BySteven Lome, MD

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Coronary Artery Disease - STEMI Topic Review

BySteven Lome, MD

Pathophysiology | Physical Examination | Diagnosis | Treatment – Revascularization • Medical Therapy | Complications

Introduction

The most serious form of the acute coronary syndrome, ST segment elevation myocardial infarction, or STEMI, most often results from complete thrombotic occlusion of a major epicardial coronary artery.

STEMI is a life-threatening, time-sensitive emergency. Early accurate diagnosis and prompt treatment to restore coronary perfusion, usually by percutaneous coronary intervention (PCI), are critical to effective management.

As the term STEMI implies, the 12-lead ECG shows significant ST segment elevation during STEMI, unlike the ST depressions and ST-T wave changes seen during unstable angina and non-ST segment elevation MI. The Figure below illustrates the ECG during an anterior ST segment elevation MI with “tombstoning” on the ECG.

With recent advances in interventional cardiology, the terms “transmural,” “non-transmural,” “Q wave MI,” and “non-Q wave MI” have fallen out of favor and are no longer recommended. The clinical differences between the types of acute coronary syndromes are discussed below.

Unstable Angina Pectoris

Three different presentations of angina qualify as “unstable”:

New-onset exertional angina; angina is considered unstable when it first occurs.
Previously stable exertional angina that now occurs with less physical exertion.
Anginal symptoms at rest, occurring without physical exertion.

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

Non-ST segment elevation myocardial infarction

Anginal symptoms/chest pain at rest that are associated with acute myocardial necrosis, as identified by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) without ST segment elevations 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 elevations on the 12-lead ECG.

Classification of Myocardial Infarction

According to the Fourth Universal Definition of Myocardial Infarction, a myocardial infarction (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 2019;2b-d(1662)] A 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.” [DeFilippis 2019;2d(1662)]

Before the routine use of acute interventions, the Killip Classification was used to predict mortality during STEMI. This system focused on physical examination and the development of heart failure to predict risk, as described below.

Class I: No evidence of heart failure (HF): mortality 6%
Class II: Findings of mild to moderate HF (S3 gallop, rales < halfway up lung fields or elevated jugular venous pressure): mortality 17%
Class III: Pulmonary edema: mortality 38%
Class IV: Cardiogenic shock defined as systolic blood pressure (BP) < 90 mm Hg and signs of hypoperfusion such as oliguria, cyanosis and sweating: mortality 67%

The original data (from 1967) showed the mortality rates listed above for each class. With advances in therapy, mortality rates have declined about 30% to 50% in each class.

Pathophysiology – CAD - STEMI

Some atherosclerotic plaques have a stable fibrous cap; others, with a thin cap, are considered “vulnerable.” Unfortunately, only a few research centers have access to the techniques and expertise required to assess plaque morphology in living patients in the catheterization laboratory.

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. There are conditions that mimic STEMI, and distinguishing these can be difficult; these are described in Diagnosis. Tissue factor, a key protein component of the clotting cascade, is located, among many other places, within the necrotic core of atherosclerotic plaques.

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

STEMI most often results from coronary thrombosis after plaque rupture rather than fixed obstruction. Unstable angina has a lower incidence of coronary thrombosis compared with non-STEMI or STEMI and is more often associated with fixed atherosclerotic stenosis (with critically low flow).

Physical Examination – CAD - STEMI

The physical examination findings during STEMI are similar to those of stable angina, unstable angina and non-STEMI, although frequently more dramatic due to the larger proportion of ischemic myocardium.

Physical examination findings are non-specific. The heart rate and BP may be elevated due to increased sympathetic tone, or the BP can be low due to reduced cardiac output (cardiogenic shock), depending on the extent of the STEMI.

An S4 heart sound may be present during myocardial ischemia due to impaired left ventricular relaxation resulting from a lack of adenosine triphosphate (ATP) production. Myocardial relaxation is an active process requiring energy (ATP), which is reduced during ischemia, and an S4 filling sound occurs when the noncompliant, stiffened left ventricle is not able to relax adequately as it receives blood during atrial contraction.

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 dual supply from the left anterior descending (LAD) and circumflex coronary artery.

When the left ventricular end-diastolic pressure (LVEDP) increases during myocardial ischemia, the right ventricle (RV) maintains cardiac output by increasing pulmonary arterial and venous pressure. This compensatory process may cause transient pulmonary edema with dyspnea and rales on lung examination.

