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Journal of Electrocardiolog

Hypothermia-induced Brugada-like electrocardiogram patternJulián Ortega-Carnicer, MD⁎, Juan Benezet, MD,

Patricia Calderón-Jiménez, MD, Jaime Yanes-Martín, MDIntensive Care Service, Hospital General de Ciudad Real, Spain

Received 12 January 2008

Abstract A patient in whom moderate hypothermia developed after prolonged cardiopulmonary resuscitation

⁎ CorrespondingE-mail address: jo

0022-0736/$ – see frodoi:10.1016/j.jelectroc

is described. Hypothermia was manifested by transient electrocardiogram changes, including longQT, precordial J waves, and downsloping ST-segment elevation ending in a negative T wave in leadsV1 and V2 resembling the Brugada syndrome. The physiopathologic mechanisms of theseelectrocardiographic findings are discussed.© 2008 Elsevier Inc. All rights reserved.

Keywords: Hypothermia; Brugada syndrome; J wave; Coved ST-segment elevation

Introduction

Although hypothermia has been listed as a cause ofBrugada-like electrocardiogram (ECG) pattern,1,2 clinicalcases of right precordial ST-segment elevation mimickingBrugada syndrome (BrS) have rarely been reported in thehypothermia setting.3,4 We report a patient with moderatehypothermia who developed a transient Brugada signcharacterized by precordial J waves and coved ST-segmentelevation ending in a negative T wave in leads V1 and V2.

Case report

A 78-year-old man with chronic obstructive pulmonarydisease was hospitalized after prolonged bystander resusci-tative effort for gasping. His relatives denied any previoushistory of malignant arrhythmias, syncope, or familyepisodes of sudden death. His family members did notshow any ECG pattern of BrS. On admission, the patientwas unconscious, bradycardic, bradypneic, and hypother-mic. There was also subcutaneous emphysema and absenceof left breath sound due to left tension pneumothorax. Herequired immediate intubation, intravenous adrenaline andatropine administration, fluid replacement, and decompres-sive thoracostomy tube insertion. After the procedure, theadmission ECG (Fig. 1A) recorded with an esophagealtemperature of 31.1°C showed normal sinus rhythm at 90

author. Tel.: +34 926 278000; fax: +34 926 278571.rtegacar@gmail.com

nt matter © 2008 Elsevier Inc. All rights reserved.ard.2008.05.001

beats/min, long QTc interval of 550 ms, and prominentJ wave followed by convex downsloping ST-segmentelevation ending in a negative in the right precordial leads,resembling a BrS. There was also a marked J wave inleads V3 to V6, characteristic of hypothermia. Initiallaboratory analysis revealed the following: glucose, 124mg/dL; sodium, 141 mEq/L; potassium, 4.2 mEq/L;magnesium, 2.3 mg/dL; calcium, 8.1 mg/dL; total protein,5.5 g/dL; creatinine, 1.8 mg/dL; urea nitrogen, 55 mg/dL;creatine kinase, 828 IU/L (MB fraction, 13.2 IU/L);troponin I, 0.11 ng/mL (normal limit value, b0.06ng/mL); white blood cells, 17.8 × 109/L, with 89.4%neutrophils; red blood cells, 4.7 × 1012/L; hematocrit,45%; hemoglobin, 14.9 g/dL; and platelet count, 244 ×109/L. Arterial blood gas values (FIO2, 1.0) were thefollowing: pH 7.35; PO2, 228 mm Hg; PCO2, 59.1.9 mmHg; and bicarbonate, 33.1 mEq/L. Two hours afteradmission, when the patient's temperature rose to 35.2°Cwith rewarming, a repeated ECG (Fig. 1B) revealed thedisappearance of J waves and ST-segment elevations.Brain CT scan was normal, and an echocardiogramdemonstrated minimal pericardial effusion and absence ofsegmental wall motion abnormalities. A peak serum ofcreatine kinase of 4216 IU/L was measured on day 2, withan MB fraction of 61.1 IU/L and a troponin I level of 0.45ng/mL. During the patient's hospitalization, all ECGs didnot reveal ST-segment elevation in the right precordialleads. Cardiac telemetry showed no malignant arrhythmias,and a provocation test with a sodium channel blocker foradequate evaluation of underlying BrS was not performed.

