ECG Interpretation in Athletes




Introduction





  • Sudden death related to cardiovascular disorders is the most common cause of death among athletes during sports and exercise.



  • Genetic cardiovascular disorders, such as cardiomyopathies and ion channelopathies, are the primary causes of sudden cardiac death (SCD) in athletes.



  • Most of these disorders can be identified through characteristic changes on a resting 12-lead electrocardiogram (ECG)



  • The heart undergoes physiologic changes in response to regular exercise (so-called “athlete’s heart”).



  • These physiologic adaptations can manifest as changes seen on an ECG.



  • Analyzing the ECG of an athlete requires careful interpreta­tion to distinguish pathologic from physiologic patterns (see Fig. 34.1 ).




    Figure 34.1


    Normal ECG findings represent physiologic adaptations and do not require additional evaluation. Abnormal ECG findings may represent an underlying pathologic cardiac disorder and warrant further evaluation. Presence of two or more borderline findings warrants further evaluation, whereas a single borderline finding found in isolation and without other clinical markers of concern does not require additional testing.



  • The evolution of modern interpretation standards that account for the physiologic changes in an athlete’s ECG have greatly improved specificity (i.e., lowered the false-positive rate) while maintaining sensitivity to detect conditions at an increased risk for SCD.





Normal Cardiac Adaptations in Athletes


Introduction





  • Cardiac adaptations develop as a result of regular, sustained exercise.



  • Electrical manifestations of this on an ECG reflect increase in cardiac chamber size and/or vagal tone.



  • ECG findings related to increased cardiac chamber size include voltage criteria for left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH) as well as incomplete right bundle branch block (RBBB).



  • Findings consistent with increased vagal tone include early repolarization, sinus bradycardia, sinus arrhythmia, first-degree atrioventricular (AV) block, Mobitz type II second-degree AV block, as well as junctional and ectopic atrial rhythms.



Specific Findings Related to Physiologic Adaptations to Exercise





  • QRS voltage criteria for LVH




    • Definition: Sokolow–Lyon criteria: sum of the S wave in V1 and the R wave in V5 or V6 (using the largest R wave) as >3.5 mV



    • 64% of athlete ECGs will meet these criteria



    • Isolated finding with no other ECG abnormalities in <2% of individuals with hypertrophic cardiomyopathy (HCM)



    • When pathologic LVH is present such as in HCM, the voltage criteria for LVH are usually associated with other abnormal ECG findings (i.e., T-wave inversion, ST-segment depression, and pathologic Q waves).




  • QRS voltage criteria for RVH




    • Definition: Sokolow–Lyon criteria: R wave in V1 + largest S wave in V5 or V6 >10.5 mV



    • 13% of athletes meet these criteria



    • Very poor correlation with arrhythmogenic right ventricular cardiomyopathy (ARVC), pulmonary hypertension, or other RV pathology




  • Incomplete RBBB




    • Definition: QRS duration 100–120 ms with an RBBB pattern: terminal R wave in lead V1 (commonly characterized as an rSR’ pattern) and wide terminal S wave in leads I and V6



    • Caused by delayed conduction owing to physiologic increase in RV size




  • Early repolarization




    • Definition: elevation of the QRS-ST junction (J-point) by ≥0.1 mV often associated with late QRS slurring or notching (J wave), often affecting the inferior and/or lateral leads



    • Common in general population and more common in young, male, and black individuals



    • Available evidence suggests that all early repolarization patterns are normal in young athletes.




  • Repolarization in black athletes




    • Up to 13% of black/African athletes demonstrate specific repolarization variant: convex ST segment and J-point elevation in the anterior leads (V1–V4) followed by T-wave inversion (see Fig. 34.2 ).




      Figure 34.2


      ECG from a 17-year-old asymptomatic black athlete. ECG demonstrates J-point elevation with a convex “domed” ST segment elevation followed by T-wave inversion confined to leads V1–V4. This is a normal repolarization variant in black athletes.



    • No association with cardiomyopathy after 5-year follow-up evaluation



    • T-wave inversion that extends to lateral leads (V5–V6) should always be considered abnormal and warrants careful evaluation to exclude cardiomyopathy.




  • “Juvenile” ECG pattern




    • Definition: T-wave inversion in anterior precordial leads



    • T-wave inversions in V1–V3 in asymptomatic athletes aged <16 years (or prepubertal) should not trigger further evaluation.



    • T-wave inversion beyond V2 in those aged >16 years should raise concerns regarding ARVC.




