Chapter 3 – Anterior Wall Myocardial Infarction

Chapter 3 Anterior Wall Myocardial Infarction

Key Points

  • Acute anterior wall ST-elevation myocardial infarction (STEMI) classically presents with ST-segment elevations in one or more precordial leads. Usually, ST-elevation in lead V1 signifies infarction of the interventricular septum. ST-elevation in leads V2–V4 indicates infarction of the anterior (or anteroapical) wall. ST-elevation in V5–V6 signals infarction of the lateral left ventricular wall.

  • Anterior wall STEMI is a high-risk event, frequently complicated by cardiogenic shock, bundle branch block and ventricular arrhythmias.

  • In the vast majority of cases of anterior, anteroseptal and anterolateral wall STEMIs, the culprit event is an acute occlusion of the left anterior descending (LAD) artery. The presence of concomitant ST-segment elevations in aVR may signify acute occlusion of the left main coronary artery (LCMA).

  • Proximal LAD occlusions may also cause ST-elevations in the high lateral limb leads (I and aVL), signifying occlusion of the LAD before the first diagonal branch (D1). Not surprisingly, high lateral infarction is usually accompanied by reciprocal ST-segment depressions in the inferior leads. Isolated, high lateral STEMIs are often missed.

  • Clinicians should also recognize the pattern of acute anterior wall STEMI accompanied by ST-segment elevations in leads II, III and aVF (concomitant inferior wall STEMI). Often, this signifies occlusion of the mid- or distal portion of a long LAD that wraps around the apex of the heart to perfuse the inferior wall. ST-segment elevations in the anterior and inferior leads may also be a sign of pericarditis, myocarditis, early repolarization or another “coronary mimic.”

  • Anterior STEMI is often complicated by development of bundle branch block; the most common pattern is right bundle branch, often with left anterior fascicular block, which may develop acutely and progress to complete heart block and life-threatening bradycardia. Bundle branch and bifascicular blocks develop when the LAD is occluded before the septal perforator branches.

  • Clinicians must recognize several early warning signs of a critical LAD occlusion: tall or abnormally broad (“hyperacute”) T-waves” in the anterior precordial leads; a biphasic T-wave in lead V2 or V3 (“Wellens’ sign” Type A); and deep, symmetric T-wave inversions (“coronary T-waves”) in the anterior precordial leads (Wellens’ sign Type B). These early warning signs may occur while the patient is pain-free and hemodynamically stable and in the presence of little or no cardiac enzyme elevation. They may represent a critically obstructed LAD that has undergone spontaneous reperfusion but that remains at risk for rethrombosis.

  • Limb lead aVR may provide critical diagnostic information. In the presence of an anterior STEMI, ST-segment elevation in aVR suggests occlusion of the left main coronary artery (LMCA) or “its equivalent.” ST-segment elevation in lead aVR is also significant in patients who have ST-segment depressions in multiple inferior and lateral leads (typically, limb leads I, II and aVL and precordial leads V4, V5 and V6). In this situation (“global” or “concentric” ischemia), ST-segment elevation in aVR is often a “STEMI equivalent,” indicating an obstructive thrombus of the LMCA or proximal LAD and the need for emergent reperfusion.

  • The presence of a LBBB makes the recognition of acute anterior wall STEMI difficult. The weighted Sgarbossa criteria are specific, but not sensitive, for the diagnosis of acute anterior wall STEMI.

  • Anterior wall STEMI must be differentiated from early repolarization pattern, left ventricular hypertrophy with repolarization abnormalities, pericarditis, takotusbo cardiomyopathy, hypothermia and other “coronary mimics.”

