Coronary Artery Disease - STEMI Topic Review

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


ST segment elevation myocardial infarction most commonly occurs when thrombus formation results in complete occlusion of a major epicardial coronary vessel.

The most serious form of acute coronary syndromes, STEMI is a life-threatening, time-sensitive emergency that must be diagnosed and treated promptly via coronary revascularization, usually by percutaneous coronary intervention.

Unlike during unstable angina and non-ST segment elevation myocardial infarction, the 12-lead ECG will show significant ST segment elevation during STEMI — as the name implies. Below is an example of an anterior ST segment elevation MI with “tombstoning” on the ECG.


The terms “transmural,” “non-transmural,” “Q wave MI” and “non-Q wave MI” are no longer recommended. The differences between the types of acute coronary syndromes are discussed below.

Unstable Angina Pectoris

Three different presentations of unstable angina exist.

  1. Exertional angina of new onset (even if relieved with rest and requiring a consistent amount of exertion to procedure symptoms, angina is considered unstable when it first occurs)
  2. Exertional angina that was previously stable and now occurs with less physical exertion
  3. Anginal symptoms at rest without physical exertion

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

Non-ST Segment Elevation Myocardial Infarction

Anginal symptoms at rest that result in myocardial necrosis, as identified by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) with no ST segment elevation on the 12-lead ECG.

ST Segment Elevation Myocardial Infarction

Anginal symptoms at rest that result in myocardial necrosis, as identified by elevated cardiac biomarkers (see Cardiac Enzymes Topic Review) with ST segment elevation on the 12-lead ECG.

The Killip Classification is frequently used to predict mortality during STEMI. This system focuses on physical examination and the development of heart failure to predict risk, as described below.

Class I: No evidence of 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 < 90 mm Hg and signs of hypoperfusion such as oliguria, cyanosis and sweating (mortality 67%)

The original data from 1967 showed the above mortality rates in each class. This was before reperfusion therapy (thrombolytics and/or percutaneous coronary intervention). With advances in therapy, the mortality rates have declined about 30% to 50% in each class.

Pathophysiology – CAD - STEMI

The “vulnerable” plaque that formed from the atherosclerotic process is responsible for acute coronary syndromes and, ultimately, coronary artery thrombosis; see Atherosclerosis Topic Review. There are conditions that mimic STEMI, and distinguishing these can be difficult; these are described in Diagnosis.

A substance known as “tissue factor” is located within the necrotic core of the plaque. When exposed to the bloodstream, tissue factor activates the clotting cascade, and thrombosis occurs. Tissue factor is exposed when the fibrous cap that covers the plaque becomes disrupted or ulcerated. This disruption of the fibrous cap is called “plaque rupture” or “plaque erosion.” Surprisingly, plaque rupture and thrombosis frequently occur at the site of modest coronary stenosis (< 50% luminal narrowing); therefore, even if stress test results are normal, the risk for an ACS is still present. Recall that stress testing detects flow-limiting stenosis of greater than 70%.

Some atherosclerotic plaques have a more stable fibrous cap. Others are thin and considered vulnerable. A clinically-useful means to distinguish these types of plaque is not currently available.

Plaque rupture and plaque erosion (ulceration) can result in coronary thrombosis. STEMI is most often from coronary thrombosis after plaque rupture and less often from fixed obstruction. Unstable angina has a lower incidence of coronary thrombosis compared with non-STEMI or STEMI and is more often the result of fixed atherosclerotic stenosis. Plaque rupture (most common) or erosion resulting in coronary occlusion is the predominant mechanism in non-STEMI and STEMI.

Physical Examination – CAD - STEMI

The physical examination findings during STEMI are similar to those of stable angina, unstable angina and non-STEMI, but they are frequently more severe due to the larger amount of myocardium experiencing ischemia.

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

A S4 heart sound may be present during myocardial ischemia due to the lack of adenosine triphosphate production impairing left ventricular relaxation. Recall that myocardial relaxation is an active process requiring ATP, which is reduced during ischemia, and a S4 heart sound occurs when the noncompliant, stiffened left ventricle is not able to relax adequately when it receives blood during atrial contraction. The S4 sound is from the blood itself striking the noncompliant ventricle.

