Infarction anteroseptal

AMI, acute myocardial infarction AS, anteroseptal infarction A, antero(lateral) infarction I, infero(posterior) infarction. Adapted from Wackers et al. (1978). 

Occasionally, the first change observed in an anteroseptal infarction, even extensive, is the increase in the T-wave amplitude in the right precordial leads, due to the acute subendocardium ischaemia in a heart without much prior ischaemia. This T-wave morphology may be interpreted as pseudonormal, and it should be readily recognised and differentiated from the normal T wave. In this case the recording of evolutionary ECG is mandatory (Figure 8.7). 

This infarction never occurs in isolation (Zimmerman, 1968). In acute phase oflarge inferolateral infarctions or, less frequently, of anteroseptal infarctions, the presence of PR-segment deviations, atrial arrhythmias and/or abnormal P waves (notched, irregular shape) suggests that atrial involvement has occurred. This probably occurs rarely, although this has to be studied with new image techniques (CE-CMR). 

Myers GB, Howard A, Klein M, Stofer E. Correlation of electrocardiographic and pathologic findings in anteroseptal infarction. Am Heart J 1948a 36 535. 

An 86-year-old woman was given adenosine 12 mg intravenously for sustained supraventricular tachycardia, which terminated but was followed by atrial fibrillation and paroxysmal ventricular tachycardia (24). Cardioversion was unsuccessful, but normal sinus rhythm was obtained with procainamide. This followed an anteroseptal myocardial infarction. 

A hypertensive crisis and myocardial infarction occurred in a 62-year-old woman after a combined injection of hydromorphone 48 mg and clonidine 12 mg subcutaneously in an attempt to refill an implanted epidural infusion pump (42). She was immediately treated with naloxone, but she subsequently had accelerated hypertension, a brief tonic-clonic seizure, and an anteroseptal myocardial infarction. Cardiac catheterization showed no coronary narrowing or blockage, but an anterior infarct was confirmed. 

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). 

Figure 2.2 (A) A patient with myocardial infarction of anteroseptal zone in a subacute phase (1) normal recording that displays extension of Q waves up to V6 (qrs). Small changes in the placement of precordial V3-V6 leads have significantly modified the morphology of QRS, now being qR in a lead V6. Therefore, according to the...

Figure 3.18 Acute infarction of anteroseptal zone with ST-segment elevation in the prefibrinolytic era. Evolutionary phases (A) at 30 min, (B) 1 day later, (C) 1 week later and (D) 2 weeks later.

Figure 4.66 Above (A) Acute phase of evolving Q-wave myocardial infarction of anteroseptal zone. There is a huge ST-segment elevation, especially in I, VL and from V2 to V5, QRS >0.12 s and morphology of complete RBBB that was not present in previous ECG. (B) Twenty-four hours later RBBB have disappeared and subacute anterior extensive infarction becomes evident. There is ST-segment elevation from V1 to V4. The transient presence of new...

In Figures 5.4 and 5.5 the changes that, as a consequence of the presence of the vector of infarction, are generated in the ventricular depolarisation loops in the presence of two prototype infarctions (anteroseptal and inferolateral areas, respectively) are represented. Said changes explain the presence of Q waves in the different leads by means of the loop-hemifield correlation. Some of the ECG morphologies and the QRS loops correlations in the seven types of infarctions, according to the classification... 

Types of infarctions in the anteroseptal area presence of Q waves or their equivalent in the precordial leads and/or I and VL (Figure 5.9A)... 

The typical apical-anterior infarction is a consequence of LAD occlusion, clearly distal to the D1 and SI. If there is anteroseptal extension, it is usually due to non-complete LAD occlusion im-... 

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... 

Figure 5.15 The ECG pattern of apical-anterior infarction (type A-2) with important anteroseptal extension as may be seen in this example but preserving the basal area of septum (D) and anterior wall (E). The lateral extension only involves the low part (D). The lack of involvement of segment 12 and lesser involvement of segment 7 are the...

This electrocardiographic pattern (QS in VI to V4-V6), as has already been mentioned, may be seen in apical-anterior MI with and without evident anteroseptal extension. In case of very distal LAD occlusion the sensitivity of this pattern is lower, since apical infarctions secondary to a very distal LAD occlusion allow for the recording of the first vector (rS in V1-V2), and the Q... 

Figure 5.16 (A, B) Example of apical-anterior infarction seen in cases of apical-anterior Ml with anteroseptal with inferior involvement equal to or greater than the involvement greater than the inferior involvement (C).

A Q wave in VI to V3-V6 may be seen in apical-anterior infarction with or without anteroseptal extension. The presence of a Q wave in II, III and VF supports that inferior infarction being equal to or more important than anterior infarction is a typical apical infarction. 

