Ischemic Patterns
Coronary Anatomy
The right and left main coronary arteries arise from the right and left aortic sinuses located at the aortic root. The left main coronary artery branches into the left anterior descending and left circumflex artery.
LAD
Septals
Diagonals
The left anterior descending artery travels down the interventricular groove toward the apex. It may wrap around the apex to supply blood to the posterior apical wall. The left anterior descending supplies blood to the anteroseptal, anterior, and anterolateral walls of the left ventricle. The LAD divides into diagonal branches that supply the base of the left ventricle and septal branches that are oriented perpendicular to the LAD to supply blood to the interventricular septum.
Circumflex
Obtuse Marginals
The circumflex artery wraps around the left atrioventricular groove and supplies blood to both anterior and posterior aspects of the lateral wall. The major branches of the circumflex are the obtuse marginal (OM) arteries. They supply blood to the lateral free wall of the left ventricle.
RCA
Acute Marginal Branch
Posterior Descending Artery
The right coronary artery (RCA) runs along the right atrioventricular groove and supplies blood to the right ventricle through its acute marginal branch. It wraps around to the posterior wall of the right ventricle before branching into the posterior descending artery (PDA). The PDA descends toward the apex along the posterior interventricular groove and supplies blood to the inferior septum and wall, the right bundle branch, and the posteromedial papillary muscle of the mitral valve.
 FIGURE 12.1 Simplified diagram of the coronary arteries and their branches depicted from an anterior view of a heart with right-dominant circulation. |
Right Coronary Dominance
In 85% of patients, the RCA is considered dominant, giving rise to the PDA and a posterolateral branch that supplies blood to the left ventricle. In 15% of patients, the PDA branches off the left circumflex artery.1
Subendocardial Ischemia
Pathophysiology
 FIGURE 12.2 A. Relationship of coronary artery to layers of the ventricular wall. B. Vectors resulting from subendocardial ischemia. |
The coronary arteries supply blood to the cardiac muscle by piercing the epicardium along which it runs and branching into the epicardial, myocardial, and subendocardial vessels. Subendocardial tissue receives the most distal branches and thus the most distal coronary blood supply, making it the layer most susceptible to coronary ischemia.
ECG Features
 FIGURE 12.3 A-C. Different types of ST depression. |
ST depression is a nonspecific finding for subendocardial ischemia. The pattern of ST depression (≥1 mm) is typically horizontal or downsloping. ST depression can also have an upsloping pattern when the J-point is depressed.
The T waves of subendocardial ischemia often remain upright but with decreased amplitude. This differs from LVH with strain pattern in which the T waves are inverted.
The leads that demonstrate ST depression do not anatomically correspond to the region of the left ventricle, which is affected by myocardial ischemia.2 Cardiac markers may be elevated with ST depression if there is associated myocardial necrosis.
ST Elevation MI
Pathophysiology
ST elevation MI (STEMI) results from complete thrombotic occlusion or persistent vasospasm of an epicardial coronary artery. Insufficient perfusion results in epicardial or transmural injury.
Prinzmetal angina: Coronary vasospasm occludes distal blood flow. When it persists for more than 20 minutes, transmural infarction can result.
Current of Injury
Acute ischemia alters the action potential of the myocardial cell in several ways. Voltage differences in the action potential between normal and ischemic cells set up a current, the vector of which results in ST elevation.
 FIGURE 12.4 Effect of ischemia on myocardial action potential. |
 FIGURE 12.5 Vector resulting from MI. |
ECG Evolution
 FIGURE 12.6 Progression of ECG changes in MI. |
Signs of Reperfusion
Resolution of ST Elevation
Early T-Wave Inversion
The appearance of early T-wave inversion has been associated with reperfusion and decreased mortality.5
ST Elevation
ST elevation in myocardial infarction (MI) can have different morphologies. It is important to recognize them all.
 FIGURE 12.7 Different morphologies of ST segments in acute MI. |
Localizing the Infarct
Different patterns of ST elevation on an ECG correlate with different sites of coronary artery occlusion. The territory and extent of MI can be inferred from the pattern of lead involvement. The diagram below is a color-coded representation of different ST elevation patterns as they correlate to the coronary anatomy of someone with right coronary dominance.
