Cardiac issues in sports medicine may encompass structural heart disease, arrhythmias, or valvular disease.
Structural heart disease may be congenital or acquired.
- Hypertrophic cardiomyopathy (HCM) describes a hypertrophied non-dilated left ventricle without evidence of any other cardiac or systemic disease that could produce the extent of hypertrophy present.1
- Myocarditis describes an inflammatory cellular infiltrate of the myocardium with or without associated myocyte necrosis.2
Arrhythmias are any abnormality or disruption to the conduction system of the heart that results in a change of the normative rate or rhythm. Arrhythmias associated with sports medicine include the following:
- Long QT syndrome (LQTS) is a channelopathy affecting the QT segment of the cardiac electrical cycle.
- Wolff-Parkinson-White syndrome (WPW) is a form of re-entrant supraventricular tachycardia from accessory electrical pathways.3
- Brugada syndrome (BrS) is a channelopathy inducing arrhythmia.
- Commotio cordis (CC) is sudden death caused by acquired ventricular fibrillation induced by a blunt blow to the chest overlying the heart.4,5
Diseases of the mitral valve, which separates the left atrium from the left ventricle, may involve mitral stenosis (MS) or insufficiency. Insufficiency can be either mitral valve prolapse (MVP) or mitral regurgitation (MR).
- Autosomal dominant mutations encoding thick and thin contractile myofilament protein components of the sarcomere or Z-disc.1
- Linked to infections with certain viruses, bacteria, or eosinophilic responses after vaccination.2
- LQTS: mutations in 10 genes encoding cardiac ion channels leading to syncope from torsades de pointes and death by evolution to ventricular fibrillation.
- WPW: accessory electrical pathway that bypasses the atrioventricular node permitting ventricular pre-excitation.3
- BrS: mutations encoding subunits of the cardiac sodium, potassium, and calcium channels inducing ventricular arrhythmias causing death.
- CC: a blow to the chest wall overlying the heart during the upstroke of the T-wave inducing ventricular fibrillation.4, 5
Mitral valve disease
- MVP: familial inherited leaflet redundancy.
- MR: caused by MVP, rheumatic heart disease, coronary artery disease, infective endocarditis, or collagen vascular disease.
- MS: caused by rheumatic heart disease.7
Epidemiology including risk factors and primary prevention
- Most common genetic cardiovascular disease.
- Most common cause of sudden cardiac death in young persons.
- Prevalence is 1 per 500 persons.1
- True incidence unknown.2
- Disease of the young with symptoms unusual in patients over 40 years of age.
- Incidence of mutations is 1 per 2000 persons.
- Acquired risk factors are hypocalcemia, hypothyroidism, and multiple drugs.
- Prevalence is 1 to 4.5 per 1000 persons.3
- Prevalence is 5 per 10,000 persons.
- Hyperthermia increases risk of arrhythmias.8
- Incidence is unknown.
- Risk increased in children and adolescents who play baseball/softball, ice hockey, lacrosse, or football.4,5
- Prevalence is 1 – 3% of the population.
- Ratio of women to men is 2 to 1.7
- Myocardial cells have aberrant shapes and chaotic connections to one another causing a disorganized myocardium structure and hypertrophy with LV wall thickness greater than 15 mm.1
- Typically, pathogen is cleared and immune reaction diminishes without sequelae. Cardiac disease occurs when intracellular antigens on cardiac myocytes results in cardiac muscle damage.2
- Accessory electrical pathways may represent embryologic remnants.3
- Results from myxomatous degeneration or proliferation of the spongiosa layer of collagen and elastic tissue in the valve leaflets, allowing the leaflets to distend back into the left atrium during systole.
- Results from ruptured chordae tendineae or papillary muscles.
- Rheumatic fever is one cause of post inflammatory scarring with leaflet thickening and calcification, leading to a funnel-shaped mitral valve with a decreased size of opening.7
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
- HCM involves left ventricular hypertrophy by early adulthood but may present at any age from infancy to old age.
- Some patients are asymptomatic but different complications may arise including sudden death, atrial fibrillation, or heart failure.
- Mortality rates in general population are ~1%/year.1
- Encompasses three phases:
- Acute injury caused by infectious source
- Innate immunologic response
- Recovery or transition to scar and dilated cardiomyopathy.2
- Patients are typically asymptomatic.
- If symptoms present, usually non-specific cardiac complaints.
