The hallmark is the presence of ST-segment elevations in the “inferior limb leads” – II, III and aVF.
In most cases, there is reciprocal ST-segment depression in the high lateral (or “superior”) leads – I and, especially, aVL. As illustrated in Chapter 1, the positive pole of lead aVL is electrically opposite to lead III.
In the earliest hours of acute IMI, the ST-segments in II, III and aVF may be normal or near-normal, but frequently, there is ST-segment depression in aVL. Thus, ST-segment depression in AVL constitutes a critical “early warning” sign of acute inferior wall STEMI.
In most cases of inferior wall STEMI (approximately 80 percent), the culprit event is an acute occlusion of the right coronary artery (RCA). In the remaining cases, the clotted vessel is the left circumflex artery (LCA). RCA (rather than LCA) occlusion is more likely if the ST-segment is elevated to a greater extent in lead III than in lead II, the ST-segment is markedly depressed (≥ 1mm) in lead aVL, or there is electrocardiographic evidence of right ventricular myocardial infarction (RVMI). Lead III is the most sensitive lead for the diagnosis of inferior wall STEMI caused by RCA occlusion.
ST-segment depressions in aVL are sometimes absent in acute inferior wall STEMI, if the culprit occluded artery is the LCA; in fact, the ST-segments in aVL may even be slightly elevated if occlusion of the LCA has caused not only the inferior STEMI but also a high lateral infarction.
In 90 percent of patients, there is a “dominant” RCA that supplies branches to the anterior and lateral walls of the right ventricle, the AV-node and the posterior left ventricular wall. Thus, acute inferior wall STEMI is often complicated by one or more of the big three: right ventricular myocardial infarction (RVMI), AV nodal block or concomitant infarction of the posterior wall. ST-segment depressions in precordial leads V1–V3 are highly suggestive of extension of the STEMI to the posterior wall.
Although inferior STEMI has a more favorable prognosis than anterior wall STEMI, the presence of RVMI, AV block or posterior wall extension helps define a high-risk subset of IMI patients; patients with one or more of these complications have a higher incidence of cardiogenic shock, ventricular and atrial arrhythmias and in-hospital and late mortality.
The right-sided leads (V4 R and V1) should be examined carefully in every patient who presents with acute inferior wall STEMI. ST-elevations in leads V4 R or V1 signify that an RVMI is present. These ECG findings: also put the culprit lesion in the proximal RCA, before the take-off the right ventricular (acute marginal) branches; identify a subset of inferior STEMI patients at heightened risk of AV block, atrial and ventricular arrhythmias, shock and death; and help avoid complications during treatment.
ECG 2.1 A 37-year-old man presented with chest pain and diaphoresis.
ECG 2.2 A 56-year-old man presented at 3:45 A.M. with nausea and epigastric pain.
The ECG shows classic features of an inferior STEMI. ST-segment elevations are present in II, III and aVF. There is obvious reciprocal ST-segment depression in the high lateral leads (I and aVL). The ST-segment elevations are much greater in III than in II; as discussed in more detail later, this helps identify the right coronary artery (RCA) as the likely infarct-related vessel. ST-segment elevation in lead III > lead II also increases the probability that a right ventricular infarction is present.
The elevated ST-segments, often called epicardial “currents of injury,” reflect transmural ischemia that extends from the endocardial to the epicardial surface (Birnbaum, Nikus et al., 2014; Wagner et al., 2009). Most importantly, ST-segment elevations announce the onset of a “STEMI” and the need for emergent reperfusion therapy. Like other acute coronary syndromes, a STEMI is usually caused by “an occlusive blood clot that is formed on a ruptured atherosclerotic plaque in an epicardial coronary artery” (Birnbaum, Wilson et al. 2014).
The ECG demonstrates an acute inferior wall STEMI. Reciprocal ST-segment depression is present in lead aVL. The ST-segments are also elevated in the lateral precordial leads (V5–V6), indicating extension of the infarct to the lateral wall. As discussed later in this chapter, involvement of the lateral leads (V5–V6) in addition to the inferior leads is a marker of a larger infarct territory.
