Q waves of necrosis

The electrocardiographic pattern or necrosis (see p. 129, Figures 2.1(4) and 5.3) is characterised by the occurrence of abnormal (pathological) Q wave (see explanation in Electrophysiological mechanisms of Q wave of necrosis p. 130 and Figure 5.3). Today we know that in many cases of MI, this pattern is not present (non-Q-wave infarction). Tissue necrosis is the highest degree of clinical ischaemia. 

Therefore, in clinical practice, the same correlation Q waves of necrosis in ECG leads and necrotic areas is used to locate injured areas (ST changes) or ischaemic ones (T-wave changes), although, very often in the acute phase, the ECG patterns of ischaemia and injury are usually visible in more leads than the ECG pattern of necrosis. However, in the chronic phase, the ECG pattern of injury usually... 

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,... 

Figures 3.18 and 3.19 show the evolution of two Mis from the acute phase with a huge ST-segment elevation until the appearance of Q wave of necrosis and negative T wave of subepicardial ischaemia. In Figure 3.20, a patient with chronic MI of inferior wall presents in the same ECG a different grade of ECG pattern of subepicardial ischaemia (negative and deep T wave in inferior leads, tall and positive T wave in right precordial leads as a mirror pattern and flat T wave in V6).

This is obtained by analysing in which leads Q wave of necrosis or R equivalents are recorded (Figure 5.9) (ECG-CMR correlation). 

The explanation of the Q wave of necrosis can be made on the basis of the theory of the electrical window of Wilson or on the formation of a vector of infarction. According to the first theory, the... 

The leads that face the vector of infarction tail record morphologies with the Q wave of necrosis (QS or QR complexes). Throughout this book we will use this concept - vector of infarction and changes that it generates in the morphology of the QRS loop and its projection in its respective... 

Proximal occlusion of a very long LAD whole anterior wall and a part of inferior and lateral wall are involved. In this situation, in some cases the ECG pattern may do not reflect the infarcted area due to the cancellation (more gray areas) of the vector of the middle segment of anterior wall (which explains the Q wave in VL) and the vector of inferior necrosis (which explains the Q wave in inferior leads). In this case only Q waves in some precordial leads may be recorded. The more basal part of anterior wall that is also usually infarcted does not generate Q wave of necrosis due to late depolarisation. 

Q wave of necrosis (QS, Qr, QR and qR) that may be seen in all three inferior leads, but never in lead II with QS pattern except in the presence of SAH. In the latter case, a QS with notches () is recorded (see Figure 5.54). 

A new infarcted area suddenly masks totally or partially previous Q waves (Madias and Win, 2000) (Figure 5.39). The ECG may seem even normal or nearly normal due to cancellation of vectors. It should be ruled out that the disappearance or decrease of the Q wave is not secondary to the development of a new intraventricular block. Also ischaemia induced by exercise may mask transiently, due to ischaemia in the opposite sites, the Q wave of necrosis (Madias et al, 1997). 

Anginal pain is not intense and/or repetitive, and the ECG is normal with no changes in the follow-up or with flattened or mildly negative T wave in leads with dominant R wave. Sometimes, small Q waves of necrosis or mildly ST-segment... 

To diagnose a chronic Q-wave infarction, the criteria that define a Q wave of necrosis should be identified. The criteria used for the diagnosis of an infarction involving the different walls into which the left ventricle maybe divided have been discussed on page 135 (Tables 5.2 to 5.4). Measurement and assessment of Q and R waves may be made according to the Minnesota code (Blackburn et al., 1960) (Figure 5.1). All these aspects have been commented on in Chapter 1. 

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. 

Each of the seven electrocardiographic patterns with a Q wave of necrosis or its equivalent that we find in daily clinical practice is shown in Figure 5.9. In the first part of this book (p. 141) we have commented on the diagnostic clues for each of the seven ECG patterns, based on the CE-CMR correlations (Figures 5.10-5.36). Now, we will briefly discuss first the comparative prognosis of ECG pattern of anteroseptal versus inferolateral pattern and later the most important prognostic implications of each pattern. 

In probably more than 50% of cases, an MI with normal intraventricular conduction and narrow QRS does not show a Q wave of necrosis or equivalent (R in V1-V2). However, it may show anomalies in the mid-late part of QRS (as low r in lateral leads, rsr , slurrings, etc. (fractionedQRS)). Also repolarisation changes may be recorded especially in the acute phase. The incidence of MI without Q wave is variable depending on whether it is detected. In the emergency department it is higher and in the CCU lower. 

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). 

Infarction located in an area, which does not generate Q wave of necrosis. 

On occasions, as it happens in MI of areas of late depolarisation, RV, atria or when the infarcted area is very small, the ECG does not generate Q wave of necrosis and may be completely normal or presents changes only in the last part of QRS or subtle... 

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