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Journal of Electrocardiology Vol. 37 No. 3 2004

Giant R Wave, Convex ST-SegmentElevation, and Negative T Wave During

Exercise Treadmill Test

Case Report

Julian Ortega-Carnicer, MD

Abstract: The giant R wave syndrome is characterized by giant R waveaccompanied by widening of the QRS complex, marked ST segment elevation,QRS axis deviation, and the formation of monophasic QRS-ST complex withobliteration of S wave in leads facing the ischemic zone. This report describesa 65-year-old-man with variant angina who had a transient giant R wavesyndrome during an exercise treadmill test. Initially, at peak exercise, therewas a convex ST segment elevation ending in a negative T wave in the same(inferior) leads which showed giant R waves. Later, in the recovery period andcoinciding with an amelioration of myocardial ischemia, there was a lessmarked increase of R wave amplitude associated with concave ST segmentelevation and positive T wave in the inferolateral leads. Subsequently, a STsegment depression in the inferolateral leads preceded the ECG normalization.The patient had also a concave ST segment elevation and positive T wave ininferolateral leads during a spontaneous episode of variant angina at rest. Anemergency coronary arteriography showed a dominant right coronary arterywith an 80% and a 75% diameter stenosis of the middle and distal segment,respectively; the other arteries and left ventriculogram were normal. Theunderlying mechanisms of the different shapes of ST segment elevation and Twaveform in the setting of acute transmural myocardial ischemia are dis-cussed. Key words: Giant R wave, convex ST-segment elevation, negative Twave, exercise treadmill test, Prinzmetal angina, Brugada syndrome.

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The giant R wave syndrome is characterized byiant R wave accompanied by widening of the QRSomplex, marked ST segment elevation (ST-E),

From the Coronary Care Unit, Hospital Alarcos, Spain.Reprint requests: Julian Ortega-Carnicer, MD, Los Alisos 10.

3002-Ciudad Real Spain; e-mail: jortegacar@wanadoo.es.© 2004 Elsevier Inc. All rights reserved.0022-0736/04/3703-0012$30.00/0

a/j.electrocard.2004.04.005

231

RS axis deviation, and the formation of monopha-ic QRS-ST complex with obliteration of S wave ineads facing the ischemic zone. It may be observedarely following coronary artery occlusion fromcute myocardial infarction (1,2), variant anginauring exercise treadmill test (ETT) (3) or sponta-eously at rest (4–6), percutaneous transluminaloronary angioplasty (7), or experimental coronaryrtery ligation (5). I report a patient with variant

ngina who developed the giant R wave syndrome

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232 Journal of Electrocardiology Vol. 37 No. 3 July 2004

ssociated with convex ST-E followed by a negativewave during an ETT.

Case Report

A 65-year-old-man with previous history of typ-cal exertional angina of seven days duration wasdmitted to the Coronary Care Unit because ofubsternal chest pain lasting 10 minutes. His cardio-ascular risk factors included cigarette smoking andypertriglyceridemia, and absence of previousyocardial infarction or left ventricular aneurysm.

hysical examination was entirely unremarkable,ith blood pressure of 120/70 mm Hg and pulse of6 beats/min. The admission ECG (Fig. 1) takenithout chest pain showed normal sinus rhythm at

ig. 1. Baseline 12-lead ECGhowing isolated T wave in-ersion in lead III and aVF.

ig. 2. Serial selected leadsCG obtained during exercisereadmill test. HR � heartate. See text for description.