Fig. 1. Serial ECG on admission. (A) ECG obtained at an esophageal temperature of 31.1°C showing J wave and coved ST-segment elevation ending in anegative T wave in leads V1 and V2 simulating the Brugada syndrome. Also note the presence of J wave in leads V3 to V6. (B) ECG recorded at an esophagealtemperature of 35.2°C revealing disappearance of both J waves and ST-segment elevations.

691J. Ortega-Carnicer et al. / Journal of Electrocardiology 41 (2008) 690–692

Four weeks later, he died of multiorganic failure. Therequest for an autopsy was denied.

Discussion

The BrS is characterized by a right precordial ST-segment elevation and a high incidence of sudden death inpatients with structural normal heart (ion channelcardiomyopathy).1,5-7 Although 3 ECG repolarizationpatterns in the right precordial leads are recognized, onlythe type 1 (coved ST-segment elevation ≥2 mm andinverted T wave) is diagnostic of BrS. This pattern can beobserved spontaneously or after the administration ofsodium channel blocks. Although hypothermia can produceJ waves associated with ST-segment elevations,8-10 wehave found only 2 case reports of hypothermia depictingECG changes in the right precordial leads simulatingBrS.3,4 Thus, Noda et al3 described a hypothermic patientwho had generalized J waves and a saddleback ST-segmentelevation in V2 only. Later, Ansari and Cook4 publishedone case of hypothermia showing a transient type 1Brugada sign in the right precordial leads, albeit withconcomitant severe diabetic ketoacidosis and hyperkalemia.In the absence of these metabolic and electrolyte dis-

turbances, our patient is the first reported case of a patientwith hypothermia who had transient precordial J wavesassociated with coved ST-segment elevation ending in anegative T wave in the right precordial leads, similar to thatseen in BrS. Conversely, hypothermia can also mask theECG manifestations of BrS. Thus, Tan and Meregalli11

reported a Brugada patient with ventricular fibrillation andwidespread ST-segment elevations after defibrillationwhose ST normalized when he was cooled to preservecerebral function.

Because the anatomical position of the right ventricle isless safe than the left ventricle in case of resuscitative effort(or external hypothermia), the elevated serum troponin Ilevels detected in our patient could be explained by a rightventricular injury during prolonged chest compressions.12

The electrophysiological mechanism by which hypother-mia may reveal Brugada pattern on ECG can be explainedby a moderate accentuation of the spike-and-domemorphology of the M and epicardial cells and a total lossof the epicardial action potential dome (plateau) leading toJ wave and coved ST-segment elevation, respectively.13-15

Thus, in a canine in vivo model of the BrS using regionalepicardial cooling of the right ventricular outflow tract,Nishida et al16 observed prominent notch and prolongation

692 J. Ortega-Carnicer et al. / Journal of Electrocardiology 41 (2008) 690–692

of the monophasic action potential in the epicardium,resulting in J-ST-segment elevation, T-wave inversion, andlong QT in the right precordial leads. Similarly, in a caninetissue model of BrS, reducing the temperature to 32°Cprolonged action potential duration and enhanced the phase1 notch of epicardial action potentials, whereas 40°Ccaused opposite changes.17 Also, in a canine arteriallyperfused right ventricle wedge preparation, Fish andAntzelevitch18 found that decreasing the temperature ofthe coronary perfusate to 29°C enhanced the epicardialaction potential spike and dome morphology, leading toheterogeneous loss of the epicardial action potential dome,phase 2 reentry within the epicardium, and ventriculartachycardia. The ionic mechanism of hypothermia-inducedJ-ST changes may be due to the effect of cold temperatureto slow the kinetics of activation of Ito less than the kineticsof the Ica.

19

In conclusion, right precordial coved ST-segment eleva-tion simulating BrS may be observed in susceptiblehypothermic patients, even in the absence of metabolic orelectrolyte disorders.

References

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