Coronary artery disease

Coronary artery disease (CAD) is characterized by the buildup of atherosclerotic plaque in the coronary arteries, leading to reduced myocardial blood flow and oxygen supply-demand mismatch. The cardinal symptom is retrosternal chest pain (angina pectoris), which may be accompanied by dyspnea, diaphoresis, nausea, and/or pain radiating to the jaw or left arm. Patients with stable CAD typically present with predictable, exertional chest pain that resolves with rest and/or nitroglycerin, while progression to acute coronary syndrome can result in myocardial infarction (MI). Diagnosis involves risk stratification using pretest probability assessment followed by testing: coronary CT angiography (CCTA) for patients under 65 years of age with intermediate-to-high pretest probability, or cardiac stress testing for older patients or those unable to undergo CCTA. Management includes comprehensive cardiovascular risk reduction (smoking cessation, diabetes and hypertension management, lipid optimization), antiplatelet therapy, antianginal treatment (e.g., with beta blockers), and revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) for high-risk anatomic lesions or refractory symptoms despite optimal medical therapy.

For approaches to acute chest pain, see “Acute coronary syndrome” and “Chest pain.” See “Chronic coronary disease” for details on other causes of stable ischemic heart disease (IHD), including diagnosis and management of ischemia with nonobstructive coronary arteries.

Coronary artery disease

• Coronary artery disease (CAD)
  • A type of IHD caused by atherosclerotic changes to coronary arteries
  • Can reduce myocardial blood supply, causing myocardial ischemia ^[1]
• Stable CAD: a non-acute form of IHD that causes reversible myocardial ischemia; often used synonymously with “chronic coronary disease” (CCD) ^[2][3]
• Obstructive CAD: typically defined as the presence of a ≥ 50% atherosclerotic coronary artery stenosis ^[1]
• Nonobstructive CAD: typically defined as atherosclerotic changes to coronary arteries without stenosis above 50% ^[1]

Chest pain and angina ^[1][4][5]

Preferred terminology for causes of chest pain or discomfort

The patient's description of their symptoms may be used to inform the suspected cause of chest pain and the probability of cardiac ischemia on a spectrum from low to high probability.

• Cardiac: likely associated with cardiac ischemia based on symptom description (e.g., central, retrosternal, squeezing, pressure, exertional)
• Possible cardiac: may be associated with cardiac ischemia based on symptom description (e.g., stabbing, tearing, ripping, burning)
• Noncardiac: unlikely to be associated with cardiac ischemia based on symptom description (e.g., pleuritic, positional, fleeting)

Historical terminology for types of chest pain

Use of the following terms is no longer recommended. ^[1][4][5]

• 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 above criteria
• Nonanginal chest pain: fulfills one or none of the above criteria

• CAD is the leading cause of death in the US and worldwide. ^[6]
• The lifetime risk of coronary artery disease at age 50 is approx. 50% for men and 40% for women. ^[7]

Epidemiological data refers to the US, unless otherwise specified.

• CAD is caused by atherosclerosis.
• See “Risk factors for atherosclerosis.”

Plaque formation and coronary artery stenosis ^[8][9]

• 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 MI (see “Acute coronary syndrome”).
• Coronary flow reserve (CFR): the difference between maximum coronary blood flow and coronary flow at rest (denoting the ability of the coronary capillaries to dilate and increase blood flow to the myocardium)
  • Expressed as a ratio of hyperemic blood flow to blood flow at rest
  • Serves as a marker for microvascular function
  • 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.

Effect of vascular stenosis on resistance to blood flow ^[10]

• 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 oxygen supply-demand mismatch ^[11]

• 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 (e.g., during physical exertion or stress, or in chronic hypertension)
  • ↑ Heart rate
  • ↑ Afterload
  • Anemia

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

Myocardial ischemia ^[11]

• Reversible ischemia: Tissue is ischemic but 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 coronary revascularization)
    • 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.

