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Unexpected Low Voltage on an ECG

A registry study of hypertrophic cardiomyopathy (HCM) patients and elite athletes in Italy revealed low voltage on ECG is not uncommon in HCM and may be a marker for more left ventricular scarring on cardiac imaging — and a poor prognosis.

By Michael H. Crawford, MD. Professor of Medicine, Lucy Stern Chair in Cardiology, University of California, San Francisco.

SYNOPSIS: A registry study of hypertrophic cardiomyopathy (HCM) patients and elite athletes in Italy revealed low voltage on ECG is not uncommon in HCM and may be a marker for more left ventricular scarring on cardiac imaging — and a poor prognosis.

SOURCE: Pelliccia A, Tatangelo M, Borrazzo C, et al. Low QRS voltages and left ventricular hypertrophy: A risky association. Eur J Prev Cardiol 2023; Feb 13:zwad035. doi: 10.1093/eurjpc/zwad035. [Online ahead of print].

Low voltage on ECG (LVE) raises concerns about pericardial effusion and infiltrative cardiac diseases. Recently, LVE has been associated with arrhythmogenic cardiomyopathy, which is relevant to athlete health screenings since this condition is a contraindication to exercise.1 In this context, there is little known about the incidence and significance of LVE in athletes and patients with hypertrophic cardiomyopathy (HCM), which is the leading medical cause of athlete sudden death.2

Pelliccia et al performed a retrospective, observational study of HCM patients from Policlinico Casilino, a hospital in Rome, and athletes from the Institute of Sport Medicine and Science, also in Rome. There were 197 HCM patients evaluated by ECG and cardiac MRI with genetic testing in selected patients (n = 47). The mean age was 58 years, and 60% were men. Patients with evidence of other conditions that could affect the heart or previous septal ablation or myectomy were excluded. There were 771 elite athletes evaluated before their participation in the Olympics by ECG, exercise ECG, and Doppler echocardiography (mean age, 23 years; 55% men). Only four athletes had undergone cardiac MRI.

The authors defined LVE as the amplitude of the QRS complex measured from the nadir to the zenith of the QRS < 0.5 mV in the limb leads, < 1.0 mV in all precordial leads, or SV1 + RV5 or V6 < 1.5 mV. All study subjects received phone follow-up calls for one to nine years. The authors found LVE in 11% of HCM patients. They did not find any difference in clinical characteristics, such as age, sex, blood pressure, or body mass index (BMI), between those with and without LVE. However, subjects who showed LVE recorded a larger extent of late gadolinium enhancement (LGE) on cardiac MRI (4.1 affected segments vs. 1.5 affected segments; P < 0.001).

During the mean 4.5-year follow-up period, LVE was associated with more incidents of functional deterioration (31% vs. 14%; P = 0.038), stroke (22% vs. 6%; P = 0.008), and implantable cardioverter defibrillator (ICD) implantation (27% vs. 10%; P = 0.015). Among athletes, 2.3% recorded LVE, and they were older (27 years vs. 23 years; P = 0.005), heavier (BMI 25 kg/m2 vs. 22 kg/m2; P = 0.001), and more frequently had documented ventricular arrhythmias (28% vs. 8%; P = 0.008). One athlete was diagnosed with arrhythmogenic cardiomyopathy, but the other 17 did not experience any clinical events during follow-up. The authors concluded LVE is not uncommon in HCM and may carry clinical implications. However, this is rare in athletes and, in the absence of cardiac disease, seems benign.


COMMENTARY

It always is interesting to appreciate what one can do clinically with the lowly-but-ubiquitous ECG. This study likely was stimulated by the unexpected observation that some athletes meet criteria for LVE. Although rare, this observation led to the diagnosis of arrhythmogenic cardiomyopathy in one athlete, which may have been lifesaving because officials disqualified the athlete from sports participation. Arrhythmogenic cardiomyopathy is rare in Italy and elsewhere,3 but HCM is more common and the leading medical cause of sudden cardiac death in athletes. Since LVE had been described in HCM patients, Pelliccia et al hypothesized this may be of clinical value for two reasons. First, if only ECG screening is conducted in athletic programs, it may miss cases of HCM. Second, lower voltage in HCM may be of unfavorable predictive significance and presage the development of reduced left ventricular systolic function and heart failure. The first was true in that about 10% of HCM patients recorded LVE; if they had been evaluated for athletics, the diagnosis may have been missed. The second hypothesis is harder to prove because of the relatively short follow-up duration of this study. In athletes, LVE was associated with ventricular arrhythmias on exercise testing. However, few of the athletes had undergone cardiac MRI, so the full implications of this association are unknown.

These issues are important in Europe because the European Society of Cardiology recommends ECG screening for all athletes, followed by echocardiography if abnormalities are detected.4 Presumably, low voltage will be added to the list of abnormalities that occasion an echo. The American Heart Association does not recommend ECG screening of athletes unless clinically indicated, but some U.S. programs do it anyway.5 Pelliccia et al noted their study population largely was Caucasian Europeans involved in European sports. Namely, there were few Black individuals, and no one who played American football. Thus, the findings in the HCM patients perhaps are more important and suggest LVE be added to the list of predictors of adverse clinical events in HCM patients, such as severe symptoms, atrial fibrillation, and left ventricular outflow tract obstruction. In addition, HCM should be added to the list of conditions associated with LVE, such as amyloidosis and pericardial effusion.


REFERENCES

1. Zorzi A, Bettella N, Tatangelo M, et al. Prevalence and clinical significance of isolated low QRS voltages in young athletes. Europace 2022;24:1484-1495.

2. Malhotra A, Sharma S. Hypertrophic cardiomyopathy in athletes. Eur Cardiol 2017;12:80-82.

3. Johns Hopkins Medicine. Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C).

4. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243-259.

5. American Heart Association. Pre-participation cardiovascular screening of young competitive athletes: Policy guidance. September 2021.