Anterior MI
When the occlusion is located at the mid or distal aspects of the LAD, ST segments will be elevated in V1-V3. Reciprocal depressions can be seen in II, III, and aVF.
Anterolateral MI
Occlusion of the proximal LAD or left main coronary can result in an extensive anterolateral MI.
The ST segment in aVR can be elevated to a greater extent than in V1 in left main coronary artery occlusion.6
Right Ventricular MI
ST elevation in V1, especially in the setting of ST elevations in the inferior leads, can represent infarction of the right ventricle. This results from occlusion of the proximal RCA. Placing right-sided leads (V3R-V5R) can help increase the sensitivity of ECG for the diagnosis of right ventricular MI.
 FIGURE 12.8 A map of ECG leads and their associated coronary artery anatomy. Colored circles represent groupings of ECG leads. |
Inferior MI
Inferior MI can result from occlusion of either the left circumflex or RCA. ST segments are elevated in II, III, and aVF. Reciprocal ST depressions occur in leads I and aVL and leads V1-V3.
Posterior MI
Lead V1 can be considered as a mirror image of posterior leads. ST depressions in V1 can be reflections of ST elevations in posterior leads (V7-V9). Occlusion of the left circumflex artery can cause this type of MI.
Lateral MI
ST elevation in leads aVL, I, V5, and V6 may represent lateral MI. However, ST elevation is commonly absent in lateral MI. This type of MI occurs with occlusion of the left circumflex or the first diagonal branch off the LAD.
Anterior MI
The LAD supplies a significant area of the left ventricular wall. Complete occlusion of the LAD can result in extensive myocardial necrosis and severely compromised cardiac output.
Septal and diagonal branches arise from the LAD. The pattern of infarction varies based on whether the occlusion occurs proximal or distal to these branches.
 FIGURE 12.9 Representative locations of different LAD lesions. |
Anterior MI Subtypes
TABLE 12.1 Different Types of Anterior MI | ||||||||||||||||||||
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Acute Complications
Heart Failure
Extensive infarction of the left ventricle can result from an anterior MI. Contractility of the left ventricle can become compromised in the acute setting, leading to cardiogenic shock.
Ventricular Dysrhythmias
Ventricular fibrillation or tachycardia occurs in a significant minority of patients with anterior MI. These rhythms are more commonly associated with anterior than with inferior MI.
AV Block
AV block associated with anterior MI is more commonly infranodal and may be permanent.
Inferior MI
An inferior MI results in ST elevations in leads II, III, and aVF.
Reciprocal ST depressions appear in leads I and aVL.
 FIGURE 12.10 Anatomy of an inferior MI. |
Anatomy
RCA
In the vast majority of patients with inferior MI, the culprit occlusion is located in the RCA.
Left Circumflex
Inferior MI can also occur from occlusion in the left circumflex or its obtuse marginal (OM) branches.
IMI Subtypes
Isolated IMI
ST elevation is confined to leads II, III, and aVF. An ECG with right-sided leads should be obtained to look for evidence of right ventricular infarction.
Inferoposterior MI
ST depression in leads V1-V3 may indicate that the posterior wall of the left ventricle is involved.
Inferolateral MI
ST elevation in the lateral precordial leads (V5-V6) indicates that the lateral wall of the left ventricle may be involved.
Right Ventricular MI
ST elevation in right-sided precordial leads (V3R-V6R) indicates that the right ventricle is infarcted.
Complications
AV Block
AV block in the setting of an acute IMI is usually at the level of the AV node and is often transient.
Papillary Muscle Rupture
The RCA supplies blood to the posteromedial papillary muscle (the anterolateral muscle is supplied by both the LAD and left circumflex). An inferior MI can lead to the fatal complication of acute mitral regurgitation from papillary muscle rupture.
Atrial Infarction
Blood flow to the right atrium is supplied by proximal branches of the RCA. Proximal RCA occlusion may result in atrial infarction and atrial fibrillation.