Angina and anginal equivalents

Angina pectoris is the cardinal symptom of CAD but may be absent, especially in older patients and patients with diabetes mellitus. ^[1][12]

Angina pectoris ^[1]

• Paroxysmal attacks or retrosternal chest pain, pressure, discomfort, or tightness caused by myocardial ischemia
• Common triggers include physical and/or mental stress and exposure to cold.
• Typical characteristics include:
  • No chest wall tenderness
  • Gradual increase in intensity
  • Radiates to adjacent areas (e.g., left arm, neck, jaw,; epigastric region, and/or back)
  • Not affected by body position or respiration
  • Typically triggered by exertion or stress but can occur at rest

Anginal equivalents ^[1][4][13]

• Symptoms of myocardial ischemia other than chest pain
• Women are more likely than men to present with accompanying symptoms. ^[1]
• Possible manifestations include:
  • Gastrointestinal discomfort
  • Dyspnea
  • Dizziness, palpitations
  • Restlessness, anxiety
  • Autonomic symptoms (e.g., diaphoresis, nausea, vomiting, syncope)
  • Acute delirium and/or unexplained falls in patients > 75 years of age

Stable angina ^[1][14]

• Symptoms are reproducible.
• Severity, frequency, and threshold for the reproduction of symptoms are predictable.
• Symptoms often subside within minutes with rest and/or administration of nitroglycerin ^[1]

• Diagnostic testing may be indicated for preoperative cardiac assessment.
• The USPSTF does not recommend using resting ECG or exercise ECG to screen asymptomatic adults with low ASCVD risk. ^[15]

The following recommendations apply to patients with no history of CAD who present with symptoms consistent with chronic stable angina. For evaluation of unstable angina (e.g., new or worsening chest pain), see “Diagnosis of ACS.”

Approach ^[1][4][16]

• Perform a clinical evaluation.
• Obtain a resting ECG.
• Determine the pretest probability (PTP) for obstructive CAD.
• Additional diagnostic testing is based on the PTP of CAD.

Physical examination findings may be normal in patients with CAD.

Clinical evaluation ^[1]

• Obtain focused patient history.
  • Determine the nature and frequency of symptoms, including angina episodes.
  • Assess for symptoms of ischemia other than chest pain (e.g., anginal equivalents).
• Identify ASCVD risk factors.
• Perform a physical examination to assess for:
  • Clinical features of peripheral vascular disease
  • Clinical features of heart failure
  • Features of valvular heart diseases

Resting ECG ^[1][3]

• Indication: all patients with angina or anginal equivalents ^[1]
• Goal: assess for ischemic ECG changes
• Findings
  • Usually normal in stable angina
  • Absence of ischemic changes does not rule out underlying ischemia (e.g., an uninterpretable ECG can mask ischemic changes).

Patients with obvious noncardiac chest pain (e.g., herpes zoster, rib fracture) and reassuring ECG do not require further cardiac testing. ^[1]

Initiate immediate diagnosis of ACS in patients with ischemic ECG changes consistent with acute ischemia.

Assessment of pretest probability for obstructive CAD ^[1][17]

Models and scores to estimate PTP for obstructive CAD include:

• Extended CAD consortium model
• PTP model for obstructive CAD

PTP model for obstructive CAD based on age, sex, and symptoms ^[1]

Other factors that independently increase PTP ^[4]

• 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 ^[1]

Approach to sequential diagnostic testing ^[1]

Patients with low PTP of obstructive CAD

• Cardiac testing is not routinely recommended.
• Studies considered in select patients
  • CAC scoring (to rule out CAD)
  • Exercise ECG testing (to rule out myocardial ischemia)

Additional cardiac testing is not routinely recommended in patients with a low PTP for obstructive CAD. ^[1]

Patients with intermediate to high PTP of obstructive CAD

• Initial test
  • CCTA: preferred for patients aged < 65 years, if less obstructive CAD is suspected, or if stress testing is contraindicated
  • OR cardiac stress testing: preferred for patients aged ≥ 65 years, if more obstructive CAD is suspected, or if CCTA is contraindicated
    • Stress imaging is usually preferred.
    • Stress ECG testing may be reasonable in the absence of an uninterpretable ECG.
• Subsequent testing
  • If CCTA or cardiac stress test results indicate CAD: Obtain invasive coronary angiography to confirm diagnosis.
  • If CCTA is inconclusive: Consider stress imaging.
  • If cardiac stress testing results are inconclusive or negative despite persistent symptoms:
    • Consider CCTA.
    • Coronary angiography may be considered if there is high clinical suspicion for CAD.
  • Intermediate to high PTP with concerning ECG findings, signs of heart failure, or heart murmur: Consider TTE to evaluate LVEF and assess for other cardiac abnormalities.

