Unusual ECG responses to exercise stress testing

Journal of Electrocardiology Vol. 34 No. 3 2001

Unusual ECG Responses to Exercise Stress Testing

John E. Madias, MD, and Himanshu Agarwal, MD

Abstract: We describe the case of a patient with coronary artery disease who developed transient ST-segment depression, right bundle branch block (RBBB), left anterior hemiblock, ST-segment elevation ⫹ST), and “giant” T-waves in her electrocardiogram (ECG), an assortment of ECG patterns heretofore unreported in conjunction with exercise stress testing (EST). The amplitude of the ⫹ST was modulated by the superimposed RBBB, as was shown by its augmentation after the abrupt disappearance of RBBB. Following recession of the latter “giant” T-waves, which usually are encountered in the hyperacute phase of myocardial infarction, developed and persisted late in the recovery period. Cardiac enzymes after EST were negative, and arteriography revealed a stenotic left anterior descending coronary artery. The present case indicates that a variety of ECG expressions of severe transmural ischemia or myocardial infarction can also be manifest in the course of EST; this also suggests a common pathophysiological mechanism in severe EST-triggered ischemia and the early phase of myocardial infarction. Key words: ECG, exercise stress testing, “giant” T-waves, right bundle branch block, left anterior hemiblock, ST-segment elevation during exercise stress testing.

Traditionally transient ST-segment depression (⫺ST) is recorded when myocardial ischemia ensues in response to exercise stress testing (1). Rarely ST-segment elevation is seen in conjunction with exercise stress testing (EST) in patients with prior myocardial infarction, ventricular aneurysm, or in absence of such antecedents (1–3). Occasionally, right bundle branch block (RBBB), left bundle branch block, left anterior hemiblock (LAH), and

left posterior hemiblock are transiently recorded in response to EST (4 –7). It is very unusual for a patient undergoing EST, and who suffers ischemia in the process, to develop more than 1 of these uncommon electrocardiogram (ECG) changes. We are reporting herein a case of a patient who showed transiently ⫺ST, ⫹ST, RBBB, LAH, and “giant” T-waves in the course of an ischemic response of an EST. A modulating effect of the RBBB on the amplitude of ischemic ⫺ST and ⫹ST was also observed.

From the Zena and Michael Wiener Cardiovascular Institute, Mount Sinai/New York University Medical Center Health System, and the Division of Cardiology, Elmhurst Hospital Center, Mount Sinai School of Medicine, New York, NY. Reprint requests: John E. Madias, MD, Chief, Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373; e-mail: [email protected]. Copyright © 2001 by Churchill Livingstone® 0022-0736/01/3403-0012$35.00/0 doi:10.1054/jelc.2001.25433

Case Report A 66-year-old woman was admitted to the hospital with complaints of chest pain attacks localized to the left lower chest, unrelated to exertion, 265

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Fig. 1. Serial 12-lead ECGs obtained during EST. Note the transient left axis shift indicative of LAH, the ⫺ST, the ⫹ST, the RBBB, and the subsequent hyperacute (“giant”) T-waves in lead V2. Numbers in the left column refer to the time of exercise (Ex) and recovery (Rec) phases of the EST.

and lasting for a few minutes. Her past medical history was significant for hypertension, hyperlipidemia, and depression. Her medications included atenolol, pravastatin, and hydroclorthiazide. She denied smoking cigarettes or using illicit drugs. Her ECG at the time of admission showed normal sinus rhythm with mild ST-segment elevation with upright T-waves in the inferior and lateral leads, suggestive of early repolarization. No changes were seen in subsequent ECGs. She was observed in the telemetry floor, and an acute myocardial infarction (MI) was ruled out by serial cardiac enzymes. The patient was discharged from the hospital, and an outpatient EST was scheduled for further evaluation. Ten days after discharge she underwent an EST in conjunction with thallium myocardial scintigraphy (TI). The resting ECG at a rate of 52 beats/min was normal at 00⬘ 00⬙ (Fig. 1). She exercised for 5⬘ and 37⬙ on the standard Bruce protocol, achieving an 83% of her predicted maximum heart rate. At 3⬘ 50⬙ of the EST, she developed 1 mm ⫺ST in 2, 3, aVF, and V5. At 4⬘50⬙, the ECG showed left axis deviation with some widening of the QRS in leads 1, and aVL, consistent with LAH. Shortly thereafter she showed ⫹ST in leads 1, aVL, and V1, and ⫺ST in 2, 3, aVF, and V5; also further widening of the QRS complex was noted with a pattern of

RBBB. At 5⬘15⬙, widening was accentuated and the QRS morphology was consistent with RBBB. The appearance of the QRS remained stable, and its duration progressively increased. At peak exercise she developed further widening of the QRS, while the QRS features were always consistent with RBBB. The above features became accentuated at 00⬘12⬙ of recovery (Fig. 1). Subsequently ⫹ST started gradually increasing in leads 1, aVL, V2-V4 with reciprocal ⫺ST in leads 2, 3, aVF, and V6, and became maximal between 02⬘05⬙ to 02⬘20⬙ of recovery. Subsequently the ⫹ST decreased, while evidence for RBBB persisted (03⬘19⬙, Fig. 1). Meanwhile at 1⬘48⬙ of recovery, a single premature atrial contraction (PAC) was conducted with a QRS in V1, similar to the one shown at 3⬘19⬙ of Fig. 1. At 04⬘00⬙ of recovery, the RBBB abruptly disappeared, and a decrease in the ⫹STs, and “giant” T-waves were noted (Fig. 2). The ECG at this point included only 2 complexes per lead, and therefore there was no way to be absolutely certain whether the long R-R interval was caused by sinus bradycardia/sinus arrhythmia, or a nonconducted PAC, which was interspersed between the 2 complexes with the different morphologies of Fig. 2, and by virtue of the subsequent pause contributed to the disappearance of the RBBB pattern. Perhaps

