Cardiac Issues in Sports Medicine

Disease/Disorder

Definition

Cardiac issues in sports medicine may encompass structural heart disease, arrhythmias, or valvular disease, as athletic training can accelerate the degenerative process and tendency for arrhythmias and sudden cardiac death (SCD).¹

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.¹

Rhythm disorders are any abnormality or disruption to the conduction system of the heart that results in a change of the normative rate or rhythm. In sports medicine, rhythm disorders predispose athletes to lethal ventricular arrhythmias at exertion. The most common arrhythmias associated with sports include⁴

• Channelopathies: Long QT syndrome (LQTS) and Brugada Syndrome (BrS).
• Supraventricular tachyarrhythmias: Wolff-Parkinson-White syndrome (WPW) is a form of re-entrant supraventricular tachycardia from accessory electrical pathways.¹
• Commotio cordis (CC) is sudden death caused by acquired ventricular fibrillation induced by a blunt blow to the chest overlying the heart.¹

Valvular heart diseases (VHD) 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).

Etiology

Structural Heart Disease

  HCM

• Autosomal dominant mutations encoding thick and thin contractile myofilament protein components of the sarcomere or Z-disc with beta-myosin heavy chain and myosin-binding protein C genes are most commonly involved.¹

  Myocarditis

• Linked to infections with certain viruses (coronavirus, coxsackievirus, adenovirus, parvovirus, and herpes virus), bacteria (Borrelia burgdorferi)⁹, eosinophilic responses after vaccination or pharmacological and environmental toxins (non-infective myocarditis).¹
• Athletes are at increased risk of infections, especially elite athletes, as they usually interact and are exposed to a considerable number of people while training, traveling, and gathering at international tournaments. In addition, high-intensity and long-duration exercises may reduce immunology competence by decreasing salivary secretory immunoglobulin A, lactoferrin, and lysozyme, which alternate the T cell response while increasing athlete vulnerability to infections.²

Rhythm Disorders

• 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.¹
• 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.⁶

Valvular Heart Disease

• MVP: caused by collagen diseases (Osteogenesis Imperfecta, Ehlers-Danlos syndrome, Marfan syndrome), genetic (fibroelastin deficiency)
• MR: caused by MVP, rheumatic heart disease, coronary artery disease, infective endocarditis, or collagen vascular disease.
• MS: caused by rheumatic heart disease.¹

Epidemiology including risk factors and primary prevention

Structural Heart Disease

HCM

• Most common genetic cardiovascular disease.
• Most common cause of sudden cardiac death in young athletes, usually between 15-25 years of age.
  • In young athletes, 20% of SCD were attributable to HCM.³
• Prevalence is 1 per 500 persons (0.2%) in echocardiography-based epidemiologic studies, but even higher – 1 per 200 if genetics, clinical diagnosis and family history are all taken in consideration.⁴

 Myocarditis

• General population incidence for acute myocarditis⁵
  • 14 people per 100,000 each year globally
  • Mortality rate of 1% to 17%
• Incidence and prevalence in athletes following COVID-19 infection range from 0.6 % to 2.3% in large registries and up to 4 % in studies using advance imaging techniques. Percentage varies depending on the screening methods employed. ⁶
• In athletes the incidence of SCD after acute myocarditis ranges from 2-12% of all fatalities.²

Rhythm Disorders

LQTS

• Most common channelopathy
• Prevalence of the disease is 1 in 2500 live births ¹

BrS

• Prevalence is 1 per 1,000 to 10,000 persons.¹
• Associated with 4% of all SCD in the general population.¹
• Hyperthermia increases risk of arrhythmias.

WPW

• Prevalence ranges from 1 to 4.5 per 1000 people in pediatric and adult studies. ¹
• Mortality risk in WPW is 0.1 – 0.45% per year.
• The risk for SCD is 1% in athletes.¹

 CC

• True incidence is unknown.
• US Commotio Cordis registry reported > 250 cases, and approximately 10-20 cases have been added yearly.
• Risk increased in children and adolescents due to vulnerability most likely due to higher elasticity at chest wall. ¹
• In certain sports, athletes are at higher risk, especially in baseball, hockey, and lacrosse due to projectile components; in fist boxing and football due to knee and chest collision; and equestrian sports (horse kick) due to direct trauma.⁷
• Survival rate increased to > 50% due to earlier CPR and defibrillation protocol improvements, as well as better protection equipment.