Exercise stress testing is preferred over pharmacological stress testing in patients who can exercise.

Diagnostic tests

The following tests can be used to diagnose CAD and/or assess risk for cardiac events.

CAC score ^[1][18]

• Use: measures the amount of calcification in the coronary arteries
• Indications
  • May be considered in select patients with low PTP for obstructive CAD to rule out CAD
  • May be used in patients who have intermediate to high PTP for obstructive CAD and are undergoing stress testing
• Interpretation: A score of 0 in patients with low PTP for obstructive CAD can eliminate the need for further testing.

CCTA ^[1]

• Use: visualizes coronary artery anatomy
• Indication
  • Symptomatic patients with intermediate to high PTP for obstructive CAD (to support diagnosis, stratify risk, and/or guide treatment decisions)
  • Select asymptomatic patients with high risk for CAD ^[19]
• Findings in CAD ^[20]
  • May show calcified or noncalcified plaques
  • May show coronary stenosis

Cardiac stress testing ^[1]

See “Cardiac stress testing” for procedure details.

• Indications
  • Intermediate to high PTP for obstructive CAD
  • May be considered in select patients with low PTP for obstructive CAD to rule out myocardial ischemia
• Findings suggesting CAD ^[3]
  • Stress ECG
    • Downsloping ST depression or horizontal ST depression of ≥ 0.1 mV (1 mm) at peak exercise intensity
    • ST elevation of ≥ 0.1 mV (1 mm) in leads with no preexisting Q waves (except in V1 or aVR) : high-risk ECG finding consistent with acute coronary syndrome
    • STEMI-equivalent ECG findings
  • Stress echocardiography
    • New or worsening wall motion abnormalities
    • Changes in global left ventricular function
  • Stress myocardial perfusion imaging: decreased myocardial perfusion
  • Stress CMR: new wall motion abnormality or perfusion abnormality

Invasive coronary angiography ^[1][16]

See “Cardiac catheterization” for details on procedure and other indications.

• Indications
  • May be considered in select patients with abnormal noninvasive cardiac testing results, e.g.:
    • Obstructive CAD on CCTA and one or more of the following:
      • Frequent symptoms
      • High-risk CAD (e.g., significant left main disease)
      • Additional findings (e.g., moderate to severe ischemia on stress testing)
    • Moderate-severe ischemia on stress testing and persistent symptoms of ischemia despite appropriate therapy
  • May be considered if clinical suspicion for CAD is high despite negative or inconclusive results on stress imaging

• Uses
  • Direct visualization of coronary arteries
  • Determine feasibility of PCI
• Interpretation ^[3]
  • Extent of disease is reported as either the number of involved vessels (1-, 2-, or 3-vessel disease) 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)

Cardiac catheterization is indicated in patients with acute chest pain and other concerning clinical findings (e.g., hypotension) or ECG changes that suggest acute coronary syndrome (e.g., new heart blocks or arrhythmias).

Other indications for invasive coronary angiography include known CCD with any of the following: either worsening symptoms or functional capacity despite optimized management, new LV dysfunction, and/or new heart failure. ^[1][16]

Description ^{[1][3][4][21][22][23]}

• The goal is to detect evidence of stress-induced ischemia.
• Heart rate is monitored throughout the study ^[24]
  • 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.

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). ^[25]

Types of stress induction

• Exercise stress tests (e.g., treadmill or bicycle): first-line ^[17][23]
• Pharmacological stress tests (e.g., vasodilator or inotropic medication): alternative in patients unable to exercise ^[4]

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. ^[25]

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). ^[17][24][25]
• 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

See “Differential diagnosis of chest pain.”

The differential diagnoses listed here are not exhaustive.

The following content applies to patients with diagnosed CAD. See “ACS management” for the management of patients with acute symptoms.

Approach ^[16][26]

• Start antianginal therapy as necessary.
• For all patients, initiate measures to prevent cardiovascular events, including:
  • Lifestyle modifications for ASCVD prevention
  • Antiplatelet therapy
  • Lipid-lowering therapy
  • Colchicine therapy may be considered.
• Manage comorbidities.
• Consider coronary artery revascularization for select patients (e.g., patients with new LV systolic dysfunction and/or heart failure).
• Offer select patients cardiac rehabilitation (e.g., after PCI or CABG).