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 and circumflex coronary artery.

When the left ventricular end-diastolic pressure, or LVEDP, increases during myocardial ischemia, that pressure can be transmitted backward to the pulmonary veins and into the pulmonary vasculature causing transient pulmonary edema that results in dyspnea and rales on lung examination.

Diagnosis – CAD - STEMI

The diagnosis of STEMI is made predominantly using the 12-lead ECG and cardiac enzymes. There is significant myocardial necrosis occurring in the setting of STEMI, resulting in elevation of the cardiac enzymes.

Cardiac enzymes — also known as cardiac biomarkers — include myoglobin, troponin and creatine kinase. Historically, lactate dehydrogenase, or LDH, was also used but is nonspecific. Cardiac enzymes are released into the circulation when myocardial necrosis occurs, as seen in MI.


Myoglobin is released into circulation with any damage to muscle tissue, including myocardial necrosis. Because skeletal muscle contains myoglobin, this measurement is quite nonspecific for MIs. The benefit is in the fact that a detectable increase is seen only 30 minutes after injury occurs, unlike troponin and creatine kinase, which can take 3 to 4 hours.


The enzymes troponin I and troponin T are normal proteins important in the contractile apparatus of the cardiac myocyte. They are released into the circulation about 3 to 4 hours after MI and are still detectable for 10 days afterwards. The long half-life allows for the late diagnosis of MI but makes it difficult to detect re-infarction as can occur in acute stent thrombosis after PCI. Although, there are a number causes for troponin elevation unrelated to MI, troponin elevation is much more sensitive and specific than myoglobin and even CK.

Creatine Kinase

Creatine kinase — also known as creatine phosphokinase, or CPK — is a muscle enzyme that exists as isoenzymes. The MB type is specific to myocardial cells, whereas MM and BB are specific to skeletal muscle and brain tissue, respectively. The CK level will increase approximately 3 to 4 hours after a MI and stays elevated for 3 to 4 days. This makes it useful for the detection of re-infarction in the 4- to 10-day window of time after the initial insult compared with troponin, which remains elevated for 10 days and is less useful for this purpose.


ST segment elevation can take many forms during STEMI; however, there some noncardiac causes of ST segment elevation that need to be recognized. Also, the development of a new left bundle branch block is considered equivalent to STEMI.

The first change ECG change during STEMI is “hyperacute T waves” that appear peaked and are related to localized hyperkalemia. These changes are rarely seen as they are transient and frequently occur prior to hospital arrival.


ST segment elevation, unlike depression, will localize to the ECG lead of the affected myocardium. Note that 1 millimeter of ST segment elevation in two contiguous leads is required to diagnose STEMI, but there are two major exceptions.

  1. Anterior STEMI requires 2 mm of ST segment elevation in V2 and V3 in men, or 1.5 mm in women, aged older than 40 years, according to the American College of Cardiology/American Heart Association definition.
  2. Posterior STEMI frequently has ST segment depression in V1 to V3 instead of elevation, as the vectors are completely reversed. 

Here is an ECG of an anterior STEMI:



The ECG findings of a posterior wall MI are different from the typical ST segment elevation seen in other MIs. A posterior wall MI occurs when posterior myocardial tissue (now termed inferobasilar), usually supplied by the posterior descending coronary artery — a branch of the right coronary artery in 80% of individuals — acutely loses blood supply due to intracoronary thrombosis in that vessel. This frequently coincides with an inferior wall MI due to the shared blood supply.

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

  1. ST segment depression (not elevation) in the septal and anterior precordial leads (V1-V4). This occurs because these ECG leads will see the MI backwards; the leads are placed anteriorly, but the myocardial injury is posterior.
  2. A R/S wave ratio greater than 1 in leads V1 or V2.
  3. ST segment elevation in the posterior leads of a posterior ECG (leads V7-V9). Suspicion for a posterior MI must remain high, especially if inferior ST segment elevation is also present.
  4. ST segment elevation in the inferior leads (II, III and aVF) if an inferior MI is also present.

Here is an ECG of an inferior STEMI with a posterior MI:



Below are ECG examples of STEMI in differing regions.