Diagnosis – CAD - STEMI

The diagnosis of STEMI is primarily based on the clinical presentation, the 12-lead ECG and laboratory measurement of specific cardiac enzymes that are released with the significant myocardial necrosis occurring in the setting of STEMI.

Cardiac enzymes — also known as cardiac biomarkers — include myoglobin, troponin and creatine kinase (historically, lactate dehydrogenase (LDH) was also used; however, LDH is nonspecific).

Myoglobin

Myoglobin is released into circulation with any damage to muscle tissue, including myocardial necrosis. Because both cardiac and skeletal muscle contain myoglobin, elevations of myoglobin are not specific for MI. However, an increase in serum myoglobin can be detected early — only 30 minutes after injury occurs — in contrast to troponins and creatine kinase, which may take 3 to 4 hours to rise to detectable levels.

Troponin

The enzymes troponin I and troponin T are proteins with important roles in the contractile apparatus of the cardiac myocyte. The troponins are released into the circulation about 3 to 4 hours after the onset of MI and can be detected for up to 10 days afterwards. The long half-life allows for late diagnosis of MI but makes it difficult to detect reinfarction (for example, with acute stent thrombosis after PCI). Although there are a number of causes for troponin elevation unrelated to MI, troponin elevation is much more sensitive and specific than myoglobin and creatine kinase.

Creatine Kinase

Creatine kinase (CK), also known as creatine phosphokinase (CPK), is a muscle enzyme that has several isoenzymes. The MB isoform is specific to myocardial cells, whereas MM and BB are specific to skeletal muscle and brain, respectively. The MB-CK level increases approximately 3 to 4 hours after a MI and may remain elevated for 3 to 4 days. This makes it useful for the detection of re-infarction in the 4- to 10-day window after the initial insult. This contrasts with troponin, which remains elevated for 10 days.

ECG findings

ST segment elevations have several different patterns with STEMI and there are also some noncardiac causes of ST segment elevation that ECG readers need to recognize. Importantly, the finding of new left bundle branch block is considered equivalent to STEMI.

The first ECG change during STEMI is the appearance of “hyperacute T waves” — T waves that appear peaked and are related to localized hyperkalemia. These changes are rarely detected, as they are transient and frequently occur prior to hospital arrival. The tracing below shows hyperacute T-wave changes in the anterior leads.

The pattern of ECG changes in STEMI reflects the anatomy of coronary arteries. LAD occlusion produces ST elevation primarily in the precordial (V1-3) leads. Right coronary occlusion produces primary ST changes in the inferior leads in the frontal plane (II-III-AVF), and left circumflex occlusions manifest with ST elevation in the lateral leads (I, AVL and V5-6). Because of the variability of individual coronary anatomy, these patterns are generalizations, not hard and fast rules. ST segment elevation of at least 1 mm in two contiguous leads is required to diagnose STEMI, but there are two major exceptions:

1. The American College of Cardiology/American Heart Association definition of STEMI sets the following criteria: Anterior STEMI requires 2 mm of ST segment elevation in V2 and V3 in men aged 40 years and older; 2.5 mm in men younger than 40 years; and 1.5 mm in women regardless of age. (Thygesen 2018;22a)

Below is an ECG with changes of an acute anterio-lateral infarct with ST-elevation in V1-V4 as well as I and AVL:

2. Posterior STEMI, usually associated with occlusion of an anatomically dominant right coronary artery, may present with ST segment depression in V1 to V3 instead of elevation, because the ST elevation vectors are oriented away from (ie, negative in) the anterior chest leads.

ECG findings of an acute posterior wall MI may include the following:

New horizontal or downsloping ST-depression of 0.5 mm or more in two contiguous anterior precordial leads and/or T-inversion greater than 1 mm in two contiguous leads with prominent R wave or R/S ratio > 1. (Thygesen 2018;22a).
R/S wave ratio greater than 1 in leads V1 or V2.
ST segment elevation in the posterior leads (leads V7-V9).
Associated ST segment elevation in the inferior leads (II, III and aVF).

Below is an ECG of an infero-posterior STEMI:

Below are ECG examples of STEMI in differing regions.

Anterior wall MI

Inferior wall MI

Posterior wall MI

The appearance of new-onset left bundle branch block (LBBB) supports the diagnosis of an acute STEMI. Sgarbossa’s ST-segment criteria may add additional confirmatory information. In patients with chronic LBBB, Chapman’s sign (a new notch in the upslope of the R wave in leads I, AVL) may be useful when previous tracings are available for comparison.

