Athlete’s Heart


New California Chapter Exercise Health And Sports Cardiology Committee
The American College of Cardiology’s California Chapter has established an Exercise Health and Sports Cardiology Committee in response to the growing need for evidence-based, standardized, comprehensive care for athletes. The committee aims to serve as a resource for consultative cardiovascular assessment of highly active individuals as well as a home for educational tools to aid in their assessment and management. This is our first educational endeavor which includes the following five sections listed in the menu with links to key subjects.

Section One: Preparticipation Evaluation of the Athlete’s Heart: Questionnaire with Videos and Resources

Authors, Alphabetical Order 

Why should you be concerned with answering these scary questions? 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 watch these videos and 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 will 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. Please share this resource with your teammates.


Athlete Cardiovascular Risk Video Questionnaire

Print out this form and watch the videos before entering your answer
Videos are courtesy of the University of Texas Southwestern Medical Center (Dr. Benjamin Levine).

1. Have you ever had discomfort, pain, tightness, or pressure in your chest during exercise?

Watch Video, then check appropriate response on printed questionnaire. 

2. Have you ever passed out or nearly passed out DURING exercise?

Watch Video, then check appropriate response on printed questionnaire.

3. Do you ever get so out of breath that you can’t continue to exercise even though your peers aren’t tired yet?

Watch Video, then check appropriate response on printed questionnaire.

4. Have you ever felt like your heart was racing, fluttering, or beating abnormally?

Watch Video, then check appropriate response on printed questionnaire.

5. Have you ever seen a doctor for a heart problem before?

Check appropriate response on printed questionnaire.

6. Has a doctor ever ordered testing for your heart, such as an EKG/ECG, x-ray, Echocardiogram, MRI or an exercise stress test?

Check appropriate response on printed questionnaire.

7. Has a doctor ever told you not to play sports before?

Check appropriate response on printed questionnaire.

8. Have you ever had an unexplained seizure?

Check appropriate response on printed questionnaire.

9. Do you take any performance supplements or energy drinks?

Check appropriate response on printed questionnaire.

Suggestions for the Physician Performing the PPE

Pre Participation Exam (PPE) Screening

The PPE is widely advocated for all youth athletes engaged in competitive sports. This year, in order to screen for the possible consequences of COVID-19, all athletes should undergo a PPE that assesses current or past symptoms of the SARS-Coronavirus-2. Testing to exclude significant cardiopulmonary disease should be based on the algorithms provided below. Most organizations suggest individual screening by a qualified clinician ( or trainer ) who has an available cardiology ( or sports medicine ) consultant. Mass screenings would require precautionary measures in order to maintain physical distancing. All screening should follow guidelines outlined by the California Department of Public Health, including cleaning of equipment (eg., ECG machines and wires to electrodes). Among athletes with  definite or possible prior infection , the use of adjunctive testing including electrocardiography, cardiac biomarkers, non-invasive imaging, and exercise testing represent potential appropriate options, depending on clinical context such as concerning symptoms.

History of new cardiac symptoms is extremely concerning and may be difficult to distinguish from deconditioning which can be due to sheltering in place. Importantly, myopericarditis related to COVID-19 should be considered in athletes with a history of new onset chest pain/pressure (even in the absence of fever and respiratory symptoms), palpitations, exercise intolerance, and/or resting or exercise related excessive tachycardia. Comprehensive clinical evaluation, regardless of ECG findings, is indicated in athletes with new onset cardiovascular symptoms or exercise intolerance. COVID-19 affected myocardial tissue can promote cardiac arrhythmias, and a major aim of the PPE is to identify those at risk for cardiac arrhythmias. At Stanford, an inexpensive ECG patch that can be automatically interpreted for PVC burden in clinic is being evaluated for this purpose in athletes recuperating from COVID-19.

Athlete COVID-19 Risk Questionnaire

Though we appear to be on the downsloping curve of the Pandemic, there may be natural seasonal surges or possibly exacerbations due to new genetic strains of SARS-Coronavirus-2  or other viruses.  Therefore, your Pre Participation exam ( PPE) must include questions regarding whether you have had COVID-19 or been exposed to it or other viral infections. The SARS-Coronavirus-2 (COVID-19) infection (as well as other viral agents) can cause damage to your heart (myopericarditis) even if you’ve only had minor exposure and not had any complaints or any symptoms. Screening for active or prior infection, with appropriate work up could prevent life threatening consequences during or after physical activity. Please complete this questionnaire, generate a pdf/copy of your responses and give it to your Doctor, coach or trainer.

Current Recommendations for Cardiac Evaluation during the Covid-19 Pandemic

Cardiac evaluation has been intensified and exercise recommendations revised during this pandemic due to concerns raised by the cardiac complications noted in severe cases of Covid-19. Even though severe cases of Covid-19 are rarely seen in younger individuals, the potential for cardiac complications remains a concern and can sometimes occur months after even mild or asymptomatic infections. As a medical community, our recommendations are empirical and must be adjusted as knowledge grows and testing techniques improve. The latest recommendation (October 2020) was commissioned by the ACC Council on Sports Cardiology who chose America’s most active and experienced Sports Cardiologists and Sports Medicine specialists with cardiology knowledge to develop the document. The recommendation has been published in a peer reviewed journal and is available as a ACC webex video. The recommendations are specific for High School athletes (Figure 1), College and Professional athletes (Adults, Figure 2) and Master athletes (Figure 3). The experts also recommended adapted criteria for Myocarditis (Table 1). They presented specific cautions regarding the routine use of Computer Magnetic Resonance Imaging (MRI or CMR) as part of post-COVID PPE algorithm until there is a better understanding of how to differentiate pathological changes from those due to exercise training. The risk level of symptoms is provided in Table 2. These experts have observed that cardiovascular consequences of Covid-19 are relatively mild and so when compared to initial recommendations at the beginning of the pandemic, they have lessened indications for cardiac testing prior to return to play.


It is assumed that the sport and exercise are performed consistent with the current level of physical distancing, appropriate hygienic measures and face mask guidelines. Age and severity of illness have been emphasized and should be taken into account when considering cardiovascular diagnostics. Note also that at this time the benefits of exercise far outweigh the risk of exercise-induced cardio-pulmonary damage in the young. Our committee promulgates these recommendations with the caveat that they may be superseded by other guidelines as new knowledge becomes available.


The pathology (fibrosis, inflammation and thrombosis) of damage to the heart and lungs has been demonstrated but the time course and severity is uncertain and appears to be mild in athletes. Also it is not certain to what degree exercise training can exacerbate the damage caused by the pathogen but the experience so far is that this appears to be minor.

Figure 1. Coronavirus Disease 2019 (COVID-19) Return-to-Play Algorithm for Athletes in Competitive High School Sports

This is the currently recommended algorithm (Oct 2020) for high school athletes with confirmed COVID-19. Note that among the cardiovascular (CV) symptoms, syncope of unclear cause identifies individuals who definitely require advanced CV testing, including cardiac magnetic resonance (CMR) imaging, exercise testing, and ambulatory ECG monitoring. Typical initial testing is obtained via a nasopharyngeal swab and polymerase chain assay for conserved regions of severe acute respiratory syndrome coronavirus–2 RNA. Multisystem inflammatory syndrome in children (MIS-C) involves fever, rash, abdominal pain, vomiting, diarrhea, lethargy, and conjunctivitis, possibly developing weeks after infection. The guidelines for RTP after myocarditis is indicated in Table 1.


CDC – US Centers for Disease Control and Prevention; ECG, 12-lead ECG/EKG; echo, echocardiogram; hs-cTn, high-sensitivity cardiac troponin-I; RTP, return to play.

Figure 2. Coronavirus Disease 2019 (COVID-19) Return-to-Play Algorithm for Collegiate and Professional Athletes in Competitive Sports

This is the currently recommended algorithm (Oct 2020) for all college and professional athletes with confirmed COVID-19. Note that among the cardiovascular (CV) symptoms, syncope of unclear cause identifies individuals who definitely require advanced CV testing, including CMR imaging, exercise testing, and extended rhythm monitoring. (see comments and legend for Table 1).

Figure 3. Coronavirus Disease 2019 (COVID-19) Return-to-Play Algorithm for Recreational Masters Athletes

This is the currently recommended algorithm (Oct 2020) for all athletes at the masters level with confirmed COVID-19. Cardiovascular disease (CVD) risk factors include hypertension, coronary artery disease, atrial fibrillation, and diabetes. (see comments and legend for Table 1).

Table 1. Adapted Criteria for Myocarditis

Myocarditis (Probable Acute Myocarditis With Both of the Following Criteria)

1. Clinical syndrome, including acute heart failure, angina-type chest pain, or known myopericarditis of less than 3 months’ duration.

2. Otherwise unexplained increase in serum troponin levels, ECG repolarization abnormalities, arrhythmias or high-grade atrioventricular block, abnormal ventricular wall motion, or pericardial effusion. Additional cardiac MRI findings that suggest myocarditis.

Sports Eligibility Myocarditis Recommendations

1. Before returning to sports, athletes diagnosed with a clinical syndrome consistent with myocarditis should undergo a resting echocardiogram, ambulatory ECG monitoring, and an exercise test no less than 3 to 6 mo after the illness.

2. It is reasonable that athletes can resume training and/or competition if all of the following criteria are met:

    A. Ventricular systolic function has normalized.
    B. Serum markers of myocardial injury, heart failure, and inflammation have returned to normal levels.
    C. Clinically relevant arrhythmias are absent.

Table 2. Risk levels of Symptoms

1. Mild Symptoms

include anosmia, ageusia, headache, mild fatigue, mild upper respiratory tract illness, and mild gastrointestinal illness;

2. Moderate Symptoms

include persistent fever, chills, myalgias, lethargy, dyspnea, and chest tightness;

3. Severe Symptoms

include dyspnea, exercise intolerance, chest tightness, dizziness, syncope, and palpitations which often require hospitalization.

Myocarditis and COVID-19

It is assumed that the sport and exercise are performed consistent with the current level of physical distancing, appropriate hygienic measures and face mask guidelines. Age and severity of illness have been emphasized and should be taken into account when considering cardiovascular diagnostics. Note also that at this time the benefits of exercise far outweigh the risk of exercise-induced cardio-pulmonary damage in the young. Our committee promulgates these recommendations with the caveat that they may be superseded by other guidelines as new knowledge becomes available.

The pathology (fibrosis, inflammation and thrombosis) of damage to the heart and lungs has been demonstrated but the time course and severity is uncertain and appears to be mild in athletes. Also it is not certain to what degree exercise training can exacerbate the damage caused by the pathogen but the experience so far is that this appears to be minor.

Myocarditis and COVID-19 in Professional Athletes

The major North American professional sports leagues were among the first to return to full-scale sport activity during the coronavirus disease COVID-19 pandemic. Martinez et al reported a retrospective analysis of return to play cardiac testing performed between May and October 2020 on professional athletes who had tested positive for COVID-19. The professional sports leagues (Major League Soccer, Major League Baseball, National Hockey League, National Football League, and the men’s and women’s National Basketball Association) implemented mandatory cardiac screening requirements for all players who had tested positive for COVID-19 prior to resumption of team-organized sports activities. The study included 789 professional athletes (98.5% males) and the majority had prior symptomatic COVID-19. Abnormal screening results were identified in 30 athletes (3.8%; troponin, 6 athletes [0.8%]; ECG, 10 athletes [1.3%]; echocardiography, 20 athletes [2.5%]), necessitating additional testing; Five athletes (0.6%) had CMR imaging findings suggesting inflammatory heart disease (3 myocarditis; 2 pericarditis, that resulted in restriction from play. No adverse cardiac events occurred in athletes who underwent cardiac screening and resumed professional sport participation.


