Coronary Artery Disease - Unstable Angina/Non-STEMI Topic Review

Pathophysiology | Physical Examination | Diagnosis | Symptoms |  Treatment – Prevention • Invasive vs. Conservative • Medical Therapy | Special Situations


The acute coronary syndromes include unstable angina, non-ST segment elevation myocardial infarction and ST segment elevation myocardial infarction. The terms “transmural,” “non-transmural,” “Q wave MI” and “non-Q wave MI” have fallen out of favor.

The differences between the three types of ACS are discussed below. The common pathophysiology in ACS occurs when an atherosclerotic coronary plaque becomes unstable, leading to a series of events that eventually results in partial or total thrombotic occlusion of an epicardial coronary artery.

Unstable Angina Pectoris 

Three different presentations of unstable angina include:

  • New-onset exertional angina, even if relieved with rest and requiring a consistent amount of exertion to produce symptoms. Angina is considered unstable when it first occurs.
  • Previously stable exertional angina that now occurs with less physical exertion.
  • Anginal symptoms at rest, that occur without physical exertion

With unstable angina, cardiac enzymes remain normal or are only very minimally elevated.

Non-ST Segment Elevation Myocardial Infarction 

Anginal symptoms/chest pain at rest that result in myocardial necrosis as identified by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) without ST segment elevation on the 12-lead ECG. ECG changes may include ST and T-wave abnormalities.

ST Segment Elevation Myocardial Infarction 

Anginal symptoms/chest pain at rest associated with myocardial necrosis, indicated by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) and ST segment elevation on the 12-lead ECG.

Classification of Myocardial Infarction

According to the Fourth Universal Definition of Myocardial Infarction (MI), an MI is defined as an acute myocardial injury accompanied by symptoms of myocardial ischemia, signs of ischemia on an ECG or evidence of a new regional wall motion abnormality. Type 1 and type 2 MIs are distinguished by pathophysiology (DeFilippis AP, et al. Circulation. 2019;2b-d). Type 1 MI is “caused by atherothrombotic coronary artery disease and usually precipitated by atherosclerotic plaque disruption (rupture or erosion),” while a type 2 MI is “caused by a mismatch between oxygen supply and demand by a pathophysiological mechanism other than coronary atherothrombosis” pathophysiology (DeFilippis AP, et al. Circulation. 2019;2d).

Pathophysiology – CAD - Unstable Angina/Non-STEMI

Some atherosclerotic plaques have a stable fibrous cap, while others are thin and considered “vulnerable.” Unfortunately, the techniques and expertise required to distinguish these is limited to a few research centers.

The “vulnerable plaque” responsible for acute coronary syndromes and, ultimately, coronary artery thrombosis, has a thin cap and a necrotic core (see Atherosclerosis Topic Review). A key protein component of the clotting cascade known as “tissue factor” is located, among many other places, within the necrotic core of the plaque.

If the thin fibrous cap that covers the plaque is disrupted or ulcerated, the result is called “plaque rupture” or “plaque erosion.” This exposes tissue factor to blood, activates the clotting cascade, and leads to intravascular thrombosis. Plaque rupture and thrombosis frequently occurs in plaques causing only modest coronary stenosis (< 50% luminal narrowing).

Patients experiencing unstable angina have a lower incidence of coronary thrombosis compared to those with non-ST segment elevation MI (non-STEMI) or ST segment elevation MI (STEMI). Unstable angina is more often the result of worsening fixed atherosclerotic stenosis. Plaque rupture or erosion with resulting intracoronary thrombus is the predominant pathophysiologic mechanism of non-STEMI and STEMI.

Physical Examination – CAD - Unstable Angina/Non-STEMI

Physical examination findings are relatively nonspecific and similar to that described in the Stable Angina Topic Review. Cardiac findings are usually only present during the ischemic episode. During an anginal attack, the heart rate and blood pressure may be elevated due to increased sympathetic tone.