Valvular Heart Disease

MS

• Developed countries: prevalence of rheumatic MS is approximately 1:100,000 worldwide and incidence of 4-10:100,000 in the USA.⁸
• Developing countries: prevalence is approximate 4-10:1,000 worldwide.
  • Rheumatic prevalence: 4-10 per 1,000 cases

MVP

• Most common valvular disease
• MVP prevalence is approximately 1 in 40 individuals of the general population⁹
• The most common cause of primary MR is this myxomatous valve disease¹⁰
  • 25% of the MVP leads to significant MR

MR

• Framingham Offspring study reported a prevalence of trivial MR was 88% of men and 92% of women.⁹
  • Mild to severe MR was seen in 19 %⁹
  • Age is associated with the severity of valve damage

Patho-anatomy/physiology

Structural Heart Diseases

HCM

• Myocyte disarray, aberrant shapes and chaotic connections combined with fibrosis and abnormal calcium kinetics cause a left ventricular disorganized and hypertrophy myocardium structure. HCM is characterized by LV wall thickness greater than 15 mm, impaired LV relaxation, and dynamic LV outflow tract obstruction (LVOTO). ¹

Myocarditis

• Typically, the pathogen is cleared, and immune reaction diminishes without sequelae.
• Cardiac disease occurs when intracellular antigen-specific adaptive immune cells invade the myocardium which provokes an acute myocardial lesion. Then the healing process (repair subepicardial-mid mural myocardial fibrosis) could promote a post-myocardial sequel.²
• Nonischemic myocardial scar could develop life-threatening ventricular arrhythmias and increased risk of arrhythmic cardiac arrest.²

Rhythm Disorders

LQTS

• Type of channelopathy caused by a genetic mutation at LQTS genes that encode for cardiac ion channel subunits involved in the ionic current modification. This prolongs the duration of the action potential, producing an abnormal EKG, with T wave abnormalities and prolonging QT interval.¹

BS

• Impaired cardiac sodium, potassium, and calcium channels induce ventricular arrhythmias, causing death.
• A recent study identified right anterior ventricular structural abnormalities as well¹¹

WPW

• Paroxysmal supraventricular tachycardias with ventricular pre-excitation, permitting accessory electrical pathways that bypass the atrioventricular node.¹  

CC

•  CC is sudden death caused by acquired ventricular fibrillation induced by a blunt blow to the chest overlying the heart.

Valvular Heart Disease

MVP

• 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.

MR

• Results from ruptured chordae tendineae or papillary muscles.

MS

• Rheumatic mitral stenosis results from autoimmune-mediated inflammation following streptococcal infection, causing leaflet thickening, commissural fusion, chordal shortening, and a characteristic “fish-mouth” valve orifice, which progressively narrows the mitral valve area and elevates left atrial pressure.¹

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

HCM

• 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 the general population are ~1%/year.¹

Myocarditis

• Encompasses three phases:
  • Acute injury caused by infectious source
  • Innate immunologic response
  • Recovery or transition to scar and dilated cardiomyopathy
• All types of exercise must be temporarily restricted, as athletes with viral myocarditis are shown to be at higher risk of adverse cardiac events and complications, especially, during intense endurance training.²
  • Clinical reassessment is indicated to return to competition, consisting of 12-lead ECG, echocardiography, exercise testing, 24-h Holter monitoring, and blood sample.²

LQTS

• Short episodes might be asymptomatic or symptomatic with episodes of dizziness.
• Long episodes with symptoms of periodic dizziness, syncopal attacks and SCD.

WPW

• Patients are typically asymptomatic.
• If symptoms present, usually non-specific cardiac complaints.
• Sudden cardiac death progression occurs when the accessory pathway conducts rapidly to the ventricle degenerating the cardiac rhythm to ventricular fibrillation.

CC

• Impacts directly over the cardiac silhouette are necessary to induce ventricular fibrillation and impacts directly over the center of the heart were the most lethal.¹
• Malignant arrhythmia may provoke unconscious, cyanosis, pulseless, convulsion and sudden cardiac arrest.

Valvular Heart Disease

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.¹

Specific secondary or associated conditions and complications

Structural diseases

HCM

• May be associated with other conditions, including Friedrich ataxia or glycogen storage diseases.
• Complications include the following¹²
  • 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, most commonly ventricular tachycardia.¹

Myocarditis

• Nonischemic dilated cardiomyopathy results from prolonged immune system response to endogenous heart antigens.

