Inferior wall infarction

It is important to obtain a baseline EKG and cardiac enzymes to evaluate the possibility of an acute myocardial infarction. The short-term (2-4 weeks) stroke risk after acute myocardial infarction (AMI) is 2.5%. Stroke is usually an early (within 14 days) complication of AMI and is more common in anterior wall (4—12%) than in inferior wall infarction (1%). Approximately 40% of patients with an anterior wall myocardial infarction develop left ventricular thrombus. 

Obtain right precordial leads in any patient with an inferior wall myocardial infarction... 

Therefore, often, the posterior wall does not exist and for this reason, the name inferior wall seems clearly better than the name inferoposterior . On the other hand, the anterior wall is, in fact, superoanterior, as is clearly appreciated in Figure 1.1 IB. However, in order to harmonise the terminology with imaging experts and to avoid more confusion, we consider that the names anterior wall and inferior wall are the most adequate for its simplification and also, because when an infarct exists in the anterior wall, the ECG repercussion is in the horizontal plane (HP V1-V6) and when it is in the inferior wall - even in the infer-obasal segment - it is in the frontal plane (FP). 

Figure 1.12 (A) The posterior (inferobasal) wall as it was wrongly considered to be placed. With this location an infarction vector of inferior infarction (segments 4 and 10 in case of very lean individuals) faces V1-V2 and explains the RS pattern in these leads. (B, C) The real anatomic position of inferior wall (inferobasal) and lateral wall...

However, (a) infarction of the inferobasal segment (posterior wall) does not usually generate a Q wave because it depolarises after 40 milliseconds (Durrer et al., 1970) (Figure 9.5). (b) Furthermore, the CMR correlations have demonstrated that the posterior wall often does not exist, because usually the basal part of the inferoposterior wall does not bend upwards (Figure 1.13). (c) In cases that the inferoposterior wall bends upwards, even if the most part of inferior wall is posterior, as may be rarely seen in very lean individuals, as the heart is located in an oblique... 

Both acute coronary syndromes (ACSs) and infarcts in chronic phase affect, as a result of the occlusion of the corresponding coronary artery, one part of the two zones into which the heart can be divided (Figure 1.14A) (1) the inferolateral zone, which encompasses all the inferior wall, a portion of the inferior part of the septum and most of the lateral wall (occlusion of the RCA or the LCX) (2) the anteroseptal zone, which comprises the anterior wall, the anterior part of the septum and often a great part of inferior septum and part of the mid-lower anterior portion of lateral wall (occlusion of the LAD). In general, the LAD, if it is large, as is seen in over 80% of cases, tends to perfuse not only the apex but also part of the inferior wall (Figures 1.1 and 1.14). 

LV is cone shaped, and, as a consequence, the four heart walls present well-defined borders at the base of the heart. However, these borders become less clear as the walls approach the apex, such that it is difficult to be sure if the infarction limited to apical area involves one or other walls. Furthermore, CMR shows that the inferobasal segment of inferior wall often does not bend upwards (Figure 1.13) thus, very fre quently all the inferior walls present the same horizontal or near-horizontal inclination. 

Furthermore, there is an inferior infarction in cases of occlusion of a large LAD artery that wraps the apex. Usually, the Q waves are only observed in leads II, III and VF when the involvement of inferior wall is equal to or greater than anterior wall (Figure 5.16). In addition, a Q wave or an ST-segment elevation in V5-V6 indicates more inferoapical than anterolateral involvement (Warner et al, 1986). 

Figure 3.17 (A) and (B) ECG-VCG correlation of the T wave and the T loop of subepicardial ischaemia in two patients with myocardial infarction (A) of the inferior wall and (B) of the inferior and lateral walls. Observe that a T loop in both cases shows homogeneous inscription and is directed upwards (see FPa) in the first case and upwards and forward in the second case (see HPa). The QRS loop of (A) rotates only clockwise and of (B) rotates first clockwise and later counter-clockwise. In the first case inferior Ml is isolated and in the second, associated to superoanterior...