  • Clinicians must also recognize several “STEMI equivalents.” These are ECG patterns that may not meet classic “threshold” definitions of “STEMI” nor standard “cath lab activation” criteria. But they often signal acute thrombotic occlusion of a major coronary artery and the need for emergent reperfusion. STEMI equivalents include ST-elevations in aVR, acute coronary syndromes with only minimal (“subthreshold”) ST-elevations, ST-elevations in fewer than “two contiguous leads,” ST-segment depressions in V1–V3 (signifying posterolateral STEMI) and other patterns reviewed in this atlas.

Anterior Wall ST-Elevation Myocardial Infarction

Anterior wall ST-elevation myocardial infarction (STEMI) is a high-risk event. Compared with inferior wall STEMIs, anterior wall STEMIs have larger infarct sizes and a higher rate of left ventricular dysfunction, congestive heart failure, ventricular arrhythmias and in-hospital and overall mortality (Stone et al., 1988).

Classically, acute anterior wall STEMI presents with ST-segment elevation in one or more precordial leads. As illustrated in Figure 3.1, ST-elevation in lead V1 signifies infarction of the interventricular septum. ST-elevation in leads V2–V4 indicates infarction of the anterior (or anteroapical) wall. And ST-elevation in V5–V6 signals infarction of the lateral left ventricular wall.

Figure 3.1 Standard placement of the six precordial leads.

Anterior Wall ST-Elevation Myocardial Infarction: A Review of the Coronary Anatomy

In the vast majority of cases of anterior, septal and anterolateral wall STEMIs, the culprit event is an acute occlusion of the left anterior descending (LAD) artery. The anatomy of the LAD is illustrated in Figure 3.2.

Figure 3.2 Anatomy of the left anterior descending coronary artery.

The most common coronary artery anatomy is illustrated in this figure. The left main coronary artery bifurcates quickly into two main branches:

  • The left circumflex artery (LCA) primarily perfuses the posterior and posterolateral wall of the heart.

  • The large left anterior descending (LAD) artery supplies blood to the anterior wall of the left ventricle. Note two critical branches of the LAD:

    • The large first diagonal branch (“D-1”) supplies blood to the upper left (high lateral) left ventricular wall; an occlusive clot within D-1 or in the LAD proximal to D1 is likely to cause a STEMI involving the high lateral leads (I and aVL), also resulting in reciprocal ST-segment depressions in the inferior leads, especially lead III.

    • The small septal perforator branches are also critically important because they nourish the interventricular septum. Since the left and right bundle branches travel within the septum, an LAD occlusion proximal to the septal perforators often causes anteroseptal infarction (ST-segment elevation in V1–V4) and development of right or left bundle branch block. The most common pattern is right bundle branch and left anterior fascicular block, which often portends the rapid development of complete heart block and life-threatening bradycardia.

See ECG 3.1, which illustrates a classic anteroseptal STEMI.

ECG 3.1 A 46-year-old man without any significant medical history presented with 2 hours of substernal chest pain.

The Electrocardiogram

The ECG demonstrates marked ST-segment elevations in lead V2–V4, as well as V1, indicating an acute anteroseptal STEMI. Left axis deviation is also present along with possible left atrial enlargement.

Deep “QS” complexes (Q-waves) are present in the anteroseptal leads. However, as emphasized later in this chapter, this does not mean that the evolving anterior STEMI is old, that there is irreversible myocardial necrosis or that myocardial salvage by reperfusion is not indicated.

Clinical Course

He was taken emergently to the catheterization laboratory, which revealed a 95 percent LAD occlusion. His peak troponin was 292. On hospital day 2, an echocardiogram demonstrated hypokinesis of the mid and distal septum and apex, but the overall left ventricular ejection fraction was normal.