Myocarditis and COVID-19 in Young Athletes

As of June, 2021 we have a better understanding of the prevalence of myocarditis in competitive athletes diagnosed with Covid-19 thanks to two large prospective multicenter studies of collegiate athletes.
ORCCA, the first large study of young athletes positive for Covid-19, included 3,018 college athletes from 42 universities. Serum troponin tests, ECG, and echocardiography identified 15 athletes (15/3,018=0.5%) with possible cardiac involvement. In a subgroup of 198 athletes who underwent a primary CMR imaging screening strategy (unselected by the other tests), a higher proportion of athletes demonstrated definite, probable, or possible cardiac involvement (n = 6 [3.0% for primary CMR strategy vs 0.5% for primary conservative strategy]).

The Big Ten registry was the second study and included 13 major universities from the Big Ten athletic conference. The strategy mandated ECG, troponin testing, echocardiography, and CMR imaging for athletes with positive COVID-19 test results, regardless of prior symptomatic status. Of 2,461 athletes,1597 (64.9%) had the complete comprehensive screening testing, including CMR imaging without prior selection. They found that 37 (2.3%) of these athletes demonstrated diagnostic criteria for myocarditis by CMR imaging, including 20 (1.2%) with normal ECG, echocardiography, and troponin test results. This leaves 17 or 1% with these positive conservative test results who would not have been identified without CMR imaging (2.3% for primary CMR strategy vs 1% for primary conservative strategy). Variability was observed in prevalence across universities, and testing protocols were closely tied to the detection of myocarditis. Variable ascertainment and unknown implications of CMR findings underscored the need for standardized timing and interpretation of cardiac testing. They propose that their CMR imaging data provide a complete prevalence of clinical and subclinical myocarditis in college athletes after COVID-19 infection. 

Comparison of the results of a conservative testing approach (symptoms, troponin, ECG and echocardiogram) vs a CMR for all athletes with COVID-19 for detecting myocarditis is best estimated using data from the 2 largest studies summarized above.  The results are 3.0-2.3% for primary CMR vs 0.5-1% for primary conservative strategy.  A “CMR for all strategy” more than doubles sensitivity but it is not clear if this added yield from a very expensive test saves lives or lessens myocardial damage.  Any comparison of a CMR strategy to another approach will favor CMR if the images are both the test result and the gold standard. The more appropriate gold standard would be the clinical outcome of the athletes; ie, do they really develop myocardial damage and/or a bad clinical outcome such as death or heart failure?

 It is revealing to consider some of the factors/variables not incorporated in these 2 studies that could affect the conclusions:  

  1. The test characteristics of the diagnostic elements to identify COVID-19 myocarditis symptoms, troponin, ECG and echocardiogram).
  2. The relative importance and characterization of the symptoms of myocarditis (including chest pain, breathing abnormalities, palpitations and fatigue)
  3. The test characteristics of the tests identifying the presence of the Sars-CoV-2 virus and how applied (nucleic acid amplification tests (NAATs) and antigen tests, nasal swab vs saliva, lab-based vs point of contact)
  4. The timing of assessment relative to the diagnosis of COVID-19 (particularly lacking is data regarding the “long-hauler” phenomena)
  5. The exact significance of the CMR findings reported in athletes (what is pathological, associated with long term damage and what is the result of exercise training?)
  6. The virulence of the causative genomic variant of Sars-CoV-2 virus 


These considerations do not detract from the available data since they could not be controlled or assessed in these studies.  However, they emphasize the need for humility and an athlete-centered, shared decision-making approach to athletes.  Furthermore, these studies require longer follow up to determine the risk of death due to the markers of myocarditis.


In an excellent Editorial responding to the Big Ten study, Udelson et al summarized the available data on return to play after COVID-19 Infection. We agree with them that the current data support a conservative approach to cardiac testing as in the guidelines and that clinical judgement be applied to individual cases. We also emphasize the need for an athlete-centered, shared decision-making approach in the management of young athletes with myocarditis post COVID-19.  These findings are consistent with our COVID-19 experience at Stanford Sports Medicine.

COVID-19 Vaccines and Myocarditis

Since April 2021, there have been increased reports to the Vaccine Adverse Event Reporting System (VAERS) of cases of called myocarditis and pericarditis happening after mRNA COVID-19 vaccination (Pfizer-BioNTech and Moderna) in the United States. These reports are rare, given the number of vaccine doses administered, and have been reported after mRNA COVID-19 vaccination, particularly in adolescents and young adults. Most patients who received care responded well to medicine and rest and quickly improved.

The cases reported are mostly in male adolescents and young adults age 16 years or older, more often after getting the second dose of one of these two COVID-19 vaccines than after the first dose, typically within several days after COVID-19 vaccination. They can usually return to their normal daily activities after their symptoms improve, and the above guidelines for management of myocarditis should be followed.Overall crude reporting for myo/pericarditis ages 12-17 is 9.1 cases per million in females and 66 per million in males. Overall reporting for ages 18-24 is 5 per million in females and 56 per million in males.  The available outcome data indicate that patients generally recover from symptoms and do well.  The CDC continues to recommend COVID-19 vaccination for everyone 12 years of age and older, given the greater risk of COVID-19 illness and related, possibly severe complications than the cases associated with vaccines.

 Additional Resources and references


Section Two: Guidelines from International Recommendations for Electrocardiographic Interpretation in Athletes

Authors, Alphabetical Order 

On Behalf Of The California American College of Cardiology Exercise Health And Sports Cardiology Committee


The present section will provide a succinct overview of the interpretation of the electrocardiogram (ECG) in the athletic population by providing select resources for a more comprehensive understanding of ECG changes occurring in athletes, supported by examples of abnormal findings.

This document does not serve to support or refute the case for pre-participation screening with an ECG, but rather as a resource to help those providers whenever they are faced with analyzing an athlete’s ECG, including team physicians, family medicine, sports medicine, cardiology, athletic trainers and others caring for athletic individuals.

1. ECGs provided in this document with brief description. ECGs obtained from Dr. Vic Froelicher.
2. “International recommendations for ECG in the athlete” provides tables and figures that clearly delineate:

Figure 2-1: Normal and Abnormal ECG Findings [PDF]
Table 2-1: Definitions of ECG Findings [PDF]
Table 2-2: Evaluation Suggested in the Setting of these ECG Findings [PDF]

Copyright Source: Journal of the American College of Cardiology; Volume 69, Issue 8, February 2017. Authors: Sanjay Sharma, Jonathan A. Drezner, Aaron Baggish, Michael Papadakis, Mathew G. Wilson, Jordan M. Prutkin, Andre La Gerche, Michael J. Ackerman, Mats Borjesson, Jack C. Salerno, Irfan M. Asif, David S. Owens, Eugene H. Chung, Michael S. Emery, Victor F. Froelicher, Hein Heidbuchel, Carmen Adamuz, Chad A. Asplund, Gordon Cohen, Kimberly G. Harmon, Joseph C. Marek, Silvana Molossi, Josef Niebauer, Hank F. Pelto, Marco V. Perez, Nathan R. Riding, Tess Saarel, Christian M. Schmied, David M. Shipon, Ricardo Stein, Victoria L. Vetter, Antonio Pelliccia and Domenico Corrado

Examples of ECGs found in Athletes

Section Three: Cardiopulmonary Exercise Testing: Indications, Interpretation & Case Examples

Authors: Gerald Bourne, MD, Elizabeth H. Dineen, DO, Jeffrey Dwyer, PhD, Victor Froelicher, MD and Jonathan Myers, PhD on behalf of the CA ACC Sports Cardiology and Exercise Health Committee*

*authors listed in alphabetical order.



The American College of Cardiology’s California Chapter has established a Sports Cardiology and Exercise Health Committee in response to the growing need for evidence-based, standardized, comprehensive care for athletes. The committee aims to serve as a resource for consultative cardiovascular assessment of highly active individuals as well as a home for educational tools to aid in their assessment and management.

The Cardiopulmonary Exercise Test ( CPET) is an extremely valuable but underutilized non-invasive examination. The Exercise and Sports Cardiology Committee would like to promote CPET as an effective tool in evaluating exercise function.

The Cardiopulmonary Exercise Test


The Cardiopulmonary Exercise Test (CPET) is an extremely valuable but underutilized non-invasive examination. The Exercise Health and Sports Cardiology Committee would like to promote CPET as an effective tool in evaluating cardiac function.

Physical activity requires the integrated performance of cardiovascular, pulmonary, metabolic, and neuromuscular systems. The Cardiopulmonary Exercise Test (CPET or CPX) evaluates the concerted response of these systems during exercise and provides an assessment of each component required for exercise performance. In contrast to standard exercise test modalities, the defining element of CPET is the continuous measurement of ventilation and gas exchange.

The relationship between oxygen consumption and carbon dioxide production and a vast array of non-invasive physiological parameters are used to determine the function of each component of physical exertion. From rest, through moderate exercise, to exhaustion, CPET enables an evaluation of overall capacity of the subject and the physiologic integrity of each system from ventilation, to circulatory transport, to tissue uptake. Although the significance of disturbances in the relationships between physiologic systems measured during CPET may be initially daunting, the utility and indications for this test are important and easy to understand.

Cardiopulmonary fitness is determined by measuring oxygen uptake (V̇O₂) at maximal exercise, while the ventilatory (anaerobic) threshold (VT) occurs at a submaximal point during exercise when pulmonary ventilation increases disproportionately to oxygen uptake. Cardiovascular limitations are exemplified by low values for peak V̇O₂ and ventilatory threshold. The ratio of oxygen uptake to work rate is reduced due to an impaired ability of the cardiopulmonary system to provide oxygen to the working muscles. A low stroke volume may be reflected by a low peak V̇O₂ per heart beat (O₂ pulse). Pulmonary limitations that may result in a reduced V̇O₂ are revealed by an abnormal breathing reserve, oxygen desaturation, CO₂ retention, or abnormal expiratory flow rate. Peripheral myopathy is suggested by a low peak V̇O₂ , with an elevated minute ventilation to V̇O₂ ratio and a high cardiac output to V̇O₂ slope. Further discrimination of the cause of exercise intolerance can be determined by evaluating the relationships between additional variables. Endurance athletes commonly will have findings on CPET that may be considered abnormal in the sedentary population. These athletes may have higher peak V̇O₂ , higher anaerobic threshold, a high O₂ pulse reflecting a higher stroke volume and a maximum exercise ventilation that nearly matches the maximum voluntary ventilation, such that the breathing reserve is nearly zero given their exceptionally high cardiovascular capacity.

Figures 1-9   Sample findings in CPET Testing


Dyspnea of unknown etiology

CPET can help differentiate between pulmonary, cardiac, neurologic, muscular and psychological basis of dyspnea that limits exercise performance.

Diagnosis and assessment of the severity of organ dysfunction, relative compensatory contributions of other organ systems, prognosis, sequential monitoring in the following disease processes.