- Mortality risk in WPW is 0.1 – 0.45% per year.
- Sudden cardiac death progression occurs when the accessory pathway conducts rapidly to the ventricle degenerating the cardiac rhythm to ventricular fibrillation.3
MVP and MR courses vary from benign and normative life expectancy to significant morbidity and mortality compared with MS symptoms, which develop 20 to 40 years after the episode of rheumatic fever and result in a continuous, rapid, and progressive course.7, 10
Specific secondary or associated conditions and complications
- May be associated with other conditions, including Friedrich ataxia or glycogen storage diseases.
- Complications include the following:
- Atrial fibrillation in 20% to 25% of patients because of left atrial enlargement.
- Heart failure secondary to diastolic dysfunction.
- Sudden cardiac death from ventricular arrhythmias.6, 11
- Nonischemic dilated cardiomyopathy results from prolonged immune system response to endogenous heart antigens.2
- Some genotypes are associated with congenital neural deafness.
- May be associated with congenital heart diseases, such as Ebstein anomaly or HCM.9
- May be associated with connective tissue disorders, such as Marfan syndrome, caused by mutations to fibrillin-1.
- Complications include the following:
- Infective endocarditis
- Mitral insufficiency
- Embolic events
- Ventricular and atrial arrhythmias
- Sudden cardiac death in isolated MVP is rare in young patients.
Severe MR and MS
- May lead to pulmonary hypertension.
- MS is sometimes complicated by the development of atrial fibrillation.5,7
2. ESSENTIALS OF ASSESSMENT
- The most common presenting symptoms are the following:
- Exertional dyspnea
- Family history of premature sudden death or syncope is also associated with HCM.11,12
- Presenting symptoms range from subclinical disease to sudden death.
- Viral prodromal symptoms of fever, myalgia, respiratory or gastrointestinal symptoms
- Disproportionate exercise intolerance
- Precordial chest pain (from pericarditis or coronary artery spasm)
- Presenting symptoms include the following:
- Presyncope or syncope
- Cardiac arrest
- Some patients are asymptomatic
- Family histories of sudden death, including drowning or sudden infant death syndrome, are important historical features that may be associated with LQTS.
- Symptoms include the following:
- Sudden cardiac death
- Usually asymptomatic until sudden death occurs.
- Patients usually collapse instantaneously after contact.4, 5,9
- Usually not symptomatic, however, some symptoms include the following:
MR and MS
- Asymptomatic, but can present with the following:
- Pulmonary edema
- MS sometimes presents with atrial fibrillation or an embolic event.7
- Wide range of auscultatory findings is possible from normative to a harsh midsystolic murmur increased with maneuvers that decrease venous return (squatting-to-standing or Valsalva), thereby decreasing stroke volume.
- Other findings include the following:
- Paradoxical S2 split that narrows on inspiration.
- Double-peak pulse.11,12
- Auscultatory findings may include a pericardial friction rub or loud S3.
LQTS, WPW, and BrS
- No physical manifestations.
- Patients are collapsed, unresponsive, and without a pulse.4,5
- Auscultatory findings include one or multiple clicks within systole, accentuated by standing.
- Auscultatory findings include a holosystolic murmur radiating to the axilla accentuated by Valsalva or an S3 sound.
- Auscultatory findings include accentuated S1 and a low-pitched middiastolic rumble accentuated by brief exercise.7,10
- Suspected patients may undergo endomyocardial biopsy to differentiate different causes of LV wall thickening.
- Genetic testing can detect 50% to 60% of HCM mutations, but it is not widely available.11
- Elevated troponin I.2
- Genetic testing may be used to determine the specific gene affected.
- Clarifies the prognosis.
- Helps rule out the disease in individuals with a family history of LQTS.13
Echocardiography is the most useful imaging modality for structural or valvular heart disease.
- In an adult athlete, maximal LV end-diastolic wall thickness of 15 mm or greater on echocardiography is consistent with HCM.
- Cardiac magnetic resonance imaging (MRI) can be used for more precise LV wall thickness measurements and imaging of myocardial scars.5
- Echocardiography used to rule out other causes of heart failure.
- Cardiac MRI may be used to identify locations for endomyocardial biopsy.2
LQTS, WPW, and BrS
- Echocardiography is normal.13
- Demonstrates a flow jet back through the MV.