Rhythm Diseases

LQTS

• Some genotypes are associated with congenital neural deafness.

WPW

• Sudden cardiac death is often precipitated by atrial fibrillation with rapid conduction over the accessory pathway, which may degenerate into ventricular fibrillation ¹
• May be associated with congenital heart diseases, such as Ebstein anomaly or HCM. ¹

Valvular Heart Disease

MVP

• 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.

Essentials of Assessment

History

HCM

• Mostly asymptomatic or only minor symptoms throughout life
• Most common presenting symptoms are the following
  • Exertional dyspnea
  • Angina
  • Syncope, especially during or immediately following exertion
  • Pre-syncope episodes
  • Palpitations
• Family history of premature sudden death or syncope is also associated with HCM. A complete medical and 3 generation family history is recommended.¹

Myocarditis

• Presenting symptoms range from subclinical disease to sudden death.
  • Viral prodromal symptoms of fever, myalgia, respiratory or gastrointestinal symptoms
  • Fatigue
  • Disproportionate exercise intolerance
  • Palpitations
  • Precordial chest pain (from pericarditis or coronary artery spasm)
  • Syncope

LQTS

• Vast majority of patients are asymptomatic and syndrome is identified solely by QT prolongation on ECG
• Of those with symptoms, the most common include the following
  • Palpitations
  • Presyncope or syncope
  • Cardiac arrest
• Family histories of sudden death, including drowning or sudden infant death syndrome, are important historical features that may be associated with LQTS.

WPW

• Patients with WPW pattern who have never developed an arrhythmia will be asymptomatic.
• Symptoms include the following
  • Tachyarrhythmias
  • Chest pain
  • Dyspnea
  • Dizziness
  • Syncope
  • Sudden cardiac death

BrS

• Usually asymptomatic until sudden death occurs
  • Commonly occurs during sleep, secondary to increased vagal activity and decreased sympathetic activity, which can trigger ventricular arrhythmias, such as ventricular fibrillation, leading to SCD.
• Exercise itself may not directly increase the risk but recovery from it can exacerbate ECG abnormalities due enhanced vagal tone.¹³
• Approximately 80% of BrS patients who developed ventricular tachycardia or ventricular fibrillation experience syncope.
• Other possible symptoms are palpation and dizziness.

CC

• Sudden impact with the anterior chest overlying the heart, followed by immediate cardiac arrest.¹

MVP

• Usually asymptomatic, but may include the following
  • Angina
  • Dyspnea
  • Palpitations
  • Syncope
  • Anxiety
  • Fatigue

MR and MS

• Asymptomatic, but can present with the following:
  • Fatigue
  • Dyspnea
  • Pulmonary edema
• MS sometimes presents with atrial fibrillation or an embolic event.¹

Physical examination

HCM

• Wide range of auscultatory findings is possible from normative to a harsh Midsystolic murmur
• Systolic murmur that begins slightly after S1
  • Heard best at apex and lower left sternal border
  • Due to left ventricular outflow tract obstruction (LVOTO)
• Holosystolic murmur
  • Heard loudest at apex which radiates to the axilla
  • Due to mitral regurgitation
• Increased with maneuvers that decrease venous return (squatting-to-standing or Valsalva), thereby decreasing stroke volume.
• Decreased with maneuvers that increase preload (squatting) or afterload (handgrip)
• Other findings include the following:
  • Paradoxical S2 split that narrows on inspiration
  • Double-peak pulse

Myocarditis

• Auscultatory findings may include a pericardial friction rub or loud S3.

LQTS, WPW, and BrS

• No physical manifestations

CC

• Patients are collapsed, unresponsive, and without a pulse.

MVP

• Midsystolic click followed by a late systolic murmur, accentuated by standing and with Valsalva maneuver. Diminished with squatting.
• Thoracic bony abnormalities (pectus excavatum, decreased anterior-posterior diameter, scoliosis), low body weight and blood pressure.

MR

• Auscultatory findings include a holosystolic murmur radiating to the axilla accentuated by Valsalva or an S3 sound.

MS

• Auscultatory findings include accentuated S1 and a low-pitched mid-diastolic rumble accentuated by brief exercise.