Differential diagnosis of ST elevation

A good mnemonic for the causes of ST segment elevation on an ECG is “ELEVATION.”

Electrolyte abnormalities
Left bundle branch block
Early repolarization
Ventricular hypertrophy
Arrhythmia disease (Brugada syndrome, ventricular tachycardia)
Takotsubo/Treatment
Injury/Infection (pericarditis or cardiac contusion)
Osborne waves (hypothermia or hypocalcemia)
Nonatherosclerotic (vasospasm or angina)

The four most common causes of ST segment elevation that may mimic STEMI are reviewed here:

1. Left ventricular hypertrophy

When left ventricular hypertrophy (LVH) is present, the voltage on the 12-lead ECG is frequently increased; however, ST segment changes can also occur with LVH, mimicking STEMI or ischemic ST segment depressions. This is referred to as “LVH with strain” or “LVH with repolarization abnormality.” Distinguishing these changes from those during STEMI is important, though often difficult. The typical pattern with LVH includes deviation of the ST segment in the opposite direction of the QRS complex (discordance), along with a typical T wave inversion pattern.

2. Early repolarization

Early repolarization is not uncommon in younger individuals. Early repolarization is seen more frequently in Black males and in athletes. There is J-point elevation and upsloping ST segment elevation that may be diffuse but is generally more prominent in the precordial leads. (Casado Arroyo 2018;2a).

3. Pericarditis

Pericardial inflammation is associated with ST elevation. Initially in pericarditis there is diffuse concave upward ST segment elevation in most leads. Subtle PR depression may also occur inmost leads. Finally, notching at the end of the QRS complex may occur; see Pericarditis ECG Review for more details.

4. Left ventricular aneurysm

ST segment elevation that persists more than 2 weeks after MI is associated with a focal wall motion disorder (“ventricular aneurysm”). If previous ECGs are not available for comparison, these persistent ECG changes may appear similar to STEMI ECG findings. The persistent ST segment elevation appears in the precordial leads with an anterior or apical aneurysm and in II-III-AVF with an inferior aneurysm.

Treatment – CAD - STEMI

The treatment of STEMI includes prompt revascularization and medical therapy. Revascularization can be performed by either primary PCI, fibrinolytic therapy (thrombolytic therapy) or surgically. Primary PCI is preferred if available within a reasonable timeframe — that is, a door-to-balloon time of less than 90 minutes.

Revascularization

The decision whether to undertake primary PCI or fibrinolytic therapy is important. Many major medical facilities have PCI capabilities, and this is the treatment of choice for STEMI. Smaller hospitals or those in rural areas may not have PCI capabilities; however, those facilities frequently have capabilities to quickly transfer patients experiencing STEMI to a primary PCI facility. When there is no primary PCI available and transfer to a primary PCI facility is not available in a timely fashion — that is, transfer in less than 60 minutes — fibrinolytic therapy is indicated.

Primary PCI

In most situations, primary PCI is strongly preferred over thrombolytic therapy; this includes primary PCI within 36 hours for patients who develop cardiogenic shock and those with Killip Class III HF. There are no situations in which fibrinolytic therapy is preferred over primary PCI, unless the patient refuses invasive procedures. Fibrinolytic therapy is most effective within 3 hours of symptom onset.

The best outcomes occur when primary PCI is performed with a door-to-balloon time of less than 90 minutes and when symptom onset was less than 12 hours before the intervention. With delayed presentation (symptom duration 12-24 hours), it is reasonable to perform a primary PCI if there is evidence of ongoing ischemia. [O’Gara 2013;13A(Table 2)] Primary PCI is not recommended when symptom onset is more than 12 hours before evaluation and the patient is asymptomatic; see Occluded Artery Trial (OAT).

Fibrinolytic Therapy

Fibrinolytic therapy must be instituted within 24 hours of symptom onset. After this time frame, fibrinolysis is contraindicated and likely to be ineffective. Note that fibrinolytic therapy is always given simultaneously with anticoagulation using unfractionated heparin or low molecular weight heparin (enoxaparin or fondaparinux).

If the preferred management for a patient with STEMI is fibrinolytic therapy because primary PCI is not available, contraindications must be considered. Suspected aortic dissection, active bleeding (excluding menses), or a bleeding diathesis are contraindications to fibrinolytic therapy. Generally, if there is high (> 4%) risk for intracranial hemorrhage (ICH), fibrinolytic therapy is also contraindicated.