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Fig. 2. 12-lead ECG during the recovery period (Rec), which includes 2 beats per each ECG lead. Note that the left axis deviation (LAH) and the RBBB disappeared abruptly, and a “giant” T-wave in V2 emerged. Of note is that the ⫺ST in leads II and III and the ⫹ST in leads aVL, and V1–V3 increased as a result of the removal of the RBBB-related “blunting” effect on the amplitude of these repolarization changes.

the latter is corroborated by the interval between a possible PAC beat superimposed on the T-wave in lead 3 and the subsequent P-wave (Fig. 2), which was identical to the P-P interval shortly thereafter. The T-wave continued to increase in amplitude particularly in lead V2 (05⬘01⬙; Fig. 1). The “giant” T-waves persisted; even at 10⬘03⬙ of recovery, the T-waves in lead V2 and V4 were 13 and 8.5 mm in amplitude, correspondingly. By that time the QRS complexes resembled the ones of resting ECG; only a biphasic T wave was noted in leads 2, aVF, and V6. The patient developed retrosternal chest pain along with the above-described ECG changes. After stabilization of her condition and completion of the post EST T1 imaging session the patient was admitted to the Coronary Care Unit where an acute MI was ruled out by serial enzymes and ECGs. The post EST T1 images revealed large anteroseptal, anterolateral, apical and moderate inferoposterior perfusion defects with reperfusion on delayed images. A large anteroapical perfusion defect with moderate reperfusion was also seen (Fig. 3). The patient underwent cardiac catheterization on the day of her EST and was found to have a long, tubular lesion with a 90% diameter stenosis of the proximal left anterior descending coronary artery. On the next day, she underwent a successful angioplasty and “stenting” of the lesion. Balloon inflation during the procedure did not result in chest discomfort or ECG changes. Two weeks later she was seen in our cardiology clinic, and she is currently totally asymptomatic 10 months after her procedure.

Discussion Transient ischemia during EST is accompanied by ⫺ST, while rarely ⫹ST is recorded (1). The latter is felt to be more severe than the one associated with ⫺ST, it is seen less frequently, and is attributed to transmural ischemic involvement (1,8). Our patient showed both varieties (Fig. 1), and at the time during which ⫹ST was recorded in precordial leads, also reciprocal ⫺ST were noted in the inferior ECG leads. A distinction needs to be made here: transient ⫹ST noted during EST in leads bearing Q-waves have been shown to reflect underlying post-MI dyskinetic territories (2,3); on the other hand, ⫹ST noted in the absence of Q-waves, or prior history of MI, exemplified by our patient, reflect severe ESTtriggered ischemia (1). In addition, our patient developed LAH followed by RBBB; these changes have been noted previously in response to EST, have been attributed to the rate increase/and or underlying ischemia (4 – 7,9,10), and have often been associated with left anterior descending coronary artery disease (4,5), which our patient was shown to have. The causative role of ischemia (as opposed to mere increase in the heart rate) was shown by pacing and druginduced tachycardia, which did not produce LAH, noted on EST, even at lower rates than the ones attained pharmacologically or by pacing (10). Also LAH did not recur on repeat EST after aortocoronary bypass grafting (6). In clinical transmural acute MI, ⫹ST has been thought to be an early ECG manifestation (11), while others believed that tall, “hyper-

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Fig. 3. Sequential “slices” left to right from apex to base (short-axis, rows 1 & 2), anterior to posterior (horizontal-long axis, rows 3 & 4), and septal to lateral (vertical long-axis, rows 5 & 6) of the T1 myocardial perfusion images. Rows 1, 3, and 5 represent post-EST images, and 2, 4, and 6 were obtained at redistribution phase of the imaging.

acute” or “giant” T-waves appear first (12). Such T-waves are accompanied by mild, on no ⫹STs. In fact in the course of the time, as the amplitude of ⫹STs increase the height of the T-waves decrease. Our patient showed transient “giant” T-waves in conjunction with ischemia of a few minutes in duration. Ischemia was severe, was associated with ⫹ST, persisted in the recovery period, and was traced to the stenotic left anterior descending coronary The “giant” T-waves followed the transient development of ⫹ST, LAH, and RBBB in our patient (Fig. 1). This sequence of ischemic manifestation, noted in a single case, is not expected to shed light in the still raging controversy as to which (⫹ST or “giant” T-waves) constitutes the earlier ECG signs of severe transmural ischemic ingury. However, the ⫹ST in conjunction with LAH and RBBB and the “giant” T-waves were seen in such tempo-

ral proximity, so that they both may represent ECG manifestations of early ischemia. Also the fact that all the above ECG changes, which were noted in our patient in response to EST, have been previously registered in patients with acute MI (11,12), variant angina culminating in MI (13), and unstable angina (14), may indicate that the electropysiological manifestations for all ischemic syndromes may be qualitatively similar at their outset, and only the extent, and duration may be the determinants of the later ECG manifestations. Finally, the increase of ⫹ST amplitude in leads V1–V3, which was noted during the abrupt disappearance of RBBB and LAH (Fig. 2) can be attributed to the removal of the “subtraction effect” (a modulating function) of the RBBB on the amplitude of ⫹STs in the right precordial leads, previously described in patients with acute MI and intermittent RBBB (15).

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