Infarction with lateral ischaemia

Figure 3.20 Old inferior infarction with lateral ischaemia (positive and symmetric T wave in V1-V3), with TV3 > TV1. The presence of flat T wave in V6 suggests that low lateral wall is also affected. Observe the negative T wave in II, III and VF (inferior ischaem ia) and the positive T wave in I and VL that appears as a mirror pattern.

The injury vector has approximately the same direction as that of the vector of ischaemia and infarction but opposite sense (see p. 35, 60 and 131 and Figures 3.6, 4.8 and 5.3). Therefore, most probably, in case of injury of the lateral wall, an ST-segment depression will be especially recorded in V1-V2, and in case of injury of the inferobasal wall, the ST-segment depression will be recorded especially in V2-V3. However, further perfusion studies, with imaging techniques in the acute phase have to be done to validate this hypothesis. 

We should remember that in some chronic coronary patients, those who present a transmural infarction classically named inferoposterior but with the new classification we define as inferolateral MI (Figure 5.9B(3)), a tall, frequently peaked, and in this case persistent, T wave may be recorded in V1-V3 as a consequence of the changes that the transmural infarction produced in repolarization (mirror pattern of inferobasal and lateral subepicardial ischaemia) (Figure 3.10). 

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...

On the contrary, in Q-wave infarction the coronary artery occlusion is usually complete, and classically it was considered that the MI was transmural and often presents homogeneous wall involvement (QS pattern) or at least the infarction involves the subendocardium and also part of the subepicardium in contact with the subendocardium (QR pattern) (Figure 5.2C). CMR has demonstrated that often Q-wave Mis are not trans-mural and, on the contrary, often are transmural non-Q-wave Mis (Moon et al., 2004). The Q-wave MI often appear in a patient without very much prior ischaemia (first infarction). Consequently, an acute ischaemia (ACS) generates a poor-quality TAP in the entire wall that is recorded, from the precordium, as subepicardial injury pattern (ST-segment elevation) (Figures 4.5 and 4.8). Later, the myocardium becomes non-excitable and Q wave of necrosis develops (Figures 5.2B and 5.3). 

Marrow ischaemia will cause signal intensity changes within marrow which can lead to infarction. Transient ischaemia can occur following an acute fracture with the marrow returning to normal weeks later. 

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