During myocardial ischemia, fourth heart sound (S4) may be present due to impaired left ventricular relaxation. Myocardial relaxation is an active, energy (ATP)-requiring process, and the supply of ATP is reduced during ischemia. Atrial contraction generates an S4 heart sound when the ischemic left ventricle becomes less compliant. With extensive or more prolonged ischemia, impaired systolic and diastolic left ventricular function with end-diastolic pressure (LVEDP) increases may result in transient pulmonary venous congestion manifesting as dyspnea and rales.

During inferior ischemia, posteromedial papillary muscle dysfunction can cause mitral regurgitation, resulting in a holosystolic murmur at the cardiac apex radiating to the axilla; see Heart Murmurs Topic Review. This rarely occurs during anterior or lateral ischemia because the anterolateral papillary muscle has a dual supply from the left anterior descending and circumflex coronary artery.

Diagnosis – CAD - Unstable Angina/Non-STEMI

The diagnosis of unstable angina and non-STEMI is primarily based on the clinical presentation supported by the ECG and laboratory assessment of specific cardiac enzymes.

The ECG may show multiple abnormalities, but, by definition, there is no ST segment elevation. The most common finding is horizontal or down-sloping ST segment depression. T waves may be inverted, usually symmetrically. These changes may vary over several hours.

Unstable angina and non-STEMI can both occur with a normal or non-specifically abnormal ECG. Observation with repeated ECGs and cardiac-specific enzyme measurements, usually 6 to 8 hours apart, is required to confirm or exclude unstable angina and non-STEMI. Cardiac enzymes (troponin and creatine kinase) may not show significant elevation until 3 to 4 hours after ischemic injury; see Cardiac Enzymes Topic Review).

The distinction between unstable angina and non-STEMI is largely based on laboratory measurement of cardiac enzymes. With unstable angina, there is no — or only very minimal — enzyme elevation, whereas a non-STEMI results in myocyte necrosis with detectable enzyme abnormalities

Symptoms – CAD - Unstable Angina/Non-STEMI

The symptoms of occlusive coronary artery disease can manifest as chronic stable angina pectoris or angina as a part of an acute coronary syndrome (ACS) — both of which are similar, with the latter frequently occurring at rest. Substernal chest pressure with radiation to the medial portion of the left arm or left jaw is the classic description.

Patients may describe angina as a “tightness,” “discomfort, not pain,” “squeezing,” “indigestion,” “heaviness,” or an “elephant sitting on my chest,” and often describe the sensations of squeezing and tightness by placing a fist in the center of the chest (Levine’s sign). Pain from angina usually begins gradually and lasts for at least 5 minutes. The pain is diffuse and difficult to localize to one part of the chest.

Less common presentations of angina include isolated shoulder pain, pain in both arms, left wrist pain, right-sided chest or jaw pain, radiation to the right arm, mid-thoracic back pain, and dyspnea without chest discomfort. Angina is rarely described as sharp.

Some associated symptoms that may occur with the classic anginal symptoms described above include dyspnea, diaphoresis (cold sweats), fatigue/weakness, nausea and dizziness. Women, elderly patients and patients with diabetes tend to have more atypical presentations of angina.

Many noncardiac disease states can also cause chest pain. Important features suggestive of noncardiac causes of chest pain include worsening with inspiration (pleuritic pain), short duration of the pain (below 5 minutes), a small pinpoint area of pain (angina is more diffuse) and lack of relief with nitroglycerine. Esophageal spasm — although a relatively uncommon cause of chest pain — can be relieved with nitroglycerine, mimicking symptoms of angina. Sharp, shooting chest pains lasting a few seconds to 1 minute are common and usually musculoskeletal in origin.

When an ACS with intra-coronary thrombosis occurs, it often produces severe prolonged anginal symptoms at rest; see Acute Coronary Syndromes Topic Review.

Treatment – CAD - Unstable Angina/Non-STEMI


Primary prevention refers to reducing the prevalence of cardiovascular disease risk factors in people without known disease in order to prevent a first CV event. Secondary prevention refers to intervention for those with known CAD that is aimed at reducing both the progression of atherosclerosis and the risk for ACS (mediated by intra-coronary thrombosis).