Heart Failure with reduced ejection fraction
Heart Failure with preserved ejection fraction
Valvular Heart Disease
Hypertrophic Cardiomyopathy
Congenital Heart Disease: Persons with CHD often have abnormal recognition of DOE
Coronary Artery Disease.


Pulmonary Artery Hypertension
Secondary Pulmonary Artery Hypertension
Chronic Obstructive Pulmonary Disease
Interstitial Lung Disease


Mitochondrial Myopathy
Neuromuscular Disease
Chronic Fatigue/ Post Exertional Malaise

Assessment of Surgical Risk

CPET responses have been increasingly applied to stratify risk as part of pre-surgical assessment. For example, peak V̇O strongly predicts risk for surgical complications, length of hospital stay, and ability to return to work across a wide spectrum of surgical interventions.

Development of Cardiac or Pulmonary Rehabilitation exercise prescriptions and guidelines

The foundation of an appropriate exercise prescription in a patient with cardiovascular or pulmonary disease is the exercise test, and because of its superior precision, the CPET provides the most accurate method to develop an individualized exercise prescription.

Assessment of safety and metrics for an exercise training program

The CPET provides a wealth of information on safety, rhythm abnormalities, ischemic responses, and symptoms that are important in developing a safe and appropriate exercise prescription.

Assessment of cardiorespiratory fitness and subsequent response to a training program or interventions in healthy individuals, athletes or those with underlying cardiovascular disease (as listed above)

The CPET provides an accurate metric to quantify changes in fitness in response to exercise training and other interventions (eg. drug, surgical or device) among both healthy individuals and those with cardiovascular disease.

How to Perform a Cardiopulmonary Exercise Test

CPET test administration requires specific equipment and personnel in order to generate accurate and reliable data.


  • Ergometer (cycle, treadmill, rowing simulator, etc)
  • Gas exchange mask/mouthpiece
  • Metabolic cart consisting of gas analyzers, expiratory gas flow and volume, and software
  • Continuous electrocardiogram
  • Blood pressure measurement device


  • Exercise physiologist to set up the exercise protocol, prepare/calibrate equipment and possibly monitor during the test
  • Medical assistant or nurse to monitor during the test
  • Qualified medical professional for interpretation of the test

Many patients can be tested on a cycle ergometer or treadmill, based on comfort level and lab availability. If testing athletes, the type and intensity of the test protocol should be matched to their sport (ex: having a sprinter perform sprints on a treadmill or a rower using the rowing ergometer) which will provide more useful test results. Cycle tests are logistically easier for monitoring blood pressure and generate electrocardiogram tracings with fewer artifacts and unstable baselines.

The exercise protocol will vary depending on the interview conducted by the ordering provider. Common exercise protocols include the step protocol (ex: Bruce-type protocol), with a step-wise or incremental increase in work rate over time, or a ramp protocol with a continuous increase in work rate over time. The exercise test should be individualized by the exercise physiologist or medical provider administering the test with a target test time between 8-12 minutes.

Key Metrics

Heart rate, blood pressure, and electrocardiographic responses to exercise should be evaluated in a similar fashion as a routine exercise test
Ventilation and Gas Exchange: Measured throughout exercise
Maximum V̇O₂ : This is the aerobic capacity or total body oxygen uptake verified by achieving a heart rate within 10 bpm of the age-predicted HRmax, a lack of change in the V̇O over two consecutive work rates, and/or a respiratory exchange ratio above 1.10 (presumably reflecting a lactate accumulation above 70-80 mg/dl). If these criteria cannot be met, the oxygen uptake at maximally tolerated exercise is referred to as peak V̇O . V̇O is often a metric that is tracked over time to monitor treatment or interventions as well as to monitor disease progression or prognosis.
V̇CO₂: Carbon dioxide elimination measured throughout the test.
Lactate Threshold V̇O₂ ≈ Anaerobic Threshold ( AT ) ≈ Ventilatory Threshold ( VT ): V̇O above which lactate accumulates in the blood. This may be a useful marker of an individual’s cardiorespiratory fitness and endurance. Often referred to as anaerobic threshold or ventilatory threshold. Can be determined by ventilatory analogs of lactate accumulation such as V̇O vs V̇CO and V̇E vs V̇O graphs. 
Respiratory exchange ratio (RER): The ratio of CO produced to oxygen consumed (V̇CO/V̇O). A marker of fuel utilization (0.70 ≈ fat utilization and ≥1.0 ≈ carbohydrate utilization). Also a reflection of the degree of physiologic effort (≥1.10 associated with maximal effort)
Oxygen Pulse (V̇O₂ /HR): Will increase at the beginning of exercise largely due to the increase in stroke volume and then will reach a plateau near the end of exercise. If this plateau is reached sooner than expected, it can be due to impaired oxygen extraction or impaired stroke volume (due to CAD or left ventricular dysfunction).
Pulmonary Ventilation (V̇E): Volume of air exhaled per unit time. Generally not a limiting factor unless there is a low breathing capacity or a disease state that impairs air flow.
Change in V̇O₂ /change in work rate: This generally has a linear relationship of 10 mL/min of oxygen uptake for every 1 Watt increase in work rate. This relationship may change in illnesses such as cardiovascular diseases where oxygen uptake may be decreased compared to change in work rate.
Heart rate recovery: Reflection of vagal reactivation. Slow heart rate recovery associated with higher adverse outcomes. Often expressed as 1-minute post exercise (HRR1) or 2-minutes post exercise (HRR2). HRR1 <12 beats/min or HRR2 <22 beats/min associated with higher risk.
V̇E/V̇CO₂: Can be expressed as a ratio (at a point in time during exercise) or as the slope of the change during exercise. Reflects ventilatory efficiency, ie. the ventilatory requirement to eliminate a given amount of CO, and is a strong prognostic marker.
Oxygen uptake efficiency slope (OUES): The relation between the change in oxygen uptake during exercise and the log of the change in ventilation. The OUES is another measure of ventilatory inefficiency, and is a strong predictor of prognosis in patients with heart disease.
Perceived exertion: A reflection of the degree of the individual’s physical effort. Often expressed using a 6-20 scale, with 6 representing a resting state and 20 representing maximal effort.

Cardiopulmonary Exercise Test Cases

Case Study – Heart failure


The patient is a 60 year old sedentary Caucasian male outpatient 71 inches tall, weighing 180 lbs. He is currently not smoking but has 23 pack years of smoking (1 pack/day for 23 years). The patient’s weight is normal (BMI=25). A history of abnormal lipids was reported (high TC, LDL, low HDL). The patient also has a history of high blood pressure. He over the past 6 months has noted increasing shortness of breath with exertion.

Reason for Referral:

Evaluation of increasing shortness of breath with regular daily activities.

Past Medical History:

There is a history of “mildly reduced ventricular function”, diagnosed approximately 6 years ago, although no imaging results are available. He reports infrequent “skipped beats”. No other history of non-cardiac or other medical problems are noted. Current medications include an ACE inhibitor, statin, and diuretic.

      CPX Test Results:


ECG: Normal sinus rhythm and left bundle branch block. 

Pulmonary Function: Forced vital capacity is 3.50 L (79% of expected) and the FEV1/FVC is 50% (Normal > 75%).

Heart rate: 71

Blood pressure: 112/68


Ventilatory threshold  
Exercise time (min:sec) 4:43
Heart rate beats/min) 98
Oxygen uptake (ml/kg/min) 7.7
Oxygen uptake (ml/min) 630
VO2 % peak 57%


Peak Exercise Reason for stopping – Shortness of breath       
Exercise time (min:sec) 11:14            
Heart rate 146            
Systolic blood pressure (mmHg) 166
Estimated METs 5.1       Ventilatory Efficiency
Oxygen uptake (ml/kg/min) 13.4 (40.4% predicted)    VE/VCO2 Slope  38.7
Oxygen uptake (ml/min) 1,096       OUES   1.18
VE (l/min) 45.0       PetCO2   31.7
VCO2 (ml/min) 1,243       Peak VE/VO2  41.0
O2 pulse (ml/beat) 7.50
RER 1.13        Breathing reserve       27.5%
SaO2 96    HRR1  = 5      
Perceived exertion  20    HRR2  = 16      


Key items:

  • Peak RER and perceived exertion suggest maximal effort
  • Limiting symptom was dyspnea; no chest discomfort reported
  • Severely impaired exercise tolerance (40.4% of age-predicted peak VO2
  • Exercise ECG not analyzable due to LBBB; infrequent PVCs occurred
  • Normal heart rate and blood pressure response; impaired heart rate recovery at 1 and 2 min post exercise
  • Ventilatory threshold occurred at low VO2 (7.7 ml/kg/min) but normal percentage of peak  
  • Normal breathing reserve; high VE/VCO2 slope and low OUES suggest ventilatory inefficiency
  • Low peak O2 pulse; plateau beginning ≈50% of peak
  • Abnormal resting PFTs suggest airflow limitation and possible pulmonary contribution to exercise intolerance



  • Severely impaired exercise tolerance 
  • Early dyspnea during exercise and daily activities, ventilatory inefficiency suggest impaired cardiac output
  • Higher than normal risk for age indicated by severely impaired peak VO2, heart rate recovery, and indices of ventilatory inefficiency


Myers J, Arena R, Cahalin L, Labate V, Guazzi M. Cardiopulmonary exercise testing in heart failure. Current Problems in Cardiology 40:322-372, 2015.

Malhotra R, Bakken K, D’Elia E, Lewis GD. Cardiopulmonary exercise testing in heart failure. JACC Heart Fail 4:607-16, 2016.

Balady GJ, Arena R, Seitsema K, Myers J, Coke L, Fletcher GF, Forman D, Franklin B, Guazzi M, Gulati M, Keteyian S, Lavie CJ, Macko R, Mancini D, Milani RV. A Clinician’s  Guide to Cardiopulmonary Exercise Testing. A Scientific Statement from the American Heart Association. Circulation 122:191-225, 2010.

Case Study – Coronary artery disease


The patient is a 68 year old sedentary Caucasian male outpatient 65 inches tall, weighing 160 lbs. The patient is currently not smoking but has a 50 pack year history of smoking (2 packs/day for 25 years). The patient is 10 lbs over the average appropriate body mass index (BMI=26.6) which qualifies as overweight. A history of abnormal lipids was reported (high TC, LDL, low HDL). The patient also has a history of high blood pressure.

Reason for Referral:

Evaluation of chest pain

Past Medical History:

The patient has the following symptoms: shortness of breath with regular daily activities and occasional mild chest discomfort. There is no other history of cardiac disease, cardiac events or dysrhythmias. No other history of non-cardiac or other medical problems are noted. Current medications include a beta blocker, ACE inhibitor, statin, and diuretic.