- Demonstrates restricted diastolic opening of the MV with gradation of the disease based on the mitral valve opening area:
- Mild: greater than 1.5 cm2
- Moderate: 1.0 to 1.5 cm2
- Severe: less than 1.0 cm2 5,7
Supplemental assessment tools
Electrocardiograms (ECGs) are useful for evaluating underlying arrhythmias.
- ECG demonstrates abnormalities in 75% to 90% of patients.
- Findings include the following:
- Voltage abnormalities
- ST-segment and T-wave abnormalities
- Prominent Q waves
- Left atrial enlargement11
- ECG sensitivity is 47%.
- Findings include nonspecific ST-segment and T-wave abnormalities.2
- Findings include the following:
- Abnormal QT interval prolongation.
- Corrected QT interval greater than 470 ms for men and 480 ms for women.13
- Classic findings include:
- Delta wave (a slurred upstroke of the QRS complex)
- Short PR interval (<120 ms).
- Other findings include:
- QRS durations longer than 120 ms
- Intermittent delta waves in the same lead.3
- Findings include the following:
- Accentuated J-wave in leads V1-V3
- ST-segment elevation
- Negative T-wave
MVP, MR, and MS
- ECG and a chest radiograph are helpful in all mitral valve abnormalities to evaluate for rhythm abnormalities as well as assess for pulmonary vascular congestion.7
Early predictions of outcomes
- Mortality rates of 1% per year, similar to the general adult population.1
- Incidence of syncope of sudden death by 40 years of age is 20%.
- Usually fatal with only 25% of resuscitations successful.4
- Ten-year survival of untreated MS patients is 50% to 60%, but once limiting symptoms develop, the 10-year survival rate drops to 0% to 15%.7
Cardiac remodeling and electrical changes in athletes who participate in intense exercise, typically at least 4 hours per week, may mimic pathologic conditions. These include left and right ventricular hypertrophy, early repolarization, and physiological arrhythmia induced by increased vagal tone.14
3. REHABILITATION MANAGEMENT AND TREATMENTS
Available or current treatment guidelines
- Athletes should be excluded from most competitive sports except for class IA sports.
- The use of pharmacologic agents or prophylactic ICDs is not recommended for the purpose of allowing participation in high-intensity sports.5
- Patients with exertional symptoms of heart failure may be started on negative inotropic medications including beta-antagonists or verapamil.
- Dual-chamber pacing has been shown to relieve symptoms and reduce outflow gradient.
- Septal myotomy-myectomy operation (Morrow procedure) may be used in those patients with symptoms refractory to medications.6
- Athletes with probable or definite myocarditis should not participate in competitive sports while active inflammation is present.5
- Treatment for acute myocarditis is supportive for left ventricular dysfunction
- Heart failure regimen:
- Angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers
- Heart failure regimen:
- Athletes may participate in competitive sports (except competitive swimming) after precautionary measures and asymptomatic with treatment for at least three months.5
- Treatment include the following:
- Long acting beta²-antagonists.
- Implantable cardioverter-defibrillator can be considered in patients at high risk of sudden death.
- Competitive sports may be considered once asymptomatic on treatments for at least three months.5
- Athletes with WPW and without structural heart disease, tachycardia, or those athletes who have undergone ablation can participate in all competitive sports.5
- Radiofrequency ablation of the aberrant pathway in WPW has potential for a definitive treatment.
- Recurrence rates between 10 – 23%.3
- Primary prevention includes softer-core balls but improved chest protection has not shown to protect against CC.
- Secondary prevention includes wider access to automated external defibrillators.4,9
- No medical or surgical therapy is required with reassurance being the mainstay of management.
- Athletes with MVP and without history or evidence of syncope, arrhythmia, severe MR, ejection fraction less than 50%, prior embolic event, and family history of sudden death may participate in all competitive sports.5
MR and MS
- Athletes with mild to moderate MR and without complications can participate in all competitive sports.
- Athletes with severe MR without complications may participate in low and some moderate-intensity sports.5
- Athletes with mild MS in sinus rhythm can participate in all competitive sports.
- Athletes with moderate MS in either sinus rhythm or atrial fibrillation can participate in low and moderate static and low and moderate dynamic competitive sports.
- Athletes with severe MS should not participate in competitive sports.5
- No medical therapy exists; however, infective endocarditis prophylaxis is recommended prior to surgical procedures.
- Surgical interventions include the following:
- Repair or replacement of the mitral valve.
