Key Points
Posterior wall ST-elevation myocardial infarction commonly occurs as a complication (or extension) of acute inferior wall STEMI. In this setting, ST-segment depressions appear in the right precordial leads (V1, V2 and V3) along with classic ST-segment elevations in the inferior leads. The precordial ST-segment depressions are the “mirror image” of ST-segment elevations over the posterior left ventricular wall. The culprit infarct-related artery is almost always the right coronary artery (RCA) (which perfuses the posterior wall of the heart by way of its posterior descending branch) or the left circumflex artery (LCA). Patients with inferior wall STEMIs complicated by ST-segment depressions in the right precordial leads (V1–V3) have larger infarct sizes and higher rates of pump failure, arrhythmias and early and late mortality.
Posterior wall STEMI may also occur in combination with lateral wall or high lateral wall STEMI. ST-segment depressions are present in precordial leads V1, V2 and V3 in combination with ST-segment elevations (or simply loss of R-wave voltage) in the lateral (V5–V6) or high lateral (leads I and aVL) regions of the heart.
Posterior wall STEMI may also occur alone. “True” or “isolated” posterior wall STEMI is not common (approximately 3–8 percent of all STEMIs) and is often missed. Usually, isolated posterior wall STEMI is caused by occlusion of the LCA or one of its branches (especially an obtuse marginal branch). The culprit artery may also be the terminal posterior descending branch of the RCA.
Most “true” or “isolated” posterior STEMIs are not isolated at all; they actually involve the posterior and lateral left ventricular walls and can include a large at-risk territory.
The right precordial leads (V1, V2 and V3) are critically important in diagnosing posterior wall STEMIs. Acute posterior wall STEMI should be suspected whenever the ST-segments are depressed in leads V1, V2 and V3. Classically, the T-waves in these leads are unusually upright, despite the markedly depressed ST-segments. ST-segment depressions and tall, upright T-waves in these right precordial leads are the electrical mirror image of ST-segment elevations and T-wave inversions over the posterior wall. Broad (≥0.04 seconds) and tall R-waves, often with a slurred upstroke, may also appear in leads V1 and V2; usually, these prominent R-waves are the reciprocal to posterior wall Q-waves, although they may reflect conduction system disturbances in some patients. The constellation of ST-segment depressions, upright T-waves and prominent R-waves in the right precordial leads (V1–V3) represents the “reciprocal sign” of true posterior wall STEMI.
By definition, isolated posterior STEMIs present without any ST-segment elevations on the 12-lead ECG. These patients present with only with anterior (right precordial) ST-segment depressions and upright T-waves. They should still be considered as candidates for immediate reperfusion therapy. According to current guidelines, right precordial ST-segment depressions suggestive of posterior wall STEMI are a STEMI equivalent.
ST-segment depressions in the right precordial leads (V1, V2 and V3) may also be caused by anterior wall ischemia. Not surprisingly, isolated posterior wall STEMI is often misclassified as “anterior wall ischemia or non-STEMI,” leading to a delay in reperfusion therapy. Acute posterior wall STEMI is likely if the anterior precordial ST-segment depressions are: most marked in the right precordial leads (V1, V2 and V3); accompanied by tall, upright T-waves in these leads; accompanied by ST-segment elevations in the lateral (V5–V6) or high lateral (I and aVL) leads; or accompanied by signs of concomitant inferior wall STEMI. Anterior wall subendocardial ischemia (or non-STEMI) is more likely if the ST-segment depressions disproportionately involve the lateral precordial leads (V4–V6) and are accompanied by T-wave inversions.
The standard 12-lead ECG is not a sensitive tool for diagnosing isolated posterior STEMI because it does not include any exploring leads that face the posterior left ventricular wall. The sensitivity can be increased by adding the three “posterior leads” (V7, V8 and V9). Clinicians should obtain posterior leads if a patient presents with symptoms that suggest an acute coronary syndrome (ACS) in the absence of diagnostic ST-segment elevations in any leads.
Posterior Wall ST-Elevation Myocardial Infarction
Posterior wall ST-elevation myocardial infarction commonly occurs as a complication (or extension) of acute inferior wall STEMI. As discussed in Chapter 2, ST-segment depressions appear in the right precordial leads (V1, V2 and V3) along with classic ST-segment elevations in the inferior leads (Ayer and Terkelsen, 2014). The precordial ST-segment depressions are the “mirror image” of ST-segment elevations over the posterior left ventricular wall. The culprit infarct-related artery is usually the right coronary artery (RCA) or, less often, the left circumflex artery (LCA).
