In 2007 we began performing ECGs as part of the pre-participation exam (PPE) for all Stanford athletes requiring athletes to provide Stanford IRB approved consents. The ECGs were digitized and entered into a database leading to three papers, the first reporting our experience with screening (Le, 2008) and then two others looking at the effect of gender (Mandic, 2009) and specific sport (Gademon, 2011) on the computerized measurements. A favorite paper was “Does size matter?” by Dewey et al. in 2008.

To ensure expertise, we published a Current Problems in Cardiology monograph entitled, “Adding the ECG to the PPE” (Perez, 2009) which provided a review of all the available research on the subject. To justify adding the ECG, we performed a cost-efficacy analysis published in the Annals of Internal Medicine (Wheeler, 2009).

The results of our study led the Athletic Department to mandate the ECG as part of the PPE in 2010. In 2010 we used a laptop analog to digital ECG system and our own software to perform the screening on Stanford collegiate athletes and the San Francisco 49ers. Our software was designed for screening athletes and the output stated whether an athlete needed further evaluation prior to participation or not. This differs from the available commercial interpretive programs which often give confusing statement when testing athletes.

Our consensus ECG recommendation (Uberoi, Ashley et al) included the agreement of an international group of sports cardiology experts that provided specific criteria for ECG diagnoses that required further evaluation prior to participation. We then addressed the confusion between classic “early repolarization” based on ST elevation and the new channelopathies classified as “early repolarization” based on R wave downslope phenomena (aka J wave syndromes), concluding that the static pattern of early repolarization was not associated with cardiac disease. See seperate menu item for this topic.

Key Points of Cardiovascular Risk Evaluation of Young Athletes


  1. Family history of sudden or unexplained death or cardiac condition should trigger detailed questioning of parents or their surrogates
  2. Previous illnesses, cardiac evaluation or restriction from sport should trigger detailed questioning of parents or their surrogates
  3. If precipitated by exercise, the following always require further evaluation: palpitations, chest pain, syncope or near syncope and/or dyspnea or unusual fatigue 

Physical Exam

  1. Soft early systolic murmurs are common but holosystolic or late systolic murmurs and all diastolic murmurs require further evaluation usually including an ECG and echocardiography
  2. Elevated heart rate or blood pressure require further evaluation
  3. Physical characteristics of connective tissue diseases require further evaluation 


  1. Traditional voltage criteria for LVH are often seen in young athletes and can be considered a normal variant
  2. ST segment elevation up to 2 mm (200 microV) is commonly seen in young athletes and if unaccompanied by symptoms do not require further evaluation
  3. ST segment depression is unusual in young athletes and requires further evaluation
  4. T wave inversion in any leads other than aVL, aVR, III, V1 or V2 are abnormal and require further evaluation
  5. Prolongation of QRS (>120msec) or QTc (fredricia >460 msec for males and >470 msec for females) require further evaluation 

Cardiopulmonary Exercise Test

  1. Unexplained exercise capacity less than expected adjusted for age, sex and exercise training level requires further evaluation 
  2. ECG abnormalities including ominous arrhythmias, and pathological ST elevation or depression require further evaluation 
  3. Drop in Systolic BP or chest pain with increasing exercise require further evaluation; diastolic BP normally drops with progressive levels of exercise while SBP rises.


  1. LV wall thickness (LVWT) is rarely greater than 13 mm in healthy young athletes and when present requires further evaluation
  2. The take-offs from the aorta of the right and left coronary arteries can be seen in the majority of athletes
  3. Relative wall thickness (RWT from 2-D echo) and the mass/EDV ratio (M/V from 3-D echo or MRI) are helpful in distinguishing HCM and athlete’s heart when LVWT is between 13 and 15 mm.
  4. LV aneurysm, abnormal LV segmental wall motion or longitudinal  strain, impaired LV diastolic function and/or systolic anterior motion of the mitral valve support the diagnosis of HCM or a myopathic process.