Importantly, there are marked ST-segment depressions in the right precordial leads (V1–V3); this indicates extension of the infarction to the posterior wall (also a marker of a larger infarct territory). Right-sided leads were negative for right ventricular infarction. The proper reading of this 12-lead ECG is “acute inferior, posterior and lateral STEMI.”
Acute inferior wall STEMI is usually caused by occlusion of the right coronary artery (RCA, 80 percent) or left circumflex artery (LCA, 20 percent). Identifying the infarct-related artery may be of clinical importance, as RVMI and heart block are more likely in RCA occlusions.
Although the 12-lead ECG is an imperfect tool to identify the infarct-related artery, there are some helpful clues (Kontos et al., 1997; Chia et al., 2000; Zimetbaum et al., 1998; Zimetbaum and Josephson, 2003; Surawicz and Knilans, 2008; Wang et al., 2009; Wagner et al., 2009).
The RCA perfuses the inferior and posteromedial portions of the left ventricle along with the right ventricle (see Figure 2.1; Wellens and Conover, 2006). This is the territory of limb lead III. Therefore:
If the ST-segment elevation is higher in lead III than in lead II, a proximal RCA clot is more likely. This is expected, as the positive pole of lead III is oriented to the right inferior segment of the heart (see Figure 2.1 and also Chapter 1). In contrast, lead II monitors the left inferior segment and is more influenced by LCA occlusions.
If the ST-segment depression in lead aVL is ≥ 1.0 mm, a proximal RCA clot is more likely. This is also understandable: in a RCA occlusion, the electrical vector of the injury current is directed toward the right side of the heart – that is, toward lead III and away from lead aVL. Leads III and aVL are near-electrical opposites.
These same ECG findings (ST-segment elevations in III > II and marked ST-segment depressions in aVL) are also strong predictors of a concomitant RVMI.
Figure 2.1 Predicting the infarct-related artery in patients with acute inferior wall STEMI.
The LCA primarily perfuses the posterior and left lateral walls of the left ventricle, which is the segment directly monitored by inferior limb lead II (see Figure 2.1; Wellens and Conover, 2006). There are three ECG clues that suggest LCA occlusion in patients presenting with an acute inferior wall STEMI:
LCA occlusion is more likely if the ST-segment elevations are equal or greater in lead II than in lead III (since the injury current is directed in a more leftward and posterior direction).
LCA occlusion is more likely if the ST-segment is isoelectric, or even elevated, in lead aVL. In the setting of IMI, this suggests an occlusion of the LCA because the injury current is directed more leftward and posterior (toward, not away from, aVL). The LCA supplies the high lateral region, typically via one or more obtuse marginal (OM) branches. Elevation of the ST-segment in aVL usually signifies an acute inferior and high lateral STEMI. Here, the ST-segment elevation in lead aVL may cancel out the expected ST-segment depression in this lead.
In some studies, the presence of concomitant ST-segment elevations in leads V5–V6 (signifying lateral wall involvement) or ST-segment depressions in leads V1–V4 (signifying posterior wall involvement) moderately increases the likelihood that the LCA is the culprit vessel (Surawicz and Knilans, 2008; Assali et al., 1998). Similarly, ST-segment depressions (> 1 mm) in lead aVR may be more common in inferior STEMIs caused by obstruction of the LCA (Tamura, 2014; Vales et al., 2011). Lead aVR is electrically opposite to lead II (see Chapter 1).
ECG 2.3 A 49-year-old female collapsed in her bathroom. On arrival in the emergency department, she was lethargic and mildly hypotensive.
ECG 2.4 A 59-year-old female, previously healthy except for hypercholesterolemia, presented after a single episode of chest pain accompanied by dyspnea and slight discomfort in both arms. After calling 911, she had a syncopal episode. In the presence of paramedics, she had a VF arrest. After defibrillation, she was hemodynamically stable and alert.
The ECG demonstrates an acute inferior wall STEMI, with extension to the posterior and lateral left ventricular wall. First-degree AV block is present. The ST-segment elevations are larger in lead III than in lead II. There is also marked ST-segment depression in aVL. Thus, the culprit infarct-related artery is almost certainly the RCA, based only on this 12-lead ECG. Right-sided leads were obtained (see next ECG).