According to the American College of Cardiology/American Heart Association guidelines, the following factors are considered absolute contraindications for fibrinolytic therapy in STEMI: [O’Gara 2013;19b(Table 6)]

Prior intracranial hemorrhage
Ischemic stroke within 3 months (EXCLUDING acute ischemic stroke within 4.5 hours)
Known cerebrovascular abnormality such as aneurysm or arteriovenous malformation
Known malignant intracranial tumor
Significant closed head trauma or facial trauma within 3 months
Intracranial or intraspinal surgery within 2 months
Suspected aortic dissection
Severe uncontrolled hypertension (unresponsive to emergency therapy)
Active bleeding or bleeding diathesis (excluding menses)
For streptokinase only, prior treatment within the previous 6 months

Relative (not absolute) contraindications to fibrinolytic therapy include:

Uncontrolled hypertension (BP > 180/110 mm Hg) either currently or in the past
Intracranial abnormality not listed as absolute contraindication (eg, benign intracranial tumor)
Ischemic stroke more than 3 months prior
Bleeding within 2 to 4 weeks (menses excluded)
Traumatic or prolonged cardiopulmonary resuscitation
Major surgery within 3 weeks
Pregnancy
Current use of anticoagulants
Noncompressible vascular puncture
Dementia

Advanced age is not listed as an absolute or relative contraindication to fibrinolytic therapy in the ACC/AHA guidelines.

“Facilitated PCI” refers to using initial fibrinolytic therapy to stabilize the patient while transport to a primary PCI facility is being arranged. This strategy failed to demonstrate a net clinical benefit in two large trials (ASSENT-4 PCI and FINESSE).

“Rescue PCI” refers to the use of PCI when fibrinolytic therapy fails. This is indicated after fibrinolytic therapy when cardiogenic shock or severe congestive HF develops (Killip Class III), or when electrical instability (ventricular tachycardia or fibrillation) or persistent ischemic symptoms are present.

Coronary Artery Bypass Grafting (CABG)

According to the ACC/AHA guidelines, urgent coronary artery bypass grafting as a means of coronary revascularization during STEMI is indicated in the following situations: [O’Gara 2013;26a(e103)]

Patients with STEMI and coronary anatomy not amenable to PCI who have ongoing or recurrent ischemia, cardiogenic shock, severe HF or other high-risk features (class I recommendation for urgent CABG)
Patients with STEMI at time of operative repair of mechanical defects such as ventricular septal defect or papillary muscle rupture (class I recommendation)

In patients with STEMI who do not have cardiogenic shock and are not candidates for PCI or fibrinolytic therapy, emergency CABG within 6 hours of symptom onset may be considered. [O’Gara 2013;26a(e103)] CABG is not indicated when there is a small area of myocardium in jeopardy and the patient is stable.

Medical Therapy

Initial medical management of STEMI consists of relief of ischemic pain with nitrates and morphine, antithrombotic measures including antiplatelet agents (aspirin, thienopyridines and glycoprotein IIb/IIIa inhibitors), and systemic anticoagulation (heparin or bivalirudin) and beta-adrenergic blockade. Supplemental oxygen should be administered if arterial desaturation is present, but not as a routine measure. [Jernberg 2018;1a] Medical therapy initiated before hospital discharge may include angiotensin converting enzyme inhibitors, angiotensin receptor blockers, sacubitril/valsartan (Entresto, Novartis), continued beta-adrenergic blockade, aldosterone antagonists and HMG-CoA reductase inhibitors.

Antithrombotic Management

Aspirin

Early antithrombotic administration at the time of STEMI diagnosis consists of non-enteric-coated aspirin 162 mg to 325 mg (unless contraindicated) p.o., chewed immediately. Lifelong therapy using 81 mg to 325 mg daily should follow.
Anticoagulation

Initial systemic anticoagulation should be started in all patients with STEMI unless a contraindication exists. Unfractionated heparin, low-molecular-weight heparin (enoxaparin or fondaparinux) or bivalirudin may be used; unfractionated heparin should be given for 48 hours total and low molecular weight heparin until hospital discharge or for 8 days.

P2Y12 inhibitors

P2Y12 receptor antagonists (clopidogrel, prasugrel, ticagrelor (Brilinta, AstraZeneca) and ticlopidine) are indicated in all STEMI cases unless urgent surgery is required. Clopidogrel can also be used as an adjunct to fibrinolytic therapy in aspirin-intolerant patients. If urgent CABG is required, these agents should not be used; these agents should be discontinued for 5 to 7 days prior to CABG, unless the benefits of surgery outweigh the risk of bleeding.