  1. Wall and chamber measurements with cardiac magnetic resonance imaging (CMR or MRI) have been shown to be more accurate than with echocardiography.
  2. Late gadolinium enhancement (LGE) on CMR is believed to represent dense replacement of myocytes with fibrosis and its pattern may help narrow the diagnosis. It is seen in roughly 50% of patients with HCM
  3. LV aneurysm, abnormal LV segmental wall motion or longitudinal  strain, impaired LV diastolic function and/or systolic anterior motion of the mitral valve support the diagnosis of HCM or a myopathic process.

Convincing Healthy Athletes to Answer the PPE CV risk Questions

  • Have you ever had palpitations or irregular heart beats during or after exercise?
  • Have you ever had Chest Pain that lasted minutes during or after exercise?
  • Have you ever had syncope or near loss of consciousness during or after exercise?
  • Have you ever had palpitations or irregular heart beats during or after exercise?
  • Have you ever had excessive shortness of breath during or after exercise?
  • Have you ever had unusual fatigue during or after exercise?
  • Have you ever had an unexplained seizure?
  • Have there ever been unexplained sudden deaths in your family including accidents and drowning?
  • Has anyone in your family had heart muscle or valvular heart disease or other familial heart conditions?
  • Has anyone in your family had a pacemaker or implanted defibrillator before age 35?

Why should you be concerned with answering these scary questions?

This paragraph is text we developed for the California chapter of the American College of Cardiology‘s website with accompanying videos and questionnaires.

Sure, heart problems and their complications including death are rare in young athletes. But what if the causes of these conditions and their complications were known and we knew their warning signs? Your parents, relatives and coaches would like you to be able to play sports safely. Modern medicine has made tools available for screening and treating heart conditions so why not take advantage of them? The first step in doing so is to answer these questions as best you can. Studies have shown us that they can be clues for recognizing the first signs of heart conditions. Your answers to these questions can be summarized for you to take to your annual screening for participation in organized sports with some suggestions for your doctor or organization to consider prior to sports participation. Even if you don’t have any of these symptoms now, you now know that if they ever occur they should be reported.

Suggested Work up of Athletes in response to Symptoms, signs or findings during a PPE

Flow Diagram for imaging options for symptoms and initial findings from a CV work up for an athlete (in collaboration with Dr Jon Wong, MD)

Interpretation of Young Athlete’s ECGs

Read the JACC Article International Guidelines for Reading Athlete’s ECGs

Examples of ECGs found in Athletes

Collection of ECGs gathered using the Cardiac Insight’s 20/20 ECG recording system

This links to the Washington University website that teaches the International ECG Guidelines for young athletes and has an optional examination.

Review of Myocardial Remodeling

The following four sections and 2 figures are adapted from the 2011 State of the Art paper by Gaasch and Zile. 

Relative Wall Thickness

In 1976 in an analysis of heart size and hemodynamics, Ford reviewed the factors influencing myocardial work and the LV workload in mammals of widely varying body and heart size. A consistent ratio of stroke volume (SV) to end-diastolic volume (LVEDV) was observed in widely varying body size. This led to the conclusion that the RWT depends solely on LV systolic pressure. The normal range for RWT was calculated to be 0.42 to 0.33 with systolic arterial pressure ranging from 140 to 110 mm Hg.

 Using M-mode echocardiographic data in 1987 from 4,975 participants in the Framingham Heart Study, Savage et al. described a spectrum of morphologic types of LV hypertrophy. Three types of hypertrophy were defined on the basis of RWT of 0.45. Eccentric hypertrophy was then divided into those with an increased LVEDd and those with a normal LVEDd. However, Huwez et al. noted problems and proposed a classification in which the geometry of hypertrophic hearts was described as either concentric (increased mass/normal volume) or eccentric (increased mass/increased volume). 

