In patients with new onset symptoms compatible with myocardial ischemia, symptoms at rest or a change in the pattern of symptoms, the ECG remains the major noninvasive imaging tool for rapid assessment, diagnosis and triage. The accuracy of the ECG interpretation increases when it is done as part of the clinical assessment of the patient rather than off line without considering demographic data, risk factors and presentation. Comparisons to previous ECG recordings improve the detection of subtle changes, especially in patients with abnormal baseline ECG. Repeat ECG recordings when changes (worsening or improvement) in symptoms are noted increases the sensitivity of detecting minor changes that otherwise could be missed.

The Fibrinolytic Therapy Trialists’ Collaborative Group analyzed data from nine large fibrinolytic trials and concluded that fibrinolytic therapy reduced mortality in patients with ST segment elevation or bundle branch block [4]. In animal models and during intracoronary balloon occlusion in patients, acute occlusion of an epicardial artery usually results in ST segment elevation. Therefore, a paradigm has emerged that ST elevation signifies transmural myocardial ischemia due to an acute occlusion of an epicardial coronary artery, whereas patients presenting without ST elevation (normal ECGs, ST depression or isolated T wave inversion) do not have ongoing transmural ischemia and therefore, may not benefit from urgent reperfusion therapy. However, many patients have nonischemic sources of ST segment elevation at baseline or show dynamic ST changes that are not caused by acute ischemia [5]. For example, ST elevation due to early repolarization that tends to diminish at higher heart rates, may be falsely interpreted as transmural ischemia. The European Society of Cardiology/ American College of Cardiology Foundation/ American Heart Federation Task Force for the Universal Definition of Myocardial Infarction sets a threshold of ST elevation in ≥2 adjacent leads measured at the J point (for patients without ECG criteria for LVH or LBBB): in leads V2-V3 ≥ 0.2 mV in men, ≥0.15 mV in women, and for all other leads ≥0.1 mV [6, 7]. Patients with compatible symptoms within the preceding 12 h, who meet these criteria are triaged for acute reperfusion therapy. In cases, where the ECG does not meet the criteria, conservative medical therapy is recommended initially. However, these thresholds should be considered as a statistical tool that help to reduce the incidence of false activation of the acute reperfusion protocols and not as strict rules. Many patients may have an acute occlusion of an epicardial artery- true STEMI (ST-elevation myocardial infarction) with ST segment elevation less than the abovementioned thresholds. On the other hand, there are many patients with compatible symptoms and ST segment elevation who meet the above criteria, yet they do not have STEMI, even if they have positive cardiac biomarkers (so called “pseudo STEMI”) [5, 8]. Recognition of specific patterns of ST elevation that are caused by nonischemic etiologies (i.e., early repolarization, normal variant, repolarization changes secondary to left ventricular hypertrophy or conduction delay, Brugada syndrome, acute pericarditis, old infarction/ aneurysm) (Fig. 9.2) is crucial. Comparison to previous ECG tracings may assist in the accurate diagnosis. However, it should be emphasized that some patterns of nonischemic ST elevation may show dynamic changes (ST elevation due to early repolarization tends to diminish with faster heart rate, whereas ST segment elevation due to old aneurysm tends to increase, etc.). In the majority of cases; however, when the ECG interpretation is done in the conjunction of the clinical examination, accurate diagnosis of STEMI can be made. Yet, there are numerous borderline cases and especially when the ECG is interpreted alone without examining the patient, false positive and false negative interpretation may occur [9].

The ECG recorded during the acute phase of ischemia reveals crucial information concerning the site of occlusion of the coronary artery, the estimated size of the ischemic area at risk and the “severity” of ischemia [8].

After an acute epicardial coronary artery occlusion T waves become tall and peaked (Fig. 9.3). Then, ST elevation develops, representing “transmural” ischemia. Without successful reperfusion, ST elevation may persist for weeks. Q waves usually develop after 4 h evolving during the ensuing 2 weeks. At 4–24 h, the terminal portion of the T wave in the leads with ST elevation becomes negative and gradually the magnitude of ST elevation diminishes in conjunction with evolution of the Q wave. The exception to this rule is the development of left ventricular aneurysm. With left ventricular aneurysm formation, Q waves develop and T waves may begin their inversion without complete resolution of ST segment elevation. ST segment abnormalities often persist for the life of the patient or until transplantation. However, with prompt reperfusion therapy (either thrombolytic therapy or primary percutaneous coronary intervention) rapid evolution is seen. In most cases with successful reperfusion, the magnitude of ST elevation diminishes rapidly and the T waves become inverted, usually with the development of Q waves. In cases with a short episode of vessel occlusion and prompt reperfusion, complete normalization of the ECG may be seen. Pathological Q waves have traditionally been considered as a sign of irreversible necrosis. However, gradual disappearance of Q waves may be seen over time, especially in patients with inferior STEMI, suggesting that following reperfusion Q waves do not always represent transmural scar [8, 10, 11].

The ECG recorded during the initial presentation predicts the size and location of the ischemic area at risk; and thus, may assist in identification of the exact size of the occlusion of the coronary artery [8].