ECG 2.3 Same patient (right-sided leads).
Although not marked by the computer, these are the right-sided leads. The lack of normal R-wave progression identifies this as a right-sided tracing.
The right-sided leads are positive for right ventricular infarction: V4 R demonstrates marked ST-segment elevation. This ECG finding alone puts the culprit lesion in the RCA, before the take-off the right ventricular (acute marginal) branches. ST-segment elevation in V4 R also identifies a subset of inferior STEMI patients at heightened risk of AV block, atrial and ventricular arrhythmias, shock and death. In fact, each of the big three complications of IMI (RVMI, posterior wall extension and AV block) is present in this patient.
Her initial troponin was normal (0.01) but later peaked at 45.5. She underwent emergency coronary angiography, which revealed a large, dominant RCA. According to the cath report, “There was a 99 percent eccentric, thrombotic stenosis in the proximal RCA that was the culprit vessel for the patient’s acute presentation.” Not surprisingly, an echocardiogram in this patient demonstrated inferior and lateral wall hypokinesis and hypokinesis of the right ventricle.
The ECG demonstrates an acute inferior and lateral wall STEMI. The ST-segment depressions in V1–V4 indicate extension of the STEMI to the posterior wall. There are several clues that suggest a left circumflex artery (LCA) occlusion. First, the ST-segments are more elevated in lead II than in lead III. In addition, the ST-segments are not depressed in the high lateral leads (I and aVL) – in fact, the ST-segments are slightly elevated in these leads. In the setting of an acute inferior wall STEMI, ST-segment elevation in leads I and aVL often indicates that the LCA or one of its branches is obstructed. Pronounced ST-segment elevations are also present in the lateral precordial leads (V5–V6), which is sometimes a marker of LCA occlusion.
Sometimes, in the earliest hours of acute inferior STEMI, the ST-segments in the inferior leads are normal or almost normal. There are no “tombstone” ST-segment elevations. Traditional “cath lab activation criteria” are not met. The computer algorithm reassures us that the ECG is normal. And we are left to wonder: Is the ECG abnormal? Are the minor ST-elevations or ST-segment straightening in lead III important? Should we activate the cath lab?
Even in the face of ambiguity, the astute clinician will recognize two important early warning signs of impending inferior wall STEMI:
One of the earliest changes in the evolution of acute STEMI is a simple straightening of the ST-segment. That is, the ST-segment loses its normal upward concavity. See Figure 2.2.
Figure 2.2 ST-segment straightening in the early evolution of a STEMI.
In Panel A, the ST-segment has a normal configuration. Panel B shows straightening of the ST-segment; even without noticeable elevation of the ST-segment, an acute STEMI may be present. Often, in the earliest stages of an acute STEMI, there is little ST-segment elevation. The only clues to an evolving STEMI may be ST-segment straightening, along with reciprocal ST-segment depressions in one or more opposite-facing leads. These are “don’t-miss” clues; we can’t wait for “tombstone” ST-segment elevations to appear (Panels C and D).
ST-segment depression in aVL and lead I may occur early in the evolution of inferior wall STEMI, even hours before there is any noticeable ST-elevation in leads II, III or aVF (Hassen et al., 2014; Birnbaum et al., 1993; Turhan et al., 2003; Bischof et al., 2016).
In 1993, Birnbaum and colleagues published an important review of 107 consecutive patients with evolving inferior wall myocardial infarctions (Birnbaum et al., 1993). They concluded:
ST depression in aVL … is found in the majority of patients with evolving inferior wall myocardial infarction and … may be the sole electrocardiographic sign of the inferior infarction … Transient ST depression in aVL is a sensitive, early electrocardiographic sign of acute inferior wall myocardial infarction.
Marriott made a similar point (Marriott, 1997):
Whenever a change resembling this is found in aVL in a patient under suspicion of angina pain, that patient should be kept under wraps until the diagnosis is clarified.
To summarize: leads III and aVL, which are electrical near-opposites, are the most critical leads for the diagnosis of early or subtle inferior wall STEMIs.