CPX Test Results:


ECG: Within normal limits

Pulmonary Function: Forced vital capacity 2.9 L (73% of expected) and the FEV1/FVC is 53% (Normal > 75%)

Heart rate: 76

Blood pressure: 146/78

Ventilatory threshold  
Exercise time 5:36
Heart rate 89
Oxygen uptake (ml/kg/min) 8.2
Oxygen uptake (ml/min) 868.4
VO2 % peak 71%
Peak Exercise Reason for stopping – Shortness of breath (with slight chest pain)
Exercise time (min:sec) 8:01            
Heart rate 99            
Systolic blood pressure (mmHg) 180
Estimated METs 6.0       Ventilatory Efficiency
Oxygen uptake (ml/kg/min) 11.5 (62% predicted)    VE/VCO2 Slope  35.9
Oxygen uptake (ml/min) 1,215       OUES   1.48
VE (l/min) 41.6       PetCO2   31.7
VCO2 (ml/min) 1,470       Peak VE/VO2  34.4
O2 pulse (ml/beat) 12.3
RER 1.21    HRR1 = 10 Breathing reserve       23%
SaO2 (%) 95    HRR2 = 16       
Perceived exertion 19            

Key items:

  • Peak RER and perceived exertion suggest maximal effort
  • Impaired exercise tolerance (62% age-predicted peak VO2 achieved)
  • Exercise ECG shows 2.0 mm downsloping ST depression; resolved by 2 min recovery; no arrhythmias observed
  • Chest discomfort (≈1 out of 4) at peak exercise resolved by 1 minute in recovery
  • Chronotropic incompetence; impaired heart rate recovery
  • Borderline breathing reserve; VE/VCO2 slope and OUES suggest ventilatory inefficiency; normal O2 sat
  • Flattening of Opulse beyond ≈50% VO2


  • Exercise intolerance attributable to high likelihood of CAD (ischemic ECG changes, chest pain, plateau of O2 pulse)
  • Pulmonary involvement suggested by low FEV1, limited breathing reserve, elevated VE/VCO2 slope and reduced OUES
  • CPET results suggest further evaluation for CAD is warranted


Chaudhry S, Arena A, Hansen JE, Lewis GD, Myers J, Sperling LS, LaBudde BD, Wasserman K. The utility of cardiopulmonary exercise testing to detect and track early-stage ischemic heart disease. Mayo Clin Proc 85:928-932, 2010.

Balady GJ, Arena R, Seitsema K, Myers J, Coke L, Fletcher GF, Forman D, Franklin B, Guazzi M, Gulati M, Keteyian S, Lavie CJ, Macko R, Mancini D, Milani RV. A Clinician’s  Guide to Cardiopulmonary Exercise Testing. A Scientific Statement from the American Heart Association. Circulation 122:191-225, 2010.

Chaudhry S, Arena R, Bhatt DL, Verma S, Kumar N. A practical clinical approach to utilize cardiopulmonary exercise testing in the evaluation and management of coronary artery disease: a primer for cardiologists. Curr Opin Cardiol 33:168-177, 2018.


HISTORY OF CURRENT COMPLAINT: Patient is a 62 y-o female who reports dyspnea on exertion of progressive intensity and frequency over the past eight months. She denies symptoms at rest and in self-care activities. Unable to climb a flight of stairs without stopping to catch her breath. Stopped exercising on her stationary cycle 4 months ago due to fatigue and SOB. She denies chest pain but reports occasional tightness or pressure when she is severely SOB.

REFERRAL: Dyspnea or unknown origin; is it cardiac, pulmonary, or deconditioning?

PAST MED HX: Four years ago, the patient had NSTEMI; symptoms were chest tightness, mid-scapular pain, and severe dyspnea. Two stents placed in culprit RCA. LAD and LCX with luminal irregularities. 90% stenosis in OM1 and OM2 treated medically. HTN, Type-2 DM, obesity; stopped smoking 8 years prior to NSTEMI. No asthma. PFTs two years ago with normal.  BMI above 30.0 for the past 20 years with recent 15-pound weight gain.


Exercise performance: 

   Time: 8:00         Watts: 80 (72% pred; mild deficit)

Reason for stopping: moderately severe dyspnea, chest tightness


PeakVO2: 18 ml/kg/min (70% pred)

Anaerobic threshold: 52% peakVO2

VO2/Watts slope: 14 ml / Watt (normal = 8.7-11.9.9)


HR @ peak exercise: 88% age-predicted maximum

No ECG changes: no ectopy or dysrhythmia

BP response: adaptive, mildly hypertensive

HR/VO2 slope: 3.6 beats/ml (normal = 3.0-4.0)

VO2/HR (analog of stroke volume: low-normal


    Vemax: 42 L/min tidal volume (Vt) 70% pred High ventilation frequency (Vf)

PetCO2: 45 mm Hg

Exercise Flow-Volume Loops: patient ventilated low in her forced vital

capacity (FVC), leaving 1.5 L of her Inspiratory Reserve Volume (IRV)

unused for tidal breathing. At peak exercise, performed 75% of each

exhalation in the Zone of Effort Independent Flow Limitation.


  • A cardiac basis of patient’s symptoms is ruled out:

PeakVO2 is only mildly reduced

Oxygen-pulse is low-normal consistent with a normal stroke volume

  • Patient is deconditioned:

Low AT and elevated VO2/Watts

  • Ventilatory Pattern is abnormal and the basis of patient’s dyspnea:

Fast Vf with reduced Vt; the result of forced expiratory efforts limited by

progressively collapsing small airways as the patient ventilated low in her

FVC. This abnormal ventilatory pattern invariably creates sensation of

SOB and may result in CO2 retention as demonstrated by this patient.

CONCLUSION: Patient’s dyspnea is pulmonary in origin. Patient is deconditioned.


Wasserman K, Hansen JE, Sue DY, Stringer WW, Whipp BJ. Clinical Exercise Testing: Principles of Exercise Testing and Interpretation Including Pathophysiology and Clinical Applications. Philadelphia: Lippincott Williams and Wilkins, 2012.

Huang W, Resch S, Oliveira RK, Cockrill BA, Systrom DM, Waxman AB. Invasive cardiopulmonary exercise testing in the evaluation of unexplained dyspnea: Insights from a multidisciplinary dyspnea center. Eur J Prev Cardiol. 2017;24(11):1190–1199.

Arena R Sietsema KE. Cardiopulmonary exercise testing in the clinical evaluation of patients with heart and lung disease. Circulation. 2011;123(6):668–680.


HISTORY OF CURRENT COMPLAINT: Patient is a 52 yo female who reports weakness in arms and legs for the past 14 years. Over the past 4 years, she has experienced profound fatigue after mild activity that may last for days. She discontinued using her stationary cycle two years ago. She felt compelled to quit her job due to fatigue and weakness. When deeply fatigued, she has short-term memory deficits and a sensation she describes as “brain fog.”

REFERRAL: Two-Day CPX (24-hour interval) to document functional capacity on Test-1 and Test-2; identify bio-markers consistent with CFS/PEM.

PAST MED HX: Patient never smoked. No DM, HTN, hyperlipidemia, renal or pulmonary disorders. Muscle CK and inflammatory markers are negative. Normal echocardiogram. No previous exercise tests. Normal blood panel and Chem-7.

CXR is normal..


   PFTs: normal pre- and post-exercise on both Test-1 and Test-2.

   Exercise: Patient cycled to volitional exhaustion on a 10 Watt ramp protocol.

PeakVO2: Supra-normal peak VO2 in both tests.

   Ventilatory threshold (V-AT): analog of lactate threshold (V-Slope method) was normal.

Cardiac: Patient achieved 88% age-predicted HRmax in both tests with normal

ECG; no ectopy or dysrhythmia, normal BP response.

Ventilation: Ventilatory response was normal and nearly identical in both Test-1

and Test-2: slope VE/VCO2 = 27, PetCO2 = 39-41.


PeakVO2     Max Work     VO2@AT      Work@AT    VO2/Watts*     VO2/HR

ml/kg/min       Watts          ml/kg/min        Watt       ml VO2/Watt  ml O2/beat _____________________________________________________________________________

Test-1       26.3             129                17.0                84                 11.5                11.0

102%pred    94%pred                                                                         118%pred

Test-2        23.0             112                16.5                76                 13.1               10.0

94%pred     82%pred                                                                          113%pred

* Normal range: 8.7-11.9 ml/min/Watt


  • peakVO2: reduced by 12% in Test-2
  • Maximal work rate: reduced by 14% in Test-2
  • Work@V-AT: reduced by 9.5% in Test-2.
  • VO2 per unit work: increased 8% in Test-2. The higher VO2/Watt in Test-2

reflects reduced mechanical efficiency, attributed by some clinicians to

muscle micro-injury, and possibly uncoupling of oxidative phosphoryl-

ation due to mitochondrial dysfunction created by test-1 exercise. These

changes are consistent with Post-Exercise Malaise (PEM), a principle

correlate of CFS.

CONCLUSION:  Exercise is limited by muscular fatigue, greater in Test-2, associated with reduced peakVO2, maximal work rate, work at V-AT, and an increased VO2 per unit work, consistent with PEM/CFS as described in the literature.


Nelson M, Buckley JD, Thomson RL, Clark D, Kwiatek R, Davison K. Diagnostic sensitivity of 2-day cardiopulmonary exercise testing in myalgic encephalomyelitis / chronic fatigue syndrome.  J Trans Med 2019;17:80-88.

Stevens S, Snell S, Stevens J, Keller B, Van Ness JM. Cardiopulmonary exercise test methodology for assessing exertion intolerance in myalgic encephalomyelitis / chronic fatigue syndrome. Frontiers in Pediatrics 2018;6:242.

Snell CR, Stevens SR, Davenport TE, Van Ness JM. Discriminative validity of metabolic and workload measurements for identifying people with chronic fatigue syndrome. Physical Therapy 2013;93(11):1484-1492.



HISTORY: Patient is a 70 yo female who requests exercise evaluation and prescription in preparation for attempts to climb to base-camp on Mount Everest (17,500 feet) and Mount Kilimanjaro (19,341 feet). She denies chest discomfort when exercising.


REFERRAL: Assess peakVO2, ventilatory anaerobic threshold (V-AT), and optimal target HR six months prior to climbing events to provide training guidelines. Perform second CPX two weeks prior to the event to assess progress and status.


PAST MED HX: No HTN, hyperlipidemia, diabetes, pulmonary disease, cardiac disease. Never a smoker. BMI = 22.48. She is active and participates in Pilates and Zumba exercise classes.


CPX TEST RESULTS:  10 Watts ramp cycle protocol


                                                     TEST-1                            TEST-2        % Change


Exercise Time                               11:07                                12:40               +17.0

Max Watts                                      111                                   126                +13.5


peakVO2 (ml/kg/min)                     24.2                                 26.0                +7.4

V-AT (ml/kg/min)                           15.3                                 17.7                 +15.7

V-AT %peakVO2                              63%                                68%                  —

Watts @ V-AT                                 60 W                               75 W               +25.0

VO2/Watts (ml VO2 / Watt)            9.5                                   11.9               +25.0

Peak RER                                       1.08                                  1.14                +5.5


HR max (bpm)                                 168                                  170                 +1.2

% age-pred HRmax                         112%                               113%                —

Oxygen-pulse (ml VO2 / HR)           8.3                                   9.2                 +10.8

HR/VO2 slope (beat / ml VO2)         3.5                                   3.9                 +8.6


HR @ V-AT                                       130                                  141                 +8.5

%HRmax @ V-AT                             77%                                 83%                 —

ECG:                                          No ECG change           No ECG change

Peak systolic BP                             142/81                            152/78              +7.0


Vemax (L/min)                                  52.2                                60.1                +15.0

PetCO2 (mm Hg)                                38                                   36                 -5.0

Peak Ve / VCO2 (LVe/LVCO2)         34.8                                35.0                +2.8




  • Maximal work capacity (Watts) increased 13.5%
  • VO2 at the V-AT increased 15.7%
  • Work (Watts) at V-AT increased 25%
  • HR at V-AT increased 8.5%
  • Oxygen-pulse (analog of stroke volume) increase 10.8%
  • Target HR for training based on Test-1 data is 130-140 77-83% measured HRmax-; target derived from Test-2 is 140-150 (83-88% measured HRmax) maintaining patient between 0-8% of V-AT. 