Anterior Wall Myocardial Infarctions

Inferior Wall Myocardial Infarctions

Posterior Wall Myocardial Infarctions

Recall that a new left bundle branch block can indicate an acute MI, commonly of the left main coronary artery or proximal left anterior descending. Sgarbossa criteriaCabrera’s sign and Chapman’s sign can be used in the setting of an old LBBB to diagnose an acute MI.

There are four major situations where ST segment elevation can be seen on an ECG when there is no STEMI present, but many other causes of ST segment elevation on the ECG exist. A good mnemonic to remember all the causes of ST segment elevation on the ECG is “ELEVATION.”

Electrolyte abnormalities
Left bundle branch block
Aneurysm of left ventricle
Ventricular hypertrophy
Arrhythmia disease (Brugada syndrome, ventricular tachycardia)
Takotsubo/Treatment (iatrogenic pericarditis)
Injury (MI or cardiac contusion)
Osborne waves (hypothermia or hypocalcemia)
Non-atherosclerotic (vasospasm or Prinzmetal’s angina)

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

1. Left ventricular hypertrophy
When left ventricular hypertrophy 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, or discordance, along with a typical T wave inversion pattern.



2. Early repolarization
Early repolarization is a common finding in young, healthy individuals. It appears as mild ST segment elevation that can be diffuse but more prominent in the precordial leads. Early repolarization frequently looks simply like “J point” elevation.


3. Pericarditis
Inflammation of the pericardium can result in pericarditis and has typical ECG findings that can mimic STEMI. These findings occur in progressive stages, all of which are seen in about 50% of pericarditis cases. Stage I consists of diffuse concave upward ST segment elevation in most leads, PR depression in most leads — though it may be subtle — and sometimes notching at the end of the QRS complex; see Pericarditis ECG Review for more details.



4. Left ventricular aneurysm
A left ventricular aneurysm can be diagnosed on ECG when there is persistent ST segment elevation occurring 6 weeks after a known transmural MI, usually anterior. Without knowing the patient’s past medical history, the ECG changes of an aneurysm may mimic STEMI ECG findings. The persistent ST segment elevation is in lead V1 and V2 with an anterior or apical aneurysm. 


In an inferior aneurysm, the persistent ST segment elevation would be in leads II, III and aVF. The only way to be sure of a LV aneurysm diagnosis on an ECG — not from an acute MI — is to have the patient’s history of prior heart attack and cardiac imaging to document the presence of an aneurysm. If the history is not known, STEMI should be assumed to be present.

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 time-frame — that is, a door-to-balloon time of less than 90 minutes.


The decision regarding primary PCI vs. fibrinolytic therapy is important. Many major medical facilities have PCI capabilities, as this is the treatment of choice for STEMI. However, smaller hospitals or those located in rural areas may not; 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 able to be done in a timely fashion — that is, transfer in less than 60 minutes — fibrinolytic therapy is indicated.

Primary PCI

In certain 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 works best when symptom onset is less than 3 hours, as fresh thrombus lysis is more readily treated than more organized, subacute thrombus. If symptoms have been present for more than 3 hours, then primary PCI is preferred.

The best outcomes occur when primary PCI is performed with a door-to-balloon time of less than 90 minutes and when symptoms onset was less than 12 hours. Primary PCI is only indicated when symptoms duration is 12 to 24 hours (delayed presentation) if severe congestive HF, hemodynamic/electrical instability or continued angina is present. Primary PCI is not recommended when symptom onset is more than 12 hours and the patient is asymptomatic; see Occluded Artery Trial, or OAT.

Fibrinolytic Therapy

Fibrinolytic therapy must be instituted within 24 hours of symptom onset. After this time frame, fibrinolytic therapy 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, as discussed under Anticoagulation in Medical Therapy.

When the decision is made to treat a patient with STEMI with fibrinolytic therapy because primary PCI is not available in a timely fashion, 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 risk for intracranial hemorrhage, defined as greater than 4%, fibrinolytic therapy is also contraindicated, and primary PCI is preferred.