  • Sinus bradycardia




    • Definition: heart rate <60 beats per minute (bpm)



    • Present in 80% of highly trained athletes



    • Heart rate >30 bpm considered normal in trained athletes



    • Sinus bradycardia should resolve with exertion.




  • Sinus arrhythmia




    • Definition: fluctuation of heart rate with breathing



    • Heart rate should correlate with breathing, without sustained acceleration or decelerations, and should resolve with exertion.



    • Not associated with symptoms to differentiate from sick sinus syndrome




  • Junctional escape rhythm




    • Occurs with QRS rate faster than resting sinus rate caused by increased vagal tone



    • Narrow complex QRS with QRS morphology similar as sinus rhythm



    • Should have a rate <100 and regular RR interval



    • Sinus rhythm resumes with exercise and increase in heart rate.




  • Ectopic atrial rhythm




    • P waves are present but different in morphology compared with sinus rhythm



    • 8% of athletes have ectopic atrial rhythm or junctional escape rhythm




  • First-degree AV block




    • Definition: PR interval >200 ms



    • Occurs in 7.5% of athletes



    • Caused by increased vagal tone and should resolve with exertion




  • Mobitz Type I (Wenckebach) second-degree AV block




    • Definition: progressive PR lengthening until a nonconducted P wave occurs (no QRS after P wave)



    • Caused by increased vagal tone: 1 : 1 P:QRS conduction should return with exertion






ECG Changes Suggestive of Cardiomyopathy


Introduction





  • Cardiomyopathies are a heterogeneous group of heart muscle diseases.



  • Collectively, they are the leading identified cause of SCD in young athletes.



  • Individuals with these diseases may be asymptomatic: often the presenting sign is sudden cardiac arrest.



  • ECG is abnormal in 85%–95% of individuals with such diseases.



Hypertrophic Cardiomyopathy (HCM)





  • Heart muscle disease characterized by asymmetric LVH or septal hypertrophy, small LV chamber size, diastolic dysfunction, and myocyte disarray on histopathology. Some cases of HCM have LV outflow tract obstruction at rest or provoked by exercise.



  • Hypertrophy is most common at the intraventricular septum but can also be found in the apex or in a concentric fashion.



  • Prevalence of approximately 1 : 500 in adults (1 : 800–2600 in young competitive athletes)



  • ECG findings are abnormal in >90% of patients with HCM.



  • ECG findings suggestive of HCM (see definitions below): T-wave inversions in the lateral or inferolateral leads, ST-segment depression, pathologic Q waves, complete left bundle branch block (LBBB), nonspecific intraventricular conduction delay, and multiple PVCs



  • Markedly abnormal ECG patterns involving deep T-wave inversion with ST-segment depression in the lateral (V5–V6, I, and aVL) or inferolateral (V5–V6, I and aVL, and II and aVF) leads warrants exclusion of apical HCM, which can be difficult to assess by echocardiogram alone; cardiac MRI is recommended when such ECG patterns are noted (see Fig. 34.3 ).




    Figure 34.3


    ECG from a patient with hypertrophic cardiomyopathy demonstrates deep T-wave inversion and ST-segment depression predominantly in the lateral leads (I, aVL, and V4–V6), left and right atrial enlargement, and left axis deviation.



Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)





  • Heart muscle disease characterized by fibrofatty replacement of RV myocardium



  • ECG findings suggestive of ARVC (see definitions below): T-wave inversion in anterior leads, ST-segment depression, multiple PVCs, epsilon wave, delayed S-wave upstroke, and low limb lead voltage




    • Epsilon wave: small negative deflection just after QRS in leads V1–V3



    • Delayed S-wave upstroke: > 55 ms from nadir of S wave to the end of the QRS complex




      • Must be in the absence of RBBB




    • Low limb lead voltage: QRS voltage <5 mm in leads I, II, and III




Idiopathic Dilated Cardiomyopathy (DCM)





  • Heart muscle disorder wherein weakened contractile function leads to heart chamber enlargement without associated increase in wall thickness and decrease in ejection fraction



  • ECG findings suggestive of DCM (see definitions below): T-wave inversions in the anterior, lateral, and inferolateral leads, ST-segment depression, pathologic Q waves, complete LBBB, and nonspecific intraventricular conduction delay




    • Goldberger’s triad (criteria suggestive of DCM): deep S waves in the anterior precordial leads, low limb lead voltage, and poor precordial R-wave progression




Left Ventricular Noncompaction (LVNC)





  • Heart muscle disorder characterized by poorly organized muscle fibers leading to deep trabeculations and thinning of the compacted myocardium



  • Hypertrabeculations are more common in male and African-American athletes; thus, the clinical diagnosis usually requires LV dysfunction.



