Physician's Perspective

Q Waves Revisited

Steven R. Gambert, MD, AGSF, MACP Editor-in-Chief, Clinical Geriatrics  

I recently saw an older woman in the hospital with significant abnormalities on her electrocardiogram (ECG). Although she had evidence of an anterolateral myocardial infarction, age undetermined, on her ECG tracing, she told me she had been recently informed by her primary care physician that her heart was healthy and that she did not have any problems. When I questioned her further about whether she had had a recent ECG, she reported that she, in fact, had one recently and was told by her physician that, although it showed abnormal findings, “electrocardiograms were unreliable and I had not had a heart attack despite it possibly showing one on the tracing.”

While it is possible that this patient had misunderstood what was being told to her or that her physician chose not to “worry” her since she had reported no clinical issues, I decided to use this case as an opportunity to review with you the literature regarding the sensitivity and specificity of ECGs and what Q waves may actually signify.

Studies report that ECGs can successfully identify patients with proven stenosis on angiography in 36% to 87% of cases.1-3 The presence of an ST elevation or Q waves can be used to accurately delineate an infarct with a specificity of between 91% and 98%; due to variations in coronary anatomy and technique of ECG testing, however, it is more difficult to determine the actual artery involved.4

One study reported that patients presenting with a history suggestive of ischemic cardiac pain but with a normal ECG still have an incidence of myocardial infarction of 7%.5 For this reason, troponin levels are obtained to correlate with serial ECG tracings.

A large meta-analysis of more than 132 studies with 24,074 patients found the overall sensitivity of an exercise tolerance test (ETT) to be 68% with a specificity of 77%.6 These data have been used to develop the American College of Cardiology/American Heart Association Guidelines for Exercise Testing.7 The specificity of the ETT was based on “true positives” or patients with significant stenosis on an angiogram. Technetium-99m isonitrile single-photon emission computed tomography–based dobutamine stress testing has been reported to be able to identify patients with coronary artery disease accurately 64% of the time.8

In a group of patients with known coronary artery disease, exercise electrocardiography had a sensitivity of only 53% for identifying those persons who would prove to have an acute coronary event within the next 2.5 years.9

The exact degree of ST elevation required for a diagnosis of an evolving acute myocardial infarction can influence the sensitivity of the ECG. An ST/junctional ST elevation of ≥0.2 mV in more than one anterior lead has a sensitivity of 56% and a specificity of 94% for acute myocardial infarction defined by clinical history and biochemical evidence. Altering the diagnostic criteria varied sensitivity between 45% and 69% but reduced specificity from 98% to 81%.10

So, going back to my patient, it is unlikely that the ECG was a false-positive for a myocardial infarction based on my findings, interpretation of the ECG, and other test results that we had available to review. The majority of abnormal Q waves are due to myocardial infarction, although other causes clearly must be considered. Non–Q-wave myocardial infarction may be transient or permanent. Transient Q waves have been produced experimentally in animals and have been observed in patients during ischemic episodes. My patient’s ECG did not change over time, making a transient cause less likely.

Q waves may accompany severe metabolic disturbances associated with shock or pancreatitis, hypothermia, and possibly even tachycardia. Non–Q-wave myocardial infarctions (pseudoinfarction) may also result from myocardial disease resulting from problems including myocarditis; AIDS; cardiac amyloidosis; neuromuscular disorders such as progressive muscular dystrophy, myotonia atrophica, and Friedreich’s ataxia; scleroderma; postpartum myopathy; myocardial replacement by tumor; sarcoidosis; left ventricular hypertrophy; and idiopathic cardiomyopathy. Pericarditis, hyperkalemia, early repolarization, intracranial hemorrhage, pneumothorax, chronic obstructive pulmonary disease with or without cor pulmonale, pulmonary emboli, traumatic heart disease, left bundle branch block, anomalous coronary artery, and coronary embolism may also present with Q waves.

As with everything else in medicine, clinical correlation and other testing may be necessary to complete the evaluation and to help delineate the most likely diagnosis. While nothing is 100% certain in clinical medicine, based on a complete evaluation of the patient and a review of all available information, a myocardial infarction occurring sometime in the past remains the most likely etiology for this patient’s Q waves.

Dr. Gambert is Professor of Medicine and Associate Chair for Clinical Program Development, Co-Director, Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Maryland School of Medicine, Director, Geriatric Medicine, University of Maryland Medical Cenyer and R Adams Cowley Shock Trauma Center, and Professor of Medicine, Division of Gerontology and Geriatric Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.

References

1. Miller RR, Amsterdam EA, Bogren HG, Massumi RA, Zelis R, Mason DT. Electrocardiographic and cineangiographic correlations in assessment of the location, nature and extent of abnormal left ventricular segmental contraction in coronary artery disease. Circulation. 1974;49(3):447-454.

2. Howard PF, Benchimol A, Desser KB, Reich FD, Graves C. Correlation of electrocardiogram and vectorcardiogram with coronary occlusion and myocardial contraction abnormality. Am J Cardiol. 1976;38(5):582-587.

3. Bodenheimer MM, Banka VS, Helfant RH. Q waves and ventricular asynergy: predictive value and hemodynamic significance of anatomic localization. Am J Cardiol. 1975;35(5):615-618.

4. Dwyer EM Jr. The predictive accuracy of the electrocardiogram in identifying the presence and location of myocardial infarction and coronary artery disease. Ann N Y Acad Sci. 1990;601:67-76.

5. Welch RD, Zalenski RJ, Frederick PD, et al; National Registry of Myocardial Infarction 2 and 3 Investigators. Prognostic value of a normal or nonspecific initial electrocardiogram in acute myocardial infarction. JAMA. 2001;286(16):1977-1984.

6. Gianrossi R, Detrano R, Mulvihill D, et al. Exercise-induced ST depression in the diagnosis of coronary artery disease. A meta-analysis. Circulation. 1989;80(1):87-98.

7. Gibbons RJ, Balady GJ, Beasley JW, et al. ACC/AHA Guidelines for Exercise Testing. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). J Am Coll Cardiol. 1997;30(1):260-311.

8. Kisacik HL, Ozdemir K, Altinyay E, et al. Comparison of exercise stress testing with simultaneous dobutamine stress echocardiography and technetium-99m isonitrile single-photon emission computerized tomography for diagnosis of coronary artery disease. Eur Heart J. 1996;17(1):113-119.

9. Sekhri N, Feder GS, Junghans C, et al. Incremental prognostic value of the exercise electrocardiogram in the initial assessment of patients with suspected angina: cohort study. BMJ. 2008;337:a2240. doi:10.1136/bmj.a2240.

10. Menown IB, Mackenzie G, Adgey AA. Optimizing the initial 12-lead electrocardiographic diagnosis of acute myocardial infarction. Eur Heart J. 2000;21:275-283.