting in a mismatch between myocardial oxygen supply and demand
• Stable CAD: a form of CAD in which patients are either asymptomatic or have stable or low-risk unstable angina; also used for patients with a history of MI whose symptoms are controlled with treatment

Chest pain and angina

Preferred terminology for types of chest pain ^[1][2][3]

• Cardiac chest pain: likely associated with cardiac ischemia based on symptoms (e.g., central, retrosternal, squeezing, exertional).
• Possible cardiac chest pain: may be associated with cardiac ischemia based on symptoms (e.g., stabbing, tearing, ripping, burning).
• Noncardiac chest pain: unlikely associated with cardiac ischemia based on symptoms (e.g., positional, fleeting).

Historical terminology for types of chest pain ^[1][2][3]

The following terms are no longer recommended for use in the 2021 AHA/ACC chest pain guidelines. ^[1][2][3]

• Typical angina fulfills all of the following criteria:
  • Retrosternal chest pain of characteristic nature and duration (e.g., transient retrosternal pressure)
  • Provoked by exertion or emotional stress
  • Relieved by rest and/or nitroglycerin
• Atypical angina: fulfills only two of the aforementioned criteria
• Nonanginal chest pain: fulfills one or none of the aforementioned criteria

• CAD is the leading cause of death in the US and worldwide. ^[4]
• The lifetime risk of coronary artery disease at age 50 is approx. 50% for men and 40% for women. ^[5]

Epidemiological data refers to the US, unless otherwise specified.

• Atherosclerosis is the most common cause (see “Risk factors for atherosclerosis”).

Plaque formation and coronary artery stenosis ^[6][7]

• For plaque formation, see “Pathogenesis of atherosclerosis.”
• Stable atherosclerotic plaque → vascular stenosis → increased resistance to blood flow in the coronary arteries → decreased myocardial blood flow → oxygen supply-demand mismatch → myocardial ischemia
• The extent of coronary stenosis determines the severity of the oxygen supply-demand mismatch and, thus, the severity of myocardial ischemia.
• Severe ischemia results in myocardial infarction (see “Acute coronary syndrome”).
• Coronary flow reserve (CFR): the difference between maximum coronary blood flow and coronary flow at rest (a measure of the ability of the coronary capillaries to dilate and increase blood flow to the myocardium).
  • In healthy individuals, the CFR can be up to 4 times higher on exertion than at rest.
  • CFR is reduced in individuals with CAD due to vascular stenosis and reduced vascular compliance.

Myocardial oxygen supply-demand mismatch ^[8]

• Definition: mismatch between the amount of oxygen the myocardium receives and the amount it requires
• Factors reducing oxygen supply
  • Coronary atherosclerosis ; and sequelae, including:
    • Rupture of an unstable atherosclerotic plaque (most common cause)
    • Thrombosis
    • Stenosis
  • Vasospasms
  • ↑ Heart rate
  • Anemia
• Factors increasing oxygen demand
  • ↑ Heart rate
  • ↑ Afterload
  • Anemia

An increased heart rate reduces oxygen supply and increases oxygen demand.

Effect of vascular stenosis on resistance to blood flow ^[9]

• The resistance to blood flow within the coronary arteries is calculated using the Poiseuille equation: R = 8Lη/(πr⁴), where R = resistance to flow, L = length of the vessel, η = viscosity of blood, and r = radius of the vessel.
• Provided the length of the vessel and viscosity of blood remain constant; , the degree of resistance can be calculated using the simplified formula: R ≈ 1/r⁴

Vascular stenosis increases vascular resistance significantly. For example, a 50% reduction in radius results in a 16-fold increase in resistance: R ≈ 1/(0.5 x r)⁴ = [1/(0.5 x r)]⁴ = (2/r)⁴ = 16/r⁴.

