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Chapter 11: THE RESTING ELECTROCARDIOGRAM ABNORMAL Q WAVES

Abnormal Q waves appearing several hours after total occlusion of a coronary artery result from necrosis secondary to the decreased blood supply. The number of affected cells has to be large enough so as to produce changes reflected at the body surface. In general, the depth of the Q wave is proportional to wall-thickness involvement.7 Thus, in lead aVF a QS complex was said to reflect transmural necrosis. On the other hand, clinical myocardial infarction (MI) without abnormal Q waves was categorized as subendocardial infarction. Presently, MIs are no longer classified as transmural or subendocardial (but as Q or non-Q MIs).36 The duration of the Q wave is proportioned to the extent of the area of necrosis parallel to the epicardial surface. If the latter is large enough, starts in the subendocardium, and extends toward (but not quitereaching) the epicardium, the corresponding unipolar leads will record QR or Qr complexes depending on the amount of living tissue located between dead tissue and the recording electrode. Therefore, abnormal Q waves may occur in MIs that are not completely transmural.7,36 The following changes have been said to be equivalent to Q waves in non-Q-wave MI: R/S ratio changes, acute frontal plane right-axis deviation, new left-axis deviation or left bundle branch block, initial and terminal QRS notching, and some types of "poor r-wave progression."36 Although the concept of non-Q-wave MI as a discrete clinicopathologic entity, different from Q-wave MI, has gained almost universal acceptance, it was challenged recently by a group of respectable electrocardiographers.36

In the course of the clinical entity known as acute myocardial infarction (MI), persisting Q waves are usually (but not invariably, as will be discussed subsequently) due to anatomic (lack of blood flow-related) necrosis. Abnormal Q waves also can occur transiently in unstable angina, Prinzmetal's angina, coronary artery spasm (without chest pain), and exercise-induced ischemia. This has been attributed to an intensity of cellular affectation ("injury") severe enough to produce a significant degree of hypopolarization (to, let us say, around 60 mV). Because the cells become electrically unexcitable (even though they are not anatomically, irreversibly necrotic),7,8,15,16 abnormal Q waves occur. Spontaneous recanalization of an occluded vessel, spontaneous reversion of the ischemia, or spasm and interventions (pharmacologic or mechanical) that improve cellular metabolism and oxygenation can restore the normal polarization. If these cells become again excitable, the abnormal Q waves may disappear or vanish.16,37 Ischemic necrosis usually takes longer to appear than the accelerated abnormal Q waves seen in the majority of patients with Q-wave MI after successful thrombolysis or effective coronary artery angioplasty performed early in the course of the process.5 The genesis of these Q waves is not well understood.37 Some authors consider them an expression of the acceleration of necrosis secondary to explosive cell swelling in already irreversibly injured tissue.31 Because some of these Q waves also tend to disappear quickly, other authors consider that they reflect factors other than myocardial necrosis, such as reversal of regional dysmetabolism or the occurrence of transient interstitial ischemia or hemorrhage.38 Profound and prolonged ischemia can cause myocardial stunning with reversible functional, metabolic, ultrastructural, and electrophysiologic abnormalities.39 Thus transient Q waves may be the ECG counterpart (electrical stunning) of the corresponding mechanical stunning.37-40 It is possible for myocardial stunning to lag behind electrical recovery.37 Myocardial stunning should be differentiated from myocardial hibernation. The latter is a term used in reference to mechanical dysfunction of an ischemic area that is not transient but chronic.41,42 Although the ECG counterpart of this type of mechanical dysfunction requires further study, it is conceivable that (in some cases) the disappearance of chronic Q waves after coronary artery bypass surgery with improvement of wall motion abnormalities indicates that these Q waves were due not to cellular death but to cellular hibernation4142 (see also Chaps. 37 and 40). Finally, abnormal Q waves need not be the end result of coronary artery disease because they may be seen after primary (due to infections or drugs) cellular necrosis and in other pathologic processes such as myocardial infiltration and certain types of interventricular septal (and LV) hypertrophy, Wolff-Parkinson-White syndrome, and muscular dystrophies.43

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