Posterior Myocardial Infarction
Posterior MIs occur in isolation in a significant minority (3%-7%) of STEMIs.7,8 Because no leads in the standard 12-lead ECG directly face the posterior wall of the left ventricle, the 12-lead ECG is an insensitive tool for diagnosing this type of infarction. Diagnosis of a posterior MI is often missed or delayed. Patients with a posterior MI benefit from early PCI and thrombolysis.
Anatomy
Posterior MIs usually result from occlusion of the left circumflex artery (or its first OM branch). The left circumflex artery supplies blood to the lateral and posterior walls of the left ventricle. Posterior MIs are commonly associated with lateral and inferior infarctions.
ECG Features
ST Depression V1-V3
These leads can be a mirrored representation of the posterior left ventricular (PLV) wall. ST depression in V1-V3, therefore, may actually represent posterior ST elevation.
Prominent R Waves V1
A tall R wave in V1 is abnormal. A tall R wave in V1 could represent the mirror image of a deep Q wave coming from the posterior wall. This, however, can be a marker of an old posterior MI.
ST Elevation in Posterior Leads
Posterior MI can only be confirmed on EKG by demonstrating ST elevation in posterior leads V7-V9. These leads are placed in the same horizontal plane as leads V4-V6. V7 is placed at the left posterior axillary line, V8 at the scapular tip, and V9 to the left of the spinal column.
 FIGURE 12.11 A. ECG appearance in anterior precordial leads. B. Axial view of a heart with posterior wall infarction. C. ECG appearance in posterior leads. |
 FIGURE 12.12 Positioning of posterior leads. |
TABLE 12.2 Differential Diagnosis of ST Depression in V1 | |||
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Right Ventricular MI
Infarction of the right ventricle occurs in approximately 50% of inferior MIs.9 Right ventricular MIs may also rarely occur in isolation. Life-threatening complications from a right ventricular infarction can occur early in the acute presentation.
Anatomy
Infarction of the right ventricle results from occlusion of the RCA proximal to the first acute marginal branch. The marginal branch is critical in supplying blood to the free wall of the right ventricle.
ECG Features
STE in V1
ST elevation in lead V1 is a relatively specific finding, but sensitivity is very poor. ST elevation is most prominent in V1 with declining degrees of elevation in V2 and V3. ST elevation in leads V1-V3 may lead to the incorrect diagnosis of an anteroseptal MI. The degree of ST elevation should increase in V2 and V3 in an anteroseptal MI.
STE in III > STE in II
ST segments in an RV MI are elevated in II, III, and aVF. Because lead III is a right-sided limb lead, ST elevation is greater in lead III than in lead II (a left-sided limb lead) in an RV MI. This may be a more sensitive finding than ST elevation in V4R.9
STE in V4R-V6R
Right-sided precordial leads should be recorded in all patients with an inferior MI. ST elevation ≥1 mm in V4R-V6R is diagnostic of an RV MI. V4R is the most sensitive lead. This is a transient finding and may be absent for 24-48 hours after symptom onset.9
 FIGURE 12.13 Proximal RCA occlusion resulting in infarction of the right ventricular lateral and posterior walls (areas shaded in blue). |
 FIGURE 12.14 ST elevation in II and III as they relate to their leftward and rightward lead positions. |
 FIGURE 12.15 Positioning of right-sided precordial leads. |
Complications of a Right Ventricular MI
Lower oxygen demand, collateral blood supply from the LAD, and a thinner myocardium are factors that limit the morbidity and mortality in right ventricular MI relative to those associated with a left ventricular MI. However, extension of an inferior MI to involve the right ventricle is associated with increased morbidity and mortality compared to inferior MIs that occur in isolation. Right ventricular MIs are also associated with their own hemodynamic complications.
Hypotension
In a minority of patients with right ventricular MI, right ventricular failure (both systolic and diastolic dysfunction of the right ventricle) results in altered hemodynamics.10 The presence of hypotension should raise concern for a right ventricular MI. Hypotension, jugular venous distention, and clear lungs are described as a clinical triad associated with RV MI.11 The classic hemodynamic finding on right-heart catheterization is a disproportionate elevation in right-sided filling pressures. Right ventricular dysfunction often resolves in several weeks, suggesting that the myocardium of the right ventricle is stunned in the acute setting and not necrotic.12 Early identification of an RV MI is critical in preventing iatrogenic hypotension by the administration of preload-reducing agents (nitroglycerin).
