Transmural ischaemia

The electrophysiological mechanism that explains the patterns of clinical ischaemia is different in cases of subendocardial and subepicardial (transmural) ischaemia. 

Figure 8.9 (A) A patient with ACS with ST-segment elevation with the pattern found in cases of severe transmural ischaemia (increase in R( disappearance of S wave, ratio J point/R wave >0.5). Troponin levels were normal. (B) The ECG after primary PCI of proximal LAD presents a deep negative T wave from V2-V4, suggestive of opened artery (reperfusion pattern).

ACS with evident ST-segment elevation suggesting a transmural ischaemia (Figure 8.7)... 

Kenigsberg D, Khanol S, Kowalski M, Krishnan S. Prolongation of the QTc interval is seen uniformly during early transmural ischaemia. JACC 2007 49 1299. 

Taggart P, Sutton PMI, Opthof T, et al. Transmural repolarisation in the left ventricle in humans during normoxia and ischaemia. Cardiovasc Res. 2001 50 454-462. 

In case of ACS with ST-segment elevation (STE-ACS), the ECG patterns of ischaemia (subendocardial), injury (transmural) and usually necrosis appear in a sequential way (see Figures 3.7 and 8.5). In the case of exercise angina, the ECG pattern of subendocardial injury is the most frequently found (see Figures 3.9A and 4.57). 

If the delay is subepicardial or even transmural (see The concept of ECG patterns of ischaemia, injury and necrosis ) (p. 20). this delay of repolarisation without change of shape of TAP generates a flattened or negative T wave. 

When acute coronary occlusion is carried out in experimental animals with closed thorax, it gives rise, during the initial phase of ischaemia, to a delay in repolarisation (TAP) in the subendocardium, which is the area that first suffers ischaemia (Lengyel et al, 1957). This subendocardial ischaemia is evidenced by a tall and peaked T wave immediately followed by ST-segment elevation (injury pattern) if the occlusion persists and the ischaemia becomes severe and transmural (see ECG pattern of injury p. 55). This pattern maybe self-limited if the occlusion is temporary, as in coronary spasm (Prinzmetal... 

Figure 3.9 In case that in basal state a certain degree of ischaemia with subendocardial predominance exists too mild to produce clear ECG changes, an increase of active ischaemia still with subendocardial predominance will produce an ST-segment depression (subendocardial injury pattern) (A). If as a consequence of ischaemia there is a delay in repolarisation predominating in subepicardium or being transmural, a flattened or negative T wave appears in leads with, but also without, predominant R wave (B-1) (subepicardial ischaemia pattern). The latter pattern is...

The ischaemia that occurs clinically secondary to an acute total coronary artery occlusion is firstpredominantly subendocardial (symmetric and usually taller T wave) and then transmural and homogeneous (ST-segment elevation), and later, in general, a Q wave of necrosis appears,... 

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). 

Electrocardiographic pattern of subepicardial ischaemia (transmural) diagnosis and differential diagnosis... 

In theory the presence of subendocardial or transmural injury in completely opposite areas of the heart may decrease or even conceal the two injury vectors (Madias, 2006). However, in practice, this does not occur usually, because the ischaemia is usually due to occlusion of only one vessel and this does not generate equal and opposed injured areas (Rautaharju, 2006). Furthermore, with the same amount of injury in two opposite areas, it is more visible in the surface ECG of the injury area that is more close to subepicardium. In the chronic phase it is more often seen that a new vector of infarction in opposed area may cancel the Q-wave pattern of a previous infarction (see Figure 5.38). 

In order to quantify the area at risk and burden of ischaemia, both ST-segment elevations and depressions should be assessed. The latter are not the expression of subendocardium injury, but the real expression ofsubepicardium (transmural) injury in a distant area. Therefore, in LAD occlusion, an ST-segment depression detected in II, III and VF, more significant compared with an ST-segment elevation in the same leads, represents more ischaemia (compare Figures 4.21 and 4.23). 

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). 

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