Myocardial ischemia ^[8]

• Reversible ischemia: Tissue is ischemic but not irreversibly dead and, therefore, still potentially salvageable.
  • Myocardial stunning: acutely ischemic myocardial segments with transiently impaired but completely reversible contractility
  • Hibernating myocardium: a state in which myocardial tissue has persistently impaired contractility due to repetitive or persistent ischemia
    • Partially or completely reversible when adequate oxygen supply is restored (e.g., after angioplasty or coronary artery bypass grafting)
    • Seen in angina pectoris, left ventricular dysfunction, and/or heart failure
• Irreversible ischemia: tissue necrosis (myocardial scars)

Coronary steal syndrome

• Definition: a phenomenon of vasodilator-induced alteration of coronary blood flow in patients with coronary atherosclerosis resulting in myocardial ischemia and symptoms of angina
• Pathomechanism
  • Long-standing CAD requires maximal coronary arterial dilation distal to the stenosis to maintain normal myocardial function.
  • In CAD, the affected coronary artery is maximally dilated distal to the stenosis to compensate for the reduced blood flow .
  • If a vasodilator (e.g., dipyridamole) is administered, the subsequent vasodilation of healthy vessels causes these to “steal” blood from the stenotic blood vessels, resulting in poststenotic myocardial ischemia.
• Clinical relevance
  • Coronary steal is the underlying mechanism of pharmacological stress testing.
  • Administration of vasodilators (e.g., dipyridamole) → coronary vasodilation → decreased hydrostatic pressure in the normal coronary arteries → blood shunting back to well-perfused myocardium → decreased flow to the ischemic myocardium → myocardial ischemia downstream to the pathologically dilated vessels → angina pectoris and/or ECG changes

Coronary steal syndrome should not be confused with coronary-subclavian steal syndrome.

Chronic ischemic heart disease

• Definition: progressive heart failure that occurs after many years of chronic ischemic damage to the myocardium

Angina

• Paroxysmal attacks of retrosternal chest discomfort, tightness, or pressure due to myocardial ischemia.
• Most commonly occurs in individuals with coronary heart disease.
• Triggers include exertion or stress, which results in increased myocardial oxygen demand.
• Angina is the cardinal symptom of CAD.
• Patients with CAD usually become symptomatic when the degree of coronary stenosis reaches ≥ 70%.
• Typically retrosternal chest pain or pressure
  • Pain is not affected by body position or respiration.
  • No chest wall tenderness
  • May gradually increase in intensity
  • May be absent, especially in geriatric and diabetic patients. ^[10]

Stable angina

• Symptoms are reproducible/predictable and severity, frequency, and threshold for reproduction of symptoms do not change.
• Symptoms often subside within minutes with rest or after administration of nitroglycerin
• Common triggers include physical/mental stress or exposure to cold

Anginal equivalents ^[1][11]

• Definition: A symptom of cardiac ischemia (other than chest pain) that is associated with exertion or stress, or relieved by short-acting nitrates or rest.
• Possible manifestations
  • Pain referred to the left arm, neck, jaw, epigastric region, or back.
  • Gastrointestinal discomfort
  • Dyspnea
  • Dizziness, palpitations
  • Restlessness, anxiety
  • Autonomic symptoms (e.g., diaphoresis, nausea, vomiting, syncope)

Patients with chest pain or anginal equivalents should be evaluated for CAD. Other indications include newly diagnosed heart failure, arrhythmia, and syncope.

The following recommendations are consistent with the 2012 and 2013 American Heart Association (AHA) guidelines for the management of stable ischemic heart disease (IHD) and the 2021 AHA chest pain guidelines. They focus on patients with chronic stable angina and no history of CAD. For patients with acute symptoms, see “Diagnostics” in “Acute coronary syndrome.” ^[1][2][12]

New onset chest pain, pain at rest, and increasing frequency or severity of pain are symptoms of unstable angina.

Symptomatic patients without known CAD ^[2][12]

Initial evaluation

• Clinical evaluation
  • Determine the pretest probability of CAD.
  • Identify traditional ASCVD risk factors.
  • Determine the nature and frequency of angina episodes.
  • Physical examination may be normal; look for:
    • Clinical features of peripheral vascular disease
    • Clinical features of heart failure
    • Features of valvular heart diseases
• Resting ECG: indicated for all patients

Additional evaluation ^[13]

Perform the following according to the pretest probability of CAD: ^[14]