The following would place a patient in the category of high risk for ICH:

  1. Prior intracranial hemorrhage
  2. Ischemic stroke within 3 months
  3. Known cerebrovascular abnormality such as aneurysm or arteriovenous malformation
  4. Known malignant intracranial tumor
  5. Significant closed head trauma or facial trauma within 3 months

Relative contraindications (not absolute) to fibrinolytic therapy include:

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

Note that advanced age is not listed as an absolute or relative contraindication to fibrinolytic therapy in the American College of Cardiology/American Heart Association guidelines.

Facilitated PCI refers to using fibrinolytic therapy to stabilize the patient while transport to a primary PCI facility is being arranged. This strategy receives a class IIb indication for high-risk patients with a low bleeding risk when primary PCI is not readily available.

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)

Coronary artery bypass grafting as a means of coronary revascularization during STEMI is indicated in the following situations:

  1. When PCI fails, and persistent symptoms or hemodynamic instability are present
  2. When a patient is not a candidate for PCI and has continued symptoms with a significant area of myocardium at risk
  3. During the time of ventricular septal defect or mitral valve repair
  4. When left main coronary disease or three-vessel coronary disease is present with cardiogenic shock or ventricular arrhythmias (ventricular tachycardia or fibrillation)

CABG is not indicated when there is a small area of myocardium in jeopardy and the patient is stable.

Medical Therapy

Initial medical therapy during STEMI consists of oxygen administration, antiplatelet therapy (aspirin, thienopyridines and glycoprotein IIb/IIIa inhibitors), anticoagulation (heparin or bivalirudin), anginal pain relief with nitrates and morphine and beta-blockade. Medical therapy upon hospital discharge may include angiotensin converting enzyme inhibitors, angiotensin receptor blockers, aldosterone antagonists and HMG-CoA reductase inhibitors.


Once STEMI is diagnosed, aspirin should be chewed at a dose of 162 mg to 325 mg immediately, unless a contraindication exists. Lifelong therapy using 75 mg to 162 mg daily should follow upon hospital discharge.


P2Y212 receptor antagonists (clopidogrel, prasugrel, ticagrelor, ticlopidine) are indicated in all STEMI cases unless surgery is needed. Clopidogrel can also be used as an adjunct to fibrinolytic therapy in patients who are intolerant to aspirin. If coronary artery bypass grafting is required, these agents should not be used; the drugs must be discontinued for 5 to 7 days prior to CABG, unless urgent and the risk for bleeding is less than the benefit of revascularization. Regardless of the type of stent used during PCI, it is preferred that thienopyridines be continued for 12 months if possible. Prasugrel is not recommended in a patient with a prior history of stroke or transient ischemic attack, or TIA. Ticlopidine is rarely used due to risk for thrombocytopenia and thrombotic thrombocytopenic purpura, or TTP.

Glycoprotein IIb/IIIa Inhibitors 

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


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


Nitrates are helpful to treat angina symptoms, hypertension and HF during STEMI; however, no clinical data exists to show a mortality benefit, and thus their use is individualized. The use of nitrates should not preclude using drugs that do show a mortality benefit.

Sublingual nitroglycerine tablets administered every 3 to 5 minutes, with a maximum dose of three tablets, can be given to relieve angina; should angina persist, intravenous nitroglycerine can be considered. Hypotension, or right ventricular infarction, is a contraindication to the use of nitrates. Phosphodiesterase inhibitors (sildenafil, vardenafil, tadalafil) — used to treat erectile dysfunction — enhance nitric oxide production and can cause potentially fatal hypotension when used in combination with nitrates. These agents should not be used together within 24 hours (sildenafil) or 48 hours (vardenafil, tadalafil) due to this interaction.


Morphine is effective in relieving anginal chest pains and the sensation of dyspnea when pulmonary edema is present. There are also some beneficial hemodynamic effects including arterial vasodilation.


Although there is little data in regards to the efficacy of beta-blockers during unstable angina and non-STEMI, there is an abundance of data during STEMI. Guidelines from the ACC/AHA recommend early intravenous beta-blockers when no contraindication exists and there is angina, hypertension or tachycardia not related to HF. Otherwise, oral beta-blocker therapy is given in the acute setting. It is important to refrain from giving beta-blockers if there are signs of cardiogenic shock, such as hypotension or pulmonary edema on chest X-ray. Long-term (lifetime) therapy has been shown to reduce MI incidence and improve mortality. Also, if LV systolic dysfunction remains after STEMI, beta-blockers are important for chronic systolic HF.

