Nigerian Journal of Cardiology

ORIGINAL ARTICLE
Year
: 2020  |  Volume : 17  |  Issue : 2  |  Page : 120--127

Electrocardiographic changes among elite athletes in Port Harcourt, Nigeria


Kanayo Mercy Odia1, Kenneth Chimbuoyim Anugweje2, Victor Datonye Dapper1, Osaretin James Odia3,  
1 Department of Human Physiology, College of Health Sciences, University of Port Harcourt, Port Harcourt, Nigeria
2 Institute of Sports, University of Port Harcourt, Port Harcourt, Nigeria
3 Department of Medicine, College of Health Sciences, University of Port Harcourt, Port Harcourt, Nigeria

Correspondence Address:
Prof. Victor Datonye Dapper
Department of Human Physiology, College of Health Sciences, University of Port Harcourt, PMB 5323, Port Harcourt
Nigeria

Abstract

Background: Due to cardiac adaptations in athletes, the normal electrocardiogram (ECG) may be altered and abnormal patterns occur. Cardiovascular-related sudden death is a leading cause of mortality during sports. ECG interpretation in athletes therefore requires careful analysis to properly distinguish changes due to physiological adaptations from those suggestive of underlying pathology. The present study describes ECG changes and attempts to identify possible adaptive and maladaptive changes among a cohort of elite athletes of different sports in Port Harcourt, Nigeria. Subjects and Methods: Cross-sectional prospective study involving 339 subjects (16–35 years) comprising 170 athletes (63 males and 107 females) and 169 nonathletes (74 males and 95 females) serving as control were recruited. Anthropometric parameters and blood pressure indices were determined and physical examination conducted to exclude associated comorbidities. Electrocardiographic parameters were determined through standard procedure using a resting 12-lead ECG. Results: No significant differences were observed for anthropometric parameters and blood pressure indices between male athletes and male nonathletes; although, female athletes had significantly higher weight and body mass index than female nonathletes. Irrespective of gender, athletes had significantly lower heart rate, T-axis and significantly higher QT-intervals compared to nonathletes; with lower P-axis and higher PR-interval among male athletes compared to male nonathletes. The left ventricular hypertrophy was the most prevalent abnormality among athletes. Conclusion: Changes described are due majorly to physiologic adaptation. However, some mal adaptations suggestive of risk factors for possible sudden cardiac death were identified. We advise sports physicians to carefully interpret ECG features of athletes to distinguish physiological changes related to athletic conditioning from findings suggestive of pathology.



How to cite this article:
Odia KM, Anugweje KC, Dapper VD, Odia OJ. Electrocardiographic changes among elite athletes in Port Harcourt, Nigeria.Nig J Cardiol 2020;17:120-127


How to cite this URL:
Odia KM, Anugweje KC, Dapper VD, Odia OJ. Electrocardiographic changes among elite athletes in Port Harcourt, Nigeria. Nig J Cardiol [serial online] 2020 [cited 2021 Dec 5 ];17:120-127
Available from: https://www.nigjcardiol.org/text.asp?2020/17/2/120/330417


Full Text



 Introduction



In athletes, the normal electrical activity of the heart may be altered and deviated patterns easily observable in the routine electrocardiogram (ECG): These alterations have been attributed to physiologic cardiac adaptation occurring as a consequence of systemic, regular, and consistent physical training.[1] Furthermore, cardiovascular-related sudden death continues to be a leading cause of mortality during sports.[2] Reports describing the sudden death of young apparently healthy athletes during an active sporting event continues to be a challenge to cardiologists working with athletes.[3],[4],[5] Previous reports from Nigeria[6] has caused a measure of national embarrassment and mourning.

The ECG is a practical tool that records the electrical activity of the heart. It is one of the simplest tools used to assess overall cardiac function and detect the presence of cardiovascular abnormalities.[7] Clearly, ECG interpretation in athletes requires careful analysis to properly distinguish physiological changes related to athletic conditioning of the heart from findings suggestive of an underlying cardiac pathology.[8] Among others, previous reports from our center have focused on QRS axis deviations among pregnant Nigerian women[9] and the effect of body mass index (BMI) on some ECG parameters in young adults.[10]

The present study describes values for some important ECG parameters among elite athletes in Port Harcourt, Nigeria, as compared to apparently healthy nonathletes of similar age and gender. This is with the view of identifying both adaptive and maladaptive ECG features suggestive of underlying cardiac pathology among our elite athletic population. This we hope would also help sports physicians reduce the occurrence of cardiovascular related sudden death among athletes in our environment most of which go unreported.