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). 

In this case, significant extensive anteroseptal involvement, especially the middle and lower portions, and also lateral involvement (mid-low wall), explains that the infarction vector is directed posteriorly rightwards and sometimes downwards (Figure 5.35), and generates a loop that usually rotates clockwise in the FP, but in HP rotates clockwise (QR in V6) (Figure 5.19) or counter-clockwise (RS in V6) (Figure 5.35). Therefore, a Q wave is seen in most of the precordial leads, VI to V4—V6 and in VL and I, QR or RS pattern maybe seen (Figures 5.19 and 5.35). The pattern of extensive anterior infarction with... 

On rare occasions apical-anterior infarctions especially with anteroseptal extension that corresponds to A-2 pattern presents with an ECG of type A-3 (extensive anterior), because an abnormal pattern is recorded not only in precordial but also in leads I and VL (QS and QR patterns). The changes caused by cardiac rotation (levorotation) or the presence of LVH, among other factors, may at least partially explain it. In the levorotated and... 

Infarctions with a Q wave in V1-V4 and sometimes qrs or qR in V5-V6 usually with a negative T wave correspond to apical-anterior infarction (distal occlusion of LAD) with or without anteroseptal extension, and most of the cases that in addition to having a Q wave in the precordial leads exhibit QS or QR patterns in VL (and/or lead I) corresponding to an extensive anterior infarction (proximal occlusion of LAD). 

Figure 5.52 The ECG of a patient with complete LBBB and associated infarction. There are ECG criteria suggestive of extensive anterior myocardial infarction (qR in I, QR in VL and low voltage of S in V3). The CMR images (A-D) demonstrated the presence of an extensive infarction of anteroseptal zone (type A-3) (proximal LAD occlusion). The inferolateral wall is free of necrosis (see (D)), because the...

We will just remind (see p. 137) that seven areas of MI detected by CE-CMR have good correspondence with seven ECG patterns (four in anteroseptal zone - septal, apical-anterior, extensive anterior and mid-anterior - and three in the inferolateral zone - inferior, lateral and infero-lateral) (Figure 5.9 Cino et al., 2006). We have also demonstrated that in clinical practice the presence of these seven ECG patterns correlates well with the corresponding infarction areas detected by CE-CMR, and therefore these have real value in clinical practice (Bayes de Luna et al., 2006a-c) (Table 5.3). Therefore, in chronic infarction the correlation between ECG changes (Q waves of necrosis) and involved area (CE-CMR) is clearly good (88% global concordance). However, the in-farcted area of apical infarction (A-2 type), mid-anterior infarction (A-3 type) and lateral infarction (B-l type) presents the lower concordance. 

Anteroseptal versus inferolateral MI prognostic implications. It is known that the MI involving LAD presents for similar area of necrosis, increased myonecrosis, reduced early and late left-ventricular function and high mortality compared with infarction in other vascular territories. However, the mechanisms underlying a worse prognosis are not completely characterised. Recently, it has been demonstrated (Kandzari et al, 2006) that prognosis after primary PCI in patient with ACS, the majority with ST-segment elevation, is different in patients with LAD occlusion than in RCA or LCX. Acute myocardial infarction due to LAD is associ-... 

Most infarctions with type A-2 pattern (QS from VI to V4-V5), especially cases without too much anteroseptal involvement, have usually a good prognosis because they are not very extensive. 

From the prognostic point of view, these usually correspond to large anteroseptal or inferolateral infarctions. In case of acute inferior MI the presence of PR-segment depression >1.2 mm in inferior leads has been demonstrated to be a marker of higher risk of in-hospital mortality and cardiac rupture (Jim et al., 2006) (Figure 10.6). Often these cases present supraventricular arrhythmias, especially atrial fibrillation. 

Selvanayagam J, Kardos A, Nicolson D et al. Anteroseptal or apical myocardial infarction a controversy addressed using delayed enhancement cardiovascular magnetic resonance imaging. J Cardiovasc Magn Reson 2004 6 653. 

Shalev Y, Fogelman R, Oettinger M, Caspi A. Does the electrocardiographic pattern of anteroseptal myocardial infarction correlate with the anatomic location of myocardial injury Am J Cardiol 1995 75 763. 

Fig. 21.11a-c. Comprehensive MR assessment of the cardiac status in a patient after myocardial infarction, a Cine imaging demonstrates normal end-diastolic thickness of the LV wall, while (b) myocardial perfusion (at rest) shows an extensive hypoperfusion within the anterior and anteroseptal LV wall... 

This 12-lead electrcardiogram shows typical characteristics of an anteroseptal-wall myocardial infarction (Ml). Note the loss of R in leads V, and Vj. Also note the ST-segment elevation in leads V, to V4. 

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