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

Either an ACE inhibitor or angiotensin receptor blocker should be given to all patients with STEMI upon hospital discharge. Caution must be used in the acute setting to avoid hypotension, which can worsen myocardial ischemia. ACC/AHA guidelines give the use of these drugs a class I indication, in the case there is LV systolic dysfunction or if the patient has diabetes. When LV function returns to normal and the patient does not have diabetes, the benefits are less clear. ARBs are generally given only if ACE inhibitors cannot be tolerated due to cough or other side effects.

Aldosterone Antagonists 

The aldosterone antagonist eplerenone was evaluated in the Epleronone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival (EPHESUS) trial, leading to the recommendation for use of the agents with an ACE inhibitor prior to hospital discharge after unstable angina and non-STEMI if there is LV systolic dysfunction (EF < 40%), either diabetes or symptomatic HF present and no contraindication (serum creatinine > 2.5 mL/min and or potassium > 5.0 mEq/L). A class effect is likely present; therefore, spironolactone is frequently used instead of eplerenone due to cost concerns, although there is no direct data to support this practice.

HMG-CoA Reductase Inhibitors 

Every patient with STEMI should receive therapy with a statin; see HMG-CoA Reductase Inhibitor Topic Review. The 2013 ACC/AHA cholesterol guidelines recommend high-intensity statin therapy (defined as LDL reduction > 50%) in patients aged younger than 75 years and moderate-intensity (defined as 30-50% LDL reduction) in those aged older than 75 years. No specific target LDL level is recommended in these guidelines — simply a reduction of LDL levels from baseline. 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 lifetime after a person has an ACS, unless a contraindication exists or the baseline LDL cholesterol is below 70 mg/dL.

Calcium Channel Blockers 

The nondihydropyridine calcium channel blockers diltiazem and verapamil can be used when there is a contraindication to beta-blockers, such as in asthma, and no HF or significant LV systolic dysfunction are present. Sublingual nifedipine is contraindicated due to a reflexive increase in the sympathetic nervous system, 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 

During cardiogenic shock in STEMI, hypotension is present from low cardiac output. This results in end-organ hypoperfusion and potentially multi-system organ failure and can be fatal. Revascularization by PCI or CABG is recommended in this setting. Hemodynamic support using intraaortic balloon counterpulsation, or IABP, known as balloon pump, may be needed and; when severe, LV assist device, LVAD, insertion may be required.

Left Ventricular Aneurysm

A left ventricular aneurysm can form after STEMI. Most commonly, the apex of the heart is involved; however, the inferior wall can form an aneurysm as well. There are four main concerns in patients with LV aneurysm.

  1. Heart failure. The portion of the heart that contains the aneurysm is not contractile and is frequently “dyskinetic.” This results in an overall decrease in heart function and the development of congestive HF.
  2. LV thrombus formation. When blood stagnates in any area of the body, there is a risk for platelet aggregation and thrombus formation; the aneurysmal portion of the LV is no different. Embolization of LV thrombi can lead to embolic stroke or other systemic embolisms.
  3. Ventricular tachycardia. The scar within the LV aneurysm is a focus for ventricular arrhythmias, which can lead to sudden cardiac death.
  4. Angina pectoris. The aneurysmal tissue can continue to cause symptoms of angina, even if revascularized.

A 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. Without knowing a patient’s past medical history, the ECG changes of an aneurysm may mimic an acute ST segment elevation MI. The only way to be sure of a LV aneurysm diagnosis on an ECG — not from an acute MI — is to have the patient’s history of a prior heart attack and cardiac imaging to document the presence of an aneurysm.

There is a surgical procedure during which the surgeon resects the aneurysm and uses a Dacron patch; this is called the “Dor procedure” or the endoventricular circular patch plasty, known as EVCPP. This procedure is indicated when medical therapy fails to control, or acceptably improve, the complications/symptoms from the LV aneurysm mentioned above.