Patient’s baseline (Test-1) indicates an exceptional fitness status:

  • Maximal work capacity is 131% of the age-predicted value
  • peakVO2 is 108% age-predicted value
  • HRmax is 109% age-predicted value
  • V-AT occurred at 60 Watts, 79% of age-predicted maximal work capacity


Training at the prescribed target intensities;

  • Oxygen pulse was increased by 10.8% with less than 2% change in max HR achieved suggesting an increase in stroke volume.
  • Work at V-AT was increased 25% while VO2 @ V-AT was increased by 15.7%, creating a greater range of activity that may be performed before onset of anaerobic metabolism.
  • Maximal work capacity (Watts) increased 13.5% with an increase in peakVO2 of 7.4%.
  • Slope of VO2 / Watt increased by 25%, consistent with increased oxygen utilization in active tissue 



Weltman A, Weltman J, Rutt R, Seip R, Levine S, Snead D, Kaiser D, Rogol A. Percentages of Maximal Heart Rate, Heart Rate Reserve, and V̇O2peak for Determining Endurance Training Intensity in Sedentary Women. Int J Sports Med 1989; 10(3):212-216. DOI: 10.1055/s-2007-1024903

Henritze J, Weltman A, Schurrer RL, Barlow K. Effects of training at and above the lactate threshold on the lactate threshold and maximal oxygen uptake

European Journal of Applied Physiology and Occupational  Physiology. 1985; 54: 84–88.


Luciene F. Azevedo, Patrícia S. Perlingeiro, Patrícia C. Brum, Ana Maria W. Braga, Carlos E. Negrão & Luciana D. N. J. de Matos (2011) Exercise intensity optimization for men with high cardiorespiratory fitness, Journal of Sports Sciences 2011;29(6):555-561, DOI: 10.1080/02640414.2010.549613.


American College of Sports Medicine. Guidelines for Exercise Testing and Prescription. Lippincott Williams & Wilkins; 10th Edition, 2017. 


Other CPET Resources: 

  1. A Practicum: Cardiopulmonary Exercise Testing and Interpretation. Includes didactic lectures, small group tutorials, and laboratory demonstrations with CPET. Usually, 3 practicums are held each year, next tentatively scheduled for October 8-10, 2020.
  2. Textbook: Principles of Exercise Testing and Interpretation 5th Edition. Authors: Karlman Wasserman, James E. Hansen et al. Marco Guazzi, Francesco Bandera, Cemal Ozemek, David Systrom, Ross Arena
  3. Marco Guazzi, MD, PHD,a Francesco Bandera, MD, PHD,a Cemal Ozemek, PHD,b David Systrom, MD,c,d Ross Arena, PHDb, Cardiopulmonary exercise testing: what is its value? J Am Coll Cardiol. 2017 Sep, 70 (13) 1618-1636.
  4. Guazzi M, Adams V, Conraads V, et al. EACPR/AHA Scientific Statement. Clinical recommendations for cardiopulmonary exercise testing data assessment in specific patient populations. Circulation. 2012 Oct;126(18):2261-2274. DOI: 10.1161/cir.0b013e31826fb946.



Author Affiliations: 


Gerald Bourne, MD,FACC

The Adaptive Behavior Institute

Kensington, CA


Elizabeth H. Dineen, DO

Assistant Clinical Professor

University of California Irvine

School of Medicine, Division of Cardiology 


Jeffrey H. Dwyer, PhD

Department of Cardiology

Kaiser Permanente Medical Center

Vallejo, CA


Victor Froelicher, MD

Professor of Medicine 

Stanford University, Palo Alto VA Medical Center

Division of Cardiology 


Jonathan Myers, PhD

Exercise Physiologist/Cardiopulmonary Specialist

Director, Cardiopulmonary Research

Stanford University, Palo Alto VA Medical Center

Section Four: Imaging of the Athlete’s Heart

Key Points

  1. The LV wall thickness is rarely greater than 13 mm in healthy athletes
  2. The LV relative wall thickness (RWT) and the LV mass to volume ratio are helpful in distinguishing hypertrophic cardiomyopathy (HCM) and athlete’s heart 
  3. The origins of the right and left coronary arteries are often seen on transthoracic echocardiography in young athletes, which may suggest anomalous coronaries 
  4. Wall and chamber measurements with cardiac magnetic resonance imaging (CMR) have been shown to be more accurate than with echocardiography
  5. Late gadolinium enhancement (LGE) on CMR is believed to represent dense replacement fibrosis and its pattern may help narrow the diagnosis. It is seen in approximately 50% of patients with HCM
  6. LV aneurysm, increased trabeculation of the LV, 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. The presence of right ventricular aneurysms or disproportionate dysfunction also suggest the possibility of arrhythmogenic right ventricular cardiomyopathy


Imaging is essential to the diagnostic algorithm when clues from an athlete’s history, an abnormal ECG or pre-participation evaluation suggest the possibility of structural heart disease. Appropriate test selection, optimal imaging protocols, and accurate interpretation are essential to distinguish between the “athlete heart” and cardiac pathology with potential clinical consequences. 

The European Association of Cardiovascular Imaging (EACVI) published an expert consensus statement on multimodality cardiac imaging approach to the Athlete’s Heart in 20151 and the American Society of Echocardiography (ASE) in collaboration with the Society of Cardiovascular Computed Tomography (SCCT) and the Society of Cardiovascular Magnetic Resonance (SCMR) published guidelines on the use of multimodality cardiovascular imaging in young adult competitive athletes in 2020 2Table 1 compares the imaging techniques we will describe in the following parts.

Table 1. Comparison of Imaging Modalities of the Athlete’s Heart described below

Imaging Modality



Cardiac Diseases


– Readily available

– Readily portable

– No radiation

– Dependent on imaging windows and technician

– Limited visualization of proximal coronaries,and ascending aorta. LV trabeculations may be challenging to visualize.

– Valvular heart disease

– Hypertrophic Cardiomyopathy

– Aortopathies

– Congenital heart disease

Cardiac CT

– Gold standard for noninvasive coronary artery assessment

– Excellent at detecting calcification

– Radiation

– Risk of contrast-induced nephropathy

– Coronary artery disease

– Coronary calcium

– Aortopathies

– Structural heart and EP procedure planning

Cardiac MRI

– Gold standard for cardiac structure and myocardial tissue

– Can assess the pattern and amount of myocardial fibrosis

– No radiation

– Cost

– Claustrophobia

– Incompatibility with implanted metal

– Hypertrophic Cardiomyopathy


– Aortopathies

– Valvular heart disease

– Congenital heart disease


Part 1. Exercise-induced Cardiac Remodeling

Exercise training can lead to cardiac remodeling, resulting in structural or functional changes that fall outside the limits of reference of non-athletes3. Athletic remodeling can be best described as proportional; LV mass often increases proportionally to left ventricular end-diastolic volume, left atrial volume often increases proportionally to stroke volume and the right heart often increases proportionally to left heart enlargement. In endurance athletes, right heart enlargement may be more prominent. Typically, LV systolic and diastolic function is preserved in elite athletes. However, endurance athletes, particularly if LV chamber dilation exists, may have a resting LV ejection fraction at the lower limits of normal or mildly reduced (LVEF 45-50%)4. Diastolic function is preserved in endurance athletes5. Just as the LV can dilate in response to endurance training, so too can the RV and atria6. In fact, endurance athletes can have RV chamber dimensions that exceed “normal” values and meet criteria for ARVC7. Isolated RV dilation (not accompanied by LV dilation) or RV regional abnormalities should raise suspicion for pathology.

Left ventricular (LV) adaptation or remodeling to prolonged exercise training was initially explained by the concept of the ‘Morganroth hypothesis’ (Figure 1)8. 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. 

While LV dilation is common in endurance athletes2, critics of the Morganroth hypothesis point to mixed evidence in strength athletes1. Also, sports and exercise is often a combination of both types of training. More recent data using MRI and serial monitoring also challenge this widely held belief. Spence et al9 examined the effects of 6 months of endurance training (3 hours per week of walking/jogging/running, n = 10) or resistance training (3 hours per week of Olympic weightlifting and supplemental strength exercises, n = 13) followed by 6 weeks of detraining on LV morphology and function, aerobic fitness, muscle strength and body composition in younger males (mean age: 27 years). In both groups, the LV mass to volume ratio (0.85 on average) did not change significantly. Using 3D echocardiography, Caselli et al10 showed that the LV mass to volume ratio was close to one in 511 Olympic athletes, irrespective of the type of sport. In college athletes (pre-season assessment), Moneghetti et al11 further demonstrates that the LV mass to volume ratio did not significantly change according to sport type although it was higher in athletes of Black race and lower in females.

Figure 1. The Morganroth Hypothesis, a recently challenged concept 

The Morganroth Hypothesis for the Cardiac remodeling of exercise training

Measuring wall thickness in echocardiography is central for evaluating LV concentric remodeling or hypertrophy. Several pitfalls should be avoided, such as the inclusion of the septal band or mitral apparatus chords in wall thickness measures. Consistency between long axis and short axis also increases reliability of measures. Using the area-length method in both diastole and systole to estimate LV mass by echocardiography can provide greater confidence in the estimates with a usual difference below 5% (Stanford athletic center). A particular attention during screening should be given to asymmetric hypertrophy (septal vs. lateral or apical vs. basal). Apical hypertrophy may be missed on routine screening and acquisition of focused apical views are helpful.

Part 2. Distinguishing HCM from Athlete’s Heart in the “Gray Zone”

LV measurements often fall within the “gray zone” between what is expected for a trained athlete’s heart and pathologic heart disease. Repeat imaging after de-training is one method to distinguish athlete’s heart from pathologic cardiac disease, as the athlete’s LV may normalize. However, de-training is seldomly embraced by the competitive athlete, their trainers or their coaches.


A study of healthy professional NBA basketball players using transthoracic echocardiography (TTE) showed that maximum LV wall thickness exceeded the upper limits of normal (10 mm) in more than half the athletes (but never exceeded 15 mm), the LV end-diastolic diameter exceeded the upper limits of normal (58 mm) in more than one third the athletes (but was often normal when indexed to body surface area), and the LV mass index exceeded the upper limits of normal (115 g/m2) in more than a quarter of the athletes12


The purpose of a study by Caselli et al13 was to consider the ability of echocardiographic and clinical variables to distinguish HCM and athlete’s heart. Twenty-eight athletes free of cardiovascular disease were compared with 25 untrained patients with HCM, matched for LV wall thickness (13 to 15 mm), age, and gender. Athletes had larger LV cavities (60 ± 3 vs 45 ± 5 mm, p <0.001), aortic roots (34 ± 3 vs 30 ± 3 mm, p <0.001), and left atria (42 ± 4 vs 33 ± 5 mm, p <0.001) than patients with HCM. LV cavity <54 mm distinguished HCM from the athlete’s heart with the highest sensitivity and specificity. Left atrium >40 mm excluded HCM with sensitivity of 92% and specificity of 71% (p <0.001). They concluded that in athletes with LV hypertrophy in the “gray zone” with HCM, LV cavity size <54 mm was the most reliable criterion to differentiate HCM from athlete’s heart. 