  • ECG findings suggestive of LVNC (see definitions below): T-wave inversions in the lateral and inferolateral leads, ST-segment depression, pathologic Q waves, complete LBBB, and nonspecific intraventricular conduction delay



Myocarditis





  • Acquired disorder and thus not an inherited cardiomyopathy, but ECG abnormalities overlap with findings found in other myocardial diseases



  • Acute presentation may include fever, chest pain, flu-like viral syndrome, and change in exercise tolerance.



  • ECG findings suggestive of myocarditis (see definitions below): T-wave inversions, ST-segment depression, pathologic Q waves, complete LBBB, and premature ventricular contractions (PVCs)



Specific ECG Findings Suggestive of Cardiomyopathy


T-Wave Inversions





  • >1 mm of depth in two or more contiguous leads V2–V6, II and aVF, or I and aVL




    • Excludes leads III, aVR, and V1



    • Excludes the repolarization variant in black athletes confined to V1–V4



    • Excludes juvenile T-wave inversion in leads V1–V3 when age is <16 years




  • Disease-specific findings




    • HCM:




      • Commonly seen in lateral (V5–V6, I, and aVL) and inferior (II and aVF) leads



      • Seen in approximately 52%–64% of individuals with HCM




    • ARVC:




      • Commonly seen in the anterior precordial leads (V1–V4); usually a flat or depressed ST segment prior to T-wave inversion, which distinguishes it from the repolarization variant in African-American athletes with J-point elevation and ST segment elevation prior to T-wave inversion



      • Seen in approximately 85% of individuals with ARVC



      • Can also be seen in lateral (V5–6) and inferior (II and aVF) leads




    • DCM




      • T-wave inversion seen in 25%–45% of individuals




    • LVNC




      • T-wave inversion seen in approximately 41% of individuals





  • Recommended follow-up evaluation:




    • In lateral or inferolateral leads: echocardiogram and cardiac MRI to exclude HCM or apical HCM; exercise ECG test and 24-hour ECG monitor in cases of grey-zone hypertrophy (13–15 mm)




      • These patients require annual re-evaluation as two separate studies have found that 6% of patients with initial normal cardiac imaging subsequently develop clinical cardiomyopathy; thus, the ECG manifestations of cardiomyopathy can occur before the morphologic changes in certain patients




    • Inferior leads alone: echocardiogram



    • Anterior leads: echocardiogram, cardiac MRI, exercise ECG test, 24-hour ECG monitor, and signal-averaged ECG to exclude ARVC




ST-Segment Depression





  • ≥0.5 mm in depth in two or more contiguous leads




    • This finding is rare in healthy athletes; thus, its presence requires the exclusion of cardiomyopathy.




  • Disease-specific findings




    • HCM:




      • Reported in 46%–50% of individuals




    • ARVC:




      • Can be seen but not a part of diagnostic criteria for ARVC




    • LVNC




      • Seen in approximately 51% of individuals





  • Recommended follow-up:




    • Echocardiogram




Pathologic Q Waves





  • Q/R ratio ≥0.25 or ≥40 ms in duration in two or more contiguous leads (except III and aVR)




    • Q waves are commonly seen in young athletes, specifically long “skinny” Q waves related to overall increases in QRS amplitude.



    • The new definition of pathologic Q waves is based on international consensus recommendations.




  • Disease-specific findings




    • HCM:




      • Reported in 32%–42% of individuals




    • ARVC:




      • Q waves are not a common finding in ARVC




    • DCM




      • Present in 10%–25% of individuals




    • Coronary artery disease (CAD)




      • Could represent premature atherosclerotic CAD; a CAD risk factor assessment is indicated





  • Recommended follow-up:




    • Echocardiogram and CAD risk factor assessment in older athletes




Complete Left Bundle Branch Block (LBBB)





  • QRS ≥120 ms, predominantly negative QRS complex in lead V1 (QS or rS), and upright notched or slurred R wave in leads I and V6



  • Disease-specific findings




    • HCM:




      • Present in approximately 2% of individuals




    • ARVC:




      • LBBB is not a common finding in ARVC




    • DCM:




      • Present in 9%–25% of individuals





  • Recommended follow-up:




    • Echocardiogram, cardiac MRI with a perfusion study; a comprehensive evaluation to exclude cardiac pathology must be performed in the presence of LBBB.



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Jul 19, 2019 | Posted by in SPORT MEDICINE | Comments Off on ECG Interpretation in Athletes

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