Primary Prevention

Primary prevention includes public health measures and patient-specific treatment focused on CVD risk factors such as LDL cholesterol, tobacco use, hypertension and obesity. Because the baseline risk of CV events is lower in the primary prevention population than in the secondary prevention population, the absolute benefit of reducing risk factors for any individual may be relatively low. However, the primary prevention population is far larger than the secondary prevention group, and the population benefits are substantial.

Treatment of lipid disorders for primary prevention include dietary and lifestyle modifications and medical therapy with HMG-CoA reductase inhibitors (statins). The American College of Cardiology/American Heart Association guidelines on the primary prevention of CVD (released in 2019) recommend lifestyle-based risk reduction for patients younger than 40, although statins may be considered in patients with family history of ASCVD and LDL cholesterol (LDL-C) of 160 mg/dL or above. For patients between the age of 40 and 75 and LDL-C ≥ 70 to < 190 mg/dL without type 2 diabetes, the guidelines recommend establishing a 10-year ASCVD risk score (pooled cohort equations (PCE) are most often used for this calculation, although other methods exist (Arnett D, et al. Circulation. 2019;8a, 9a). For low-risk patients (< 5%) lifestyle interventions are recommended; for borderline-risk patients (5% to < 7.5%), statins may be considered. A moderate-intensity statin (e.g., atorvastatin 10 mg, rosuvastatin 10 mg, or simvastatin 20-40 mg (Grundy SM, et al. J Am Coll Cardiol. 2019;10a) is recommended for intermediate risk patients (≥ 7.5%-< 20%) if ASCVD risk “enhancers” are present. Statins are recommended for patients whose 10-year ASCVD risk if 20% or higher. A high-intensity statin (e.g., atorvastatin 80 mg, rosuvastatin 40 mg; Grundy SM, et al. J Am Coll Cardiol. 2019;10a) is also indicated in all patients with LDL-C of 190 mg/dL or higher. Patients with type 2 diabetes between the age of 40 and 75 should be started on a moderate-intensity statin, although a high-intensity statin may be considered in those with higher risk. For patients older than 75, a clinical assessment and a physician-patient discussion around risk are needed to decide on the appropriateness of statin therapy (Arnett D, et al. Circulation. 2019;20a).

Antiplatelet therapy is not recommended for all patients for primary prevention of CVD; however, an individualized approach should be taken. If the risk for bleeding is low, yet there is a significant risk for CVD that does not meet a coronary risk equivalent — putting the patient in the secondary prevention category (see below) — antiplatelet therapy can be considered. According to the 2019 Guidelines on the primary prevention of CVD, low-dose (75 to 100 mg orally daily) aspirin might be considered (Class IIb recommendation) for the primary prevention of ASCVD among select adults 40 to 70 years of age who are at higher ASCVD risk but not at increased bleeding risk (Arnett D, et al. Circulation. 2019;28a(e204)).

Secondary Prevention

Coronary risk equivalents (10-year risk for cardiac event > 20%) include the following:

  • Non-coronary atherosclerotic disease: Peripheral arterial disease (PAD), carotid artery disease, renal artery disease, abdominal aortic aneurysm
  • Type 2 diabetes
  • Multiple risk factors: Using the Framingham risk score, a 10-year risk for a cardiac event is greater than 20%
  • Chronic kidney disease

Patients meeting the coronary risk equivalents above should be considered as having established asymptomatic coronary artery disease.

Secondary prevention includes antiplatelet therapy and a HMG-CoA reductase inhibitor regardless of the serum LDL-C level. Smoking cessation, BP control, HDL/triglyceride therapy, exercise and weight loss are discussed elsewhere.

