Middle-Aged Man With an Incidental ECG Abnormality

March 12, 2011

A 44-year-old man presents for a preemployment physical examination. He is healthy, and he currently takes no long-term medications. A detailed review of systems reveals no ischemic chest pain, dyspnea with exertion, orthopnea, or any other symptoms of either coronary artery disease (CAD) or heart failure.

A 44-year-old man presents for a preemployment physical examination. He is healthy, and he currently takes no long-term medications.

HISTORY

A detailed review of systems reveals no ischemic chest pain, dyspnea with exertion, orthopnea, or any other symptoms of either coronary artery disease (CAD) or heart failure. The patient does not smoke. He plays a round of golf weekly and participates in activities such as company softball games without any symptoms. He reports that his uncle “died of a heart attack” at the age of 54.

PHYSICAL EXAMINATION

The patient weighs 72 kg (159 lb). Vital signs are normal, including blood pressure (108/72 mm Hg). Results of the cardiac and pulmonary examinations are normal.

LABORATORY, IMAGING, AND ECG RESULTS

The hemogram, serum chemistry values, and glucose level are all normal. Total cholesterol level is 159 mg/dL, with a low-density lipoprotein cholesterol level of 90 mg/dL and a high-density lipoprotein cholesterol level of 51 mg/dL. A chest radiograph is normal, and results of a purified protein derivative skin test are negative.

An ECG reveals normal sinus rhythm and a QRS axis of +60°. The only abnormality is a J-point elevation of 0.23 mL in the inferior leads. Troponin levels are normal. The ECG is essentially identical 5 weeks later.

(Answer and discussion on next page)

CORRECT ANSWER: D

Poll Results

Online Poll

Powered By

WebsiteGear

: Requires Javascript Enabled On Your Browser.


The patient exhibits early repolarization (elevation of the QRS-ST junction, or J point) in leads other than V1 through V3. In the past, J-point elevation, particularly in leads V1 through V3 and in young persons, was considered an innocent finding.1 More recent studies have linked J-point elevation, especially in leads other than V1 through V3, to an increased risk of ventricular fibrillation.2-4

One recent study recorded incidence, epidemiology, and prognosis with a 30-year follow-up.5 The findings were impressive and seem to indicate that J-point elevation is an independent and significant cardiac risk factor. Among the more than 10,000 patients who were followed up in the study, the incidence of inferior lead J-point elevation was about 4%, while that of lateral lead J-point elevation was about 2.5%. The mean age at initial diagnosis was 44 years, and the group was normotensive and had the same risk factors as the “control” population without early repolarization.

THE TAKE-HOME MESSAGE:

J-point elevation, particularly in the inferior leads, seems to be an independent risk factor for arrhythmia, cardiac death, and all-cause mortality. Specifics of pathophysiology and treatment require further study.

When study participants were followed up for death from cardiac causes, ventricular arrhythmias, and all-cause mortality, a statistically significant risk was independently attributed to the presence of J-point elevations. In particular, an inferior location and an elevation of greater than 0.2 mL were associated with a relative risk of arrhythmia-related death of 3.94, cardiac death of 4.92, and all-cause death of 2.24. These risks surpass those of ECG evidence of left ventricular hypertrophy and the ECG finding of prolonged QT interval.5 Thus, choice D is correct here. The Kaplan-Meier curves are impressive, and the reader is referred to the reference for review.

The mechanism by which the ECG finding of J-point elevation becomes a marker for adverse prognosis remains poorly understood for now. It appears that early repolarization is a stable phenomenon rather than a fluctuating one, since most patients, like the man in this case discussion, show the same pattern on long-term, serial ECGs. The leading hypothesis is that J-point elevation is a marker for some cellular-level structural defect that results in a tendency for abnormal ventricular repolarization and arrhythmogenicity, either alone or in conjunction with ischemic disease that develops later in life.

Aggressive diagnostic evaluation for CAD (choice B) is not appropriate here. A careful history taking revealed no evidence of classic or, for that matter, unstable angina. The patient is able to exert himself quite strenuously without any anginal or heart failure symptoms. Moreover, the risk associated with J-point elevation seems more related to arrhythmias and electrophysiological instability than to an increase in the development of ischemic disease.

Beta-blocker therapy and avoidance of startle situations (choice C) are useful in the treatment of another electrophysiological disorder-prolonged QT interval. This condition is currently better understood than J-point elevation; it is a disorder of ion channel physiology in the myocardium. This patient, however, has on 2 occasions had a normal QT interval; thus, choice C is not the best answer here.

Outcome of this case. Because there is currently no evidence-based specific therapy for J-point elevation, this patient will be carefully monitored at 4- to 6-month intervals. It is hoped that in time the specific pathophysiology that predisposes to arrhythmia and to all-cause cardiac death will be defined and will be amenable to treatment and prevention.

References:

REFERENCES:



1.

Klasky AL, Oehm R, Cooper RA, et al. The early repolarization normal variant electrocardiogram: correlates and consequences.

Am J Med.

2003;115:171-177.

2.

Haïssaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization.

N Engl J Med.

2008;358:2016-2023.

3.

Nam GB, Kim YH, Antzelevitch C. Augmentation of J waves and electrical storms in patients with early polarization.

N Engl J Med.

2008;358:2078-2079.

4.

Rosso R, Kogan E, Belhassen B, et al. J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: incidence and clinical significance.

J Am Coll Cardiol.

2008;52:1231-1238.

5.

Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with early repolarization on electrocardiography.

N Engl J Med.

2009;361:2529-2537.

FOR MORE INFORMATION:

•  Baggish AL, Hutter AM Jr, Wang F, et al. Cardiovascular screening in college athletes with and without electrocardiography.

Ann Intern Med.

2010;152:
269-275.