Often, in the early phases of inferior STEMI, the only abnormality may be ST-segment straightening or minimal ST-elevation in lead III.
ST-segment depression in aVL (and sometimes in lead I) is the other critical “early warning” sign of acute inferior wall STEMI.
Therefore, carefully examine lead aVL in all patients where STEMI is a possibility. Lead aVL can help us notice and interpret subtle and ambiguous ST-segment abnormalities in the inferior leads. And importantly, when there are ST-elevations involving the inferior or the anterior leads (or both), the finding of ST-segment depressions in lead aVL eliminates any consideration that these ST-elevations are the result of pericarditis or benign early repolarization (Bischof et al., 2016).
Examine ECGs 2.5 and 2.6 for clear examples of Birnbaum’s and Marriott’s lesson. Each of these tracings is diagnostic of acute inferior wall STEMI. However, the ST-segment elevations in the inferior leads are subtle. In each case, the diagnosis of acute inferior wall STEMI was missed or delayed. But each case also demonstrates clear ST-segment depression in aVL, which should have alerted the clinicians to the correct diagnosis.
ECG 2.5 A 55-year-old man presented with intermittent chest pain and mild dyspnea. The computer reading was “Sinus bradycardia, otherwise normal ECG.” He was admitted for “Possible Acute Coronary Syndrome, Rule-out M.I.”
ECG 2.6 A 41-year-old female presented with 3 days of chest pain and cough, which she attributed to “sitting in front of the computer all day.” She reported mild chest discomfort and was slightly anxious.
The clinicians did not immediately recognize the early inferior wall STEMI, probably because the ST-segment in lead III is barely elevated. The computer reading was also reassuring. However, upon careful inspection, there is straightening of the ST-segments in leads III (and also in leads II and aVF); the normal, upward concavity in these leads is gone. There is also subtle ST-segment elevation in III and aVF. If, at the bedside, there was any doubt about these abnormalities, lead aVL provides a telltale clue: the ST-segment is depressed. While at first glance the sagging ST-segment in aVL may seem minor, it is actually quite pronounced when considered in light of the very small R-wave in the same lead. The disproportionate ST-depression in aVL provides proof that the subtle ST-segment abnormalities in the inferior leads represent a true, “actionable” STEMI.
The computer cannot make this diagnosis, but we have to. At the very least, the patient needs a repeat ECG within 10–15 minutes. In the words of Marriott, he must be “kept under wraps.” Note: sinus bradycardia is also present. Sinus bradycardia is common in acute inferior STEMI, since the SA node is supplied by the RCA in 60 percent of individuals (and by the LCA in the remaining 40 percent). Inferior wall STEMIs are also frequently accompanied by increased parasympathetic tone.
Initially, this healthy young female was felt to have atypical chest wall pain. The clinicians interpreted her ECG as either “benign early repolarization or pericarditis.” But it cannot be either one of these. Reciprocal changes are present: the ST-segment depressions in the high lateral leads (I and aVL) are incompatible with early repolarization or pericarditis. ST-segment depression is also present in the anterior and lateral precordial leads.
Most importantly, there is ST-segment elevation in lead III. Sure, the ST-segment in lead III is only 1 mm elevated, and it has a reassuring, “smiley face,” upward concavity. But don’t be fooled. This ECG demonstrates an early, subtle inferior wall STEMI. Her initial troponin was 4.25. The next figure shows her repeat ECG, taken 17 minutes later.
ECG 2.6 Same patient (follow-up ECG, taken 17 minutes later).
This would be an appropriate time to consider whether “upward concavity” or “downward concavity” is a helpful clue in distinguishing between STEMI and other, more benign causes of ST-segment elevation (for example, early repolarization pattern, pericarditis or the ST-segment elevations associated with left ventricular hypertrophy). In general, ST-segments that are straightened, concave downward, “dome-shaped” or “tombstone” in appearance are much more common in STEMI. And smooth, upwardly concave ST-segments (with “J-point elevation”) are more characteristic of benign conditions. But the shape of the ST-segment is simply not a reliable ECG sign in differentiating between the two. A smoothly contoured, concave-upward, “smiley face” ST-segment does not exclude acute ST-elevation myocardial infarction, as illustrated in this case (Brady et al., 2001; Birnbaum, Nikus et al., 2014).