For STEMI patients who have undergone PCI with coronary stenting, it is recommended that P2Y12 inhibitors be continued for 12 months, if possible, regardless of the type of stent used. Prasugrel is not recommended in patients with a history of stroke or transient ischemic attack (TIA). Ticlopidine is now used rarely due to risk of thrombocytopenia and thrombotic thrombocytopenic purpura (TTP).

Glycoprotein IIb/IIIa Inhibitors

These drugs include abciximab, eptifibatide and tirofiban. Glycoprotein IIb/IIIa inhibitors very strongly inhibit platelet function by blocking fibrinogen binding to the activated glycoprotein IIb/IIIa receptor complex. Any of these agents may be used in addition to aspirin, a P2Y12 inhibitor and anticoagulation (except with bivalirudin) at the time of PCI in high-risk patients with STEMI. There are no strong data to support the use of glycoprotein IIb/IIIa inhibitors prior to PCI at the present time.

Nitrates

Nitrates may be useful in the management of post-MI anginal symptoms, hypertension and HF; however, no clinical data exist documenting a mortality benefit. The use of nitrates should not preclude using the neurohormonal blocking agents that have mortality benefits.

Sublingual nitroglycerine tablets administered every 5 minutes, with a maximum dose of three tablets, can be given to relieve angina; should angina persist, intravenous nitroglycerine can be considered. Systemic hypotension and/or suspected right ventricular infarction are contraindications to the use of nitrates.

Phosphodiesterase-5 inhibitors (sildenafil, vardenafil, tadalafil) enhance nitric oxide production and can cause potentially fatal hypotension when used in combination with nitrates. Nitrates should not be used together with PDE-5 inhibitors within 24 hours (sildenafil) or 48 hours (vardenafil, tadalafil) due to this interaction.

Morphine

Morphine effectively relieves anginal chest pain and reduces the sensation of dyspnea when pulmonary edema is present. Morphine may cause respiratory depression and hypotension.

Beta-blockers

Although there are few data regarding the efficacy of beta-blockers during unstable angina and non-STEMI, there is an abundance of data supporting beta-adrenergic blockade with STEMI. ACC/AHA guidelines recommend early intravenous beta-blockers when no contraindication exists. Otherwise, oral administration of beta-blocker therapy may be initiated in the acute setting. Beta-blockade is contraindicated in cardiogenic shock, with systemic hypotension or with acute left heart decompensation. Long-term (lifetime) beta-blocker use reduces the incidence of recurrent MI and reduces post-MI mortality rates.

Angiotensin Converting Enzyme Inhibitors/Angiotensin Receptor Blockers

The ACC/AHA guidelines state that angiotensin converting enzyme (ACE) inhibitors are reasonable (class IIa recommendation) for all patients with STEMI and no contraindications. Importantly, in patients with impaired LV systolic function or diabetes, ACE inhibitors have a class I indication. Angiotensin receptor blockers (ARB) are the recommended alternative agents if the post-MI patient cannot tolerate ACE inhibitors due to cough.

Aldosterone Antagonists

In the EPHESUS (Epleronone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival) trial, the aldosterone antagonist eplerenone added to an ACE inhibitor was associated with lower mortality after an MI. This led to the recommendation for use of aldosterone antagonists with an ACE inhibitor and beta-blocker in patients with STEMI with LV systolic dysfunction (EF < 40%) and either diabetes or symptomatic HF (and no contraindication, ie, serum creatinine > 2.5 mL/min and/or potassium > 5.0 mEq/L). 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 STEMI patient (without contraindications) should receive a statin; see HMG-CoA Reductase Inhibitor Topic Review. The 2018 American College of Cardiology/American Heart Association cholesterol guidelines recommend (class I) high-intensity statin therapy (defined as a regimen to achieve LDL reduction ≥ 50%) in patients aged younger than 75 years. For age older than 75 years, high- or moderate-intensity statin therapy (defined as 30-49% LDL reduction) should be initiated (class IIa recommendation) depending on individual risk factors and preferences. No specific target LDL level is recommended in the guidelines — only a reduction of LDL levels from baseline. [Grundy 2018;10a;11a(e294, e295)] The Multicenter InSync Randomized Clinical Evaluation (MIRACLE) trial and Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 (PROVE-IT TIMI 22) trial used atorvastatin (80 mg/day given orally) with good results. Statin therapy should be lifelong after an acute coronary syndrome, unless a contraindication exists or the baseline LDL cholesterol is below 70 mg/dL.

