1. In left ventricular hypertrophy, there is often a QS deflection or poor R wave progression in the right precordial leads that suggests anterior myocardial infarction. The secondary ST-segment elevation in these leads may be mistaken as a current of injury.
2. In pulmonary emphysema, the R waves in the right precordial and sometimes midprecordial leads become quite small or are absent, suggesting anterior myocardial infarction. These QRS changes are explained by the vertical displacement of the heart secondary to a low-lying diaphragm and the intervention of hyperinflated lungs.
3. The pseudoinfarction pattern may also be seen in patients with pneumothorax. The voltage of the QRS complex may be reduced. QS deflection may appear in the right precordial leads.
4. In pulmonary embolism, the Q waves in lead III (as part of the S1Q3 pattern), and sometimes in lead aVF, that are accompanied by ST-segment and T-wave changes are often interpreted as inferior myocardial infarction. In addition to T-wave inversion, with or without an rSr′ pattern in the right precordial leads due to acute right heart strain, QS complexes with ST-segment elevation may occasionally develop in these leads and mimic acute anterior myocardial infarction.
5. In hypertrophic cardiomyopathy, abnormal Q waves are often seen, especially in the left precordial leads and lead I. These Q waves have been attributed to ventricular septal hypertrophy.
6. Myocardial fibrosis is often responsible for the pseudoinfarction pattern in patients with dilated cardiomyopathy, progressive muscular dystrophy, Friedreich’s ataxia, scleroderma, amyloidosis, and primary and metastatic tumors of the heart.
7. QS deflections are often seen in the right precordial leads in patients with complete left bundle branch block in the absence of myocardial infarction.
8. Left anterior hemiblock is occasionally associated with small Q waves in the precordial leads that mimic anterior myocardial infarction.
9. The delta waves in Wolff-Parkinson-White syndrome are frequently interpreted as abnormal Q waves of myocardial infarction.
10. Pheochromocytoma may be associated with striking ECG changes masquerading as ischemic heart disease.4
11. Other conditions that may be associated with ECG changes simulating myocardial infarction include intracranial hemorrhage, hyperkalemia and, as mentioned above, acute pericarditis.3
- Copyright © 2001 by American Heart Association
We are grateful to Drs Kessler and Cheng for their insightful comments regarding our article.R1 The possibility of artifact in this ECG recording came to our minds, too. However, the follow-up ECGs, which were performed with another ECG machine, revealed similar findings. The likelihood of interference by other extrinsic factors, such as an arterial pulse (suggested by Dr Kessler), in producing the observed bizarre T waves cannot be completely excluded. The bizarre T waves disappeared several hours later, and the subsequent ECGs, which were not shown, still revealed ST segment elevation with positive T waves in V1 to V3, and inverted T waves in V4 to V6. We think the key finding was the ST segment elevation in the right precordial leads, especially V3, and we consider it a good example of pseudo-myocardial infarction.
The possibility of acute pericarditis, as suggested by Dr Cheng, should be considered as well. However, the ST segments in several leads, including leads I, II, and aVL, show depression instead of elevation, a finding uncommon for pericarditis. The list of causes of pseudoinfarction raised by Dr Cheng is important. Moreover, an intriguing ECG finding in the contemporary era of interventional electrophysiology is the ST-T change after radiofrequency catheter ablation of the accessory atrioventricular pathway; such a change includes an elevated ST segment and tented T waves in the right precordial leads after elimination of the left accessory pathways. The repolarization changes after successful ablation of accessory pathway is presumably due to “cardiac memory.”R2