Concentric LVH is less common in athletes than eccentric or normal geometry but can occur in up to 12% and is often mild14. The process of making a diagnosis involves a comprehensive investigation that typically includes ECG, functional indices from echocardiography, and CMR. Some of the findings used to distinguish athlete’s heart from HCM are represented in Table 2.

Table 2. Findings in the Patterns of Training and Hypertrophic Cardiomyopathy




(distance runners, wide receivers, backs, basketball)

Resistance training/isometric

(wrestlers, linemen, gymnasts)

Hypertrophic Cardiomyopathy

LVEDV (end diastolic volume)



Normal – Reduced* 

(LVEDD < 54 mm)

LVWT (wall thickness)







LVM (mass)




RWT (relative wall thickness)**




Mass/Volume ratio

< 1.0

< 1.0

> 1.0 males


* In “burned-out HCM”, the LV becomes dilated and LV systolic function reduced

** RWT = 2 * posterior LV wall thickness/LV end-diastolic diameter

# In the paper by Caselli et al10, RWT was defined as the ratio of the septal and free wall thickness normalized to LV end-diastolic diameter

Part 3. Selecting the Appropriate Cardiac Imaging Modality in Athletes

Athletes Without Known Cardiac Disease

Cardiac imaging is not routinely incorporated as a component of pre-participation screening for cardiac disease in athletes. The decision to pursue cardiac imaging is primarily driven by suspicious findings from the medical history (e.g. exertional chest pain or syncope), physical exam (e.g. murmur), or EKG (e.g. LBBB, frequent PVCs, pathologic Q-waves, ST-segment depression, T-wave inversion) that increase the athlete’s likelihood of cardiac disease. When cardiac pathology is suspected, TTE is often the initial cardiac imaging modality of choice, since it is widely accessible and comprehensively evaluates the structure and function of the heart without any risks to the athlete2.

However, TTE may be insufficient in diagnosing certain cardiac conditions due to image quality and/or its inherent limitations. Therefore, we propose a targeted imaging approach that depends on the cardiac pathology that is suspected (Figure 2). For example, master’s athletes who engage in higher intensity exercise and have a risk of coronary disease may be considered for cardiac imaging to evaluate for ischemia or electrical instability with maximal exercise testing, perfusion imaging, or coronary CT angiogram. The use of cardiac MRI has become an integral tool in many scenarios in the evaluation of the Athlete’s heart15. Cardiac CT also has an important role in imaging the athlete. 

Athletes With Known Cardiac Disease

For any given cardiovascular condition, deciding which cardiac imaging test to pursue (if any) and when to test can be complex. There are multiple appropriate use criteria expert statements that give guidance on when a particular imaging modality is appropriate by modality (echocardiography16, cardiac CT17) and by disease (stable ischemic heart disease18, heart failure19, valvular heart disease20, structural non valvular heart disease21, and congenital heart disease22). There are also recent updated guidelines for hypertrophic cardiomyopathy23.

Part 4.  Case Examples

CASE 1.  A 20 year-old African American female basketball player presents to cardiology clinic for evaluation of chest pain and syncope during athletic activity. Two years ago she began experiencing fatigue during practice and games, but progressed to the point that she would develop these symptoms when she was ascending stairs. She also had a syncopal event during the middle of basketball practice without prodrome. She spontaneously regained consciousness. There was no family history of cardiac disease. 

Physical exam was normal. EKG demonstrated normal sinus rhythm and T wave inversions in III and avF. TTE showed LVEF that grossly appeared low-normal with normal LV global longitudinal strain (-18.9%), severe LV diastolic dysfunction, and hypertrabeculation of the LV apex. Cardiac MRI demonstrated mildly dilated LV with increased trabeculation at the apex with non-compacted to compacted myocardial ratio of 2.5 in diastole with a calculated LVEF of 55%. There was absence of abnormal delayed myocardial enhancement to suggest scar or infiltrative disease. 

Case 1 Figure 1. TTE 2 chamber view. Increased trabeculations in LV apex and anterolateral wall concerning for non-compaction. EF estimated at 35%

Case 1 Figure 2 and 3: Cardiac MRI 2 chamber and short-axis views of the left ventricle. Noncompacted to compacted myocardial ratio 2.5.


If LV hypertrabeculations with borderline LV ejection fraction are discovered on imaging in a competitive athlete, what is the strongest element that will distinguish true cardiomyopathy from physiologic changes in the athletic heart? 

  • A. Ratio of noncompacted to compacted myocardial layer thickness is >2.0 at end-systole by TTE
  • B. Ratio of noncompacted to compacted myocardial layer thickness is >2.3 at end-diastolic by CMR
  • C. Impaired systolic and/or diastolic function
  • D. Positive family history of cardiomyopathy
  • E. Presence of LGE on CMR
View the Correct Answer

Answer: C

Impaired systolic and/or diastolic function

Findings of borderline LV systolic function in conjunction with symptoms were concerning for a diagnosis of LV noncompaction. She completed an exercise treadmill test and there were no inducible arrhythmias. A 14-day event monitor demonstrated 1 run of ventricular tachycardia lasting 6 beats. She was referred for genetic evaluation, started on a low-dose beta blocker for suppression of her NSVT, and told to abstain from athletic activity in the short term with plans for serial reassessment with imaging and heart rate monitoring over time. 

Among competitive athletes, especially those of African American ethnicity, hypertrabeculation of the LV and RV apex is more common. The hypothesized explanation is that a chronic increase in cardiac preload in the setting of isotonic physiology will produce enlargement of the intertrabecular recesses which may regress on detraining8. About 15% of those who meet the diagnostic cutpoints for pathologic noncompaction by TTE or CMR (ratio of noncompacted to compacted myocardial layer thickness is >2.0 at end-systole by TTE, and ratio of noncompacted to compacted myocardial layer thickness is >2.3 at end-diastole by CMR) will be overdiagnosed with LV noncompaction.  In order to distinguish physiologic changes in the athletic heart from a true diagnosis of LV noncompaction, the strongest element to support the diagnosis of a myocardial disease is impaired systolic or diastolic function1. A cutoff of EF <50% has been suggested. In borderline cases where the EF is between 50-54%, a reduction in global longitudinal strain of < -15% may be suggestive of an underlying cardiomyopathy.

Other features that distinguish true noncompaction cardiomyopathy from physiologic changes in the competitive athlete include very thin compacted layer (<5 mm), marked impairment of LV systolic function, presence of LGE on CMR, and clinical findings suggestive of the diagnosis such as heart failure, tachyarrhythmias, and embolic events1.

CASE 2. A 40 year-old male long distance runner and mountain biker with paroxysmal atrial fibrillation presented with decreased exercise capacity during episodes of atrial fibrillation. His exercise regimen consists of 75-100 miles of mountain biking a week. He is taking propafenone, metoprolol succinate, and rivaroxaban, which were prescribed post-cardioversion, and in the past he had tried flecainide but did not maintain sinus rhythm. His family history is significant for coronary artery disease in two second degree relatives. There is no personal history of congenital heart disease.  

Physical exam was normal. EKG demonstrated normal sinus rhythm and an incomplete RBBB. A 14-day event monitor demonstrated 0% atrial fibrillation burden and his CHADSVASC score was 0. TTE showed LVEF of 65%, normal LV diastolic function, a moderately enlarged RV with preserved systolic function, a mildly dilated LA with a size of 45 mL/m2, a severely dilated RA with a size of 38 mL/m2, trace tricuspid regurgitation, and normal pulmonary pressures. Cardiac MRI demonstrated right ventricular dilation and mild right ventricular hypertrophy without ARVC/D criteria, normal right ventricular function, mild dilation of the LV, and biatrial enlargement (Figure below). Both ventricles did not demonstrate anatomic abnormalities such as sacculations, aneurysms, or focal thinning. 

The differential diagnosis for an athletic patient with RV dilation includes arrhythmogenic RV cardiomyopathy, toxic cardiomyopathies, primary and secondary pulmonary hypertension, and congenital heart diseases1. Ultimately because the RV did not demonstrate any structural or functional abnormalities, the majority of the patient’s findings were attributed to physiologic adaptations of the heart in an endurance athlete. The patient was told to continue to exercise without limitations, and was referred to electrophysiology for consideration of ablation in light of his recurrent need for cardioversions and insufficient treatment with different antiarrhythmic and rate control strategies.

Case 2 Figure. TTE 4 chamber view. Moderately enlarged RV, a mildly dilated LA with a size of 45 mL/m2, a severely dilated RA with a size of 37.7 mL/m2


What would be the next best step in management in this endurance athlete with paroxysmal atrial fibrillation?

  • A. Continue current management
  • B. Uptitration of beta blocker to a resting heart rate of 30
  • C. Retrial of pill-in-the-pocket approach with a higher dose of flecainide
  • D. Referral for ablation
  • E. Recommendation for detraining
View the Correct Answer

Answer: D. Referral for ablation

Athletes have higher vagal tone resulting in resting sinus bradycardia. Rate control can have the effect of slowing the resting heart rate while also reducing performance during exercise by lowering the heart rate, producing unwanted side effects both during rest and during exercise. Therefore, a rhythm control strategy is often preferred8.

Antiarrhythmics such as flecainide and propafenone, when used alone, can organize atrial fibrillation into 1:1 atrial flutter due to slowing of atrial myocardial conduction without the use of an additional AV blocking drug. Therefore, AV nodal blockers are used in combination with flecainide and propafenone and are rarely tolerated in athletes,given the AV nodal blocker slowing of heart rate that can inhibit performance. A pill in the pocket approach with 200-300 mg of flecainide can be considered for athletes with low AF burden and absence of sinus node disease, but is not always effective, as in the case of this patient. Given the frequent intolerance or aversion to medications in athletes, ablation is often considered early. Success rates are similar for athletes and nonathletes, with 84% freedom from recurrence after 3 years following multiple procedures24

Detraining is effective at reducing AF in an athlete, but significant deescalation of athletic regimen is not desirable for many athletes and often is not recommended until all other options are exhausted24.

In our particular case, the patient was deemed to have echo findings consistent with endurance athlete changes and not a cardiomyopathy. He was told to continue to exercise without limitations, and was referred to electrophysiology for consideration of ablation in light of his recurrent need for cardioversions and insufficient treatment with different antiarrhythmic and rate control strategies.

CASE 3. A 40 year-old woman competitive bodybuilder was referred to cardiology for a systolic murmur and transthoracic echocardiogram showing LVH. She had prior syncope associated with blood draw and with stress while taking a hot shower. In addition to competitive weightlifting, she also does high intensity interval training (HIIT) and exercises in total about 3 hours 6 days per week. Her family history is significant for HCM in her cousin, who underwent myectomy and primary prevention ICD. Continuous rhythm monitoring showed no ventricular arrhythmia. Her TTE demonstrated asymmetric septal hypertrophy with LV septal thickness of 20 mm, systolic anterior motion of the mitral valve with an LVOT gradient of 48 mmHg with Valsalva and these findings were consistent with HOCM. Cardiac MRI showed 5-10% LGE in the LV septum without evidence of aneurysm. 