Calcium Channel Blockers

The non-dihydropyridine calcium channel blockers diltiazem and verapamil can be used for symptomatic management of angina when there is a contraindication to beta-blockers, such as in asthma, and no HF or significant LV systolic dysfunction are present. However, an analysis of 28 trials showed no beneficial effect of calcium channel blockers on infarct size or the rate of reinfarction with STEMI. [O’Gara 2013;29a(e106)] Sublingual nifedipine, which is sometimes used in hypertensive emergencies, is contraindicated in patients with CAD due to a reflex increase in sympathetic nervous system activity, which can be harmful.

Complications of STEMI

There are quite a few mechanical and nonmechanical complications of STEMI, many of which are life-threatening.

Cardiogenic Shock

Cardiogenic shock in STEMI results from low cardiac output, leading to hypotension, end-organ hypoperfusion and multi-system organ failure.

Optimal management involves a multidisciplinary shock team that includes an interventional cardiologist, cardiothoracic surgeon, cardiac intensivist and advanced HF specialist, and consists of mechanical cardiac support (MCS) in suitable patients with acute severe or refractory cardiogenic shock. (Tehrani 2020;9a)

Acute Arrhythmias

a. Ventricular Fibrillation

The most common cause of prehospitalization deaths with STEMI is ventricular fibrillation. The widespread availability of automated external defibrillators (AEDs) has decreased mortality. Life-threatening ventricular tachycardia (VT) can also occur during and after STEMI. See the Ventricular Tachycardia ECG Review for more detail and multiple ECG examples.

Below is an ECG tracing of sustained monomorphic VT.

Accelerated idioventricular (AV) rhythm (“slow ventricular tachycardia”) may also occur after STEMI. See the Idioventricular Rhythms ECG Review for more detail and multiple ECGs.

The tracing below shows an example. AV dissociation is evident in the V1 rhythm strip.

The management of patients at risk for syncope and sudden death due to post-STEMI ventricular arrhythmia is beyond the scope of this section. See the Automated Implantable Cardioverter Defibrillator (AICD) Topic Review.

b. Atrial Fibrillation

Although not a common complication of STEMI, atrial fibrillation (AF) after STEMI is associated with older age, Killip class, higher heart rates and female sex. AF can occur if atrial infarction, sinus node ischemia or atrial ischemia occurs. In addition, AF is often a complication of acute increases in left atrial pressure and volume associated with LV dysfunction and/or mitral regurgitation. The median time of onset of AF is about 2 days post-MI. Prompt control of the ventricular response rates is important (myocardial oxygen demand increases as heart rate increases). Beta-adrenergic blockade is indicated. Cardiologists and critical care physicians often use intravenous amiodarone off-label in the setting of AF and STEMI. Emergency cardioversion may be required, although precipitating factors should be corrected (if possible) prior to attempting cardioversion. [Pokorney 2012]

Myocardial Rupture Syndromes

a. Ventricular Septal Defect

Ventricular septal defect (VSD) develops as a complication of STEMI in about 0.2% of patients. The incidence has decreased from 1% to 3% in the pre-reperfusion era to 0.17% to 0.31% after primary PCI. Older age, female sex, higher heart rate, higher Killip class and delayed (or lack of) reperfusion are associated with an increased likelihood of postinfarct VSD. The lower third of the septum is perfused by the right coronary artery and the upper two-thirds by multiple septal perforators from the LAD. The incidence of post-STEMI VSD is roughly the same with anterior and inferior infarctions.

A post-MI VSD results in left-to-right shunting of blood and can be life-threatening. On physical exam, a holosystolic murmur at the left lower sternal border occurs. Right heart catheterization will show an increase in oxygen saturation from the right atrium to the right ventricle. 2D and Doppler echocardiography is essential for diagnosis and evaluation of post-MI VSD. Transesophageal echocardiography (TEE) may be necessary if transthoracic imaging is unsatisfactory.