Calculation of Relative Wall Thickness with 2D Echocardiography

Koren et al. were among the first in 1991 to use M-mode echocardiography to study the relationship of RWT to clinical outcomes. They studied LV remodeling in 230 hypertensive patients and reported different morbidity and mortality in those with different patterns of structural remodeling. They used the term “concentric hypertrophy” to describe hearts exhibiting increased LV mass (125 g/m2) with a high RWT (0.45), and they introduced the term “concentric remodeling” to describe those with a normal mass and high RWT. Thus, they were able to include hypertensive patients who had abnormal geometry, but no hypertrophy. This study confirmed that concentric remodeling had an adverse prognostic impact despite the lack of an absolute increase in LV mass. This was followed by several large studies all of which confirm the importance of distinguishing the various patterns of ventricular remodeling in populations with hypertension. Concentric remodeling exhibits a trend toward higher LV mass than is seen with a truly normal geometry. Thus, the various geometric patterns of remodeling are related to systemic hemodynamics, cardiovascular risk factors, and adverse cardiovascular outcomes. The upper limit of normal or cutpoint for RWT is now recommended to be 0.42.

RWT= (2xPWT or PWT+IVST)/LVID, PWT= posterior wall thickness, LVID = Left ventricular Internal dimension, IVST = Intraventricular septal thickness

Mass/Volume Ratio

The ratio of LV mass to end-diastolic volume (M/V) is closely related to the RWT and should carry the same implications as changes in RWT. The relationship of M/V and RWT shown in Figure 1 was developed by specifying thickness and the corresponding RWT, and then calculating the mass, volume, and the corresponding M/V using standard methods. This method assumes a uniform LV wall thickness, which is a limitation in the presence of coronary heart disease and forms of hypertrophic cardiomyopathy.The normal RWT range of 0.32 to 0.42 corresponds to an M/V range of approximately 1.0 to 1.5. These estimates are consistent with angiographic, echocardiographic, and cardiac magnetic resonance imaging (MRI) data indicating average normal values of M/V ranging from 1.1 to 1.3. 

In 2010 in the Dallas Heart Study, Khouri et al. used cardiac MRI to measure LV mass and volume in 2,803 subjects, and they describe 4 “distinct geometric patterns” of LV remodeling. Their 4-tiered classification was based on whether concentricity and end-diastolic volume were increased or not.  Of subjects with LVH (n=875), the most common geometric pattern (n=468) was termed “eccentric and indeterminate” (increased mass with a normal end diastolic volume, and normal concentricity). Only 53 had typical eccentric hypertrophy, while concentric hypertrophy was present in 361. A small group (n =13) exhibiting an increase in mass, volume, and concentricity was classified as “thick and dilated”. These 4 geometric patterns were associated with different clinical characteristics, biomarkers, and ejection fractions. The group with eccentric (dilated) or concentric hypertrophy exhibited lower LV ejection fractions than the other 2 groups. The researchers concluded that identification of these “distinct phenotypes” may predict prognosis. This study differed from previous publications in that modern cardiac MRI was used to assess LV volume, mass, and geometry. The definitions of concentric and eccentric geometry also differed from those previously used making comparisons difficult.

Despite differences in methods and definitions, the M/V is a parameter that, like the ejection fraction and RWT, does not require consideration of or correction for body size. This can be a major advantage, especially as there is little agreement as to the appropriate allometric scaling and normalization of LV volume or mass (Dewey, et al). 

RWT= (2xPWT or PWT+IVST)/LVID, PWT= posterior wall thickness, LVID = Left ventricular Internal dimension, IVST = Intraventricular septal thickness

Classification of LV Remodeling

In an attempt to provide an inclusive classification of a wide variety of ventricular remodeling patterns, Gaasch and Zile devised the scheme shown in Figure 2. To be inclusive , this classification of remodeling considers LV volume, mass, and RWT (or M/V). Their classification limits the term “concentric” to those without chamber dilation. Therefore, a normal end-diastolic volume and an increased RWT (or M/V) pattern would be classified as concentric hypertrophy if LV mass is increased, and as concentric remodeling if LV mass is normal. These terms are currently used by the American Society of Echocardiography. The term “eccentric” is applied exclusively to patterns with enlarged (dilated) ventricles. Thus, eccentric geometry includes those with physiologic hypertrophy, eccentric hypertrophy, and eccentric remodeling. These eccentric patterns are distinguished by differences in LV mass and RWT (or M/V). Mixed hypertrophy exhibits increased volume, mass, and RWT.