Figure 3.19 Evolution of inferior wall infarction due to RCA occlusion after RV branches treated with fibrinolysis. Observe the ST-segment deviations depression in lead I,...

In the chronic phase in case of dominant RCA occlusion, there is involvement of inferior wall and some part of the lateral wall. This explains the Q wave in inferior leads and sometimes V5— V6 but not in lead I and aVL. Also, it explains the RS morphology in VI because the vector of infarction of lateral wall points to VI (see Figure 1.9). In case of occlusion of very dominant LCX, as all the lateral wall maybe infarcted, we may find in chronic phase QR morphology in lead I and aVL, but usually not QS (see Figure 5.34), which is seen much more often in cases of occlusion of D1. 

In some infarctions with QS pattern from VI to V4, the presence of a Q wave is observed in II, III, and VF, with qr or QS pattern. This occurs in typical apical infarctions, but not in case of important anteroseptal extension (Figure 5.16), since in the former, inferior infarction is frequently as important or more than anterior infarction, with the infarction vector of inferior wall and the corresponding loop in the FP, being directed upwards (Figure 5.16A). In... 

A thorough assessment of II, III and VF provides useful information about anteroseptal involvement in the cases of apical-anterior MI. If infarction Q waves are present in II, III and VF, the infarction of inferior wall probably equally or predominantly involves this wall with respect to the anterior wall (very long LAD). If tall R waves are present in II, III and VF, the inferior involvement is probably small or absent (short LAD). 

It is called lateral infarction, because the infarction is limited to the lateral wall, sometimes with small extension to the inferior wall. There... 

Consequently, the infarction that is presented with RS pattern in VI, with or without small qr in lateral leads, is not the result of infarction of the most basal (posterior or inferobasal) portion of the inferior wall, but is, in fact, a lateral infarction (Figures 5.23-5.25). Figure 5.26 shows the diagnostic criteria of lateral MI found in lead VI. 

It is called inferior infarction though it usually also involves part of the inferior septum. Thus, when a Q wave is present in at least two contiguous inferior leads (see Table 5.1), as the sole electrocardiographic abnormality, the involvement of part of the inferior septum is frequently associated with an inferior wall infarction that also very often includes the inferobasal segment (segment 4) of the inferior wall, classically named posterior wall ... 

In inferolateral infarction due to RCA occlusion, there are more signs of inferior than of lateral infarction, and, in any case, the latter may be manifested by an RS in VI and in some cases by abnormal q wave in the left precordial leads, but not by q wave in leads I and VL (Figure 5.33). In turn, in inferolateral infarction due to LCX occlusion, the lateral wall is more involved than the inferior wall, and this explains why a Q wave may be recorded in I, VL, V5 and V6, though usually a QR, instead of a QS, pattern is seen. Also, according to the loop-hemifield correlation, the Q wave in II, III and VF may be more important... 

This corresponds to an inferior and/or lateral wall infarction (Figure 5.9B(l-3)). In this book, segment 4, which was traditionally known as the posterior portion of the inferoposterior wall, is named inferobasal segment of the inferior wall. The RS morphology in VI is due to an infarction of the lateral wall. 

The VCG has been used to locate the presence of multiple infarctions. However, this technique is rarely used in daily practice. Furthermore, as we have already stated, it has been demonstrated that practically the same information may be obtained if the ECG-VCG correlation is used to understand ECG morphologies, as is done in this book (Warner et al., 1982). We need to also have in mind that, in some cases of single infarction, Q waves in leads of different areas may be seen, e.g. in an apical infarction due to a distal LAD occlusion, in addition to Q waves in the precordial leads these may also be seen in the inferior wall when the LAD is very long and there is infarction of the inferior wall that may be even greater than the anterior involvement (Figure 5.16). 

Figure 5.55 Inferior infarction associated with an IPH (A) the vector of the first part of the activation (the sum of the normal activation initiating vector in the case of an IPH -see B(l) plus the infarction vector - Inf. V) moves away from the inferior wall more than that would be seen in an isolated IPH and is opposite to the final vector of ventricular depolarisation that is directed downwards...

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