To detect subtle STEMIs, focus on whether the ST-segment elevations are regional (in an anatomic territory, such as the inferior, lateral or anterior wall) and focus on the presence of reciprocal ST-segment depressions (here, in leads I and aVL). This topic is considered in more detail in Chapter 7, Confusing Conditions: ST-Segment Elevations and Tall T-Waves (Coronary Mimics).
The lesson from the preceding cases is clear: do not wait for the ST-segments to exceed “2 mm in elevation in at least 2 contiguous leads.” Do not wait until the ST-segments look like “tombstones.” Do not wait until the 12-lead ECG meets “cath lab activation criteria.” And do not wait for the computer to get it right. We must make the diagnosis of acute inferior wall infarction early. Learn to detect subtle straightening and minor elevations of the ST-segments in II, III and aVF. And always check for ST-segment depressions in leads I and aVL, which can serve as a trusted ally.
This atlas is filled with examples of acute ST-elevation myocardial infarctions in their early stages, where the ST-segment elevations are barely noticeable. Remember, there should not be a strict “minimum threshold” for the ST-segment elevation to make a diagnosis of acute STEMI (Chan et al., 2005; Birnbaum, Wilson et al., 2014; Birnbaum, Nikus et al., 2014; Nikus et al., 2014; Nikus et al., 2010). The often-repeated standard of “ST-segment elevation of at least 1 mm in at least two contiguous leads” (with various age, gender and lead variations) was derived from population-based studies and also served as the criteria for entry into the original, large randomized trials of thrombolytic therapy. It remains a cornerstone of the American Heart Association/American College of Cardiology/European Society of Cardiology criteria for the diagnosis of STEMI (Chan et al., 2005; American College of Cardiology Foundation, 2013; Thygesen et al., 2012; Birnbaum, Wilson et al., 2014).
But virtually all current consensus statements regarding the definition of STEMI include the caveat that “lesser degrees of ST-[elevation] … do not exclude acute myocardial ischemia or evolving MI” (Thygesen et al., 2012). In clinical practice, any ST-segment elevation may be sufficient, especially when the ST-segment elevations are regional and are accompanied by reciprocal changes in the electrically opposite leads. In addition, even minimal ST-segment elevations may be significant, when they are found in leads where the QRS amplitude is very low (for example, lead aVL) (Birnbaum, Wilson et al., 2014). Straightened or minimally elevated ST-segments, when accompanied by reciprocal ST-segment depressions, are often a “STEMI equivalent.” See Chapter 3 for additional discussion and examples of these and other “STEMI equivalents.”
Even as we stress the importance of ST-segment depression in lead aVL as an early warning sign of inferior STEMI, we should not overstate our case. There is an important electrocardiographic caveat: occasionally, patients with early inferior wall STEMIs will present without any reciprocal ST-segment depressions in aVL. This is an uncommon exception, but it is important. As noted earlier, these patients often have ST-segment elevations that are more pronounced in lead II than in lead III, and the culprit coronary artery occlusion is usually the LCA rather than the RCA. Typically, the LCA is occluded proximal to the takeoff of the first obtuse marginal (OM) branch. In this circumstance, a concurrent high lateral STEMI is often present along with the inferior wall STEMI. The expected ST-segment depressions in aVL that are reciprocal to the inferior wall STEMI are “canceled out” by the ST-segment elevations in the high lateral leads (I and aVL) (Birnbaum, Wilson et al., 2014). ST-segment elevations are also frequently present in the lateral precordial leads (V5 and V6). Refer again to ECG 2.4, presented earlier, for an example of an inferior and lateral wall STEMI without ST-segment depression in aVL (due to an LCA occlusion). Additional examples are included in the self-study ECGs in this chapter.
In caring for patients with acute inferior wall STEMI, it is not enough to simply identify the inferior ST-segment elevations. In every case, the clinician must examine the tracing carefully for the following big three complications:
ST-elevations in lead V1 or V4 R, signifying right ventricular myocardial infarction (RVMI);
ST-segment depressions in the right precordial leads (V1–V3), indicating extension of the STEMI to the posterior wall; and
The presence of first-degree, second-degree or third-degree AV nodal block.