All patients with CAD should receive education on risk factor reduction as well as treatment with antiplatelet agents and statins; antianginal medications are indicated if symptomatic. ^[16]

Antianginal therapy for CAD ^[16]

• Short-term relief and/or prevention of exertional angina: short-acting nitrates (e.g., sublingual nitroglycerin )
• Longterm management
  • First-line agents:
    • Beta blockers (e.g., carvedilol , metoprolol , bisoprolol )
    • OR CCBs (e.g., amlodipine , nifedipine , verapamil )
    • OR long-acting nitrates (e.g., isosorbide dinitrate , isosorbide mononitrate )
  • If symptoms persist, begin combination therapy with a second first-line agent, i.e.:
    • A beta blocker PLUS a long-acting nitrate or a dihydropyridine CCB
    • A CCB PLUS a long-acting nitrate
  • Consider ranolazine if first-line agents are ineffective or not tolerated.
• Cautions
  • Nondihydropyridine CCBs (e.g., verapamil) can cause worsen cardiac conduction and function in patients on beta blockers or with LV dysfunction. ^[16]
  • Concomitant use of nitrates and PDE-5 inhibitors (e.g., sildenafil) can cause severe hypotension.
  • Avoid partial beta agonists (e.g., pindolol, acebutolol) as their sympathomimetic activity can increase MVO₂. ^[3][27]

Beta blockers should only be given if there is a specific indication (e.g., post-MI, angina pectoris, or LVEF ≤ 50%). ^[16]

Prevention of cardiovascular events ^[16]

Coronary artery disease is a type of ASCVD. See also “Management of ASCVD.”

General measures ^[16]

• Age-appropriate immunizations (e.g., COVID-19 vaccination, pneumococcal vaccine, and annual influenza vaccination)
• Lifestyle modifications for ASCVD prevention
  • Diet emphasizing healthy plant-based foods and lean protein (e.g., plant-based diet)
  • Smoking cessation
  • Increased physical activity
  • Limiting alcohol consumption
  • Obesity management if indicated
  • Minimizing exposure to air pollution

Antiplatelet therapy ^[16]

• Start single-agent antiplatelet therapy with either:
  • Aspirin (preferred) ^[16]
  • OR clopidogrel (if aspirin is not tolerated)
• Dual antiplatelet therapy (DAPT) with aspirin and clopidogrel for a limited time may be used if indicated (e.g, for 6 months after PCI followed by single antiplatelet therapy).
• DAPT may be extended in certain patients (e.g., 1–3 years after MI in patients with low bleeding risk).
• Aspirin PLUS vorapaxar may be considered in select patients with low stroke risk in consultation with a cardiologist
• Aspirin PLUS low-dose DOAC (e.g., rivaroxaban ) can be considered for patients at high risk of MACE and low to moderate bleeding risk but no other indication for DAPT or therapeutic DOAC. ^[16]
• In patients on DOAC therapy who require antiplatelet therapy, consider treatment strategy based on bleeding risk and thrombotic risk in consultation with a cardiologist.

Long-term NSAIDS should not be used in patients with CCD, as they can increase cardiovascular complications.

Proton pump inhibitors can reduce the risk of GI bleeding in patients on DAPT.

Lipid-lowering therapy

• Start high-intensity statin therapy.
• Consider addition of nonstatin lipid-lowering agents (e.g., ezetimibe), in patients with both of the following:
  • Very high risk of future ASCVD events
  • Inadequate response to statin monotherapy
• See “Lipid-lowering therapy for ASCVD” for details, including agents and dosages.

RAAS inhibitor therapy

• Indication: patients with co-occuring hypertension, diabetes mellitus, LVEF ≤ 40%, and/or CKD ^[16]
• Preferred: ACE inhibitors (e.g., lisinopril , ramipril )
• Alternative (if ACE inhibitors are not tolerated): angiotensin receptor blockers (e.g., losartan , valsartan )

Colchicine

• Colchicine (off-label) may be considered in patients with high risk of ASCVD events despite adequate management. ^[16]
• Monitor patients for adverse effects.