Aspirin significantly reduces the risk for ACS events in patients with established coronary disease. The data to support risk reduction in patients with coronary risk equivalents are not as robust, but aspirin is still recommended. There is a dose-related risk for major bleeding with aspirin, especially from the gastrointestinal tract. This risk is acceptable at low doses (70 to 100 mg per day) considering the CV benefits of aspirin in secondary prevention patients. The risk-benefit ratio is not as favorable in primary prevention patients ― with lower baseline CV risk than a secondary prevention patient, but a similar bleeding risk. Clopidogrel is guideline-recommended (Level of Evidence B) for secondary prevention in aspirin-intolerant patients following an NSTE-ACS event.

A moderate dose of an HMG-CoA reductase inhibitor such as atorvastatin 40 mg or simvastatin 40 mg is recommended initially. In most patients with CAD or coronary risk equivalent, the actual goal LDL cholesterol is less than 100 mg/dL. However, if high-risk features including prior ACS, poorly controlled risk factors (hypertension, tobacco use) and type 2 diabetes are present, the goal is less than 70 mg/dL. Data from both the Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) trial and Treating to New Targets (TNT) trial support these recommendations.

Early Invasive vs. Initial Conservative

Two distinct treatment pathways exist for the treatment of unstable angina/non-STEMI: the “early invasive” strategy and the “ischemia-guided” strategy (formerly known as “initial conservative management”).

An early invasive strategy is defined as proceeding to coronary angiography with a decision for revascularization — percutaneous coronary intervention (PCI; also known as coronary stenting) or coronary artery bypass graft surgery (CABG) based on angiographic coronary anatomy — within 24 hours of hospital admission. An ischemia-guided strategy is defined as initial medical therapy, only, deferring coronary angiography and possible revascularization unless or until there is evidence of recurrent ischemia. In both strategies, patients receive dual antiplatelet therapy (DAPT) and anticoagulation therapy, although the downstream management differs. (Amsterdam EA, et al. J Am Coll Cardiol. 2014;28b(e166).)

Factors associated with appropriate selection of a treatment strategy include: (Amsterdam EA, et al. J Am Coll Cardiol. 2014;30a(e168),Table 8)

Immediate invasive strategy (within 2 hours):

  • Refractory angina
  • Signs or symptoms of heart failure or new or worsening mitral regurgitation
  • Hemodynamic instability
  • Recurrent angina or ischemia at rest or with low-level activities despite intensive medical therapy
  • Sustained ventricular tachycardia or ventricular fibrillation

Ischemia-guided strategy:

  • Low-risk score (e.g., TIMI [0 or 1], GRACE [< 109])
  • Low-risk troponin-negative female patients
  • Patient or clinician preference in the absence of high-risk features

Early invasive strategy (within 24 hours):

  • None of the factors associated with immediate invasive or ischemia-guided strategies, but GRACE risk score > 140
  • Temporal change in troponin
  • New or presumably new ST depression

Delayed invasive strategy (within 25 to 72 hours):

  • None of the above factors but diabetes
  • Renal insufficiency (glomerular filtration rate < 60 mL/min/1.73 m2)
  • Reduced left ventricular systolic function (ejection fraction < 40%)
  • Early postinfarction angina
  • PCI within 6 months
  • Prior CABG
  • GRACE risk score 109–140; TIMI score ≥ 2

The Invasive vs. Conservative Treatment in Unstable Coronary Syndromes (ICTUS) trial showed no difference in the early invasive and ischemia-guided approaches over 3 years. The third Randomized Intervention Treatment of Angina (RITA-3) trial showed no difference at 1 year, but there was a reduction of death or MI at 5 years in the early invasive arm, seen mainly in high-risk patients. These data support the approach mentioned above, to only perform angiography/PCI on high-risk patients.