Parasternal long and short images, which demonstrate asymmetric septal hypertrophy with a thickness of ~ 20 mm.

Parasternal long and short images, which demonstrate asymmetric septal hypertrophy with a thickness of ~ 20 mm.

Apical 5 chamber view without color Doppler, which demonstrates systolic motion of the anterior mitral leaflet and flow acceleration through the left ventricular outflow tract.

Apical 5 chamber view with color Doppler, which demonstrates systolic motion of the anterior mitral leaflet and flow acceleration through the left ventricular outflow tract.

Peak LVOT gradients at rest, with Valsalva maneuver, and at peak exercise

T1-weighted cardiac magnetic resonsance image with gadolinium contrast showing the left ventricle in short axis. Within the left ventricular septum (dark), there is evidence of late gadolinium enhancement (bright), which constituted 5-10% of the left ventricular myocardium

Question 1 of 3: Which of the following cardiac imaging findings are NOT associated with increased risk of sudden cardiac death?

  • A. LGE > 15% on cardiac MRI
  • B. Presence of LV aneurysm
  • C. Maximal LV wall thickness > 30 mm in any segment
  • D. Mitral regurgitation
  • E. LVEF < 50%
View the Correct Answer

Answer: D. Mitral regurgitation

Question 2 of 3: Should she undergo prophylactic ICD implantation?

  • A. Yes
  • B. No


View the Correct Answer

Answer: No

She has 0 “major” risk factors (sudden death in a first degree relative, LVH > 30 mm, recent unexplained syncope, LV aneurysm, and LVEF < 50%). Other risk factors that may aid in the decision-making, extensive LGE or CMR (>15% of LV mass) and NSVT, were also absent.

Question 3 of 3:  How should she be counseled in regards to her exercise regimen?

  • A. Refrain from all physical activity
  • B. No exercise restrictions
  • C. Shared discussion about participation in moderate or high-intensity sports


View the Correct Answer

Answer: C

After a discussion with this athlete, we decided that she avoid her weightlifting and high-intensity interval training. Previous guidelines recommended against moderate or high-intensity competitive sports in athletes with clinical expression of HCM. However, recent evidence of HCM patients showed a similar ventricular arrhythmia burden in competitive athletes versus non-athletes20. Current HCM guidelines21 suggest a shared discussion about participation in moderate or high-intensity competitive sports for individuals with HCM, recognizing that the risk of SCD may be increased. 


  1. Gladerisi M, et al. The multi-modality cardiac imaging approach to the Athlete’s Heart: an expert consensus of the European Association of Cardiovascular Imaging. Eur Heart J 2015;16:353.
  2. Baggish AL, et al. Recommendations on the use of multimodality cardiovascular imaging in young adult competitive athletes: a report from the American Society of Echocardiography in collaboration with the Society of Cardiovascular Computed Tomography and the Society of Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr 2020;33:523-549.
  3. Lang RM, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2015;28:1-39.
  4. Abergel E, et al. Serial left ventricular adaptations in world-class professional cyclists:implications for disease screening and follow-up. J Am Coll Cardiol 2004;1:144-149.
  5. Finocchiaro G, et al. Role of doppler diastolic parameters in differentiating physiologic left ventricular hypertrophy from hypertrophic cardiomyopathy. J Am Soc Echocardiogr 2018;5:606-613.
  6. Oxborough D, et al. The right ventricle of the endurance athlete: the relationship between morphology and deformation. J Am Soc Echocardiography 2012;25:263-271.
  7. Iskander A, et al. Left atrium size in elite athletes. J Am Coll Cardiol Imag 2015;8:753-62.
  8. Morganroth J, et al. Comparative left ventricular dimensions in trained athletes. Ann Int Med 1975;82:521-524.
  9. Spence AL, et al. A prospective randomized longitudinal MRI study of the left ventricular adaptation to endurance and resistance exercise training in humans. J Physiol 2011;589.22:5443-5452.
  10. Caselli S, et al. Three-dimensional echocardiographic characterization of left ventricular remodeling in Olympic athletes. Am J Cardiol 2011;108:141-147.
  11. Moneghetti KJ, et al. Echocardiographic assessment of left ventricular remodeling in American style footballers. Int J Sports Med 2020;41:27-35. 
  12. Engel DJ, et al. Athletic cardiac remodeling in US professional basketball players. JAMA Cardiol 2016;1:80-87.
  13. Caselli S, et al. Differentiating left ventricular hypertrophy in athletes from that in patients with hypertrophic cardiomyopathy. Am J Cardiol. 2014;114:1383-9.
  14. Finocchiaro G, et al. Effect of sex and sporting discipline on LV adaptation to exercise. J Am Coll Cardiol Imag 2017;10:965-72.
  15. Rowin E and Maron MS. 2016, March 10. Cardiovascular magnetic resonance imaging in the assessment of athletes with heart disease. <>
  16. Douglas PS, et al. 2011 Appropriate use criteria for echocardiography.J Am Soc Echocardiogr 2011;24:229-67.
  17. Taylor AJ, et al. 2010 Appropriate use criteria for cardiac computed tomography. J Cardiovasc Comp Tomogr 2010;4:407.e1-407.e33.
  18. Wolk MJ, et al. ACCF/AHA/ASE/ASNC/HFSA/HRS/SCAI/SCCT/SCMR/STS 2013 multimodality appropriate use criteria for the detection and risk assessment of stable ischemic heart disease. J Am Coll Cardiol 2014;63:380-406.
  19. Patel MR, et al. 2013 ACCF/ACR/ASE/ASNC/SCCT/SCMR appropriate utilization of cardiovascular imaging in heart failure. J Am Coll Cardiol 2013;61:2207-2231.
  20. Doherty JU, et al. ACC/AATS/AHA/ASE/ASNC/HRS/SCAI/SCCT/SCMR/STS 2017 appropriate use criteria for multimodality imaging in valvular heart disease. J Am Coll Cardiol 2017;70:1647-1672.
  21. Doherty JU, et al. ACC/AATS/AHA/ASE/ASNC/HRS/SCAI/SCCT/SCMR/STS 2019 appropriate use criteria for multimodality imaging in the assessment of cardiac structure and function in nonvalvular heart disease. J Am Coll Cardiol 2019;73:488-516.
  22. Sachdeva R, et al. ACC/AHA/ASE/HRS/ISACHD/SCAI/SCCT/SCMR/SOPE 2020 appropriate use criteria for multimodality imaging during the follow-up care of patients with congenital heart disease. J Am Coll Cardiol 2020;75:657-703.
  23. Ommen SR, et al. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 2020;76:e159-240.
  24. Pelliccia A, et al. 2020 ESC guidelines on sports cardiology and exercise in patients with cardiovascular disease. 2021;42:17-96.

* Imaging modalities that may supplement exercise testing include echocardiography, nuclear (PET or SPECT), and MRI

ARVC = arrhythmogenic right ventricular cardiomyopathy; BNP = basic natriuretic peptide; CAD = coronary artery disease; CTA = computed tomography angiography; CMR = cardiac magnetic resonance imaging; HCM = hypertrophic cardiomyopathy; IVCD = interventricular conduction delay; LBBB = left bundle branch block; LGE = late gadolinium enhancement; MRA = magnetic resonance angiography; PVC = premature ventricular tachycardia, SCD = sudden cardiac death; TEE = transesophageal echocardiogram; TTE = transthoracic echocardiogram;

Section Five: Case Reports of the Athletic Heart

In this educational section for CA ACC Sports and Exercise Health Committee, test your knowledge with clinical case reports and multiple choice questions. Further information and references provided in the discussion sections.

Athletes with Coronary Artery Calcifications: A Case Report

Authors: Deepak Ravi, MD; Timothy Canan, MD, Division of Cardiology, Department of Medicine, University of California, Los Angeles

A 58-year-old male with history of prostate adenocarcinoma, treated with robotic prostatectomy without the need for androgen deprivation therapy, was referred to cardiology for evaluation of coronary artery calcifications that were noted incidentally during staging computed tomography (CT) imaging. He has otherwise been healthy and takes only vitamins regularly. His parents both smoked and died of lung cancer and has no family history of early coronary artery disease. He stopped eating fast food as a teenager, gave up red meat, and has now been following a plant-based diet for many years. He has exercised his entire adult life, including weightlifting, running, high-intensity circuit training, and has now switched mainly to cycling due to knee arthritis. His current exercise routine includes 60-minute rides on a stationary bike with high-intensity power intervals six days per week. He denies any chest pain, pressure, dyspnea, or drops in exercise capacity or power output recently. He does endorse some palpitations during early recovery that last less than 10 seconds without lightheadedness or syncope. His blood pressure in clinic is 121/60 mmHg, BMI 25.7 kg/m2, with no abnormalities on physical exam. Labs show a total cholesterol of 244 mg/dL, HDL 91 mg/dL, LDL 137 mg/dL, and triglycerides 80 mg/dL. Resting electrocardiogram shows sinus bradycardia at 50 bpm without ectopy, ST or T wave abnormalities.

Question 1 of 2 What would you do next?

  • A. Lifestyle modifications of diet and exercise
  • B. Medical management with aspirin, low dose statin, and beta blocker
  • C. Further risk stratification needed
  • D. Invasive coronary angiography
View the Correct Answer

Question: What would you do next? Answer: C

Further risk stratification needed The patient has already optimized his lifestyle and is exceeding current physical activity guidelines.1 He is asymptomatic without clear evidence of ischemia or acute coronary syndrome, so jumping to invasive coronary angiography for his coronary artery calcifications would not be appropriate at this time. Medical management may be indicated, so his 10-year ASCVD Risk is calculated and found to be borderline at 5.1%. Initiation of a low dose aspirin and a moderate intensity statin therapy are both IIb recommendations and can be considered if other risk-enhancing factors are present.2 He is therefore sent for labs and studies for further risk stratification. Lipoprotein (a) is elevated at 198 nmol/L, high sensitivity CRP <0.2 mg/L, and hemoglobin A1c is 5.3%. A two-week external rhythm monitor to assess his symptomatic palpitations demonstrated sinus rhythm ranging from 37 bpm to 162 bpm with an average rate of 56 bpm. Patient triggered events on the monitor during episodes of post-exercise palpitations showed brief runs of an irregular supraventricular tachycardia with a maximum rate of 200 bpm and the longest run lasting 14 beats at average rate of 94 bpm. There are rare premature ventricular contractions seen but no ventricular runs. A CT coronary calcium score reveals a total Agatston score of 2085, placing him in the 99th percentile. The distribution shows no calcium in the left main, 461 in the left anterior descending, 347 in the left circumflex, and 1278 in the right coronary artery.

Question 2 of 2 What is the next appropriate step?