Revascularization for stable CAD ^[16][26]

Revascularization is not routinely indicated for patients with stable CAD; tailor decisions with a multidisciplinary team (e.g., interventional cardiologists, cardiac surgeons).

• Indications
  • Activity-limiting symptoms due to significant coronary artery stenosis despite optimized pharmacological treatment
  • High-risk anatomic lesions, e.g.:
    • Multivessel disease, especially in patients with LVEF ≤ 35% ^[16][26]
    • Significant LMCA stenosis
    • May be considered for significant 3-vessel disease in patients with normal LVEF ^[26]
  • Newly diagnosed HFrEF or clinical heart failure ^[16]
• Options ^[26]
  • CABG is generally preferred in complex situations, e.g.:
    • Significant LMCA stenosis or multivessel disease in patients with complex CAD
    • Multivessel disease with proximal LAD involvement and concomitant diabetes mellitus ^[28]
  • PCI
    • May be preferred in patients with high surgical risk
    • Reasonable alternative to CABG in select patients

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

Antianginal medications relieve symptoms by reducing myocardial oxygen demand (MVO₂); and/or increasing myocardial blood supply. ^[16]

Beta blockers and nitrates

Ranolazine

• Ranolazine is a metabolic modulator that reduces MVO₂ without altering heart rate or BP. ^[29]
  • Inhibition of late inward sodium channels on cardiac myocytes → reduced calcium influx via sodium-calcium channel pump → reduced wall stress and MVO₂ ^[30]
  • Decreased rate of fatty acid beta-oxidation (aerobic process) with a simultaneous increase in glycolysis (anaerobic process) ^[31]
• Adverse effects include nausea, constipation, headache, dizziness, bradyarrhythmias, and QT prolongations.

Management of hypertension ^[16][27]

• Recommend lifestyle changes for managing hypertension as first-line treatment for all patients.
• Target BP in hypertension: < 130/80 mm Hg ^[27]
• First-line pharmacological therapy: beta blockers, ACE inhibitors, or ARBs
• Second-line options include dihydropiridine calcium channel blockers (CCBs), long-acting thiazide diuretics, and mineralocorticoid receptor antagonists.
• See “Antihypertensive therapy” for details, including agents and dosages.

Management of diabetes mellitus ^[16]

• Individualized glycemic goals (e.g., HbA1c < 7%; for patients aged < 65 years) ^[16]
• Use noninsulin diabetes medications with known protective cardiovascular effects (i.e., GLP-1 receptor agonists or SGLT-2 inhibitors). ^[32]
• See “Antihyperglycemic treatment of diabetes mellitus” for details and dosages.

Management of heart failure ^[16]

• All patients: SGLT-2 inhibitor therapy
• Patients with HFrEF
  • Beta blockers: Carvedilol, metoprolol succinate, and bisoprolol are preferred agents in patients with LVEF < 50%.
  • ACE inhibitors (e.g., lisinopril) or ARBs (e.g., losartan).
• See “Pharmacotherapy for heart failure” for details and dosages.

Management of CKD ^[16]

• ACE inhibitors (e.g., lisinopril) or ARBs (e.g., losartan)
• See “Pharmacotherapy for CKD" and “Antihypertensive therapy” for details and dosages.

In patients with CKD who require PCI, take measures to avoid contrast-related acute kidney injury (e.g., adequate hydration, minimized volume of contrast media, high-dose statins). ^[16]

Management of mental health conditions ^[16]

• Targeted mental health screening for adults (e.g., major depressive disorder, anxiety disorder)
• Screening for substance use (e.g., alcohol, cocaine)
• Treatment (nonpharmacological and/or pharmacological) of comorbid mental health conditions

Management after MI ^[16]

• Start beta blockers after MI to reduce recurrence. ^[33]
• Long-term use (> 1 year) of beta blockers may not provide continued benefit in patients with no other indications. ^[16]

Beta blockers reduce the risk of MI, relieve symptoms, and may improve exercise tolerance.

• Prognostic factors
  • Left ventricular function: increased mortality if EF < 50% ^[34]
  • 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% ^[3]
  • 25% of patients will develop acute MI within the first 5 years. ^[35]
  • High-grade stenosis is associated with an unfavorable prognosis.

See “Primary prevention of ASCVD.”

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