When an ischemia-guided strategy is chosen for initial management, additional risk stratification must be done to evaluate whether high-risk features that would warrant changing to an invasive approach are present. If the high-risk features outlined above develop during observation, an invasive approach should be undertaken

Medical Therapy

The armamentarium of medical management of unstable angina and non-STEMI includes beta-blockers, angiotensin converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs), aldosterone antagonists, HMG-CoA reductase inhibitors, calcium channel blockers, nitrates, antiplatelet therapy and anticoagulation therapy. Treatment with fibrinolytics, or tissue plasminogen activator (tPA), is not recommended for unstable angina and non-STEMI management — and only in certain instances for STEMI; for more details, see STEMI Topic Review.


Early administration of beta-blockers in unstable angina/non-STEMI patients decreases myocardial ischemia, reinfarction and the frequency of complex ventricular dysrhythmias and increases long-term survival (Amsterdam EA, et al. J Am Coll Cardiol. 2014;21b-c(e159)). The 2014 ACC Guidelines on unstable angina/non-STEMI recommend (Class I recommendation) initiating beta-blocker therapy within the first 24 hours of hospitalization, except in patients who show: 1) Signs of heart failure; 2) Evidence of low-output state; 3) Increased risk for cardiogenic shock (> 70 years of age, heart rate > 110 beats per minute, systolic BP < 120 mm Hg and late presentation); and 4) Other contraindications to beta-blockers (such as PR interval > 0.24 second, second- or third-degree heart block without a cardiac pacemaker, active asthma or reactive airway disease). The guidelines warn against administering intravenous beta-blockers (Class III: Harm) in unstable angina/non-STEMI patients who have risk factors for shock, as beta-blockade may increase the likelihood of shock (Amsterdam EA, et al. J Am Coll Cardiol. 2014;21a,21d(e159)).

Angiotensin Converting Enzyme (ACE) Inhibitors/Angiotensin Receptor Blockers (ARBs)

There are fewer data to support the use of ACE inhibitors in unstable angina/non-STEMI than in STEMI, where definite benefits have been demonstrated. Nonetheless, ACC/AHA guidelines recommend that ACE inhibitors should be included in the hospital discharge medications for patients with hypertension, diabetes, LV systolic dysfunction (EF < 40%) and/or heart failure symptoms. Data are limited for individuals who do not meet these indications. An ARB is an acceptable alternative for patients who develop cough or other side effects related to ACE inhibitors.

Aldosterone Antagonists (Mineralocorticoid Receptor Antagonists – MRAs)

In the EPHESUS trial, eplerenone added to an ACE inhibitor was associated with lower mortality after an MI. This led to the recommendation for the prescription of eplerenone with an ACE inhibitor prior to hospital discharge after unstable angina/non-STEMI for individuals with left ventricular systolic dysfunction (EF < 40%) and either diabetes or symptomatic heart failure who have no contraindications (serum creatinine > 2.5 and or potassium > 5.0). Some clinicians prescribe spironolactone instead of eplerenone due to cost concerns; however, there are no head-to-head trial data to support this practice.

HMG-CoA Reductase Inhibitors

Every patient with unstable angina and non-STEMI should receive high-intensity statin therapy, unless contraindicated (Amsterdam EA, et al. J Am Coll Cardiol. 2014;22a). The Myocardial Ischemia Reduction With Acute Cholesterol Lowering (MIRACL) and Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 (PROVE-IT TIMI 22) trials used atorvastatin (80 mg per day given orally) with good results. Statin therapy should be lifetime after a person has an ACS, unless a contraindication exists.

Calcium Channel Blockers

The non-dihydropyridine calcium channel blockers diltiazem and verapamil may be used for patients without clinical heart failure or LV dysfunction and a contraindication to beta-blockers (asthma). Sublingual nifedipine is contraindicated due to a reflexive increase in sympathetic nervous system activity, which can be harmful.


Individualized nitrate dosing may be useful for the treatment of angina symptoms, hypertension and HF during unstable and non-STEMI; however, no clinical data have shown a mortality benefit associated with chronic nitrates. The use of nitrates should not preclude using drugs that do show a mortality benefit.

Antiplatelet Therapy

There are three main categories of antiplatelet therapy.

Aspirin: Aspirin acts by irreversibly blocking the enzyme cyclooxygenase resulting in decreased thromboxane A2 production and platelet inhibition.