STEMIs Involving the “High Lateral” Wall

Proximal LAD occlusions may cause ST-elevations not only in the anterior, septal and lateral precordial leads but also in the high lateral limb leads (I and aVL). When concomitant ST-segment elevation is present in leads I or aVL, it usually signifies occlusion of the LAD before the first diagonal branch (D1) (see Figures 3.2 and 3.3). Not surprisingly, high lateral infarction is usually accompanied by reciprocal ST-segment depressions in the inferior leads. Even if there are no noticeable ST-elevations in I or aVL, the presence of ST-segment depressions in the inferior leads, in a patient with an acute anterior wall STEMI, carries the same significance: one can predict that a high lateral STEMI is evolving and that the LAD is occluded proximal to the takeoff of D-1 (Yip et al., 2003; Arbane and Gay, 2000; Engelen, 1999; Birnbaum et al., 1994; Eskola et al., 2009; Birnbaum, Wilson et al., 2014; Wagner et al., 2009; Wang et al., 2009).

A STEMI involving leads I and aVL likely signifies either an obstructive occlusion of the LAD, prior to or within the first diagonal branch; or occlusion of the left circumflex artery (LCX) or its first major branch (the obtuse marginal artery). Logically, and as illustrated in this figure, the reciprocal inferior leads, especially lead III, will show ST-segment depressions.

Figure 3.3 Perfusion of the high lateral wall of the left ventricle.

Leads I and aVL monitor the high lateral portions of the left ventricle. As illustrated in Figure 3.3, the high lateral myocardium is usually supplied by the first diagonal artery (the first large, proximal branch of the LAD) or the left circumflex artery (or an obtuse marginal branch).

Figure 3.4 Position of the limb leads.

ECG 3.3 A 75-year-old man developed chest pain while shoveling snow. He also complained of dizziness and shortness of breath. On ED arrival, he was in respiratory distress, and his initial systolic blood pressure was 80 mm Hg.

ECG 3.3 The same patient, 1 hour later.

ST-segment elevations in the high lateral leads, without ST-elevations in V1–V4, may also be caused by occlusion of the left circumflex artery (LCA) or one of its major branches, especially the obtuse marginal (OM). See Figure 3.3.

See the following ECG tracing (ECG 3.2) for a typical example.

ECG 3.2 A 61-year-old man with chest pain reported “not feeling well” for 10 hours.

The Electrocardiogram

The ECG demonstrates an extensive STEMI involving the anteroseptal, lateral and high lateral regions of the heart. The inferior ST-depressions are reciprocal changes associated with acute injury to the high lateral wall (I and aVL).

Clinical Course

The angiogram findings were predictable: “The left anterior descending coronary artery was totally occluded proximal to the origin of the first diagonal branch.”

Early Warnings of LAD Occlusion and Impending Anteroseptal STEMI

When patients present with chest pain, shortness of breath or related symptoms, one critical goal is to identify patients likely to have a critical LAD obstruction. Even without clear ST-segment elevations that meet standard “cath lab activation” criteria, a critical LAD occlusion may be present. Hyperacute T-waves, Wellens’ syndrome and ST-segment elevations in lead aVR are among the “don’t-miss” clues.

Hyperacute T-Waves

When a major epicardial coronary artery is suddenly occluded, the first change on the electrocardiogram is a sudden increase in the amplitude of the T-waves. Although these “hyperacute T-waves” may be transient, they represent a critical warning sign of coronary artery (especially LAD) occlusion (Birnbaum, 2014; Sommers, 2002; Ayer and Terkelsen, 2014; Rokos et al., 2010; Nikus et al., 2010; Nikus et al., 2014; Thygesen et al., 2012).

In the anterior precordial leads (V1–V4), hyperacute T-waves appear abnormally tall, and often they are broad-based or “bulky” (Marriott, 1997). They can be symmetric or asymmetric. One useful clue to abnormal, hyperacute T-waves is found in precordial lead V1. The T-wave in V1 is usually small or even inverted. If the T-wave in V1 is taller than the T-wave in V6, it is usually abnormal and may be “hyperacute.”

Hyperacute T-waves signify severe transmural ischemia and an impending STEMI due to a critical LAD occlusion. Although immediate reperfusion may not be indicated for hyperacute T-waves alone, repeat electrocardiograms at short intervals are required (Birnbaum, 2014).