Posterior wall STEMI may also appear in conjunction with a lateral wall or high lateral wall STEMI. Here, the ST-segment depressions in the right precordial leads (V1, V2 and V3) are accompanied by ST-elevations in leads V5 and V6 (lateral wall STEMI) or in leads I and aVL (high lateral STEMI).
“True” or “isolated” posterior wall STEMIs are the subject of this chapter. True posterior STEMIs are not especially common (perhaps 3–8 percent of all myocardial infarctions), but they are often missed. Long delays in reperfusion therapy are almost the rule. This is not surprising because in posterior wall myocardial infarctions, the current of injury develops in an electrically “silent” region of the myocardium, where there are no exploring electrodes (Brady et al., 2001; Ayer and Terkelsen, 2014; Lawner et al., 2012; Brady 2007). Nonetheless, these are true STEMIs.
Typically, true posterior wall STEMIs present with only ST-segment depressions in one or more of the right precordial leads (V1–V3), sometimes accompanied by development of tall or broad R-waves. As befits any other STEMI, there is an occluded infarct-related artery, most often the LCA or one of its major branches. Acute posterior STEMI can also be caused by occlusion of the posterior descending artery, the terminal posterior branch of the RCA.
Recent echocardiographic and cardiac magnetic resonance imaging studies now make it clear that “true” or “isolated” posterior wall STEMI is, in fact, not isolated at all. In most patients with STEMIs characterized as “true posterior,” there is extensive lateral wall ischemia and a large area of myocardium at risk (Nikus et al., 2010; Wagner et al., 2009; Ayer and Terkelsen, 2014; Rokos et al., 2010; Brady, 2007).
In some patients who present with right precordial (V1–V3) ST-segment depressions, the diagnosis is anterior wall subendocardial ischemia or non-STEMI. In other patients with right precordial lead ST-segment depressions, the correct diagnosis is posterior wall STEMI. It is our job to tell one from the other (Rokos et al., 2010; Birnbaum, Nikus et al., 2014; Birnbaum, Wilson et al., 2014).
The Coronary Anatomy
Usually, “isolated” posterior wall STEMI is caused by a thrombotic occlusion of the left circumflex artery (LCA) or one of its major branches, most often a large obtuse marginal (OM) branch. Isolated posterior wall STEMI may also occur if the posterior descending artery (PDA), the large terminal branch of the right coronary artery, is occluded. Review Figures 3.3 and 4.1; it is no surprise that “true” posterior wall STEMIs almost invariably extend to the lateral left ventricular wall when the LCA or OM is the culprit vessel.
Figure 4.1 Culprit artery occlusions in true posterior wall STEMI.
This figure shows the posterior wall of the left ventricle. True (isolated) posterior wall STEMI may be caused by occlusion of the left circumflex artery (or one of its major branches) or, occasionally, by occlusion of a terminal branch of the RCA (usually the posterior descending artery).
Posterior Wall STEMI: The ECG “Reciprocal Sign”
Figure 4.2 illustrates the electrocardiographic hallmarks of a true posterior wall STEMI. There are dominant (tall and wide) R-wave in leads V1 and V2, which are the mirror image of posterior Q-waves. The ST-segments are depressed in the right precordial leads (V1, V2 and V3), the reciprocal to the posterior wall ST-segment elevations. And the T-waves are unusually tall, as if they are “determined” to stay upright, despite the sagging ST-segments. In this atlas, we refer to these as “bolt upright” T-waves. These are the mirror image of posterior wall T-wave inversions. Together, these ECG abnormalities represent the “reciprocal sign” of posterior STEMI. The reciprocal sign is usually limited to the right precordial leads (V1, V2 and V3), but they sometimes extend to V4 (Lawner et al., 2012; Brady 2007; Brady, 1998; Boden et al., 1987).
Therefore, true posterior wall STEMI should be considered whenever the following ECG abnormalities are present:
ST-segment depressions in the right precordial leads (V1–V3), accompanied by upright T-waves.
Tall or broad R-waves in precordial leads V1 and V2. The R-wave is noticeably broad (≥0.04 seconds wide) and often has a slurred upstroke. The R:S ratio in lead V2 is ≥ 1.0. Like the mirror image Q-waves, prominent R-waves may not appear on the initial ECG1 (Brady, 2007; Brady, 1998).
