Myocardial Infarction

Differential Diagnosis of Q Waves

  

Non infarction Q Waves
While the vast majority of abnormal Q waves are due to myocardial infarction, a significant number are due to other causes.
Noninfarction Q waves may be transient or permanent. Transient Q waves have been produced experimentally in animals and observed in patients during ischemic episodes. Such Q waves have been explained by a transient loss of electrophysiological function, but without irreversible cellular damage, a phenomenon referred to by some as “myocardial concussion.” Q waves have been recorded with severe metabolic disturbances accompanying shock or pancreatitis. Similarly, transient Q waves have been noted during cardiac surgery and ascribed variously to transient ischemia and hypoxia, coronary spasm, localized metabolic and electrolyte disturbances, and possible hypothermia. Rarely a transient Q wave may result from tachycardia.
The largest group of noninfarction Q waves is due to myocardial disease, including myocarditis, AIDS , cardiac amyloidosis, neuromuscular disorders such as progressive muscular dystrophy, myotonia atrophica, Friedreich’s ataxia, scleroderma, postpartum myopathy, myocardial replacement by tumor, sarcoidosis, idiopathic cardiomyopathy, anomalous coronary artery, and coronary embolism.
Noninfarction Q waves are common in hypertrophic cardiomyopathy and may simulate anterior or inferior myocardial infarction. Although the exact mechanism of the abnormal Q waves in this condition is unclear, increased septal mass or abnormal depolarization because of anomalous architecture of the septal myocardium, or both, have been proposed as the cause.
Abnormal Q waves can be associated with chronic obstructive lung disease (COLD) with or without cor pulmonale, pulmonary embolism, and pneumothorax. In COLD, findings in the precordial leads frequently simulate anterior myocardial infarction. The mechanism responsible for the QS complex is clockwise rotation and downward displacement of the diaphragm and of the heart. As a result, the electrodes are located superior to the initial vector; when this vector is directed inferiorly, a QS pattern results. By placing the electrode one interspace lower, it is often possible to record an R wave and thus provide strong evidence against myocardial infarction. Occasionally in COLD the Q wave may simulate inferior myocardial infarction. The positional origin of the anterior or inferior Q waves may be suspected when the Q wave is accompanied by other EKG findings of COLD. However, since both COLD and myocardial infarction frequently coexist, differential diagnosis may at times be difficult or impossible.
Abnormal Q waves, especially in lead III and rarely in lead aVf, with an S wave in lead I, can be recorded in acute cor pulmonale due to pulmonary embolism. Clockwise rotation with superior orientation of the initial vector is most likely responsible for the Q waves in lead III. A Q wave in lead II is rarely recorded. Occasionally acute pulmonary embolus may simulate anterior myocardial infarction.
Spontaneous pneumothorax, particularly on the left, may result in a pattern simulating anterior myocardial infarction with occasional absence of the R wave in all the precordial leads.
In LBBB the initial forces are directed from right to left and either superiorly or inferiorly. When the inferiorly directed forces dominate, a QS complex may be recorded in the precordial leads, simulating an anterior myocardial infarction. If the initial vector is oriented to the left and superiorly, a QS complex may be registered in the inferior leads, suggesting inferior myocardial infarction.
With left anterior divisional block, the transitional zone is shifted to the left, and an initial Q wave may appear in the right precordial leads. Loss of the forces normally contributed by the left anterior division results in a vector directed inferiorly, posteriorly, and to the right. Consequently, right precordial leads may register a qrS complex suggestive of an anteroseptal infarction. By placement of the electrodes one interspace lower, an rS complex can be recorded attesting to the positional nature of the Q wave.
Noninfarction Q waves are frequent in WPW. WPW type B, with the initial forces directed from right to left, registers a QS complex in the right precordial leads and may be mistaken for anteroseptal or anterior myocardial infarction. Rarely, preexcitation of the left lateral wall, with the vector oriented anteriorly and to the right, simulates lateral infarction. Most often, however, WPW simulates inferior infarction. The Q waves recorded in leads II, III, and aVf are due to superior orientation of the initial vector and may be seen with either type A or type B WPW.
In LVH, failure to record an R wave in leads V1 to V4 may suggest an anteroseptal myocardial infarction. Similarly, reciprocal elevation of the ST segments in these leads may contribute to an erroneous diagnosis of myocardial infarction. The exact mechanism of the initial negative deflection of the QRS is not clear, but it may be related to posterior rotation or inferior orientation of the initial vector.

In the majority of patients with AMI, some change can be documented when serial electrocardiograms (EKGs) are compared. However, many factors limit the ability of the EKG to diagnose and localize MI: the extent of myocardial injury, the age of the infarct, its location, the presence of conduction defects, the presence of previous infarcts or acute pericarditis, changes in electrolyte concentrations, and the administration of cardioactive drugs. Nevertheless, serial standard 12-lead EKGs remain a clinically useful method for the detection and localization of MI. Even when left bundle branch block is present on the EKG, MI can be diagnosed when striking ST-segment deviation is present beyond that which can be explained by the conduction defect.
Although general agreement exists on electrocardiographic and vectorcardiographic criteria for the recognition of infarction of the anterior and inferior myocardial walls, less agreement is found on criteria for lateral and posterior infarcts; here even the terminology may be confusing. It has been reported that patients with an abnormal R wave in V1 (0.04 sec in duration and/or R/S ratio >1 in the absence of preexcitation or right ventricular hypertrophy) with inferior or lateral Q waves have an increased incidence of isolated occlusion of a dominant left circumflex coronary artery without collateral circulation; such patients have a lower ejection fraction, increased end-systolic volume, and higher complication rate than patients with inferior infarction due to isolated occlusion of the right coronary artery.
More sophisticated forms of EKG recordings including high-resolution electrocardiography, body surface potential mapping of ST segments, and continuous vectorcardiography have all been reported in small series of patients to augment the 12-lead EKG in diagnosing AMI, but the lack of ready availability of equipment and the special expertise required limits the use of these techniques. Of potentially more widespread clinical applicability is a clinical and EKG algorithm for predicting the presence of AMI that provides a computerized reading of the tracing along with a statement of the patient’s risk of adverse cardiovascular events with and without reperfusion therapy.
Although most patients continue to demonstrate the EKG changes from an infarction for the rest of their lives, particularly if they evolve Q waves, in a substantial minority the typical changes disappear, Q waves can regress, and the EKG can even return to normal after a number of years. Under many circumstances Q-wave patterns may simulate MI. Conditions that may mimic the electrocardiographic features of MI by producing a pattern of “pseudoinfarction” include ventricular hypertrophy, conduction disturbances, preexcitation, primary myocardial disease, pneumothorax, pulmonary embolus, amyloid heart disease, primary and metastatic tumors of the heart, traumatic heart disease, intracranial hemorrhage, hyperkalemia, pericarditis, early repolarization, and cardiac involvement with sarcoidosis.

Back to top     Go to Quiz