Laboratory studies

HCM

• Suspected patients may undergo endomyocardial biopsy to differentiate different causes of LV wall thickening.
• Genetic testing can detect HCM mutations, but it is not widely available. Genetic testing panels can demonstrate an extensive heterogeneity and multiple molecular pathways (approximately 2000 sarcomere mutations had been identified)¹

Myocarditis

• Elevated troponin I, more sensitive than specific.
• Endomyocardial biopsy

LQTS

• 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.¹

Imaging

Echocardiography is the most useful imaging modality for structural or valvular heart disease.

HCM

• Transthoracic Echocardiography (TTE)
  • Left ventricular wall thickness >15mm without a nondilated left ventricle is necessary for diagnosis
  • A septal/posterior wall thickness ratio over 1.3 in normotensive patients or over 1.5 in hypertensive patients is also diagnostic of HCM
  • Diastolic dysfunction
  • Left atrium enlargement
  • Systolic dysfunction
  • LVOTO
  • Exercise stress testing
• Cardiovascular Magnetic Resonance (CMR) shows in detail the septum, mitral valve, and papillary muscles
  • Useful for the preoperative evaluation before ventricular septal myectomy
  • Differentiate HCM from other non-sarcomere causes that could mimic HCM
  • Can also detect myocardial fibrosis, an important prognostic indicator

Myocarditis

• Echocardiography used to rule out other causes of heart failure.
• In echocardiography, both acute and chronic myocarditis can present with an increase in the size of the ventricular chambers
• Cardiac MRI may be used to identify locations for endomyocardial biopsy.²

LQTS, WPW, and BrS

• Echocardiography is normal

MR

• Demonstrates a flow jet back through the MV.

MS

• 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

Supplemental assessment tools

Electrocardiograms (ECGs) are useful for evaluating underlying arrhythmias.

HCM

• ECG demonstrates abnormalities up to 90% of patients (do not predict clinical course).¹⁴
• Findings include the following
  • Voltage abnormalities
  • Left axis deviation
  • ST-segment and T-wave abnormalities
  • Prominent Q waves in inferior and lateral leads
  • Left atrial enlargement

Myocarditis

• ECG sensitivity is 40%.
  • Findings include nonspecific ST-segment elevations and T-wave abnormalities.

LQTS

• Findings include the following
  • Abnormal QT interval prolongation.
  • Corrected QT interval greater than 470 ms for men and 480 ms for women (440 ms and 460ms, respectively, in non-athletes).¹

WPW

• 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

BrS

• Findings include the following
  • Accentuated J-wave in leads V1-V3
  • ST-segment elevations greater than 2mm with:
    • Inverted T waves (type I)
    • Saddleback-shaped ST elevation greater than 2mm (type II)
  • Saddle-back shaped ST elevations less than 2mm (type III)

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.

Early predictions of outcomes

HCM

• Mortality rates of 1% per year, similar to the general U.S. population overall mortality (0.8 % per year).¹

LQTS

• Incidence of syncope of sudden death by 40 years of age is 20%.

CC

• Usually fatal with only 25% of resuscitations successful.¹

MS

• 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

Professional issues

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.¹

Rehabilitation Management and Treatments

Available or current treatment guidelines

Structural Heart Disease

HCM^12,14

• Exercise stress testing is advised in pediatric patients with HCM to assess functional capacity and prognosis.
• Vigorous exercise may be considered following shared decision-making and annual expert evaluation.
• In athletes with HCM, mild- to moderate-intensity recreational exercise should be recommended to improve general health following the guidelines of general population.
• The use prophylactic ICDs is not recommended for the purpose of allowing participation in high-intensity sports.
• Asymptomatic patients (genotype-positive, phenotype-negative for HCM): participation in competitive sports of any intensity is reasonable.
• Patients with exertional symptoms of heart failure may be started on negative inotropic medications including beta-antagonists or verapamil.
• Participation in high-intensity recreational activities or moderate-to high-intensity competitive sports activities “may be considered after a comprehensive evaluation and shared discussion, repeated annually with an expert provider who conveys that the risk of sudden death and ICD shocks may be increased”.
• Mavacamten treatment is effective for symptomatic obstructive hypertrophic cardiomyopathy that improves exercise capacity, LVOT (left ventricular outflow tract) obstruction, NYHA functional class and health status in patients.¹⁵
• Septal reduction therapy (surgical or percutaneous) is indicated for refractory obstructive cases, ideally at experienced centers. ^12,17