Hyperacute T-waves signifying occlusion of the LAD and impending STEMI must be differentiated from other causes of prominent T-waves, including hyperkalemia, left ventricular hypertrophy, early repolarization, bundle branch block (or a ventricular paced rhythm), hypertrophic cardiomyopathy and stroke. For examples of some of these confusing conditions, see Chapter 7, Confusing Conditions: ST-Segment Elevations and Tall T-Waves (Coronary Mimics).

Figure 3.5 illustrates hyperacute T-waves in the precordial leads. The T-waves are tall and wide; Marriott has described these hyperacute T-waves as “broad-based” and “bulky” (Marriott, 1997). His term “wishbone effect” is also apt, as the arms of the T-wave appear to be widely splayed apart. Note that the T-wave in V1 is much taller than the T-wave in V6. This is almost never normal and serves as a clue to acute coronary insufficiency.

Figure 3.5 Hyperacute T-waves.

This figure illustrates Wellens’ syndrome (Type A), which is an early warning sign of a critical LAD occlusion. In leads V2, V3 and V4, the ST-segment is essentially normal. However, the T-wave is biphasic, becoming negative in its terminal portion.

Figure 3.6 Wellens’ syndrome.

Wellens’ Syndrome

Another important early warning sign of a critical LAD occlusion is “Wellens’ syndrome” (“Wellens’ warning”). Two patterns are recognized.

  • First, precordial leads V2, V3 or V4 may show a biphasic T-wave. Classically, the ST-segment is normal or near-normal, but the T-wave is inverted in the terminal portion. This pattern, sometimes referred to as “Wellens’ Type A,” is usually a reflection of an acute or chronic proximal LAD occlusion. It may signify recent reperfusion of an obstructed LAD (but the obstructed LAD remains at risk).

  • Deep, symmetric T-wave inversions (“coronary T-waves”) in the anterior or lateral precordial leads may also signify LAD occlusion. This pattern is sometimes referred to as Wellen’s sign, Type B (Tandy et al., 1999; Wagner et al., 2009; Ayer and Terkelsen, 2014; Birnbaum, 2014). These must be differentiated (clinically) from the T-wave inversions that accompany intracranial hemorrhage. Importantly, anterior precordial T-wave inversions are also a common ECG finding in patients with acute pulmonary embolism. (See Chapter 5, The Electrocardiography of Shortness of Breath.)

The ECG abnormalities of Wellens’ syndrome – biphasic T-waves or deep T-wave inversions – may appear while the patient is pain-free and hemodynamically stable and in the presence of little or no cardiac biomarker elevation. Nonetheless, they are characteristic of an acute, tight LAD occlusion. Angiographic studies suggest that patients who are pain-free and who present with these biphasic or inverted T-waves in V2–V4 may have undergone spontaneous reperfusion of the LAD; that is, they are in a somewhat later, “evolutionary” phase of their acute coronary insufficiency syndrome (Nikus et al., 2014; Birnbaum, Wilson et al., 2014; Nikus et al., 2010). Nevertheless, it is likely that the proximal LAD has a ruptured plaque with residual clot and is still at risk for re-occlusion and development of a classic anterior wall STEMI within hours or days (or, possibly, weeks). These patients should not be discharged or subjected to exercise stress testing. Admission and cardiology consultation, at the very least, are indicated (Wagner et al., 2009; Birnbaum, Wilson et al., 2014; Nikus et al., 2014; Nikus et al., 2010; Birnbaum, Nikus et al., 2014).

The Electrocardiogram

The ECG shows a classic biphasic T-wave in leads V2 and V3; this is Wellens’ warning. The ST-segment is essentially normal before the T-wave reverses direction and becomes inverted. The T-waves are also inverted in leads V4 and V5. In fact, both types of Wellens’ syndrome (A and B) are present on this single tracing. This pattern is strongly associated with a critical proximal LAD occlusion, even if the patient is pain-free and even if the troponin is normal. One hour later, the patient had a repeat ECG.

