The association between abnormally wide Q waves and MI was established by historical works in the 1930s–1940s [13, 14]. Originally, Q-wave MI was considered strongly associated with transmural infarction. Later on, moderate sensitivity and good specificity for Q waves to detect myocardial necrosis at autopsy in patients with a narrow QRS complex was reported [15]. Adverse post-MI outcome was evident from studies conducted before the introduction of reperfusion therapy – fibrinolysis or PCI. Q-wave duration, Q/R ratio, and Q waves in multiple infarct locations were associated with worse long-term outcome [16].

In the chronic phase of MI, Q waves are regarded as a sign of irreversible necrosis. However, about 50 % of patients presenting within 1 h of onset of ST-elevation acute coronary syndrome (STE-ACS) already have Q waves in the leads with ST elevations, especially in the anterior leads. These Q waves may be transient and not necessarily represent irreversible damage. It is believed that intense ischemia may cause a transient loss of electrical activity in the region at risk. Thus, Q waves on presentation may reflect either irreversible damage and/or a large ischemic zone and thus portend a large final infarction. On the other hand, in inferior STE-ACS, preexisting Q waves may disappear during acute ischemia – the Q waves may be “pulled up” by the injury current – and reappear during reperfusion.

The traditional view that Q waves represent transmural MI, while subendocardial MI is reflected by ECG changes other than Q waves, was questioned in the 1980s [17]. It was evident from autopsy studies that about half of subendocardial MIs caused pathological Q waves, while about half of transmural MIs did not [18]. Accordingly, the terms Q-wave and non-Q-wave MI replaced the former designations. The most recent golden standard of myocardial injury, cardiac magnetic resonance imaging (CMR), has shown that the Q-wave/non-Q-wave distinction is determined by the total size rather than by the transmural extent of the underlying scar [19].

Braunwald’s group introduced the concept of reduction of infarct size by pharmacologic agents in the late 1960s–1970s, and that resulted in a need for refinement of the classification of acute coronary events [20]. The term unstable angina (acute ischemia without resultant detectable necrosis) was introduced in the early 1970s and was classified according to severity by Braunwald in the late 1980s [21, 22].

After the introduction of the three original ECG leads, I, II and III, by Einthoven in 1912, investigators began to classify MIs based on changes in the QRS complex according to their location into anteroapical and posterobasal MI. With the development of the unipolar leads and multiple chest lead technique, additional locations were introduced. Monumental work with systematic autopsy studies in the 1930s and 1940s established the theoretical and empirical basis for the association between different ECG patterns and the location of myocardial necrosis [14]. Based on pathological correlation, a relationship between the location of infarcted areas and Q waves on the ECG was, until recently, accepted and, with minor modifications, implemented in scientific statements and textbooks.

Already in the 1930s, studies showed different premortal ECG patterns depending on the MI location at autopsy. In patients, who survived the acute infarction, coronary angiography enabled the correlation of ECG signs of myocardial necrosis with this new technique. Reperfusion therapy, initially by intracoronary thrombolysis in the 1980s, resulted in a clear need to improve the ECG diagnosis to be able to predict the culprit artery and the estimated size of the area at risk by observing changes from the acute occlusive phase (ST/T changes). Since then, many ECG algorithms for the prediction of the culprit artery and the level of vessel occlusion have been introduced. The results of the studies evaluating these algorithms vary; they are dependent on factors such as time from ECG recording to angiography, individual variation of coronary artery anatomy, and coronary artery dominance.

More recently, the correlation between Q waves in various ECG leads and the affected myocardium has been studied by CMR. Based on these findings, a new terminology for LV walls and location of Q-wave MIs was proposed [23]. The consensus group recommended to classify the different MI locations based on the following six most commonly occurring patterns of abnormal Q waves and Q-wave equivalents (Fig. 19.2). In septal MI, the septal wall and often a small part of the adjacent anterior wall are involved, and the ECG shows Q waves in leads V1 and V2 [24]. The term mid-anterior was recommended for MIs located especially in the mid-low segments of the anterior wall. This MI subtype is typically caused by occlusion of the first diagonal branch, and in the ECG Q waves are present in leads aVL (I) and sometimes V2. Compared with septal infarction, in apical-anterior MI, the abnormal Q waves extend into the more leftward precordial leads – typically V3 and V4 and sometimes V5 and V6. There are no abnormal Q waves in leads aVL and I. Extensive anterior infarction is essentially a combination of the three previously mentioned types. Consequently, the ECG shows abnormal Q waves in the precordial leads and lead aVL (sometimes also in lead I). In lateral MI, the ECG may produce the Q-wave equivalents of abnormally prominent R waves in leads V1 and V2. There may also be abnormal Q waves in lead I, aVL, and/or V5 and V6. Finally, inferior MIs produce Q waves in leads II, III, and aVF, but without increased R waves in leads V1 and V2. When the infarct-related artery (right coronary or left circumflex artery) is very dominant and the occlusion is proximal, the infarction encompasses both the inferior and the lateral wall, and then the ECG pattern is the association of criteria of inferior and lateral MI (inferolateral MI).