A.  Mirror Patterns [H]

In the acute phase of STEACS mirror patterns may appear (ST depression) in opposite leads.

The correlation of the leads with ST elevation and mirror patterns allow, in cases of LAD occlusion (ST elevation in precordial leads), the site of occlusion to be located (Fig. 9.8). In cases of ST elevation in II, III and VF (right coronary [RC] or circumflex [CX] occlusion), this correlation allows the occluded artery to be identified (Fig. 9.11).

Locating the site of occlusion in LAD. (Figs 9.8–9.10): In ACS due to LAD occlusion and ST elevation in precordial leads, the mirror pattern allows the site of occlusion to be located (Figs 9.8–9.10). If the occlusion is high, proximal to the first diagonal (D_I), and the LAD is long, wrapping the apex which is something that frequently occurs, the vector of severe transmural ischemia (injury vector) moves upward (↑ of ST in V2-V4-5) and from II, III, and VF we see its tail. Thus, an ST depression is recorded in the inferior leads (Fig. 9.10A). If the occlusion is also proximal to the first septal (S_I), ST would also be elevated in V₁ (Bayés & Fiol-Sala, 2008).

However, if the occlusion is distal to the first diagonal (Figs 9.8 and 9.9), the vector of severe ischemia (injury vector) would also be directed forward but downward instead of upward, and thus II, III, and VF would record an isoelectric or positive ST segment (Fig. 9.10B).

It is important to remember the rare cases of total occlusion of the left main trunk (LMT) that arrives alive to the hospital, present STEACS resembling proximal LAD occlusion to D1 and S1. Very frequently in these cases RBBB+LAH appear, that sometimes may make it difficult to evaluate the ECG changes.

The hemodynamic presentation in total occlusion of LMT is much serious that in LAD proximal occlusion. Approximately 50% of patients die from cardiogenic shock (Fiol et al., 2012). Later on we will see that in most cases LMT involvement is shown by subocclusion, not total occlusion, originating NSTEACS, with a depression of ST in seven or more leads.

In conclusion, the algorithm of Figure 9.9 can be used to locate the site of occlusion in the LAD in the case of STEACS (Fiol et al., 2009). We must look at (1) the appearance of ST in II, III, and VF to determine if the occlusion is proximal or distal to D1 and (2) whether occlusion is proximal to the first septal (S1) (Fig. 9.9B). Figure 9.10 shows the ECG in two cases of LAD occlusion, one proximal and one distal to D1.

CX occlusion versus RC occlusion in the case of ST elevation in II, III, and VF (Fig. 9.11–13): In ACS with ST elevation in II, III, and VF the occluded artery is RC at the proximal or distal level if a depression in the ST segment is seen in lead I. This occurs because the severe ischemia vector (injury vector) is directed more toward the right since the affected area in RC occlusion is located more in this zone (Figs 9.11 and 9.13A and B). By contrast, if occlusion is in the CX artery, the severe ischemia vector (injury vector) is directed more to the left because it is the most affected area and then in lead I we may see ST elevation (Figs 9.11 and 9.13C).

In case of doubt or when the ST is isoelectric, we may use other criteria to identify the culprit artery (Fig. 9.12) (Fiol-Sala et al., 2004). This figure shows the successive steps that allow the location of the involved artery with high SP and SE, in case of STEACS with ST elevation in II, III and VF.

In addition to typical patterns of ST elevation, there are some ECG patterns seen in the evolving course of an STEACS considered atypical and that we discuss below (De Winter et al., 2008; Nikus et al., 2010; Bayés de Luna, 2012; Birnbaum et al., 2012). [I]

• STE equivalent (Figs 9.14 and 9.15): Is a mirror image of true STEACS. It corresponds to a mirror pattern of severe transmural lateral ischemia due to occlusion in CX, that originates an ST elevation in the back leads but are recorded in V1–V2 as mirror pattern (ST depression in V1–V2). Often they are considered to be a true ST depression and they are incorrectly diagnosed as NSTEACS. The presence of sometimes very small ST elevations in inferior and/or lateral leads and in V7–V9 (Fig. 9.15), and above all to know that this pattern exists, is useful to make the correct diagnosis.
  
• In the hyperacute phase a final positive T wave is not present at the end of the ST depression (Fig. 9.14). However, a positive T wave usually appears after a few hours coinciding with a decrease in the ST depression. This change of pattern corresponds to the mirror image that appears in the back leads; less ST elevation and the appearance of a negative T (Fig. 9.15). Also often, a high R of lateral infarction appears in V1 that is the mirror pattern of Q in back lead. These considerations are important in making the differential diagnosis with the pattern of severe subocclusion in the proximal LAD (Figs 9.15 and 9.23A).
  
• Peaked, symmetric and tall T wave (Fig. 9.16) may appear in the hyperacute phase of STEACS and is caused by the isolated initial subendocardial ischemia that is present in this phase in STEACS. It occurs usually in case of LAD occlusion, (V₁ to V₂–V₃), but rarely may be seen in cases of LC or CX occlusion.
  The presence and duration depends on when the first ECG is taken. It is generally brief (Fig. 9.16A) and usually is recorded during this first ECG because already an ST elevation is present. There are times, however, that the duration is longer and it may rarely (≈2% of LAD occlusion cases) be accompanied by a generally small ST depression, especially if subendocardial ischemia was already present previously (De Winter, 2009) (see before and Fig. 9.16B).
  