  • A. Medical management with aspirin, low dose statin, and beta blocker
  • B. Exercise stress testing
  • C. CT coronary angiogram
  • D. Invasive coronary angiography
View the Correct Answer

What is the next appropriate step? Answer: B

Exercise stress testing Given his significant coronary calcium burden in the 99th percentile, a high dose statin is more appropriate. A beta blocker is certainly reasonable but requires an informed discussion with athletes as it can be tolerated poorly with a reduction in exercise heart rate and capacity. CT coronary angiography could be useful to evaluate plaque morphology, but can be challenging in the setting of a high calcium burden with reduced sensitivity and positive predictive value due to extensive blooming artifact. Invasive angiography would be preferred if the patient had chest pain, decreased systolic function, ischemia on stress testing, or ventricular arrhythmias, which have not been demonstrated in this patient. He agreed to start taking aspirin 81 mg daily and high intensity statin therapy with rosuvastatin 20 mg daily. He then underwent cardiopulmonary exercise testing with stress echocardiography imaging. He exercised on a recumbent bicycle with ramp protocol, reaching a peak work rate of 262 W, heart rate of 163 bpm (101%MPHR), and a VO 2 Max of 41.1 ml/kg/min (141% predicted). Anaerobic threshold was calculated at 206 W using the V-slope method and occurred at a heart rate of 146 bpm. He experienced no symptoms or arrhythmias during or after peak exercise and had no evidence of ischemia by electrocardiogram or echocardiography. Repeat lipid panel on statin therapy showed a reduction in total cholesterol to 168 mg/dL, HDL 88 mg/dL, LDL 69 mg/dL, and triglycerides 56 mg/dL. He is cleared to continue his current level of exercise, predominantly in the aerobic range based on his CPET test results. He is given instructions on symptoms to monitor for during exercise, as well as precautions for when to seek emergency care. He has done well so far with no statin-induced myopathy symptoms, ischemic symptoms or events.

Athletes with COVID-19: A Case Report

Authors: Christine P. Shen, MD; Sandeep R. Mehta, MD, Division of Cardiology, Scripps Clinic

A 29-year-old female tested positive for coronavirus disease 2019 (COVID-19) after presenting to outpatient COVID testing with cough, chills, and body aches. Her course was complicated by left-sided numbness, and MRI brain showed left frontal and parietal lobe abnormal hyperintense signals. She was treated with a course of prednisone for presumed viral leukoencephalopathy. Prior to her infection, she was a competitive athlete in weightlifting and performed high-intensity workouts 2-3 hours per day, 5-6 days per week. She had no prior medical history. Family history was significant for myocardial infarction in two first-degree relatives. Within 3 weeks of being diagnosed with COVID-19, she developed severe exertional intolerance. Upon standing or walking for a few minutes, she experienced lightheadedness, shortness of breath, and tachycardia with heart rates of 120s-150s as measured on a consumer-grade wearable device. Her heart rate decreased to the 70s, her usual resting heart rate, upon lying down. She reported generalized fatigue and difficulty concentrating. She presented for cardiologist consultation three months after her initial COVID-19 diagnosis. At that time her blood pressure was 122/78 and her heart rate was 90 while sitting. She did not have orthostatic hypotension. On physical exam, she did not have any abnormalities. Her most recent lipid panel showed LDL 57 mg/dL, HDL 62 mg/dL, triglycerides 53 mg/dL, and total cholesterol 130 mg/dL. BMP, CBC, and TSH were normal. EKG showed sinus rhythm with sinus arrhythmia. Resting echocardiogram showed normal ejection fraction of 65%, normal wall thickness, normal diastolic function, and normal valvular function. CT angiography of the chest showed no evidence of pulmonary embolus.

Question 1 of 2 Which of the following tests will most likely show the cause of her symptoms?

  • A. Exercise treadmill stress test
  • B. CT coronary cardiac
  • C. Tilt table testing
  • D. Cardiac MRI
View the Correct Answer

Question: Which of the following tests will most likely show the cause of her symptoms? Answer: C

Tilt table testing The patient’s symptoms are concerning for autonomic dysfunction after a viral infection. She has atypical features not concerning for angina, so a stress test or cardiac CT would not likely show ischemia. A cardiac MRI could be useful in showing inflammation but would not likely explain her symptoms. She was therefore sent for autonomic reflex testing. Valsalva maneuver also reproduced symptoms, but beat-to-beat blood pressure response was normal. Tilt table testing showed severe symptomatic orthostatic intolerance with lightheadedness, blurry vision, chest tightness, and shortness of breath with head-up tilt at 70º. End-tidal CO2 was reduced after 3 minutes in head-up tilt. She remained in regular sinus rhythm. Her heart rate increased from 61 to 116 bpm, and her blood pressure rose inappropriately, from 106/68 to 110/76 mmHg. She had reduced mean cerebral blood flow velocity in the right middle cerebral artery as much as 35% during head up tilt at 70 degrees compared with baseline, consistent with postural orthostatic tachycardia syndrome (POTS).

Authors: Christine P. Shen, MD; Sandeep R. Mehta, MD, Division of Cardiology, Scripps Clinic

Question 2 of 2 What is the next appropriate step for this patient?

  • A. Lifestyle management with salt and fluid loading, compression stockings, and graded exercise.
  • B. Beta-blocker
  • C. Fludrocortisone
  • D. Midodrine
View the Correct Answer

Question: What is the next appropriate step for this patient? Answer: A

Lifestyle management with salt and fluid loading, compression stockings, and graded exercise. POTS is best treated initially with lifestyle management with salt and fluid loading, compression stockings, and graded exercise. Patients should drink 2-3 L of water per day, consume salt 10-12 g/day, and wear compression stockings. Patients should start a graded, structured, and supervised exercise program. Propranolol at a low-dose can help with sinus tachycardia and palpitations. Fludrocortisone and Midodrine have been used if symptoms persist after lifestyle management. Authors: Christine P. Shen, MD; Sandeep R. Mehta, MD, Division of Cardiology, Scripps Clinic

Deciding Return to Play in the Grey Area of Guidelines

Neal M. Dixit MD1, Ali Nsair MD1,2, Jeffrey J. Hsu MD, PhD1,2 1Department of Medicine, 2Division of Cardiology David Geffen School of Medicine at UCLA Los Angeles, California 90095

Case Presentation

A 20-year-old male presents to the office seeking a third opinion regarding his risk of playing competitive American-style football. He was a star athlete in high school and excelled in his first year of college football last year. Prior to his sophomore year, electrocardiogram (ECG) screening was implemented at his university, and his ECG revealed T-wave abnormalities that prompted further workup. Echocardiogram by report showed normal left and right ventricular (RV) ejection fraction, wall thickness, and size. An exercise treadmill test and coronary angiogram revealed no abnormalities. The patient had no exercise induced symptoms or ectopy and achieved 16 metabolic equivalents. He was allowed to resume participation in football activities and a two-week ambulatory electrocardiographic monitor was placed as a precaution.

However, the ambulatory monitor showed 3 episodes of non-sustained ventricular tachycardia (NSVT), all of which occurred at night without symptoms and lasted 5 beats or less. The total PVC burden was less than 1%. He was referred for a second opinion, and subsequently underwent further testing with cardiac magnetic resonance imaging (MRI) (Figure 1), which revealed left ventricular (LV) apical wall hypokinesis with associated wall thinning characterized by fatty metaplasia, mid-myocardial delayed gadolinium enhancement, and a normal RV. The left ventricle was mildly enlarged (LV end-diastolic dimension = 126.4 ml/m^2, LV end-systolic dimension = 60.3 ml/m^2, LV ejection fraction = 52%) and the RV was normal in size (RV end-diastolic dimension = 93.9 ml/m^2, RV end-systolic dimension = 38.1 ml/m^2, RV ejection fraction = 59%). 

He was advised that participation in high intensity competitive athletics would put him at increased risk of ventricular arrhythmia and sudden cardiac death and subsequently stopped football activities. He now comes seeking a third opinion regarding participation in the upcoming football season.

His past medical history is only notable for a pre-mature birth at 27 weeks due to placental insufficiency. He takes no medications. He has no family history of cardiomyopathy or sudden death. He drinks alcohol only occasionally and has never smoked or used drugs.

His cardiac exam reveals a regular, bradycardic rhythm, normal S1/S2, and a I/VI systolic murmur along the left sternal border. Jugular venous pressure is estimated at 7cm of water. He was not noted to have any hair or skin abnormalities. The remainder of the exam is normal.

Electrocardiogram (Figure 2) shows sinus bradycardia at 45 beats per minute, biphasic T-waves in leads V1-V5,, inferolateral ST segment depressions, no axis deviation or interval prolongation, no evidence of chamber enlargement, and a QRS duration of 108ms. Prior imaging is described as above.


Figure 1: Cardiac MRI. Post gadolinium, inversion recovery, T1-weighted gradient echo image (A) and steady state free precession (SSFP) image (B) both show high signal (arrows) due to extensive fat infiltration in the apex of the left ventricle.

Figure 2: 12-lead Electrocardiogram showing sinus bradycardia, precordial T-wave inversions, and inferolateral ST segment depressions

Question 1 of 2 How should you counsel him on whether he should play in the upcoming football season?

  • A. Advise against resuming high intensity competitive athletics and recommend placement of an implantable cardiac defibrillator (ICD)
  • B. Discuss the risk of continued high intensity competitive athletics and come to a shared-decision 
  • C. Advise to sit out the season with symptom follow up and repeat cardiac imaging in 1 year
  • D. Allow continued participation of competitive athletics under close cardiology follow up
View the Correct Answer

Question 1 of 2 How should you counsel him on whether he should play in the upcoming football season? Answer is B

Given the features that raise significant concern for ACM, the patient should be advised that participation in high intensity competitive athletics increases his risk of ventricular arrhythmia and sudden death (2,3). ICD may be reasonable for some patients with ACM and a history of sudden cardiac arrest, sustained ventricular tachycardia, LV ejection fraction <45%, and those with multiple major and minor disease criteria (2). In patients without an ICD, beta blockers are a reasonable therapeutic option to reduce the risk of arrhythmia (Class IIa, Level of Evidence: C).

Question 2 of 2 Which of the following may be helpful in establishing a formal diagnosis?

  • A. Identification of a second-degree relative with confirmed ACM
  • B. Identification of the morphology of ventricular ectopy
  • C. Identification of a likely pathogenic mutation for ACM by genetic testing
  • D. None of the above 
View the Correct Answer

Question 2 of 2 Which of the following may be helpful in establishing a formal diagnosis? Answer is C

The patient meets several of the 2020 Padua criteria for LV variant of ACM (known as ALVC) (4). However, in patients with normal RV findings, it is suggested that ACM not be diagnosed solely off LV phenotypic criteria due to overlap with conditions such as dilated cardiomyopathy, hypertrophic cardiomyopathy, and cardiac sarcoidosis. In this patient with several clinical findings suggestive of arrhythmogenic cardiomyopathy (ACM), identification of a pathogenic mutation association with ACM would allow for the diagnosis of ALVC by Padua criteria. Identification of first and second degree relatives with confirmed ACM consist of major and minor Padua criteria, respectively, however, they are insufficient to confirm diagnosis of ALVC. A right bundle branch block pattern of ventricular tachycardia is a minor Padua criteria, insufficient to confirm diagnosis of ALVC.  

In our patient, genetic testing of the Arrhythmia and Cardiomyopathy Comprehensive Panel (Invitae) of 67 inherited genes did not reveal any mutations associated with ACM or other cardiomyopathy. Thus, a formal diagnosis of ALVC was not able to be made by Padua criteria.