Ventricular Arrhythmia 

The most common cause of pre-hospital death during STEMI is ventricular fibrillation; the widespread availability of automated external defibrillators, or AEDs, has been of benefit in this situation. Ventricular tachycardia also commonly occurs as well during and after STEMI and can be life-threatening. Treatment includes amiodarone and/or lidocaine. See the Ventricular Tachycardia ECG Review for more detail and multiple ECG examples.

Below is one example of sustained monomorphic VT.



An accelerated idioventricular rhythm is a common post-STEMI rhythm; it is also termed “slow ventricular tachycardia” because it meets morphology criteria for VT, but it has a heart rate below 100 beats per minute. This is a benign, hemodynamically stable rhythm, and no treatment is necessary. See the Idioventricular Rhythms ECG Review for more detail and multiple ECGs.

Below is one ECG example. Note the AV dissociation in the rhythm strip in lead V1 at the bottom; this is diagnostic for VT in the setting of a wide QRS complex tachycardia, but not always seen.


The prophylactic administration of lidocaine to suppress premature ventricular contractions or prevent ventricular tachycardia/fibrillation is not recommended. The Cardiac Arrhythmia Suppression Trial (CAST) demonstrated increased mortality using encainide, flecainide and moricizine to suppress PVCs after an ACS.

Atrial Fibrillation 

Although not a common complication of STEMI, atrial fibrillation can occur when atrial infarction occurs — as indicated by PR depression on the ECG. Rapid control of heart rates is crucial to limit the extent of ischemia. Recall that oxygen demand increases as heart rate increases. Emergent cardioversion and amiodarone therapy are frequently needed in the setting of atrial fibrillation and STEMI.

Ventricular Septal Defect 

When infarction of the interventricular septum occurs, this area can thin with the remodeling process and, on occasion, a complete defect between the right and left ventricles can develop. This results in left-to-right shunting of blood and can be life-threatening when acute. A holosystolic murmur at the left lower sternal border occurs. Right heart catheterization will show an “oxygen step-up” between the right atrium and right ventricle, as oxygenated blood will be present in the right ventricle.

The ventricles are good at adapting to hemodynamic stress when gradually introduced, as in worsening aortic regurgitation; however, when acute, ventricular failure and shock occurs — as is present with acute VSD formation. Emergency surgical repair is warranted in this setting. Without surgical intervention, the mortality rate is greater than 90%. Fortunately, with the early revascularization techniques now employed (PCI), acute VSD formation is less common.

Acute Mitral Regurgitation 

Acute severe mitral regurgitation is a life-threatening disorder. Papillary muscle rupture after acute MI can occur as a complication of an inferior MI (right coronary artery supply), as the posteromedial papillary muscle is the most likely to rupture.

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. Mortality approaches 100% if not surgically fixed. As a bridge to surgery, intraaortic balloon counterpulsation can be helpful hemodynamically to reduce afterload and lessen the mitral regurgitation. Right heart catheterization will show prominent “V waves” in the pulmonary capillary wedge pressure tracing.

Left Ventricular Thrombus 

After MIs, especially anteriorly, 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 I, level of evidence B recommendation to warfarin therapy for 3 months when there is a cardiac source of embolus suspected after a MI.

Left Ventricular Free Wall Rupture 

This is a fatal complication of MI and occurs when thinning of the left ventricular free wall occurs as a part of remodeling. A complete defect results in blood from the left ventricle filling the pericardium. This usually occurs rapidly, resulting in cardiac tamponade, pulseless electrical activity, or PEA, and death. Treatment is emergent surgical repair.

Right heart catheterization will show increased right heart pressures and decreased left heart pressures with inspiration. Also, the diastolic pressures will be elevated and equal. Normally, the pericardium can expand as the heart fills; however, with cardiac tamponade from a large pericardial effusion or constrictive pericarditis, this is not able to occur. As a person inspires, venous return is increased to the right heart and the interventricular septum bulges to the left; this impairs LV filling, reducing left heart cardiac output and thereby decreasing systemic pressure (increasing the “pulsus paradoxus”). As a person exhales, right ventricular filling decreases and the left heart fills, causing the interventricular septum to bulge to the right and impairing right ventricular filling. The diastolic pressures are elevated and equal because every cardiac chamber pressure influences the other —considering the heart is not able to expand as mentioned above.