1 beats/min, frontal QRS axis about �80°, QRSidth of 0.06 s, and an isolated T wave inversion in

ead III and aVF. Therapy was begun with atenolol25 mg/12h), aspirin (250 mg), subcutaneous enox-parine (60 mg/12h) and intravenous nitroglycerin.Four days later, following discontinuation of theedication, the patient performed a graded ETTsing the standard Bruce protocol (Fig. 2). At thehird minute of exercise, the ECG showed an in-rease of the R wave voltage coinciding with oblit-ration of the S wave and slight ST-E in thenferolateral leads. At the fourth minute of exercise,t a heart rate of 95 beats/min (61% of maximalredicted heart rate) and a blood pressure of 180/00 mm Hg, the ECG (Fig. 3) demonstrated right-ard QRS axis deviation (�120°) causing giant Rave in leads II, III and aVF and deep S wave in

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Exercise Treadmill Test • Julian Ortega-Carnicer 233

eads I and aVL; QRS width of 0.10-0.11 s with aR’ pattern in V5-6; convex ST-E followed by neg-tive T wave (without isoelectric separation) ineads II, III, aVF and V5-6; and ST-depression ineads I, aVL, and V1-3. Although the patient deniedhest discomfort, the ETT was stopped and a sub-ingual nitroglycerin was administered. At the first

inute of the recovery period, at a heart rate of 72eats/min, the ECG showed further increase in Rave amplitude and convex ST-E in the inferolat-

ral leads. At the second minute of the recovery

ig. 3. Twelve-lead ECG recorded at the fourth minutef exercise showing rightward QRS axis deviation to120° and giant R waves associated with ST segment

levation in inferior leads. Note the convex ST segmentlevation ending in a negative T wave in leads II, III, aVFnd V5-6.

ig. 4. Twelve-lead ECG re-orded at the second minutef the recovery period dem-nstrating frontal QRS axisbout �105°, and prominent

waves associated with STegment elevation in inferioreads. Note concave ST seg-

ent elevation followed by aositive T waves in inferioreads.

eriod, at a heart rate of 67 beats/min, the ECGFig. 4) showed frontal QRS axis about �105°, QRSidth of 0.07-0.08 s, a decrease in the R wave

mplitude and a concave ST-E accompanied ofositive T wave in the inferolateral leads. At thehird minute of recovery phase, the ECG revealedeappearance of S wave, and upsloping ST segmentepression along with peaked upright T wave in thenferolateral leads. Finally, at 4 minutes after post-xercise phase, the ECG returned to baseline con-guration. The patient did not complain of anyhest pain throughout the ETT. Serial cardiac en-yme determinations were normal.Two days later, the ECG monitor showed an

symptomatic ST-E. The ECG (Fig. 5A) revealed theame appearance as in the second minute of theecovery period. Later, a sublingual nitroglycerineas administered and the ECG (Fig. 5B) returned to

he baseline configuration. An emergency coronaryrteriography showed a dominant right coronaryrtery with an 80% and a 75% diameter stenosis ofhe middle and distal segment, respectively; thether arteries and left ventriculogram were normal.wo coronary stents were deployed in the rightoronary artery. The patient made an uneventfulecovery and was discharged two days later onreatment with amlodipine and aspirin.

Discussion

This patient had two asymptomatic episodes ofransient inferolateral ST-E during an ETT andpontaneously at rest. Since the patients with Prin-metal’s angina may have painless attacks of myo-ardial ischemia (8) and a 30% of transient ST-E

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234 Journal of Electrocardiology Vol. 37 No. 3 July 2004

uring ETT (9), I believe that a coronary spasmuperimposed on an atherosclerotic lesion in theominant right coronary artery could be responsi-le of the ECG findings recorded in this patient. Theresent patient and the case reported by Jim et al.3) showed striking ECG resemblances during theTT, especifically related with changes in ST seg-ent morphology and T waveform. Initially, at

eak exercise, there was a convex ST-E ending in aegative T wave in the same (inferior) leads whichhowed giant R waves. Later, in the recovery periodnd coinciding with an amelioration of myocardialschemia, there was a less marked increase of Rave amplitude associated with concave ST-E andositive T wave in the inferolateral leads. Subse-uently, a ST segment depression in the inferolat-ral leads preceded the ECG normalization. Theresent patient had also a concave ST-E and posi-ive T wave in inferolateral leads during a sponta-eous episode of variant angina at rest.Transient giant R wave syndrome associated with

onvex ST-E and negative T wave due to acute

ig. 5. Twelve-lead ECG recorded during an asymptom-tic episode of myocardial ischemia at rest reveals con-ave ST segment elevation accompanied of positive Taves in inferior leads (A). After sublingual nitroglycer-

ne, the ECG returned to the baseline configuration (B).