Another clue to a posterior wall STEMI is the presence of a concomitant lateral or high lateral or inferior STEMI. Therefore, whenever the ST-segments are depressed in V1–V3, raising the possibility of a posterior STEMI, check for:
Concomitant ST-segment elevations in the lateral (V5–V6) or high lateral (I and aVL) leads. Lateral wall infarction may also manifest as loss of R-wave amplitude in leads V5 and V6 (the lateral wall “voltage drop-off” sign).
Concomitant ST-segment elevations in the inferior leads (or simply ST-segment depressions in lead aVL).
An Approach to Chest Pain Patients Who Have Anterior Wall ST-Segment Depressions
All too often, patients with chest pain, shortness of breath, dizziness or other related symptoms – who have ST-segment depressions in the right precordial leads (V1, V2 and V3) – are labeled as having “unstable angina” or anterior wall ischemia or a “non-STEMI.” Some of these patients are experiencing acute posterior wall STEMIs, not anterior wall ischemia, and they could benefit from emergent reperfusion therapies (Pride et al., 2010; Brady et al., 2001).
ST-segment depressions in the anterior precordial leads may be caused by a posterior wall STEMI. Or they may be caused by anterior wall ischemia (unstable angina or a non-STEMI). Or anterior wall ST-segment depressions may be a sign of acute or chronic pulmonary hypertension (for example, in the setting of acute pulmonary embolism). Our objective is to discern when right precordial ST-segment depressions are a posterior wall “STEMI equivalent” (Brady et al., 2001; Wagner et al., 2009; Thygesen et al., 2012; Nikus et al., 2010; Rokos et al., 2010; Fesmire et al., 2006; Birnbaum, Nikus et al., 2014; Birnbaum, Wilson et al., 2014; Smith et al., 2002). The ECG features of acute pulmonary embolism are discussed in detail in Chapter 5, The Electrocardiography of Shortness of Breath.
One important point first: Any ST-segment depression in V1, V2 and V3, even subtle deviations, should be taken seriously. Remember that most normal individuals have some degree of ST-segment elevation in one or more of the right precordial leads. This means that any degree of anterior precordial ST-segment depression should raise the possibility of posterior wall STEMI or anterior wall ischemia. Also keep in mind that the anterior precordial leads are at some distance from the posterior wall of the left ventricle. Not surprisingly, even in the presence of an evolving posterior STEMI, the ST-segment depressions in V1, V2 and V3 may appear modest. Use old, baseline ECGs for comparison, if they are available.
Following are several important clues that can help to differentiate anterior wall ischemia or non-STEMI from posterior wall STEMI.
Acute posterior wall STEMI is likely if the anterior precordial ST-segment depressions are limited to or are most prominent in the three right precordial leads (V1, V2 and V3). Anterior wall ischemia (unstable angina or a non-STEMI) is more likely if the anterolateral leads (V4–V6) are most affected by the ST-segment depressions and if the ST-T-wave changes are transient or dynamic (Smith et al., 2002).
Acute posterior wall STEMI is also more likely if the right precordial ST-segment depressions are accompanied by tall, upright T-waves. T-wave inversions are more common in anterior wall subendocardial ischemia (and in acute pulmonary embolism). Again, the “bolt upright” T-waves in V1–V3 are the mirror image of posterior wall T-wave inversions. See Figure 4.3.
Posterior wall STEMI is more likely if the R-waves in leads V1 or V2 are tall, are broad or have a slurred upstroke.
Posterior STEMI is more likely if the ECG demonstrates: (a) signs of concomitant lateral wall STEMI (ST-segment elevations or loss of R-wave voltage in the lateral precordial leads V5 or V6); (b) signs of concomitant high lateral STEMI (ST-segment elevations in leads I and aVL); or (c) signs of evolving inferior wall STEMI (Nikus et al., 2010; Lawner et al., 2012).
Figure 4.3 Differentiating anterior wall ischemia from posterior wall STEMI.
Posterior wall STEMI is highly likely when the right precordial ST-segments are accompanied by upright T-waves (Panel A). Panel C demonstrates symmetric T-wave inversions and is more characteristic of anterior wall ischemia (unstable angina or non-STEMI). Panel B has features of anterior ischemia and posterior STEMI; posterior leads should be obtained, along with echocardiography, whenever the diagnosis is in doubt. Remember: Panels B and C are also characteristic of acute pulmonary embolism (see Chapter 5).
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