Myocarditis^16,17

• Athletes with probable or definite myocarditis are restricted from participating in all physical activities, including competitive sports, while active inflammation is present.
• RTP is only considered when there is normal LV function, no significant arrhythmias, and resolved myocardial injury, for which athletes should undergo comprehensive reevaluation, including Echocardiogram, 24-hour Holter monitoring, exercise stress testing.
• A 3–6-month exercise abstinence period is recommended post-acute phase, with reassessment based on symptom resolution, normalized cardiac biomarkers, and imaging (e.g., cardiac MRI).
• Athletes should receive preparticipation screening every 6 months, and annual follow-ups post-clearance to monitor for recurrence.
• COVID-19 patients should follow a return to physical activity protocol of 5 phases once the patient is asymptomatic for at least 7 days.¹⁸
• Treatment for acute myocarditis is supportive for left ventricular dysfunction
  • Heart failure regimen:
    • Angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers
    • Beta-antagonists
    • Diuretics

Rhythm Disorders

LQTS^19,20

• Rehabilitation and lifestyle modification:
  • Focus on trigger avoidance (QT-prolonging drugs, dehydration, electrolyte imbalances, hyperthermia).
  • Maintain hydration and monitor electrolytes.
  • Regular follow-up with a heart rhythm specialist for treatment adjustments.
• Return to Sport (RTP)
  • Shift toward shared decision-making (SDM) in selected LQTS athletes.
  • RTP criteria: >3 months asymptomatic on therapy, stress test + Holter monitoring, AED access, and EAP in place.
• Asymptomatic athletes may return to most sports (except competitive swimming) if stable for > 3 months with precautions.
• Treatment includes the following ^20,21
  • Long-acting beta²-antagonists (nadolol, propranolol) are first-line therapy, especially in LQT1 and LQT2.
  • Mexiletine, a late sodium channel blocker, is useful in LQT3 to shorten QT interval and reduce arrhythmic risk.
  • Implantable cardioverter-defibrillators are considered for patients with high risk of sudden death.
  • Left cardiac sympathetic denervation (LCSD) if fails to B-blockers or ICD is contraindicated.

BrS ^20,22

• Lifestyle and Medical care
  • Avoid BrS-exacerbating drugs (e.g., sodium channel blockers), maintain hydration and electrolytes, and prevent hyperthermia.
  • Ongoing cardiology follow-up for risk assessment and therapy adjustment.
• Return to Sport
  • Requires individualized evaluation: ECG, Holter, and stress testing.
  • Genotype-positive/phenotype-negative athletes may return if asymptomatic and safety measures (e.g., AED access, trigger avoidance) are in place.
  • Athletes with prior arrhythmias must be asymptomatic on therapy for >3 months.
  • Follow-up ensures ongoing risk assessment and therapy optimizations

WPW²⁰

• Rehabilitation Post-Ablation
  • Rest for 1-2 weeks to allow healing; monitor with ECG to assess success and detect recurrence.
• Return to Sport (RTP):
  • Based on EP study and stress testing.
  • Athletes without structural heart disease, tachycardia, or post-ablation can participate fully.
  • High-risk young athletes with concerning conduction features are disqualified from competition.
• Treatment
  • Radiofrequency ablation offers definitive management; recurrence rates range from 10-23%.

CC²²

• Primary prevention includes softer-core balls. Chest protection has not shown to protect against CC.
• ICDs not recommended if no underlying cardiac disease.
• Secondary prevention for SCD: wider access to automated external defibrillators.

Valvular Heart Disease

MVP^23,24

• No medical management is required. Reassurance is key.
• Low-risk athletes (no syncope, arrhythmia, severe MR, low EF, embolism, or family history of SCD) can compete in all sports.
• High-risk MVP requires close monitoring, possible restriction, and a multidisciplinary “sports heart team” which shared decision-making (SDM) for advised.

MR¹²

• Athletes with mild–to-moderate MR: full participation allowed.
• Athletes with severe MR: allowed in low-to-moderate intensity sports only after evaluating symptoms and LV function.
• Surgical options: valve repair or replacement.

MS²⁵

• 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.
• No medical therapy exists; however, infective endocarditis prophylaxis is recommended prior to surgical procedures.
• Surgical interventions include the following
  • MS
    • Percutaneous mitral balloon valvotomy
    • Mitral commissurotomy
    • Mitral valve replacement ^25,26
• Individuals that require surgical valve replacement with mechanical prosthesis plus anticoagulation are recommended to avoid contact sports or sports associated with trauma.