ransmural myocardial ischemia has not received s

elevant and specific comments in the literature,ut I have found several illustrations from pub-ished works showing similar ECG changes duringTT (10,11), acute myocardial infarction (1,12,13),ariant angina (4–6,14), percutaneous translumi-al coronary angioplasty (15), experimental coro-ary artery ligation (5), or certain nonischemiconditions, as the injection of potassium into theoronary arteries (5). In the absence of giant Rave, acute myocardial ischemia causing J wave,

onvex ST-E and negative T wave in the rightrecordial leads may simulate the Brugada syn-rome—a hereditary cardiac disease (with a geneutations affecting cardiac sodium channel func-

ion) characterized by a prominent J wave followedy an elevated coved or occasionally saddle-back STegment and a negative T wave in right precordialeads, and high risk of sudden cardiac death inatients with structural normal heart (16). Isch-mia-induced ECG abnormalities mimicking Bru-ada pattern has been described rarely in associa-ion with the hyperacute phase of right ventricularnfarction or ischemia (17,18), but I have also foundwo additional cases published by Lew et al. (19)nd Surawicz et al. (15) showing transient J wave,onvex ST-E and negative T wave in right precor-ial leads during transmural myocardial ischemiaecondary to ETT and percutaneous transluminaloronary angioplasty, respectively.The clinical significance of the shape of ST-E

convex or concave type) in patients with transmu-al myocardial ischemia is not well established. Inatients with reperfused acute anterior myocardialnfarction, using the shape of ST-E in lead V3,osuge et al. (20) reported that left ventricular

unction was relatively poor in patients with con-ex type ST-E, and excellent in those with concaveype at discharge. In contrast, in patients with prior

wave myocardial infarction and ST-E during ETT,abuchi et al. (21) reported that the concave ST-E

ad a higher incidence of stenosis of the infarct-elated artery and myocardial ischemia in the in-arct region. In this patient and the case reported byim et al. (3), the occurrence of convex ST-Ecompanied by giant R wave and broadening of theRS complex at peak of ETT and their disappear-nce with the amelioration of myocardial ischemiauggests that this ECG pattern is an accompanimentf the severe myocardial ischemia.The underlying mechanisms of the different

hapes of ST-E and T waveform in the setting ofcute transmural myocardial ischemia are unclear,ut I hypothesized that the ECG similitude betweenhe acute myocardial ischemia and the Brugada

yndrome might have a similar mechanism. It has

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Exercise Treadmill Test • Julian Ortega-Carnicer 235

een reported that acute myocardial ischemiaauses an increase of extracellular K� with mem-rane depolarization, depletion of intracellular ATP,nd action potential shortening (22). Reduced levelf ATP due to hypoxia activate IKATP (22–24). Dueo greater ATP sensitivity of IKATP in epicardium25), together with a large transient outward K�

urrent (Ito)-mediated notch (spike and dome)26), the epicardial action potential dome or pla-eau is suppressed and action potential duration isbbreviated much more than in the endocardium27). Because the ST segment corresponds tempo-ally to the action potential plateau phase, theifference in plateau potentials within the ventri-les results in a pronounced ST-E (28,29). Completeoss of the epicardial action potential dome may beccompanied by a prolongation of the epicardialction potential, which lead to the development ofconvex ST-E and inversion of T wave (30,31).In conclusion, the giant R wave syndrome may

ccur in conjunction with convex ST-E and nega-ive T wave during severe attacks of acute transmu-al myocardial ischemia.

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