The Electrocardiogram

It is usually a good idea to heed Wellens’ warning. This follow-up ECG demonstrates an extensive anterior, lateral and high lateral STEMI, as evidenced by dramatic ST-segment elevations in precordial leads V2–V6 as well as leads I and aVL. As expected, there are reciprocal ST-segment depressions in lead III. There is ventricular ectopy as well.

Clinical Course

The peak troponin was, fortunately, only 42. The ECG (with a combined anterior, septal and high lateral STEMI) is virtually diagnostic of an obstructing clot in the proximal LAD, before the first diagonal. Indeed, angiography demonstrated a 100 percent LAD occlusion proximal to D-1.

ECG 3.4 A 46-year-old man with untreated hypertension and tobacco use reported intermittent chest pain for 2 months. The pain became suddenly worse, and he awoke on the morning of his ED visit with substernal burning. The initial troponin level was 0.7.

The Electrocardiogram

The ECG demonstrates T-wave inversions in the anterior precordial leads (as well as T-wave abnormalities in the high lateral leads I and aVL). The precordial T-wave inversions are deep and symmetric, very suggestive of ischemia and an acute, high grade LAD occlusion. These symmetrically inverted, anterior precordial T-waves are called “coronary T-waves” or Wellens’ sign, Type B. They frequently serve as an early warning sign of a critical LAD occlusion and an impending STEMI. The differential diagnosis of these deep anterior precordial T-wave inversions also includes subarachnoid hemorrhage, acute pulmonary embolism, stress (takotsubo) cardiomyopathy and, occasionally, a juvenile variant. Refer to Chapter 6, Confusing Conditions: ST-Segment Depressions and T-Wave Inversions, for further discussion.

Clinical Course

In this case, the second troponin level was mildly elevated at 4.8. He was sent emergently to angiography, which revealed a 100 percent LAD occlusion. The troponin leak did not continue, and he did not experience a STEMI.

ECG 3.5 A 49-year-old man with 4–5 hours of dull chest and interscapular pain that awoke him from sleep. He also reported several episodes of emesis and shortness of breath. He had no prior cardiac history, although he was a heavy smoker. In the emergency department, he had imaging studies to rule out pulmonary embolism or thoracic aortic dissection. His initial troponin level was normal. His serum potassium level was also normal. He was treated with nitroglycerin and morphine sulfate, and he was admitted to the intensive care unit. Catheterization was scheduled for the next morning.

The Electrocardiogram

Hyperacute T-waves are present in precordial leads V1–V4. The T-wave in V1 is much taller than the T-wave in V6, an additional signal that the T-waves are abnormal. There are also formed Q-waves in the anterior and septal precordial leads, along with QT prolongation. There is one other important abnormality: the ST-segments are depressed in the inferior leads; as discussed earlier, this is highly predictive of a high lateral STEMI, caused by a critical LAD occlusion in the proximal segment, before the take-off of the first diagonal branch (and before the septal perforators). The ST-segments are also depressed in the lateral precordial leads, and there is mild ST-segment elevation in aVR. All of these changes are suggestive of a critical LAD or left main coronary artery occlusion or their “equivalent” (severe three-vessel disease).

Clinical Course

Several hours after the preceding ECG was obtained, he had a witnessed episode of ventricular fibrillation that was managed successfully with a single defibrillatory shock. The following ECG was obtained.

ECG 3.5 The same patient – 15 hours later, after an episode of ventricular fibrillation as an inpatient.

The Electrocardiogram

As predicted by the initial hyper-acute T-waves, he has developed ECG evidence of an extensive anteroseptal myocardial infarction, with probable involvement of the high lateral leads. As noted previously, in the presence of an anterior wall STEMI, the mere presence of ST-segment depressions in the inferior leads suggests that the culprit occlusion is in the LAD proximal to D-1. This tracing indicates loss of R-wave voltage in lead aVL; and despite the low voltage in aVL, there is slight ST-segment straightening and elevation, along with the depressed ST-segments in II, III and aVF. The ST-segment depressions in V5–V6 are no longer apparent.