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. Also, the patient will benefit from a cardiac rehabilitation program in which the exercises are adjusted to the condition and goals established to improve his/her fitness.²⁸

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 cardiovascular 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 remains the foundation of pre-participation cardiac screening.²⁸
• 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.^27,28
• ECG is included in European guidelines while American guidelines suggest that ECG should only be considered in relatively small cohorts.²⁸
• Multimodality imaging (Echocardiography or MRI) is not recently recommended for universal pre-participation cardiac screening.²⁸

Cutting Edge/Emerging and Unique Concepts and Practice

HCM

Cardiac Myosin Inhibitors (CMIs) such as Mavacamten, the first FDA-approved CMI, reduce the number of myosin heads available to bind to actin, aiming to decrease hypercontractility. Clinical benefits include improved exercise capacity, reduced LVOT obstruction, and symptom relief. Gene editing and RNA-based therapies remain experimental.²⁹

Myocarditis

Recent treatment advances stem from cardio-immunology, including trials with agents like Anakinra, Abatacept, and PD-L1-loaded nanoparticles to modulate immune response and oxidative stress.³⁰

LQTS and BrS

In LQT1, beta-blockers and LCSD remain key treatments. For Brugada Syndrome, epicardial substrate ablation effectively reduces ventricular arrhythmias and can normalize ECG patterns.³¹

Valvular Heart Disease

Transcatheter mitral edge-to-edge repair devices like MitraClip and PASCAL show non-inferior outcomes compared to surgery in patients with mitral regurgitation, including similar rates of mortality and heart failure rehospitalization.³²

Gaps in the Evidence-Based Knowledge

The American Heart Association/American College of Cardiology does not recommend universal ECG screening in healthy young athletes. However, European medical societies recommend 12-lead ECG in addition to history and physical examination for pre-participation screening in competitive athletes due to an increase in the detection of cardiovascular diseases, and an estimated of 60% of disorders associations with SCD may be detected.³³ For example, the national screening program of Italy showed a significant decrease in SCD after its establishment in 1982 (3.6/100,000 in 1979-1980 decrease to 0.4/100,000 in 2003-2004).³³

Congenital Heart Disease

Correlation between exercise intensity and the risk of developing arrhythmias in patients with congenital heart disease is unknown and future studies are needed.³⁴

Heart Failure

Physical activity is known to provide quality of life and improve cardiovascular capacity in heart failure patients, nonetheless, there is insufficient data associating the benefits of regular exercise on survival in chronic disease. In addition, the impact of high intensity exercise in asymptomatic heart failure individuals with reduced and preserved systolic function is also lacking. Future multicenter clinical trials are needed to design personalized and effective exercise programs in this population.³⁴

Little to no evidence exists with reference to the ideal start time of a moderate to high intensity rehabilitation exercise program after an acute heart failure event.

Arrhythmias

In atrial fibrillation patients who have undergone successful catheter ablation, it remains unknown if there is a relationship concerning vigorous exercise participation at the same intensity before and after the procedure, with the risk of atrial fibrillation recurrence.³⁴

Valvulopathies

Long-term effects of strenuous exercise on the aortic root and aortic valve also remain unknown. Competitive exercise does not seem to have deleterious effects on the morphology and function of the left ventricle and aortic valve.³⁴

Aortopathies

Exercise’s effect on aortic dissection and rupture risk as well as its impact on the evolution of aortic disease is still undetermined and warrants experimental studies.

References

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Original Version of the Topic

Bradley M. McCrady, DO, Marc Gruner, BS. Cardiac issues in sports medicine. 9/20/2013

Previous Revision(s) of the Topic

Bradley M. McCrady, DO, Marc Gruner, BS. Cardiac issues in sports medicine. 9/20/2013

Previous Revision(s) of the Topic

Bradley M. McCrady, DO, Marc Gruner, BS. Cardiac issues in sports medicine. 8/3/2017

Odrick R Rosas, MD, PhD, Victor Rosado, MD, Daniel Almodovar-Frau, MD, Martin Roldan-Auffant, MD. Cardiac Issues in Sports Medicine. 4/27/2022

Author Disclosure

Martin Roldan-Auffant, MD
Nothing to Disclose

Humberto Ramirez, MD
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Kevin De Jesus, MD
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Gerardo Miranda-Comas, MD
Nothing to Disclose