P2Y12 receptor blockers/inhibitors: These include clopidogrel, prasugrel, ticagrelor, cangrelor and ticlopidine. Clopidogrel has delayed onset of action, no means of reversing the effects, and a significant percentage of nonresponders. Prasugrel and ticagrelor have a rapid onset of action and few — if any — nonresponders, but both carry a higher risk for bleeding. Prasugrel is not recommended in patients with prior TIA or stroke, as it may cause harm (class III). Cangrelor is a potent, rapidly acting, IV-administered P2Y12 platelet inhibitor that received FDA approval on the basis of superior results in reducing thrombotic events in patients undergoing PCI when compared to clopidogrel (De Luca L, et al. J Am Heart Assoc. 2021;1c-d). In the prescribing information, cangrelor is indicated “as an adjunct to PCI to reduce the risk of periprocedural MI, repeat coronary revascularization, and stent thrombosis in patients who have not been treated with a P2Y12 platelet inhibitor and are not being given a glycoprotein IIb/IIIa inhibitor.” (Chiesi USA. Kengreal package insert;1a.)

Glycoprotein IIb/IIIa inhibitors: This category includes abciximab (no longer available), eptifibatide and tirofiban. These agents very strongly inhibit platelet function by blocking the binding of fibrinogen to the activated glycoprotein IIb/IIIa receptor complex.

Initial Antiplatelet agents: As mentioned above, whether an early invasive or an ischemia-guided approach is chosen, all patients with unstable angina and non-STEMI should initially receive aspirin, a P2Y12 receptor blocker and an anticoagulant. Of the P2Y12 inhibitors, clopidogrel is frequently used; however, ticagrelor may be given instead of clopidogrel, as there are fewer nonresponders and it has a more rapid onset of action. The AHA/ACC Guidelines state that it is reasonable (Class IIa recommendation) to use ticagrelor in preference to clopidogrel (Amsterdam EA, et al. J Am Coll Cardiol. 2014;24b(e162)). Even when no revascularization is performed, as in the ischemia-guided strategy, a P2Y12 receptor blocker should be continued for 12 months. Anticoagulant options include unfractionated heparin, enoxaparin and fondaparinux (for both early invasive and ischemia-guided strategies), and bivalirudin (for early invasive strategy only; (Amsterdam EA, et al. J Am Coll Cardiol. 2014;29a(e167),Figure 3).

When an early invasive strategy is used, a glycoprotein IIb/IIIa inhibitor could be given in addition to aspirin and a P2Y12 inhibitor based on the patient’s risk. When high-risk features are present, such as delay to angiography and early recurrent anginal chest pains, a glycoprotein IIb/IIIa inhibitor should definitely be utilized prior to angiography. Eptifibatide and tirofiban are the preferred glycoprotein IIb/IIIa inhibitors in this setting. If a patient in the ischemia-guided category develops high risk features and PCI is planned, a glycoprotein IIb/IIIa inhibitor should be started.


Unless contraindicated, all patients with unstable angina and non-STEMI should receive anticoagulation. Based on available data and current guidelines, the choice of anticoagulant differs between early invasive and ischemia-guided management strategies.

With an ischemia-guided strategy, anticoagulation is initiated with either unfractionated heparin or low-molecular-weight heparin (enoxaparin or fondaparinux). Unfractionated heparin therapy should be continued for 48 hours; guidelines based on clinical trials state that low molecular weight heparin (enoxaparin or fondaparinux) should be continued for the entire length of hospitalization (Amsterdam EA, et al. J Am Coll Cardiol. 2014;24a(e162),Table 7).

If an early invasive strategy is employed, initial anticoagulation may be accomplished with unfractionated heparin, low molecular weight heparin or bivalirudin (Angiomax). Bivalirudin is not recommended for the ischemia-guided approach (Amsterdam EA, et al. J Am Coll Cardiol. 2014;24a(e162),Table 7).