Remodeling patterns also appear to be different by sex and ethnicity (Hispanic and African Americans). The specific method used to determine LV mass and volume is also important. Using cardiac MRI, some investigators exclude the papillary muscles from the LV mass , whereas others report that the papillary muscles are included in the mass and excluded from the chamber volume. That could result in relatively small, but significant differences in the M/V. Even within the same study there may be discrepancies between RWT and M/V if the LV volume is derived according to the modified biplane Simpson’s rule and the LV mass and RWT are derived from linear measurements.  

Physiologic hypertrophy

The change in LV architecture seen in physiologic hypertrophy can be considered a form of eccentric remodeling/hypertrophy in that both chamber size and LV mass are increased. However, in physiologic hypertrophy, a normal RWT is maintained. An example of physiologic hypertrophy is the athlete who exhibits modest LV chamber enlargement and increased LV mass with a normal RWT (0.36) and normal LV function. Even athletes with substantial LV enlargement exhibit an average RWT (approximately 0.33) that is within the range of normal. In athletes with physiologic hypertrophy, stroke volume is increased, while ejection fraction and mean circumferential fiber shortening velocity are normal. 

Normal responses of the Athlete’s Heart to Exercise Training

Left ventricular (LV) adaptation or remodeling to prolonged exercise training in humans has been explained by the sport-specificity concept of the ‘Morganroth hypothesis’ (1975). Using non-guided M-mode echocardiography, Morganroth et al. (1975) observed that endurance athletes (swimmers, long-distance runners) possessed increased LV end-diastolic volume (LVEDV), normal LV wall thickness and increased LV mass compared to sedentary subjects. In contrast, resistance-trained athletes (wrestlers) exhibited increased LV wall thickness and LV mass with no change in LVEDV compared to sedentary controls. These divergent patterns were later described as ‘eccentric’ and ‘concentric’ left ventricular hypertrophy, respectively, and resulted from episodic elevations in preload during endurance exercise and afterload during resistance exercise. Actually all exercise has isotonic and isometric components and modern athletes use both types of exercise training emphasizing the type needed most for their sport.  The figure below illustrates the Morganroth hypothesis. Availability of 3-D echocardiography and MRI have led to controversy regarding these differences in the response to training.

The magnitude of concentric LVH depends upon the ethnicity and sex of the athlete. Concentric LVH is less common in athletes than eccentric or normal geometry but can occur in up to 12% and is usually of a low magnitude. It is not feasible to assume pathology without further investigations including 12-lead ECG and MRI….plus functional indices from echo will help to differentiate physiological from pathological.

Endurance training or isotonic (distance runners, wide receivers, backs, basketball)Resistance training or isometric (wrestlers, linemen, gymnasts)Hypertrophic Cardiomyopathy
LVEDV (end diastolic volume)Increasednormal<54 mm
LVWT (wall thickness)Normal <13mmIncreased <13mmIncreased >13mm
LVM (mass)increasedincreasedincreased
RWT (relative wall thickness)<0.42<0.42>0.42
Mass/Volume ratio< 1.0< 1.0> 1.0 males
RWT= (2xPWT or PWT+IVST)/LVID, PWT= posterior wall thickness, LVID = Left ventricular Internal dimension, IVST = Intraventricular septal thickness

Distinguishing HCM from Athlete’s Heart in the Grey Zone with Echocardiography

Clinically, a RWT >0.42 is considered abnormal and thus a sign of dysproportional increase in LV muscle wall mass, and a warning sign of non physiological hypertrophy. When only 2-D echocardiography was available, RWT was the best available surrogate for pathological hypertrophy. However, MRI and 3D echo provided more accurate measurements than 2D echo such that volumes and mass replaced linear 2D-measures and M/V ratio was favored. 2D echos required assumptions of LV geometry when converting to mass and volume and have proven to be less accurate. Since linear 2D-measures such as  RWT did not require assumptions it appeared more reliable when using 2-D techniques. Furthermore, the 2-D Echo exam requires proper beam alignment to make correct measurements while this is not the case with 3D echo and MRI. These advances have made the volume/mass ratio and measurements favored.