Clinical Course

Catheterization revealed severe three-vessel coronary artery disease, including complete occlusions of the RCA and LCA and subtotal occlusion of the proximal LAD. His peak troponin was 242. He underwent coronary artery bypass grafting 3 days later.

The Importance of Lead aVR

Limb lead aVR, although often ignored, may provide critical diagnostic information in patients suspected of having an acute STEMI (Tamura, 2014; Yamaji et al., 2001; Zhong-qun et al., 2008; Eskola et al., 2009; Nikus and Eskola, 2008; Gorgels et al., 2001; Rokos et al., 2010; Lawner et al., 2012; Aygul et al., 2008; Wagner et al., 2009; Williamson et al., 2006; Wang et al., 2009; Nikus et al., 2014; Birnbaum, Wilson et al., 2014).

ST-segment elevation in lead aVR may indicate an acute obstruction of the left main coronary artery (LCMA) or, alternatively, severe three-vessel disease. As explained beautifully by Wellens, “When the left main coronary artery is occluded acutely, ischemia will occur both in the territory supplied by the LAD and CX, resulting in an ST-deviation vector pointing toward lead aVR” (Wellens and Conover, 2006).

A more detailed discussion follows. The days of ignoring lead aVR have come to an end.

  • In patients with electrocardiographic evidence of an anterior wall STEMI (ST-segment elevations in leads V1–V4), ST-segment elevation in aVR may signify acute occlusion of the left main coronary artery (LMCA). LMCA occlusion is especially likely if the ST-segment elevation is greater in aVR than in V1. In patients with acute anterior wall STEMI, the higher the ST-segment elevation in aVR, the higher the mortality rate. Complete occlusion of the LMCA is a rare occurrence; however, the LMCA perfuses at least 75 percent of the left ventricular mass, and critical LMCA occlusion is often followed by hemodynamic collapse and malignant ventricular arrhythmias (Nikus and Eskola, 2008; Yamaji et al., 2001; Tamura, 2014);

  • ST-segment elevation in aVR may also be present in association with ST-segment depressions in multiple (sometimes six or more) inferior and lateral leads. Lead aVR examines the heart “from the right shoulder”; it is also reciprocal to leads I, II and aVF and leads V4, V5 and V6. Therefore, when the ST-segments are depressed in these lateral and inferior leads, it could signify “only” inferior and lateral wall ischemia. But if the ST-segment is also elevated in aVR – and especially if the widespread inferior and lateral ST-segment depressions are accompanied by inverted T-waves – the pattern is highly suggestive of an acute thrombotic occlusion of the LAD or LMCA (left main “equivalent” disease). Stated differently, this pattern is a “STEMI equivalent” (Nikus et al., 2014). According to Nikus et al., “if this ECG pattern of circumferential subendocardial ischemia also encompasses ST-elevation in lead aVR … and especially when associated with inverted T-waves … [these patients] should have high priority for urgent invasive evaluation because of high probability of severe angiographic coronary artery disease” (Nikus et al., 2014; Birnbaum, Wilson et al., 2014).

  • ST-segment elevation in aVR has also been observed in patients with posterior wall STEMI, in patients with severe multivessel coronary artery disease and in patients with right heart strain due to acute pulmonary embolus.