Surgical repair is the definitive treatment for post-MI VSD. The ACC/AHA guidelines recommend emergent surgical repair regardless of hemodynamic status; however, this remains controversial and a multidisciplinary team at an experienced center should create a management strategy that is tailored to the individual patient. (Goyal 2018;4a)

b. Acute Mitral Regurgitation due to Papillary Muscle Rupture

Acute mitral regurgitation (MR) due to papillary muscle rupture after acute MI typically occurs between 48 hours and 1 week after an inferior STEMI. The incidence (2003-2015) of post-STEMI papillary muscle rupture is about 0.05%. (Elbadawi 2019;5a)

The posteromedial papillary muscle is often by a single coronary artery, either a distal branch of a dominant RCA or an obtuse marginal branch of the circumflex, and is the most common site of the rupture. Nishimura et al hypothesized that papillary muscle rupture occurs more often in single-vessel coronary disease because better preserved LV function generates greater shearing forces.

Acute MR secondary to papillary muscle rupture manifests with the rapid onset of pulmonary edema and often with cardiogenic shock. The diagnosis requires a high degree of suspicion and prompt evaluation with echocardiography or contrast left ventriculography. Optimal management involves a dedicated team approach and early right heart catheterization. (Taleb 2019;3a)

There are two papillary muscles that comprise part of the complex anatomy of the mitral valve. The anterolateral papillary muscle receives dual blood supply — from the left anterior descending coronary artery and the left circumflex coronary artery — in most individuals, whereas the posteromedial papillary muscle receives its sole blood supply from the right coronary artery.

Complete infarction of the posteromedial papillary muscle can occur during an inferior MI but only partial, or no, damage will be done to the anterolateral papillary muscle during an anterior (left anterior descending) or lateral (circumflex) infarction, as there is dual blood supply to this papillary muscle. Thus, the posteromedial papillary muscle is the most likely to rupture.

Emergent surgical repair or replacement of the mitral valve is indicated. In a surgical series reported from the Netherlands, operative mortality was about 4% and in-hospital mortality was 25%. (Bouma 2014;6a) Support devices for cardiogenic shock include Impella, TandemHeart, extracorporeal membrane oxygenation (ECMO) and intra-aortic balloon pump (IABP): the choice, use and management of these devices requires a specialized team with the resources of a cardiovascular center.

c. Left Ventricular Free Wall Rupture

In a recent series, post-MI rupture of the free wall of left ventricle occurred in about 1% of patients. Risk factors associated with LV rupture included advanced age, female sex and the absence of prior MI. Although surgical repair was attempted in slightly more than half of the patients with free wall rupture, the overall in-hospital mortality was greater than 80%. (Nozoe 2014;3a)

The acute physiologic consequences of free wall are similar to cardiac tamponade with the rapid onset of low cardiac output, narrow pulse pressure, tachycardia, and high, equalized filling pressures.

Left Ventricular Aneurysm

ST segment elevation persisting for more than 2 weeks after a STEMI suggests LV aneurysm formation. Echocardiography is the preferred initial imaging modality to confirm the diagnosis and evaluate LV function. LV aneurysms most commonly involve the cardiac apex, although inferior wall or lateral wall aneurysms may occur as well. Patients with post-MI left ventricular aneurysm may experience complications that include:

a. HF. The portion of the heart that forms an LV aneurysm is non-contractile or “dyskinetic.” This results in impaired LV systolic function and the development of HF.
b. LV thrombus formation. HF is the most common precipitating factor for LV thrombus formation. The diagnosis of LV thrombus is usually made by echocardiography, and LV thrombus discovered within 3 months of MI is usually attributed to the MI. The vast majority of patients with LV thrombus have an ejection fraction (EF) ≤ 40%.
c. Ventricular tachycardia. LV aneurysms often include extensive scar formation that may serve as a substrate for ventricular arrhythmias. Electrophysiologic mapping and surgical or catheter-based ablation now offer management alternatives to automated implantable cardioverter defibrillator (AICD) implantation.

LV aneurysm can be diagnosed on ECG when there is persistent ST segment elevation occurring 6 weeks after a known transmural MI, usually anterior; these ECG findings were previously discussed above. Without knowing a patient’s medical history, the ECG changes due to an aneurysm may mimic an acute ST segment elevation MI. The only way to conclusively distinguish an LV aneurysm from an acute MI diagnosis on an ECG — not from an acute MI — is to have the patient’s history of a prior MI and cardiac imaging to document the presence of an aneurysm.