These three complications are common in patients with inferior STEMI, and they are readily apparent from the surface ECG. Importantly, each of these complications is also an independent marker of a larger infarction, and each is associated with a heightened risk of pump failure, post-infarct angina, heart block, atrial and ventricular arrhythmias and in-hospital and 1-year mortality.
The electrocardiographic features and the complications of IMI (the big three) are completely predictable, based on the anatomy of the right coronary artery (Figure 2.3).
Figure 2.3 Anatomy of the right coronary artery.
The anatomy of the RCA helps to explain the frequent occurrence of RVMI, AV nodal block and posterior wall extension (the big three complications) in patients with acute inferior wall STEMI.
In 90 percent of individuals, there is a dominant RCA1 that supplies:
The inferior wall of the left ventricle;
The anterior and lateral walls of the right ventricle, via the acute marginal (right ventricular) branches, which exit from the proximal to mid-portion of the RCA;
Large portions of the posterior wall of the left ventricle and the posterior interventricular septum, via the large posterior descending artery (PDA); and
The AV nodal artery, which is a tiny branch of the PDA (explaining the common association between inferior STEMI and AV nodal block).
One last clinical-anatomic correlation: the PDA usually supplies blood to the posteromedial papillary muscle of the mitral valve. (The anterolateral papillary muscle is involved less often in patients with ST-elevation myocardial infarction because it usually has a dual blood supply, from the left anterior descending and the left circumflex arteries.) Therefore, acute inferior wall myocardial infarction is often accompanied by papillary muscle dysfunction. It is routine to hear a soft, apical, holosystolic murmur of mitral insufficiency in patients with acute inferior wall STEMI. A loud holosystolic murmur, in a patient with an inferior STEMI and pulmonary edema, signifies acute papillary muscle rupture, a rare but potentially devastating complication. A case of inferior wall STEMI, complicated by papillary muscle rupture, is included in the self-study ECGs later in this chapter.
RVMI occurs in 25–50 percent of patients with acute inferior STEMI (Goldstein, 2012; Wellens, 1993; Tsuka et al., 2001; Del’Itallia, 1998; Moye et al., 2005; Kakouros and Cokkinos, 2010; O’Rourke and Dell’Italia, 2004; Zehnder et al., 1993). Almost always, RVMI results from occlusion of the RCA proximal to the acute marginal (right ventricular) branches (see Figure 2.2). Thus, RVMI is usually recognized in the context of, and as a complication of, an acute inferior wall STEMI.
The most important complication of RVMI is hypotension due to low cardiac output. Impaired cardiac output results primarily from progressive hypokinesis and dilatation of the right ventricle. Dilatation of the RV also causes bowing of the interventricular septum, which then intrudes into the left ventricular chamber, further impairing LV filling and systolic function (Goldstein, 2012; Inohara et al., 2013).
Less frequently, RVMI may result in other complications, including atrial fibrillation (due to right atrial dilatation), ventricular tachycardia or fibrillation, RV thrombus formation with subsequent pulmonary thromboembolism, ventricular septal rupture, tricuspid valve regurgitation, pericarditis or hypoxemia (caused by high RV pressures and right-to-left shunting through a patent foramen ovale).
Even though the right ventricular dysfunction is often transient (and the term right ventricular infarction may be a misnomer), the occurrence of RVMI is associated with an increased risk of early mortality, cardiogenic shock, ventricular tachyarrhythmia and advanced heart block compared with IMI alone (Goldstein, 2012; Zehnder et al., 1993; Inohara et al., 2013; Hamon et al., 2008).
Once RVMI is recognized on the ECG, clinicians know to avoid drugs that will reduce right ventricular preload, such as nitroglycerin, morphine and diuretics. Intravenous fluids are typically administered in order to optimize right ventricular filling and improve cardiac output (Goldstein, 2012). Inotropic agents (for example, dobutamine or dopamine) are often used for hypotension that is refractory to moderate volume resuscitation. Overzealous fluid administration in patients with RVMI can cause further bowing of the septum into the left ventricular cavity and, paradoxically, impair left ventricular function. Correction of bradycardia and heart block, which often coexist in patients with RVMI, is also critical. Emergent reperfusion speeds recovery of right ventricular function.