 Subjects and Methods



Ethical approval was obtained from our Institutional Research Ethics Committee. Participation was entirely voluntary. The study was carried out over a period of 19 months from November 2016 to June 2018. The objective and nature of the study was explained and informed consent was sought and obtained from each participant before recruitment into the study. The study was conducted in accordance with the Helsinki Declaration of 1975 as amended in 2000.[11]

Subjects

Using the Morris' formula for small (hyper geometric) population,[12] the minimum suitable sample size was estimated to be 118 subjects. Therefore, a total of 339 subjects consisting of 170 athletes (63 males and 107 females) and 169 nonathletes (74 males and 95 females) serving as controls were recruited into the study. The study was a cross-sectional prospective study. Subjects were aged between 16 and 35 years. All subjects were Nigerians by birth comprising predominantly of subjects from the various ethnic nationalities in Southern Nigeria. All athletes were elite athletes involved in competitive sports for at least 1 year. All athletes of the Sports Institute, University of Port Harcourt and Rivers State Sports Council, Port Harcourt, Nigeria, who voluntarily gave informed consent and met the inclusion criteria were recruited into the study. All nonathletes were randomly selected from among apparently healthy undergraduate students of the University of Port Harcourt, Nigeria. Attempt was made to match athletes and nonathletes for sex, age, and BMI.

Subjects with positive history and clinical features suggestive of heart disease, hypertension and/or diabetes were promptly excluded from the study. Subjects with recent history of ill health including episodes of stooling, vomiting, and recent intravenous fluid therapy or blood transfusion within 3 months of the study were also excluded from the study. All subjects, especially athletes, who admitted to positive history of taking anabolic steroids were promptly excluded from the study. Subjects who gave a positive history of alcohol consumption (more than 8 pints of beer or more than 1 pint of spirit) within the past 2 weeks were excluded from the study. As defined by Centers for Disease Control and Prevention, 1992,[13] all current, previous or occasional smokers were also excluded from the study. Febrile subjects and subjects on inotropic agents were also excluded from the study.

Determination of anthropometric parameters and blood pressure indices

Standard heights without shoes and weights wearing light clothes of all participants were measured in meters (m) and kilograms (kg) respectively using a standard scale (Seca model). BMI was calculated by dividing body weight in kilogram by the square of the height in meter (kg/m2). In all subjects, diastolic blood pressure (DBP) and systolic blood pressure (SBP) were measured manually using a standard mercury sphygmomanometer with an appropriate cuff size. On arrival, subjects were allowed to rest on a comfortable chair for about 30 min before blood pressure measurement. During measurements, readings were taking until two consecutive similar measurements were obtained. The blood pressure measurements were determined from the right upper arm by the same observer with the subject seating comfortably and left arm resting on a table at the level of the heart. The SBP was regarded as the first phase of the Korotkoff sound, whereas the fifth phase was regarded as the DBP. The mean arterial pressure (MAP) was calculated using the formula: MAP = (SBP + 2DBP)/3.

Determination of electrocardiographic parameters

A thorough physical examination was next conducted to exclude the presence of associated co-morbidities. A Cardiovit AT-2plus model (Schiller AG, Altgasse 68 CH-6341, Bear Switzerland) standard resting 12 – lead electrocardiographic machine with a paper speed of 25 mm/s and standardized at 0.1 mV/mm was used for the determination of ECG parameters.

Subjects were allowed to relax in supine position at least 10 min on the examination couch before determination of ECG. No form of physical activity or routine training was allowed prior to determination of ECG. The limb leads were then appropriately fastened to the limbs after application of a nonirritant electrode gel. The chest leads were also placed on the chest wall on identifying its different placement positions according to the recommendations of the American Heart Association and the American College of Cardiology.[14],[15] The ECG was then determined for each subjects and appropriate tracings obtained. All recordings were done by the same person.