In 2006, Williamson et al. published a review of the utility of lead aVR in emergency medicine and critical care (Williamson et al., 2006). The authors listed each of the following as a proven or potential application of lead aVR: (a) ST-segment elevations in lead aVR, suggesting left main coronary artery or proximal LAD obstruction in patients with suspected acute coronary syndromes; (b) detection of incorrect placement of the limb leads (reversal of the normal P-wave, QRS and T-wave patterns in leads I and aVR); (c) recognition of a tall, terminal R-wave in aVR, suggesting sodium channel blocker (especially tricyclic anti-depressant) poisoning; (d) supporting the diagnosis of acute pericarditis, where the PR-segment in lead aVR is commonly elevated; (e) helping to differentiate atrioventricular nodal re-entrant tachycardia (AVNRT) from atrioventricular reciprocating tachycardia (AVRT); (f) detecting inverted P-waves and AV-dissociation in aVR, confirming the diagnosis of ventricular tachycardia; and, possibly, (g) suggesting acute right heart strain and pulmonary embolus by finding ST-segment elevation in aVR.

Understanding “STEMI Equivalents”

One of the key decision points in the emergency care of patients with chest pain, dyspnea or similar symptoms is recognition of regional ST-segment elevations (STEMIs). This ECG finding is critical because it identifies a subset of patients with acute coronary syndromes (ACS) who are highly likely to have an acute occlusion of one of the main epicardial coronary arteries. Emergent percutaneous coronary intervention (PCI), or, in many settings, thrombolytic therapy, is indicated in these patients. ACS patients who have ECG changes limited to ST-segment depressions or T-wave inversions are, for the most part, excluded from these reperfusion recommendations. So, among all the chest pain and ACS patients who present to emergency departments, finding a STEMI changes everything.

National guidelines have established “findings consistent with ST-elevation myocardial infarction (STEMI),” and these have been translated into hospital-based and prehospital “catheterization laboratory activation criteria.” For the most part, these standard definitions have been derived from population-based epidemiologic studies and several large thrombolysis clinical trials. According to the 2012 Joint European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Health Federation Task Force, a STEMI exists if the following criteria are met (Thygesen et al., 2012): new ST-segment elevation at the J-point in two anatomically contiguous leads, with the following threshold criteria: ≥ 1 mm (0.1 mV) in all leads other than leads V2–V3; and in precordial leads V2–V3, the following diagnostic criteria apply: ≥ 2 mm (0.2 mV) in men 40 years or older, ≥ 2.5 mm (0.25 mV) in men < 40 years, and ≥ 1.5 mm (0.15 mV) in women. All other ischemic changes, including regional ST-segment depressions and T-wave inversions, are, in the absence of ST-segment elevations meeting these accepted criteria, classified as “non-STEMIs or unstable angina.”

Importantly, however, most experts, including the panels referenced previously, agree that the accepted definitions do not define the entirety of all ACS patients who have occluded infarct coronary arteries and who need emergent reperfusion therapy. For example, as Thygesen, Nikus and others have pointed out, “lesser degrees of ST [elevation] … do not exclude acute myocardial ischemia or evolving MI” (Thygesen et al., 2012; Nikus et al., 2014).

In recent years, in an effort to improve ECG interpretation and emergency cardiac care, the indications for emergent reperfusion have been expanded. Some additional ECG patterns have been identified, typically called “STEMI equivalents.” These ECG patterns are easily missed, and they are unlikely to be recognized by computer algorithms. Patients with these patterns do not fit the usual, “textbook” criteria for “cath lab activation;” however, these patients are highly likely to have an acute obstructing thrombus in a major coronary artery, and they are, like their counterparts with more classic ST-segment elevations, candidates for emergent reperfusion therapy.

In patients who have chest pain, dizziness, dyspnea or other symptoms compatible with an acute coronary syndrome, the following patterns are the most widely recognized “STEMI equivalents” (Rokos et al., 2010; Thygesen et al., 2012; Wagner et al., 2009; Nikus et al., 2010; Birnbaum, Nikus et al., 2014; Birnbaum, Wilson et al., 2014; Nikus and Eskola, 2008; Ayer and Terkelsen, 2014; Lawner et al., 2012).