The most sensitive and specific sign of RVMI is ST-segment elevation in the right-sided precordial lead V4 R (Moye et al., 2005; Zehnder et al., 1993; Inohara et al., 2013). Indeed, ST-segment elevation in V4 R is a more sensitive and specific test for RVMI than bedside physical findings, including the classic triad of hypotension, jugular venous pressure elevation and clear lungs. The ST-segment elevation in V4 R may be quite transient (Wagner et al., 2009). Also, the ST-segment elevation in V4 R may be quite small – sometimes no more than 0.1mV. This is understandable, given that the right ventricle has only one-sixth the muscle mass of the left ventricle (Kakouros and Cokkinos, 2010).
ST-segment elevation in V4 R is strongly predictive of a mid- or proximal RCA occlusion. In addition, this ECG finding alone – ST-segment elevation in V4 R – is a strong, independent predictor of complications and early mortality. In Zehnder’s classic review of 200 consecutive patients with acute IMI, the finding of ST-segment elevation in V4 R of ≥ 1 mm increased the in-hospital mortality rate five-fold, from 6 to 31 percent (Zehnder et al., 1993). Patients with ST-elevation in V4 R had a higher incidence of major in-hospital complications, including ventricular tachycardia and fibrillation, high-grade AV block that required pacing, atrial fibrillation, hemodynamic instability, pump failure and cardiogenic shock.
Larger ST-Segment Elevations in Lead III Compared with Lead II
Disproportionate ST-elevation in lead III (> II) and pronounced (≥ 1 mm) ST-segment depression in lead aVL are also valuable markers of accompanying RVMI (Turhan et al., 2003; Moye et al., 2005). As summarized earlier in this chapter, these are the same ECG clues that are used to predict the proximal RCA as the infarct-related artery.
ST-Segment Elevation in Lead V1
Every standard 12-lead ECG comes with one right-sided lead – for free. Precordial lead V1 is located in the fourth intercostal space, just to the right of the sternum (see Chapter 1). Thus, it is a right-sided lead, and it routinely monitors the right ventricle as well as the interventricular septum. In the setting of inferior wall STEMI, the presence of ST-segment elevation in lead V1 is highly suggestive of concomitant RVMI, accompanied by acute right ventricular dilatation (rather than, by chance, a second, anteroseptal STEMI) (Zimetbaum and Josephson, 2003; Tsuka et al., 2001; Moye et al., 2005; Wagner et al., 2009). Patients with acute inferior wall STEMI and ST-segment elevation in V1 almost always have a proximal RCA occlusion. Sometimes, in these patients, reciprocal ST-segment depressions appear in leads V5 and V6.
Keep in mind that, in patients with acute inferior STEMI, two opposing forces may be tugging on the right precordial lead ST-segments (including V1). Right ventricular infarction causes ST-segment elevation in V1. At the same time, posterior wall extension is a common complication of IMI and causes right precordial ST-segment depression. Ultimately, the position of the ST-segments results from a summing of these forces; RVMI can hide the signs of posterior wall involvement, and vice versa.
A final caveat: there is another circumstance where patients may present with simultaneous ST-segment elevations in the inferior leads and in the anteroseptal leads (including V1). This occurs in the setting of anterior wall STEMI and, specifically, when the occluded artery – the left anterior descending – includes a long, terminal branch that “wraps around” the apex of the heart to perfuse the inferior left ventricular wall. However, occlusion of a “wrap-around” LAD is likely to cause more extensive ST-segment elevations involving the anterior and lateral precordial leads, including V6. In the setting of inferior wall STEMI, accompanying ST-segment elevation limited to precordial lead V1 usually signals RV infarction (Alzand and Gorgels, 2011). Examples of concurrent anterior and inferior STEMI caused by occlusion of a “wrap-around LAD” are included in Chapter 3, Anterior Wall Myocardial Infarction.