Special Situations – CAD - Unstable Angina/Non-STEMI

Wellens’ Syndrome 

Although no formal guidelines exist specifically for this ECG change, an early invasive strategy is attractive due to the high-risk nature of critical proximal left anterior descending artery (LAD) disease. Patients with Wellens’ Syndrome ECG changes may show biphasic T waves in the anterior precordial leads or deep T-wave inversion throughout the precordial leads.

Non-cardiac Chest Pains

There are multiple causes of chest pains, and when the diagnosis is in question, a cardiac etiology must be assumed initially due to the life-threatening nature of ACS. A diagnosis of “unstable angina” is used frequently in patients with chest pain when the primary reason for continued observation in the hospital is to assure that an ACS is not present.

Platelet Assays 

Some institutions use platelet assays to identify clopidogrel nonresponders. Those patients are treated with prasugrel or ticagrelor instead. These platelet assays are not recommended in the ACC/AHA guidelines, but do not appear to pose any harm.

Arrhythmia During ACS 

Life-threatening ventricular tachycardia and ventricular fibrillation may complicate the ACS. Atrial fibrillation and atrial flutter occur frequently with ACS, particularly in older patients. Routine preventive measures to prevent arrhythmias during an ACS include beta-blocker treatment and attention to maintaining serum electrolytes (potassium and magnesium) within normal limits (total body electrolyte depletion may be a concern in patients who have been maintained on chronic loop-blocking diuretics).

Prophylactic administration of lidocaine to suppress premature ventricular contractions (PVCs) or prevent ventricular tachycardia/fibrillation is not recommended. The Cardiac Arrhythmia Suppression Trial (CAST) demonstrated increased mortality associated with anti-arrhythmic drugs including encainide, flecainide and moricizine for suppression of post-MI PVCs.

Atrial fibrillation may pre-exist or occur de novo with an ACS, including unstable angina and non-STEMI. Patients with AF who require anticoagulation for stroke prophylaxis must receive appropriate combination antithrombotic therapy to minimize bleeding risk (Kumbhani DJ, et al. J Am Coll Cardiol. 2021;3a-b). According to the 2020 ACC expert consensus decision pathway, ACS patients with AF receiving anticoagulation who require PCI should continue anticoagulant stroke prophylaxis indefinitely, and in addition receive a P2Y12 inhibitor (clopidogrel preferred) for up to 12 months (Kumbhani DJ, et al. J Am Coll Cardiol. 2021;9a). Patients with newly diagnosed AF who are already receiving antiplatelet therapy because of a previous ACS should either: 1) replace aspirin with a P2Y12 inhibitor (clopidogrel preferred) and start an oral anticoagulant (if within 12 months of an ACS event and/or a PCI); or 2) stop antiplatelet therapy altogether and start an oral anticoagulant (if more than 12 months have elapsed since an ACS event and/or a PCI). (Kumbhani DJ, et al. J Am Coll Cardiol. 2021;12a,13a-c.) Current data support the use of a direct-acting oral anticoagulant with a P2Y12 inhibitor (Lopes RD, et al. JAMA Cardiol. 2019;1a).

Anemia During ACS

There are no official guidelines regarding the threshold for transfusion in patients who are anemic during an ACS. In general, the hematocrit should be maintained at greater than 21% and preferably above 30%.

Wearable Cardioverter-Defibrillator (WCD) Devices

The 2017 ACC Guidelines on the prevention of sudden cardiac death state that the use of a wearable cardioverter-defibrillator (such as LifeVest) may be reasonable (Class IIb recommendation) in patients “at an increased risk of sudden cardiac death but who are not ineligible for an implantable cardioverter-defibrillator, such as awaiting cardiac transplant, having an LVEF of 35% or less and are within 40 days from an MI, or have newly diagnosed NICM, revascularization within the past 90 days, myocarditis or secondary cardiomyopathy or a systemic infection.” (Al-Khatib SM, et al. Circulation. 2017;77a(e348).)