ST-Segment Elevations That Do Not Reach the Accepted Threshold Amplitudes

Minimal (subthreshold) ST-segment elevations may be significant, but they are easy to overlook, especially in lead aVL or other leads where the QRS voltage may be low. Even minimal ST-elevations are likely to indicate a true STEMI when there are anatomically reciprocal ST-segment depressions. As Birnbaum, Nikus and others have warned, “Not every patient with positive biomarkers and with ST-elevation lower than the threshold should be defined as having a non-STEMI, as many of them have acute occlusions of an epicardial coronary artery” (Birnbaum, Nikus et al., 2014).

ST-Segment Elevations in Fewer Than “Two Contiguous Leads”

Early, subtle inferior wall STEMIs may present with ST-segment elevation or straightening only in lead III. Early high lateral STEMIs may present with ST-elevation limited to lead aVL. Again, the specificity for true STEMI is markedly increased when reciprocal ST-segment depressions are present.

ST-Segment Depressions in Precordial Leads V1–V3, Indicating Posterior (or Posterolateral) Wall STEMI

As discussed in Chapter 4, these patients must not be classified as having a non-STEMI or “just anterior wall ischemia.” ST-segment depressions in the right precordial leads (V1–V3), accompanied by upright T-waves, makes an acute posterior wall STEMI highly likely.

de Winter’s ST/T-Wave Complex

The de Winter complex includes upsloping ST-segment depressions in precordial leads V1–V3 that begin as sharp depressions of the J-point and then transition into an upsloping ST-segment and finally terminate in a tall, upright T-wave. Sometimes, these abnormalities are associated with ST-elevations in aVR. Although uncommon, the de Winter complex is highly suggestive of acute obstruction of the proximal LAD or, occasionally, an occlusion of the LCA (de Winter, 2015; Birnbaum, Nikus et al., 2014; Birnbaum, Wilson et al., 2014; Verouden et al., 2009). This de Winter form of hyperacute T-waves is often a persistent, rather than transient, abnormality.

A Pattern of Inferior (Leads II and aVF) and Lateral (I, aVL, V5, V6) ST-Segment Depressions, Accompanied by ST-Segment Elevations in Lead aVR

These “global” or “concentric” or “circumferential” ST-segment depressions, when accompanied by ST-segment elevation in aVR, may indicate left main coronary artery or left anterior descending artery occlusion (discussed earlier in this chapter). These patients must not be erroneously classified as “non-STEMI” (Birnbaum, Wilson et al., 2014).

Patients Who Have Had Return of Spontaneous Circulation (ROSC) after Out-of-Hospital Cardiac Arrest (OHCA)

Many patients with ROSC after OHCA have an occluded infarct-related vessel and are candidates for emergent reperfusion. However, ROSC after OHCA is not always a STEMI-equivalent.

One common alternative diagnosis is subarachnoid hemorrhage (SAH). Recent studies suggest that, among comatose survivors of OHCA, subarachnoid hemorrhage is more likely than an acute coronary syndrome (ACS) if: (a) the initial arrest rhythm was “unshockable (asystole or pulseless electrical activity, rather than VT or VF); (b) immediate echocardiography demonstrates a preserved (≥ 50 percent) left ventricular ejection fraction; (c) the history (if available) included pre-arrest headache rather than chest pain; and (d) if ST-segment elevations are present, they are not accompanied by reciprocal ST-depressions. None of these findings, including the history, is 100 percent discriminatory. In recent studies, T-wave inversions and QT-interval prolongation were similar in patients with ACS and SAH. The bottom line is that some patients who have ROSC after OHCA will need an emergent CT scan prior to undergoing reperfusion therapy (Lewandowski, 2014; Yamashina et al., 2015; Arnaout et al., 2015; Mitsuma et al., 2011).

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Sep 22, 2020 | Posted by in CARDIOLOGY | Comments Off on Chapter 3 – Anterior Wall Myocardial Infarction

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