- Percutaneous mitral balloon valvotomy
- Mitral commissurotomy
- Mitral valve replacement7,10
Coordination of care
It is essential that the sports medicine physiatrist work with the cardiologist to properly obtain treatment recommendations and create a safe return to play program.
Patient & family education
It is critical that athletes, family, and coaches are educated properly on any potential risks that return to play might bring to the cardiacvascular system.
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
Standardized history questions and physical examination techniques should be used, because cardiovascular abnormalities are difficult to detect.
Parents of young athletes should also be involved in answering history questions.
History questions should include cardiac-related symptoms during exercise, previous cardiac medical history or workup, and family history of cardiac symptoms or conditions.
Cardiovascular assessment during pre-participation examinations should include blood pressure measurement, palpation of radial and femoral pulses, dynamic cardiac auscultation (including squat-to-stand and/or Valsalva maneuvers), and evaluation for Marfan syndrome.12
4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE
Cutting edge concepts and practice
Alcohol septal ablation in HCM utilizes 1 to 4 mL of alcohol placed into a septal perforator coronary artery branch to produce a small controlled myocardial infarction, which decreases septal thickness and motion, enlarging the LV outflow tract and improving cardiac muscle function in persons with HCM.6
Minimally invasive cardic valve-replacement and suture-less valve replacement may allow patients a faster return to baseline but return to play is still based upon anticoagulant use, valvular function, and ventricular systolic function.5,15
5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE
Gaps in the evidence-based knowledge
The American Heart Association/American College of Cardiology recommends against universal ECG screening in healthy, young athletes because of poor sensitivity, high-false positive rates, poor cost-effectiveness, lack of physician oversight, and concern of overall cost.5
However, European medical societies recommend 12-lead ECG in addition to history and physical examination for pre-participation screening in competitive athletes.16
Further studies into the long-term effects of strenuous exercise in patients with MS on pulmonary artery pressure are needed.7
- Maron BJ and Maron MS. Hypertrophic Cardiomyopathy. Lancet 2013; 381:242-55.
- Cooper LT Jr. Myocarditis. N Engl J Med 2009 Apr 9;360(15):1526-38.
- Rao AL, Salerno JC, Asif IM, et al. Evaluation and Management of Wolff-Parkison-White in Athletes. Sports Health 2014 Jul;6(4):326-32.
- Maron BJ, Estes NA 3rd. Commotio cordis. N Engl J Med. 2010;326:917-927.
- Maron BJ, Zipes DP, Kovacs RJ; on behalf of the American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology, Council on Cardiovascular Disease in the Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and the American College of Cardiology. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: preamble, principles, and general considerations: a scientific statement from the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015 Dec 1;66(21):2343-9.
- Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA. 2002;287:1308-1320.
- Bonow RO, Carabello BA, Chatterjee K, et al. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118:e523-e661.
- Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the second consensus conference. Circulation. 2005;111:659-670.
- Pediatric and Congenital Electrophysiology Society (PACES); Heart Rhythm Society (HRS); American College of Cardiology Foundation (ACCF), et al. PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern. Heart Rhythm. 2012;9:1006-1024.
- Shipton B, Wahba H. Valvular Heart Disease: review and update. Am Fam Physician. 2001;63:2201-2208.
- Soor GS, Luk A, Ahn E, et al. Hypertrophic cardiomyopathy: current understanding and treatment objectives. J Clin Pathol. 2009;62:226-235.
- Giese EA, O’Connor FG, Brennan FH, Depenbrock PJ, Oriscello RG. The athletic preparticipation evaluation: cardiovascular assessment. Am Fam Physician. 2007;75:1008-1014.
- Roden DM. Clinical practice. Long-QT syndrome. N Engl J Med. 2008;358:169-176.
- 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, Domenico Corrado; International recommendations for electrocardiographic interpretation in athletes. Eur Heart J 2017 ehw631. doi: 10.1093/eurheartj/ehw631
- Pope NH and Ailawadi G. Minimally invasive valve surgery. J Cardiovasc Transl Res. 2014;7(4):387-94.
- Corrado D, Pelliccia A, Bjørnstad HH et al. Cardiovascular preparticipation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol: Consensus Statement of the Study Group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J. 2005;26:516-524.
Original Version of the Topic
Bradley M. McCrady, DO, Marc Gruner, BS. Cardiac issues in sports medicine. 09/20/2013
Bradley M. McCrady, DO
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