• Deep inverted T wave (Fig. 9.17). This is a pattern often seen in STEACS if the artery, usually LAD, opens spontaneously or under treatment (PCI or fibrinolysis) before the ST elevation pattern evolves to Q-wave MI. Therefore, a deep negative T wave from V1-V2 to V4-V5 may appear, generally with some lengthening of QT, indicating that the artery is more or less open (T wave of reperfusion), although it may close again (Fig. 9.17). In these cases it is necessary to carry out PCI as an urgent, but not emergent, procedure. At this time the negative T wave pattern indicates that there is no active ischemia (no pain). Therefore, this is mainly a reperfusion pattern as seen following fibrinolysis or PCI, or coronary spasm. However, without treatment the process can resume (Fig. 9.17), presenting pseudonormalization or even if angina persists, an ST elevation.

This post-ischemic T wave that appears in the clinical course of STEACS or coronary spasm (see later) occurs because a slower repolarization persists in the affected transmural zone when compared to neighboring areas due to a slowing in the ionic exchange during repolarization (Fig. 9.18). This may be explained (A) (Fig. 9.18-1) by the sum of the longest TAP in the affected transmural zone and the shortest TAP of the neighboring areas, and (B) because a vector is generated in the affected transmural zone in the second part of repolarization (not yet completely repolarized and with a longer TAP) that goes from this to the neighboring areas (vector of ischemia) (Fig. 9.18-2). MRI in small series of these cases has shown transmural edema with the negative T wave disappearing conjointly with the edema (Migliore et al., 2011) (Fig. 9.18-3).

Later in this chapter, we will explain the basis for other negative T waves that appear during the clinical course of ischemic heart disease (e.g. NSTEACS, Q wave infarction) (see Figures 9.25, 9.34, 9.38).

• Other patterns. On rare occasions, a negative U wave may be seen when a negative T wave is pseudonormalized or a residual negative U wave may remain in an aborted STEACS.

A.  Extensive Involvement (Circumferential) [O]

(See Figs. 9.22 and 9.23; Nikus et al., 2010; Kosuge et al., 2011.)

1. This is usually due to subocclusion of the main trunk (LMT) or two or three proximal vessels. Less frequently it is due to proximal LAD severe subocclusion, and rarely to proximal occlusion of the dominant LCX artery.
   
2. In all cases, ST depression exists in ≥7 leads (for some authors in ≥8 leads). When the subocclusion occurs in the left main trunk (Fig. 9.22) the ST depression in precordial leads does not present a final positive T wave, or it is only minimal. The final positive T wave is usually more evident if the subocclusion is in the proximal LAD or in two to three vessels (Fig. 9.23).
   
3. In all cases ST elevation in VR exists and often in V1; this is more evident in LMT/2–3 vessel disease.
   
4. Differentiating between subocclusion in 2–3 vessels and in proximal LAD (Fig. 9.23) is difficult in the ECG, because in both cases there is ST depression in the right or middle precordial leads. In our experience, patients with subocclusion in 2–3 vessels present more ST elevation in VR than in the isolated subocclusion of proximal LAD, and the final T wave in mid-precordial leads is less evident (Fig. 9.23A and B). Cases of severe subocclusion of the proximal LAD may evolve more often to Q-wave myocardial infarction if not treated in time (Fig. 9.23A), and are equivalents of atypical pattern B2 of STEACS (Fig. 9.16B).
   
5. The differential diagnosis between critical proximal LAD subocclusion and CX occlusion is not easy, especially after the hyperacute phase. In both cases (see before) an ST depression in V1–V3 may be seen, but in LCX occlusion the T wave is usually negative in the hyperacute phase, although in the follow-up a final positive T wave appears as a mirror pattern of evolving lateral MI (Fig. 9.15B). In the critical subocclusion of the LAD the final T wave is positive already in the early phase. This is relevant to evaluating the degree of urgency in performing PCI.

As a summary: If the final positive T wave appears late in the evolving phase of an ACS when the ST depression is not very evident, much probably the occluded artery is the LCX. In case of subocclusion of LAD, the final positive T wave already is present from the first moment, and often evolves to complete occlusion (STEACS and Q wave MI) (compare Figs 9.15 and 9.23A).

B.  Regional Involvement (Fig. 9.24)

1. Usually there are 1-2 vessels involved.
   
2. The most ECG criteria are the following:
   
   
   
   • ST depression in less than seven leads.
     
   • ST elevation in VR, if present, is usually <1 mm
   
   
3. The ST depression may be seen (Pride et al., 2010):
   
   
   
   • V1 to V4. In 80% of cases, it is explained by LAD subocclusion. In these cases there is usually, as has been explained in the case of circumferential involvement (Fig. 9.23), a final positive T wave, and in V1 there is nearly no ST depression. There may be slight depression in some leads of the FP. The regional involvement in the case of proximal LAD subocclusion is more frequent than the circumferential involvement already discussed (Fig. 9.23A).
     
   • It should be emphasized that in 20% of patients the presence of ST depression in V1–V4 is due to total CX occlusion, in which case the ECG pattern is equivalent to STEACS (atypical pattern A) (Pride et al., 2010). In this case, the acute phase of ST depression generally occurs without a final positive T wave, at least in V1 and V2, and almost always a slight ST elevation in inferior or lateral leads (Fig. 9.13A) (see before). We have already commented on the differential diagnosis between LCX occlusion (STEACS) and LAD subocclusion (NSTEACS) that often evolves to STEACS (see before).
     
   • In II, III, and VF. Very infrequent. Due to RC/CX subocclusion.
     
   • In V3-V5-6 and some FP leads. Frequently there is 2–3 vessel disease, but it is very difficult to identify the culprit artery, although if ST depression is present in lead I, more frequently the RCA is affected (Fig. 9.24).