For all subjects, the heart rate, P-axis, QRS-axis, T-axis, PR-interval, QRS-interval, and QT-interval were automatically determined by the electrocardiograph machine and the values recorded. The QT-intervals were corrected for heart rate (QTc) using Bazett's formula to obtain the value for each subject.[16] A QTc- interval was considered abnormally prolonged if ≥470 ms.[17] The presence of right ventricular hypertrophy, left ventricular hypertrophy, right atrial hypertrophy, left atrial hypertrophy, cardiac ischemia, and sinus arrhythmia were next determined from the ECG tracing of each subject using the Seattle criteria.[8] The right ventricular hypertrophy was defined by the sum of the R-wave in V1 and the S-wave in V6 exceeding 1.05 mV. The left ventricular hypertrophy was calculated using Sokolow–Lyon voltage criteria (sum of amplitude of the S-wave in lead V1 and the R-wave in lead V5 or V6 ≥3.5 mV).[18] Right atrial hypertrophy was defined as a P-wave voltage ≥0.25 mV. The left atrial hypertrophy was defined as a biphasic P-wave in V1 where the terminal portion was more negative than − 0.1 mV and ≥4.0 m in duration. Ischemia was regarded as T-wave inversion or ST-segment depression ≥2 mm in more than 2 contiguous leads other than leads V1, aVR, and III. Sinus arrhythmia was determined as a variation of P-P interval, from one beat to next, at least 120 ms.

The ECG changes particular to athletes were next determined from the ECG tracings obtained from each subject. These were divided into common (adaptive) and uncommon (maladaptive) features using the Seattle criteria.[8] The common (adaptive) ECG features were determined thus: adaptive left ventricular hypertrophy was defined as QRS-voltage criteria for the left ventricular hypertrophy in isolation without any other accompanying ECG changes. Sinus bradycardia is determined on the ECG when there is a normal upright P-wave in lead II preceding every QRS-complex with a ventricular rate of <60 beat per minute. ST-segments elevation refers to an ST-segment that is abnormally high above the baseline. The left axis deviation was defined as a QRS-axis more negative than −30° and right axis deviation as a QRS-axis more positive than +120°. A PR interval ≥200 ms was considered as first-degree atrioventricular (AV) block. Early repolarization pattern was defined as an elevation of the QRS-ST (J-point) ≥0.1 mV from baseline in at least two peripheral or precordial leads. Short QT-interval is defined as QT-interval ≤330–340 ms.[1],[8] The uncommon (maladaptive) ECG features were determined as follows: abnormal left ventricular hypertrophy was defined here as left ventricular hypertrophy accompanied by other ECG changes such as left atrial hypertrophy, left axis deviation, ST-segment depression, T-wave inversion, or pathological Q-waves; repolarization abnormality was determined from the ECG tracings as abnormalities in ST-segment (ST-segment elevation) and T-wave (inverted T-wave). A Q-wave was considered abnormal (pathological Q-wave) if it exceeded 4 ms in duration and/or if the depth of the Q-wave exceeded 25% of the height of the R-wave. Left bundle branch block was defined as QRS duration ≥120 ms, whereas an RSR' pattern in anterior precordial leads of ≥120 ms was consistent with complete right bundle branch block (RBBB) or RSR' pattern in V1 <120 ms consistent with incomplete RBBB. Atrial fibrillation is defined as a quivering or irregularly irregular ventricular rate (arrhythmia) with absence of P-wave and baseline is characterized by either fibrillatory waves ranging from 300 to 600 waves per minute or just minute oscillations.

All abnormal ECGs were repeated in order to minimize methodological errors. All ECG tracings were interpreted by a single observer and then cross checked for accuracy independently by a trained cardiologist with requisite experience in ECG interpretation. The ECG findings in athletes were all interpreted using the Seattle Criteria as a standardized ECG tool.[8]

Statistics

Results obtained are presented as mean ± standard deviation or as proportions where appropriate. The analysis was made using SPSS version 20.0 statistical package (IBM, Armonk, New York, USA). The Z-test was used to compare continuous variables while the categorical variables were analyzed using Chi-square test or two-tailed Fisher's exact test (when expected cell frequencies were <5). Variance was set at infinity and a P < 0.05 was considered statistically significant.