• Obvious noncardiac cause: : No cardiac testing required
• Low PTP of obstructive CAD
  • Additional diagnostic testing is not routinely recommended.
  • CAC scoring or cardiac exercise stress testing may be considered in select cases.
• Intermediate to high PTP of obstructive CAD
  • Coronary CT angiography (CCTA): Preferred for patients aged < 65 years
  • OR cardiac stress testing: Preferred for patients aged ≥ 65 years
    • Patients able to exercise: Exercise stress testing is preferred.
      • Interpretable ECG: Obtain exercise ECG testing or exercise stress imaging.
      • Uninterpretable ECG: Obtain exercise stress imaging.
    • Patient unable to exercise: Pharmacological stress testing (i.e. with imaging) is appropriate.
• Further diagnostic testing: Tailor additional testing decisions to individual patients. ^[14]
  • Additional noninvasive cardiac testing : preferred for most patients
  • Invasive coronary angiography (gold standard): usually reserved for specific clinical scenarios

Either cardiac stress testing or CCTA can be used to risk stratify patients with intermediate to high PTP of obstructive CAD. ^[2]

Additional diagnostic testing is not routinely recommended for patients with a low pretest probability of obstructive CAD. ^[2]

Asymptomatic patients

• Diagnostic testing may be indicated for preoperative cardiac assessment in select patients.
• The U.S. Preventive Services Task Force does not recommend screening asymptomatic adults with low ASCVD risk using resting ECG or exercise ECG. ^[15]

Resting ECG ^[12]

• Best initial test for chest pain
• Usually normal in stable angina
• Findings that suggest previous MI or unstable angina: These typically necessitate further workup (see “Acute coronary syndrome”).
  • ST-segment depression
  • T-wave inversion or T-wave flattening
  • Wellens pattern
• Uninterpretable ECG: one that does not allow identification of stress-induced ischemic changes, typically due to preexisting abnormalities that affect interpretability, such as: ^[1][14]
  • Resting ST depression ≥ 0.1 mV (1 mm)
  • Complete LBBB
  • Digoxin use
  • Preexcitation (e.g., WPW)
  • Ventricular paced rhythm
  • LVH

Resting ECG results are usually normal in patients with stable CAD.

The 2021 AHA chest pain guidelines recommend using validated scores published within the past 10 years to predict the pretest probability of obstructive CAD. ^[2]

Pretest probability of obstructive CAD by age, sex, and symptoms

• The following is one of several possible methods suggested in the 2021 AHA guidelines for estimating the pretest probability of obstructive CAD based on age, sex, and symptoms. ^[2]
• Patients with obvious noncardiac chest pain and reassuring ECG do not require cardiac testing or calculation of pretest probability of CAD. ^[2]

Other factors that independently increase PTP ^[1]

• Presence of traditional ASCVD risk factors (e.g., diabetes mellitus)
• Concerning ECG findings (e.g., Q waves that suggest prior infarction)
• Previously documented coronary artery calcium (CAC) scores or visual estimation of CAC on prior noncardiac chest CT. ^[2]

Overview

• Noninvasive testing
  • Provocative: cardiac stress testing
    • Exercise stress testing
      • Exercise ECG testing
      • Exercise stress imaging: e.g., echocardiography, myocardial perfusion scan, cardiac MRI (CMR)
    • Pharmacological stress testing: cardiac imaging (e.g., echocardiography, myocardial perfusion scan, CMR) combined with pharmacological stressor (e.g., dobutamine) under ECG monitoring
  • Nonprovocative: cardiac anatomic testing, e.g., CCTA, CAC scoring
• Invasive testing: coronary angiography

Cardiac stress testing ^{[1][2][12][16][17][18]}

Description

• The goal is to detect evidence of stress-induced ischemia.
• Heart rate is monitored throughout the study ^[19]
  • Estimated maximum heart rate = 220 – age (in years)
  • Target heart rate = 85% of the maximum heart rate
• 12-lead ECG is used for monitoring throughout the study.

Indications ^[20]

• Chronic stable angina: most useful for risk stratification in patients with an intermediate-to-high PTP of obstructive CAD.
• Provocation of arrhythmia
• Evaluation of patients who experience other exertional symptoms (e.g., palpitations, syncope)
• Risk assessment for patients who are due to undergo cardiac revascularization

Types of stress induction

• Exercise stress tests (e.g., treadmill or bicycle): first-line ^[14][18]
• Pharmacological stress tests (e.g., vasodilator or inotropic medication): alternative in patients unable to exercise ^[1]

Modalities and diagnostic endpoints

General criteria for test termination

Some clinical and ECG criteria vary between exercise stress tests and pharmacological stress tests (see “Comparison of cardiac stress tests” for details). General criteria include the following:

• A diagnostic endpoint is reached (preferred). ^[14][19][20]
• A target heart rate threshold is achieved (i.e., if no diagnostic endpoint is reached)
• Significant cardiac arrhythmia
• Technical issues with patient monitoring
• Patient request

Test preparation

• Hold methylxanthines (e.g., caffeine, aminophylline) for 12 hours prior to testing (no need to hold for dobutamine testing).
• Hold dipyridamole for 48 hours prior to adenosine and regadenoson stress tests.
• Beta blockers, CCBs, and nitrates can affect diagnostic value and may be held prior to testing at the treating clinician's discretion. ^[20]

Achievement of 85% of the patient's estimated maximum heart rate, no exaggerated BP response, and no ST-segment abnormalities during exercise stress testing confer a low probability of CAD (i.e., a normal test). ^[20]

Cardiac anatomic testing ^[12]

• Coronary CT angiography (CCTA): can visualize anatomic CAD ^[21]
  • Indications
    • Patients with an intermediate to high PTP of obstructive CAD
    • Patients with contraindications to cardiac stress testing
    • Patients who have previously had a cardiac stress test with:
      • Persistent symptoms and no abnormalities detected during previous tests
      • Inconclusive cardiac stress test results
  • Supportive findings ^[22]
    • Calcified or noncalcified plaques
    • The degree and extent of coronary stenosis can be measured and is usually reported using CAD-RADS.
• Coronary artery calcium (CAC) scoring: measures the amount of calcification in the coronary arteries ^[1]
  • Rarely used to assess for CAD in symptomatic patients; usually reserved for asymptomatic patients (see “Diagnostics” in “Lipid disorders”)
  • Consider in patients with a low pretest probability of CAD to rule out the disease.

Coronary angiography ^[12][23]

• Indications
  • Chronic stable angina
    • Contraindications for or inability to perform noninvasive testing
    • High clinical suspicion for CAD and ambiguous results on noninvasive testing
    • Abnormal results from noninvasive testing, such as: ^[24]
      • ST elevation during cardiac stress testing
      • Perfusion abnormalities involving 10% of the myocardium after stress
      • Significant coronary artery stenosis on CCTA
      • Inducible wall motion abnormalities
    • Persistent symptoms of angina despite appropriate therapy
    • Initial testing for survivors of sudden cardiac arrest
    • Consider as initial testing for patients with signs of heart failure.
  • Other indications: e.g., acute coronary syndrome and certain valvular diseases (see “Cardiac catheterization”)
• Uses
  • Direct visualization of coronary arteries
  • To determine the feasibility of direct therapeutic intervention using percutaneous coronary intervention (see “Treatment” below)
  • Cardiac catheterization can provide information on several parameters; (e.g., coronary blood flow; , pressure within heart chambers, cardiac output, oxygen saturation). ^[25]
• Supportive findings: ^[12]
  • The extent of the disease is reported as either the number of involved vessels (1, 2, or 3 vessels) or involvement of the left main coronary artery (LMCA).
  • Significant coronary artery stenosis is usually defined as one of the following:
    • ≥ 50% narrowing of the LMCA
    • ≥ 70% narrowing of other coronary arteries, e.g., RCA, LCx, LAD

Patients with acute chest pain and other concerning clinical findings (e.g., hypotension) or ECG changes that are suggestive of acute coronary syndrome (e.g., new heart blocks or arrhythmias) should undergo cardiac catheterization.

See “Differential diagnosis of chest pain.”

The differential diagnoses listed here are not exhaustive.

The following recommendations are consistent with the 2012, 2014, and 2021 American Heart Association (AHA) guidelines on the management of patients with stable IHD and coronary artery revascularization. ^[12][23][26]

Approach ^[12]

The goal of treatment is to reduce cardiovascular morbidity and mortality, improve ischemic symptoms, and maintain quality of life.

• All patients: pharmacotherapy for CAD
  • Start prevention of recurrent CAD, i.e., antiplatelet agents, statins, and management of comorbidities.
  • Start antianginal medication.
• Select patients: revascularization
  • Not routinely recommended for stable CAD
  • Techniques
    • Percutaneous coronary intervention (PCI)
    • Coronary artery bypass grafting (CABG)

All patients with CAD should receive education on risk factor reduction, as well as treatment with antiplatelet agents and antianginal medications

Pharmacotherapy for CAD

Pharmacotherapy for CAD has two main therapeutic goals, prevention of recurrent CAD and symptomatic relief with antianginal treatment. Specific indications and potential effects should be taken into account before prescribing the different drug classes.