Right Ventricular Infarction 

This can occur simultaneously with an inferior STEMI, as the right coronary artery supplies the right ventricle. Acute right ventricular failure can occur, leading to hypotension and cardiogenic shock. Because the right ventricle is unable to contract, the cardiac hemodynamics become “preload dependant.” If preload is high enough, blood can be “forced” through the right heart. Nitrates decrease preload by venodilation and can cause profound hypotension in the setting of right ventricular infarction. The treatment of choice is IV fluids to help increase preload. A right-sided ECG will show ST segment elevation and should be done in all inferior STEMI patients.

Systolic Heart Failure 

The left ventricular systolic dysfunction potentially resulting from STEMI can cause chronic systolic congestive HF; see Congestive Heart Failure (Systolic) Topic Review.

Pericarditis and Dressler’s Syndrome 

Pericarditis can occur when a transmural infarct also causes pericardial infarction. This occurs 1 to 3 days after MI. Dressler’s syndrome — also known as post-MI syndrome — is an autoimmune phenomenon that can occur after MI and another cause of post-MI pericarditis. Dressler's syndrome manifests 2 to 3 weeks after MI as pericarditis and a pericardial effusion. The diagnosis is clinical and based on ECG changes of pericarditis. Treatment includes aspirin and colchicine to decrease inflammation. Anticoagulation should be avoided in order to prevent hemorrhage into the pericardium and cardiac tamponade.

Special Situations – CAD - STEMI

Aortic Dissection 

During ascending aortic dissection, the right coronary ostium may be involved, causing an inferior STEMI. This is relatively uncommon but must be recognized quickly, as surgical intervention is crucial for survival.


When coronary angiography is performed late after symptom onset during STEMI, there is a risk for  “no-reflow” or “microvascular obstruction.” This results in a significant decrease in forward blood flow in the coronary circulation despite the major vessel remaining patent. Because the distal, smaller vascular bed is occluded with thrombus, there is no circulatory channel for the blood to leave the coronary arteries. Catheter-based thrombus aspiration, or thrombectomy, can help prevent no-reflow, but data is limited. More aggressive use of glycoprotein IIb/IIIa inhibitors may help as well, but this data is again limited. The presence of no-reflow does predict worse outcomes after STEMI.


ST segment elevation MI is rare during pregnancy but can occur. Atherosclerotic plaque rupture in women with typical risk factors is the most common etiology. Spontaneous coronary dissection risk is increased during pregnancy, as well. PCI is the primary treatment option, as thrombolytics and glycoprotein IIb/IIIa inhibitors are contraindicated during pregnancy.

Mimicking STEMI 

Many disorders can mimic STEMI in both the symptomatic presentation and the ECG findings, as previously discussed. Remember STEMI is an ACS, which implies an unstable atherosclerotic plaque and thrombosis. There are several other disorders that can cause anginal symptoms and ischemic ST segment elevation on the ECG, but are not from atherosclerotic plaque rupture include. These include coronary spasm, aortic dissection, vasculitis, Takotsubo cardiomyopathy (stress-induced cardiomyopathy), radiation therapy, coronary embolus, non-cardiac chest pain with chronic ECG changes (LBBB or LVH), myocarditis, cocaine use, trauma or cardiac contusion, and congenital coronary anomalies.

Non-steroidal Anti-inflammatory Drugs (NSAIDs) 

These agents (ibuprofen, naproxen, rofecoxib) have many negative effects on the heart, both during and after STEMI. They can interfere with the beneficial actions of aspirin, increase the risk for MI (COX-2 selective inhibitors), exacerbate HF, and increase BP. These drugs should be discontinued immediately when STEMI is diagnosed.

Glucose Control 

Tight control of blood sugar levels has become the standard of care during ACS. There is currently insufficient data to support a reduction in morbidity or mortality with more intensive control, such as insulin drips.

1. ACC/AHA STEMI Guidelines
2. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine
3. Hurst’s the Heart, 13th Edition
4. Kumar A and Cannon CP. Acute Coronary Syndromes: Diagnosis and Management, Part 1. Mayo Clin Proc. 2009;doi:10.4065/84.10.917.