 Results



The values of age and various anthropometric parameters: height, weight, BMI, and blood pressure indices: SBP, DBP and MAP are presented in [Table 1]a for all athletes and nonathletes and in [Table 1]b and [Table 1]c for male and female athletes and nonathletes, respectively. The values for heart rate, P-axis, T-axis, QRS-axis, as well as PR-interval, QRS-interval, QT-interval, QTC–interval, are as presented in [Table 2]a and [Table 2]b for male and female athletes and nonathletes respectively. Similarly, the prevalence of some common ECG abnormalities is as shown in [Table 3]a and [Table 3]b for male and female athletes and nonathletes respectively. Finally, the prevalence of some adaptive and mal adaptive ECG features of chronic exercise among athletes is presented in [Table 4] and [Table 5] for male and female athletes and nonathletes, respectively.{Table 1}{Table 2}{Table 3}{Table 4}{Table 5}

Expectedly, athletic subjects were only found to have significantly higher height, weight, and BMI compared to nonathletic subjects (P < 0.05); with no significant differences in age and blood pressure indices between athletes and nonathletes (P > 0.05). No significant differences were observed for age, weight, BMI, and the blood pressure indices between male athletes and male nonathletes (P > 0.05); however, male athletes were found to be significantly taller than male nonathletes (P < 0.05). By comparison, female athletes were found to have significantly higher weights and BMI compared to female nonathletes (P < 0.05). No differences were observed for age, height, and the blood pressure indices among female athletes and female nonathletes.

A comparison of the electrocardiographic parameters: Heart rate, P-axis, QRS-axis, T-axis, PR-interval, QRS-interval, QT-interval and QTc-interval is shown in [Table 2]a and [Table 2]b for male and female athletes and nonathletes, respectively. Irrespective of gender, athletes were found to have significantly lower heart rate and T-axis and significantly higher QT intervals compared to nonathletes (P < 0.05). However, a significantly lower P-axis and higher PR interval were observed only between male athletes and nonathletes (P < 0.05); suggesting possible gender variations for some ECG parameters investigated amongst our cohort of subjects. No significant differences were observed for QRS-axis, QRS-interval, and QTc-interval among athletes and nonathletes in both male and female subjects (P > 0.05).

Expectedly, as shown in [Table 3]a and [Table 3]b, male and female athletes showed a similar pattern of prevalence of some of the common ECG abnormalities investigated: left ventricular hypertrophy, sinus arrhythmia, and left atrial hypertrophy (P-mitrale). However, left ventricular hypertrophy was most prevalent and left atrial hypertrophy least prevalent among athletes of both gender. Despite the essentially similar pattern observed for nonathletes (male and female) as compared to athletes (male and female) in the present study: Chi-squared analysis did not show any significant association between athletic status and the prevalence of some common ECG abnormalities investigated among either male or female subjects involved in the present study (P > 0.05); reducing the possibility of gender variations for these parameters.

The five most prevalent adaptive electrocardiographic features of chronic exercise seen among subjects in the present series are: adaptive left ventricular hypertrophy (using the isolated QRS voltage criteria), sinus bradycardia, T-wave inversion (the normal variant), sinus arrhythmia, and ST-segment elevation; while the corresponding five most prevalent maladaptive electrocardiographic features of chronic exercise are: abnormal left ventricular hypertrophy, repolarisation abnormality, left axis deviation, left atrial hypertrophy (P-mitrale), and ST-T elevation abnormality. The overall prevalence of the other ECG features (adaptive and maladaptive) of chronic exercise is summarized in [Table 4] and [Table 5], respectively. [Table 4] suggests possible gender variations of the adaptive features: adaptive left ventricular hypertrophy and sinus bradycardia being more prevalent among female athletes; while T-inversion (normal variant) and first-degree AV block being more prevalent among male athletes (P < 0.05). [Table 5] suggests a possible gender bias of the maladaptive features among our subject population: female athletes apparently having a significantly higher prevalence of abnormal left ventricular hypertrophy, repolarization abnormality, left axis deviation, and left atrial hypertrophy compared to male athletes (P < 0.05).

