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A 59-year-old woman with hypertension, hyperlipidemia, and gastroesophageal reflux reported exertional angina that resolved with rest and nitroglycerin. Nuclear stress test results revealed a small, reversible inferior-wall defect and a left ventricular ejection fraction (LVEF) of 0.67. A coronary angiogram showed diffuse 3-vessel disease. The patient underwent elective 4-vessel coronary artery bypass grafting (CABG) with no complications and was extubated the next day. On postoperative day 2, a routine electrocardiogram (ECG) showed an rSr′ pattern in leads V1 and V2, and ST-segment elevation (STE) in leads V2 through V4 (Fig. 1).

Fig. 1. Fig. 1. Fig. 1.
Fig. 1

Citation: Texas Heart Institute Journal 46, 2; 10.14503/THIJ-18-6783

The patient reported no chest pain or dyspnea and had no murmurs, gallops, or rubs. A bedside echocardiogram showed preserved LVEF and no wall-motion abnormalities. Her initial troponin I level of 29.74 ng/mL decreased to 19.05 ng/mL 12 hours later.

The ECG shows which of the following?

  • A) Brugada phenocopy

  • B) Brugada type 2 pattern

  • C) Pericarditis

  • D) Acute anterior STE myocardial infarction (STEMI)

Focus on ECGs: Answer #18

Answer

C) Pericarditis.

The ECG shows concave STE in leads V2 through V4, and mild reciprocal ST-segment depression and PR elevation in lead aVR (Fig. 2), probably signifying postsurgical pericarditis.

Fig. 2. Fig. 2. Fig. 2.
Fig. 2

Citation: Texas Heart Institute Journal 46, 2; 10.14503/THIJ-18-6783

Brugada ECG patterns are classified as type 1 (a coved STE pattern >2 mm in leads V1 through V3 followed by a negative T wave) and type 2 (a saddleback STE pattern >2 mm).1 Either pattern can be seen in patients with Brugada phenocopy, a phenomenon in which a true congenital Brugada syndrome is not present. The diagnostic criteria for Brugada phenocopy include the following2,3: a type 1 or 2 Brugada pattern and a medical condition to explain it, resolution of that pattern when the underlying condition resolves, no symptoms (such as syncope), no family history suggesting Brugada syndrome, and negative provocative testing with a sodium-channel blocker.

Although our patient had saddleback STEs in lead V2, her clinical presentation was more consistent with pericarditis. In addition, rSr′ patterns in Brugada type 2 indicate different phenomena. Benign patterns, typically when the initial r wave is taller than r′, occur in athletes, pectus excavatum, or partial right bundle branch block, and after higher chest-lead placement of electrodes V1 and V2. In pathologic rSr′ patterns (as in right ventricular enlargement or arrhythmogenic dysplasia, Wolff-Parkinson-White syndrome, or hyperkalemia), r′ tends to be taller than r.4 Furthermore, the β angle (which the r′ wave makes with the ST segment) can be used to diagnose type 2 Brugada syndrome by measuring the duration of the base of the triangle of r′ at 5 mm from the high takeoff. A β angle >3.5 mm suggests type 2 Brugada syndrome,1 and our patient's pattern did not meet this criterion.

Acute STEMI was excluded: the patient was hemodynamically stable without chest pain and had preserved LVEF, normal wall motion, and decreasing troponin I levels (their elevation was probably secondary to recent CABG). Before her discharge from the hospital, the ST changes in the anterior leads resolved (Fig. 3).

Fig. 3. Fig. 3. Fig. 3.
Fig. 3

Citation: Texas Heart Institute Journal 46, 2; 10.14503/THIJ-18-6783

References

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    Bayes de Luna A
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    GoldwasserD
    , et al. Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report [published erratum appears in J Electrocardiol 2013;46(1):76]. J Electrocardiol2012;45(
    5
    ):433–42.

  • 2.

    Perez-Riera AR
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    ):1976–8.

  • 3.

    Ferrando-Castagnetto F
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    Brugada phenocopy as a dynamic electrocardiographic pattern during acute anterior myocardial infarction. Ann Noninvasive Electrocardiol2016;21(
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  • 4.

    Baranchuk A
    ,
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    Differential diagnosis of rSr′ pattern in leads V1-V2. Comprehensive review and proposed algorithm. Ann Noninvasive Electrocardiol2015;20(
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    ):7–17.

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Contributor Notes

Section Editors: Yochai Birnbaum, MD, FACC, Mohammad Saeed, MD, FACC, James M. Wilson, MD

From: Section of Cardiology, Department of Medicine (Drs. Birnbaum and Borgaonkar), Baylor College of Medicine; and Department of Cardiology, Texas Heart Institute and Baylor–St. Luke's Medical Center (Dr. Birnbaum); Houston, Texas 77030

Address for reprints: Sanket Borgaonkar, MD, Suite 1100D, 6620 Main St., Houston, TX 77030, E-mail: sanket.borgaonkar@bcm.edu