The purpose of a study by Caselli et al was to consider the ability of echocardiographic and clinical variables for the differential diagnosis of hypertrophic Cardiomyopathy (HC) versus athlete’s heart. Twenty-eight athletes free of cardiovascular disease were compared with 25 untrained patients with HC, matched for LV wall thickness (13 to 15 mm), age, and gender. Clinical, electrocardiographic, and 2-D echocardiographic variables were compared. Athletes had statistically significant larger LV cavities (60 vs 45 mm), aortic roots (34 vs 30 mm), and left atria (42 vs 33 mm) than patients with HC. LV cavity <54 mm distinguished HC from athlete’s heart with the highest sensitivity and specificity. Left atrium >40 mm excluded HC with sensitivity of 92% and specificity of 71%. Absence of diffuse T-wave inversion on ECG (specificity 92%) and negative family history for HC (specificity 100%) also proved useful for excluding HC. They concluded that in athletes with LV hypertrophy in the “gray zone” with HC, LV cavity size appears the most reliable criterion to help in diagnosis, with a cut-off value of <54 mm useful for differentiation from athlete’s heart. Other criteria, including LV diastolic dysfunction, absence of T-wave inversion on electrocardiography, and negative family history, further aid in the differential diagnosis.  

Can ECG QRS voltage Estimate Hypertrophy in Young Athletes?

Electrocardiography (ECG) is used to screen for left ventricular hypertrophy (LVH) with the assumption that mass roughly equals QRS voltage. But to quote Bacharova and Estes, “the assumption that mass can be predicted from amplitude resembles the erroneous assumption that the size of a battery can predict its output”. We have previously demonstrated that the QRS voltage criteria are poorly predictive of CV death in clinical populations (Ha et al, 2018) and recent guidelines have not been recommended for use in athletes. The purpose of a study from our group by Hedman et al was to comprehensively evaluate the value of ECG for identifying athletes with LVH or a concentric cardiac phenotype.

A retrospective analysis of 196 male Division I college athletes routinely screened with ECG and echocardiography within the Stanford Athletic Cardiovascular Screening Program was performed. Left-ventricular mass and volume were determined using echocardiography. LVH was defined as left ventricular mass (LVM) >102 g/m²; a concentric cardiac phenotype as LVM-to-volume (M/V) ≥1.05 g/mL. Twelve-lead electrocardiograms including high-resolution time intervals and QRS voltages were obtained. Thirty-seven previously published ECG-LVH criteria were applied (see Figure below). Multiple regression, receiver operating curve (AUC) and likelihood ratios were calculated.

ECG lead voltages were poorly associated with LVM (r = 0.18-0.30) and M/V (r = 0.15-0.25). The proportion of athletes with ECG-LVH was 0%-74% across criteria, with sensitivity and specificity ranging between 0% and 91% and 27% and 99.5%, respectively. The average AUC of the criteria in identifying the 11 athletes with LVH was 0.57, and the average AUC for identifying the 8 athletes with a concentric phenotype was 0.59. RWT was normal in all of them.

The diagnostic capacity of all ECG-LVH criteria were inadequate and, therefore, not clinically useful in screening for LVH or a concentric phenotype in athletes. Setting specificity high enough to limit false positives resulted in useless sensitivities. This is probably due to the weak association between LVM and ECG voltage even when corrected for BSA.

This Figure details the discriminate test characteristics (AUC, sensitivity and specificity) of the 37 traditional scores for ECG-LVH. It becomes very clear that setting specificity high enough to avoid too many false positives results in a very low sensitivity and likelihood ratio.

Hedman et al. below

Selected Resources



  • Hadley D, Hsu D, Pickham D, Drezner JA, Froelicher VF. QT Corrections for Long QT Risk Assessment: Implications for the Preparticipation Examination. Clin J Sport Med. 2019 Jul;29(4):285-291.
  • Hedman K, Moneghetti KJ, Christle JW, Bagherzadeh SP, Amsallem M, Ashley E, Froelicher V, Haddad F. Blood pressure in athletic preparticipation evaluation and the implication for cardiac remodelling. Heart. 2019 Aug;105(16):1223-1230.