 Discussion



During the study, echocardiography services were not readily available at our center. We were therefore unable to immediately screen our subjects for the presence of other occult cardiac diseases. However, this limitation does not detract from the import our findings. Second, appropriate matching of each athletic subject with a nonathletic was a further limitation; however, statistical analysis showed an essentially similar pattern of interaction between age and BMI with the various ECG parameters investigated in both sexes among both our athletic and nonathletic population.

Expectedly, the present study describes a physiological bradycardia among our athletes irrespective of gender. This is typically true for athletes and serves as a physiologic adaptation to ensure a more efficient heart: with a larger stroke volume with fewer cardiac contractions during each cardiac cycle.[1],[8] The results also show significantly lower values of both P-axis among male athletes as compared to male nonathletes (P < 0.05). In the presence of structural remodeling, the P-wave morphology on a 12 lead ECG can be altered.[19] The P-wave axis is a routine measure reflecting the net vector component of atrial depolarization in the frontal plane and has been associated with the risk of atrial fibrillation.[19] Although the P-wave axis of male athletes fell within normal ranges (0°–+75°), it has significantly lower degrees when compared with that of nonathletes; implying that the electrical activity of the atrial chamber is tilted leftward in male athletes compared to male nonathletes. Noteworthy, results obtained from this study shows that in both male and female athletes, the T-wave axis has significantly lower values when compared to the corresponding values for either male or female nonathletes (P < 0.05).

PR-intervals in male athletes were significantly higher than male nonathletes (P = 0.001). First-degree heart block is said to be present when the PR interval exceeds 200 ms in duration.[8] This first-degree AV or heart block is one of the common adaptive features found in athletes and is consistent with results found in the present study among male athletes.[8] QT-intervals in both male and female athletes were significantly higher than corresponding nonathletes (P = 0.001). QT interval is prolonged by training and long QT-syndrome is an inherited channelopathy that exposes athletes to a risk of sudden cardiac death. Since the QT-interval is also dependent on heart rate;[20] the identification of an inherited long QT interval and that arising from prolonged physical training is critical.[20],[21] QT-interval is longer in athletes than in nonathletes because of the lower resting heart rates associated with training. Noteworthy, the QTc-interval seen amongst athletes in the present study is within normal limits: despite being in the bounds of the upper limits of normal.[20],[21]

The Seattle Criteria continues to serve as a guide to distinguish adaptive and maladaptive ECG features in athletes and should be used to separate and identify these abnormal features in order to preempt risk factors of sudden cardiac death in athletes. When found in isolation, left ventricular hypertrophy is known to be a common adaptive ECG finding in athletes.[22] However, left ventricular hypertrophy if found along with pathologic Q-wave, inverted T wave at V4–V6, and/or left axis deviation is an abnormal nonadaptive feature and thus may pose a risk factor for sudden cardiac death. This study found 34% of athletes having the isolated left ventricular hypertrophy (adaptive left ventricular hypertrophy) and 27% of maladaptive left ventricular hypertrophy, i.e., left ventricular hypertrophy accompanied by other specified ECG changes according to the Seattle criteria.[8]

ECG features indicative of pathological left ventricular hypertrophy in the assessment of an athlete with a left ventricular wall thickness between 13 and 16 mm includes pathological Q-waves, ST-segment depression, left bundle branch block, and T-wave inversions in the lateral/inferior leads.[23] The present study found similar features: 2% pathological Q-waves, 2% complete left bundle branch block, 9% T-wave abnormality among others. Two subjects were also found to have a short QT-interval. We opine that these features are likely risk factors of arrhythmia which could be potential causes of sudden cardiac death among our subjects.[23] These particular subjects were referred for further evaluation and careful observation.

 Conclusion



The ECG changes found in this study are not only due to physiological adaptation but also include some mal adaptive features suggestive of potential risk factors for sudden cardiac death. We suggest routine ECG assessment of athletes and advise cardiologists and sports physicians to be cautious when interpreting ECG changes in athletes to properly determine changes due to physiological adaptation (remodeling) from changes due to maladaptation or pathology.[24] The study could be of value since previous reports in this regard have been relatively scarce.

Acknowledgment

The authors would like to acknowledge the assistance of Dr O. Maduka and Dr T. F. Ilodibia both of the University of Port Harcourt Teaching Hospital, Port Harcourt, Nigeria.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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