Systolic Dysfunction
Decreased cardiac output from the right ventricle results in decreased preload delivered to the left side of the heart. Left ventricular output suffers and results in hypotension. Treatment is aimed at increasing right ventricular preload by delivering intravenous crystalloid.
Diastolic Dysfunction
Decreased compliance of the right ventricle leads to increased diastolic filling pressures of both the right ventricle and atrium. This can result in the bowing of the interventricular septum into the left ventricular space during diastole. The amount of left ventricular diastolic filling becomes limited.
Hypoxemia
R-to-L Shunt
Patients with a patent foramen ovale in the setting of elevated RV and RA pressures can develop a right-to-left shunt leading to hypoxemia.
Pulmonary Emboli
Embolization of a right ventricular thrombus from the cavity of an infarcted right ventricle to the pulmonary circulation is another important cause of hypoxemia to consider.
Bradycardia
Vagal Stimulation
Reflex stimulation of afferent vagal fibers that run along the RCA may result in sinus bradycardia.
AV Block
In most patients, the blood supply to the AV node is from the AV nodal branch of the RCA. Persistent AV block may indicate AV nodal dysfunction in an ischemic AV node. However, in many cases, AV block in the acute setting of an RV MI is from vagal stimulation.
Atrial Fibrillation
Occlusion of the proximal RCA can lead to right atrial infarction. This can increase the risk of supraventricular tachyarrhythmias including atrial fibrillation.
Acute Pulmonary Edema
The RCA is the single blood supply to the posteromedial papillary muscle of the mitral valve. Proximal RCA occlusion can result in papillary muscle rupture and subsequent life-threatening mitral regurgitation.
Lateral MI
Electrocardiographic signs of lateral MI are often subtle or completely absent. ST elevation is absent in acute lateral MI 50% of the time. The lateral wall of the left ventricle is often in an electrocardiographically silent location.
 FIGURE 12.16 Anatomy of lateral MI. |
Anatomy
Left Circumflex
The left circumflex artery wraps around the AV groove posteriorly. Obtuse marginal arteries branch from the circumflex and supply the lateral wall of the left ventricle. Occlusion of the circumflex or one of its obtuse marginal branches results in a lateral MI. In the 10%-15% of the population with a left-dominant coronary circulation, the left circumflex feeds into the PDA. Occlusion of the left circumflex in patients with a left-dominant coronary circulation will appear as ST elevations in leads II, III, and aVF.
Diagonal Branch
Occlusion of the first diagonal branch of the LAD results in lateral MI.
Associated ECG Patterns
ST Elevation
May be completely absent. ST elevation may be present in lead aVL only or may be accompanied by ST elevation in lead I. ST elevation in these leads is often less than 1 mm in height, especially when the QRS amplitude is low. ST elevation may also be present in leads V5 and V6.
ST Depression
Reciprocal ST depression may be the only electrocardiographic sign of a lateral MI. Reciprocal ST depressions appear in leads II, III, and aVF.
ST depressions may also appear in leads V1-V3 when circumflex occlusion results in infarction of the posterior wall (posterolateral MI).
Pericarditis
Pericarditis accounts for approximately 5% of the causes of nonischemic chest pain in the emergency department.13 In the vast majority of cases, this cause is unknown or secondary to viral infection. Less common causes include malignancy, uremia, chest wall irradiation, chest trauma, autoimmune disease, medications, recent myocardial infarction, and bacterial infections.
Clinical Characteristics
The chest pain of acute pericarditis often has a sudden onset. It is described as retrosternal (or left sided), pleuritic, and positional (relieved by sitting forward, worse supine). The pain can radiate to the trapezius ridge or down the left arm. Symptoms typically last less than 2 weeks.