Antianginal drugs

• Goal: : reduction of myocardial oxygen demand (MVO₂)
• First-line agent: beta blockers
• Second-line agents: CCBs, nitrates, ranolazine
  • Consider as initial monotherapy for patients with contraindications to beta blockers (e.g., vasospastic angina).
  • Consider as combination therapy; with beta blockers to improve symptom control , e.g., a beta blocker PLUS a nitrate, dihydropyridine CCB , OR ranolazine.
  • CCB (nondihydropyridine) PLUS a nitrate (nondihydropyridine CCBs such as verapamil have a similar effect to beta blockers on cardiac conduction) ^[27]
• Third-line agent: Consider ranolazine if beta-blockers, CCBs, and nitrates are ineffective or not tolerated. ^[12]

Overview of pharmacotherapeutic agents for CAD

Beta blockers are used to reduce the risk of MI and death and for symptom relief (antianginal treatment) in patients with CAD.

Revascularization for stable CAD ^[12][26]

Decisions regarding revascularization are complex and should be made with a multidisciplinary team of specialists (e.g., interventional cardiologists, cardiac surgeons) on an individual basis. See “Acute coronary syndrome” for revascularization indications of patients with acute symptoms.

• Indications
  • High-risk anatomic lesions involving multiple or critical vessels, such as:
    • Complex CAD
    • 3-vessel disease
    • LMCA stenosis without patent bypass grafts
  • High-risk physiological conditions, such as:
    • LVEF < 50%
    • Prior sudden cardiac arrest with suspected ischemia-induced VT
  • Activity-limiting symptoms due to any significant coronary artery stenosis that persist:
    • Despite optimal medical treatment
    • OR due to contraindications to pharmacotherapy
• Options
  • CABG is generally preferred in patients with:
    • > 50% LMCA stenosis without patent bypass grafts
    • Complex CAD or three-vessel disease PLUS low surgical risk
    • Multivessel disease with either proximal LAD stenosis or concomitant diabetes mellitus ^[23]
    • LV dysfunction
  • PCI : may be preferred in select patients

The choice of revascularization technique should take into account patient preference, coronary anatomy, left ventricular function, prior history of revascularization, and the presence of concomitant chronic conditions.

Revascularization is harmful in patients who do not meet anatomical or physiological criteria for intervention.

• Prognostic factors
  • Left ventricular function: increased mortality if EF < 50% ^[33]
  • Involvement of left main coronary artery or involvement of more than one vessel is associated with a worse prognosis
• Stable angina
  • Annual mortality rate: up to 5% ^[12]
  • 25% of patients will develop acute MI within the first 5 years. ^[34]
  • High-grade stenosis is associated with an unfavorable prognosis.

Primary prevention of CAD

See “Primary prevention of ASCVD.”

Prevention of recurrent CAD

See also “Prevention of recurrent ASCVD.”

• Lifestyle modifications for ASCVD prevention
  • Smoking cessation
  • Increased physical activity
• Lipid-lowering therapy for ASCVD
  • Start moderate- or high-intensity statin therapy.
  • Consider addition of nonstatin lipid-lowering agents if there is a poor response to statin monotherapy.
• Antiplatelet therapy: single-agent antiplatelet therapy with aspirin or clopidogrel
• Management of comorbidities
  • Management of hypertension
    • Target BP in hypertension: < 130/80 mm Hg ^[29]
    • First-line treatment: beta blockers
    • Alternative: ACE inhibitors or angiotensin receptor blockers (ARBs), especially in patients post MI
  • Management of diabetes mellitus
    • Individualized glycemic goals (e.g., HbA1c < 7%)
    • Consider the use of antihyperglycemics with known protective cardiovascular effects in patients with T2DM, e.g., metformin, SGLT-2 inhibitors. ^[35]

Vasospastic angina

Description

• Angina caused by transient coronary spasms (usually due to spasms occurring close to areas of coronary stenosis)
• Not affected by exertion (may also occur at rest)
• Typically occurs early in the morning ^[36]

Epidemiology ^[37]

• Highest prevalence in the Japanese population (especially young women)
• Average age of onset: 50 years

Etiology

• Cigarette smoking; use of stimulants (e.g., cocaine, amphetamines), alcohol, or triptans
• Stress, hyperventilation, exposure to cold
• Associated with other vasospastic disorders (e.g., Raynaud phenomenon, migraine headaches) ^[38]
• Common atherosclerotic risk factors (except smoking) do not apply to vasospastic angina.