Left Ventricular Thrombus

After MI, especially anterior, the myocardial stunning that occurs can result in blood pooling toward the akinetic segment — frequently, the cardiac apex — resulting in thrombus formation. Embolization of this thrombus can cause a stroke. There are no good data regarding prevention of LV thrombi; however, the ACC/AHA guidelines give a class IIa, level of evidence C recommendation to warfarin therapy for 3 months when there is a cardiac source of embolus suspected after a MI. (O’Gara 2013;33a)

Right Ventricular Infarction

Even in the era of early PCI for ACS, advanced echocardiography and MRI imaging demonstrate transient acute right ventricular (RV) dysfunction is common after acute MI.

(Gorter 2016;1b) Clinically recognized RV infarction generally occurs in the setting of an acute inferior STEMI, because the right coronary artery supplies the free wall of the right ventricle. An ECG that includes right-sided chest leads will show ST segment elevation and should be done in all inferior STEMI patients. Right bundle-branch block and complete atrioventricular block are the most frequent conduction abnormalities associated with RV infarction. (Haji 2000;3a)

Acute right ventricular failure can occur, leading to hypotension and low forward cardiac output. Until recently, volume expansion to increase RV filling pressures was the primary approach to management. However, recent major advances in percutaneous RV support including a percutaneous RVAD (Impella RP, Abiomed), have changed this situation dramatically. (Harjola 2016;8a,9a)

In contrast to LV infarction, recovery of RV function often occurs over a few months after RV infarction. (Gorter 2016;1a)

Systolic HF

The development of impaired LV systolic function after acute MI represents a complex combination of myocardial necrosis and scarring, stunning, and remodeling. Ischemic heart disease is a major underlying cause of chronic HF. See Congestive Heart Failure (Systolic) Topic Review.

Pericarditis and Dressler’s Syndrome

Before the advent of reperfusion for ACS, acute post-MI inflammatory pericarditis was reported in up to 25% of anterior STEMI patients.

By the early 1990s, thrombolysis had reduced the incidence of post-MI pericarditis by one-half, and a more recent registry study reported an incidence of 110 per 10,000 in 2013. The authors commented that post-MI pericarditis had become “a relatively rare complication of STEMI in the coronary reperfusion era.” (Lador 2018;1a)

Dressler's syndrome is an autoimmune post-MI pericarditis, manifest clinically by pleuropericardial pain, fever and a high erythrocyte sedimentation rate (> 40 mm) a week or more post-MI. Before the reperfusion era, about 3% of patients developed post-MI pericarditis, the majority within 3 months. The diagnosis is clinical and based on ECG and echocardiographic evidence of pericarditis. Treatment includes aspirin and colchicine to decrease inflammation. Anticoagulation should be avoided in order to prevent intra-pericardial bleeding and cardiac tamponade.

Special Situations – CAD - STEMI

Aortic Dissection

An ascending aortic dissection that occludes the right coronary ostium may result in an inferior STEMI. This is relatively uncommon but must be recognized quickly, as surgical intervention is crucial.

No-reflow

When coronary intervention is performed for STEMI, there is a risk of “no-reflow” or “microvascular obstruction.” Despite conduit vessel patency, myocardial perfusion may be reduced due to multiple mechanisms including ischemia, reperfusion, endothelial dysfunction, distal thromboembolism and microvascular arteriolar spasm.

There are both patient-related and lesion-related risk factors for no-reflow. The patient-related factors include delayed presentation to the catheterization laboratory, hyperglycemia and hypercholesterolemia. Lesion-related factors include the composition of the plaque and the amount of intravascular thrombus present. (Rezkalla 2017;2a-b)

Management of no-reflow events is controversial and beyond the scope of this section.

Pregnancy

ST segment elevation MI is rare during pregnancy but does occur. Atherosclerotic plaque rupture in women with typical risk factors is the most common etiology. The risk of spontaneous coronary artery dissection risk also increases during pregnancy. PCI is the primary treatment option; thrombolytics and glycoprotein IIb/IIIa inhibitors are contraindicated during pregnancy.

STEMI Mimics

Many disorders can mimic STEMI in both the symptomatic presentation and the ECG findings, as previously discussed. STEMI is an ACS, involving an unstable atherosclerotic plaque and thrombosis. Other disorders may cause chest pain symptoms and ischemic ST segment elevation on the ECG, but are not caused by atherosclerotic plaque rupture. These include coronary spasm, cocaine abuse, aortic dissection, coronary vasculitis, Takotsubo cardiomyopathy (stress-induced cardiomyopathy), emboli to the coronaries, myocarditis, trauma or cardiac contusion and congenital coronary anomalies.