ECG Features
Diffuse ST elevation is the classic finding in acute pericarditis. ST segments are elevated in all leads except aVR and often V1. Elevated ST segments are typically concave. The ECG characteristics of acute pericarditis evolve through four stages.14
 FIGURE 12.17 Progression of ECG changes in pericarditis. |
Diffuse ST Elevation
Represents epicardial inflammation.
Diffuse PR Depression
Leads V1 and aVR
ST segments can be depressed in these leads. The PR segment in V1 and aVR can be elevated, representing an atrial current of injury.
Normal ST Segments
Normal PR Segments
T-Wave Flattening
The PR segment can normalize before the ST segment, making pericarditis even more difficult to distinguish from acute coronary syndrome (ACS).15
Diffuse T-Wave Inversions
T-wave inversions may persist indefinitely in some patients.
T Wave Normalizes
TABLE 12.3 ECG Findings More Consistent with Ischemia | |||||
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Diffuse ST Depressions
ST depressions that are deep and diffuse reflect diffuse subendocardial ischemia. Diffuse ST depressions are often accompanied by reciprocal ST elevation in lead aVR. The specificity of this pattern for acute coronary occlusion is unknown, as patients with this pattern are less likely to undergo emergent coronary angiography. The differential for this pattern includes coronary occlusion and noncardiac causes.
Coronary Occlusion
Subtotal Proximal LAD Occlusion
Acute coronary thrombosis is a dynamic process of clot formation and lysis. Diffuse ST depression may appear when occlusion of the proximal LAD is near complete. This pattern may quickly evolve into a large ST elevation MI representing complete coronary occlusion.
Complete Proximal LAD Occlusion with Collateral Flow
Diffuse ischemia may be the consequence of complete LAD occlusion in a heart with good collateral flow supplying the left ventricle from branches of other coronary vessels.
Noncoronary Causes
Recent Defibrillation or Cardioversion
ST segment changes are typically transient after resuscitation following cardiac arrest or cardioversion.
Significant Tachycardia
Atrial fibrillation with rapid ventricular response and reentrant narrow complex tachycardias can be associated with diffuse ST depressions. Rate-related ischemia typically resolves with restoration of sinus rhythm or rate control.
Neurocardiogenic Causes
Subarachnoid Hemorrhage
Subarachnoid hemorrhage is a less common cause of cardiac arrest. Diffuse ST depression with reciprocal ST elevation has been described in a case series.16 This pattern is thought result from excessive catecholamine release and neurogenic stunning of the myocardium. Elevated troponin levels occur in more than one third of patients with subarachnoid hemorrhage.17
Stroke
Seizure
Diffuse ST depressions have also been described in case reports of ischemic stroke and seizure.18
Left Ventricular Aneurysm Morphology
Persistent ST elevation following myocardial infarction is referred to as left ventricular aneurysm morphology given its association with aneurysmal distortion of the ventricle seen on autopsy studies. LV aneurysms most commonly complicate large anterior MIs and occur in the anterior or anterolateral wall of the left ventricle. Less often, aneurysms can occur in the inferior or posterior walls after infarction involving these areas.
Persistent ST elevation, however, is also associated with ventricular dyskinesis and akinesis in the absence of aneurysm formation. Some morphologic characteristics may help distinguish persistent ST elevation from the acute MI pattern.
ECG Features of Aneurysmal Morphology
Deep Q Waves
Deep Q waves commonly accompany the elevated ST segments resulting from a dyskinetic area of the ventricle.
STE
ST elevation occurs most often in the anterior precordial leads. The ST segment is often concave. Elevation of the ST segments is thought to be secondary to traction on the normal myocardium by the scarred or necrotic tissue.
Absent Reciprocal Depression
Reciprocal ST depression will be notably absent.
Absence of Dynamic Changes
The morphology of the QRS waves will be unchanged over time. ST elevation will appear fixed and unrelated to the patient’s complaint or resolution of chest pain.
T:QRS Ratio
The best way to discriminate between LV aneurysm and acute anterior MI thus far is to sum the T-wave amplitude in leads V1-V4 and divide by the QRS amplitude sum from V1 to V4. A ratio greater than 0.22 predicts acute MI with 95% sensitivity.19
 FIGURE 12.18 Anterior LV aneurysm.
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