Diagnosis ^[11][39]

The goal of diagnostic testing is to detect transient ischemic changes and/or coronary artery spasm during anginal episodes, as well as concomitant coronary artery stenosis. Specialist consultation is advised. ^[11]

• Initial testing ^[11][40]
  • Resting ECG: Obtain during an acute anginal attack.
  • Consider Holter monitor in patients with: ^[40]
    • No ischemic changes documented on resting ECG
    • Syncope or bradyarrhythmias ^[11][40]
  • Exercise stress test
    • Consider if ischemic changes have not been identified using other methods.
    • Approx. one-third of patients with vasospastic angina show no ST segment changes during an exercise stress test. ^[11]
• Cardiac biomarkers
  • Measure serial troponin I and/or troponin T levels during periods of acute chest pain (i.e., at arrival and 1–6 hours later) if acute coronary syndrome is suspected (see also “Complications”).
  • Serial troponin levels are unlikely to be elevated in patients with transient ischemic changes. ^[36][41]
• Advanced testing ^[11][39]
  • Coronary angiography: commonly indicated in vasospastic angina with ST-segment elevation to rule out underlying coronary artery stenosis
  • Coronary artery spasm provocation testing ^[11][39]
    • Usually only performed to help inform a diagnosis or treatment decision when further information is required after completion of other tests
    • Not recommended for patients with severe coronary artery stenosis or advanced heart failure ^[36]
    • Spasms are usually induced pharmacologically.
    • Nitrates and calcium channel blockers (CCBs) should be held before testing.
    • Noninvasive coronary artery spasm provocation testing is not advised. ^[39]

Noninvasive bedside coronary artery spasm provocation testing can lead to significant adverse effects and even death. Provocative testing to diagnose vasospastic angina should only be attempted by a specialist, and usually only during coronary angiography. ^[39]

Treatment ^[11][42]

• General recommendations
  • Smoking cessation
  • Avoid beta-blockers (particularly nonselective beta blockers) , and other agents that induce vasoconstriction, such as: ^[40][42]
    • Triptans
    • High-dose aspirin (> 325 mg) ^[40][42]
    • Certain chemotherapeutic agents
    • Alcohol and recreational drugs
  • Atherosclerotic risk factor modification, as appropriate (see “Prevention”) ^[36]
• Pharmacotherapy: The goal is to prevent spasms and arrhythmias, and to improve symptoms during acute attacks. ^[11][40]
  • First-line therapy: calcium channel blockers, e.g., verapamil , diltiazem , or nifedipine ^[11]
  • Alternatively:
    • Long-acting nitrates: e.g., isosorbide dinitrate
    • Combination therapy for symptom control: nitrates with up to two CCBs from different classes ^[11]
• Additional pharmacotherapy
  • Short-acting nitrates: e.g., nitroglycerin
    • May be used during acute attacks
    • Patients should seek medical attention if pain persists after three doses of nitroglycerin taken over 15 minutes.
  • Statins: e.g., fluvastatin can further prevent coronary artery spasm when added to CCB treatment. ^[36][43]
  • Alpha blockers: The addition of prazosin to CCBs or long-acting nitrates may reduce episodes of spasm. ^[36][42]
  • Magnesium supplementation may help to prevent spasms. ^[36][40][44]

Complications ^[11][40]

• Myocardial infarction
  • May occur with prolonged spasms or in patients with concomitant coronary artery stenosis
  • See “Acute coronary syndrome.”
• Arrhythmias ^[11]
  • AV block: A pacemaker may be required (see “Management approach to patients with AV block”).
  • Ventricular arrhythmia and sudden cardiac death: An implantable cardioverter defibrillator may be required.

Prolonged coronary artery spasms can lead to MI or fatal arrhythmias. ^[11]

Prognosis

• 5-year survival rate is > 90% (with treatment). ^[45]
• The persistence of symptoms is common.

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