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.2,3
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. Most common arrhythmias associated with sports include:4
- 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.5
- Commotio cordis (CC) is sudden death caused by acquired ventricular fibrillation induced by a blunt blow to the chest overlying the heart.6
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).
Structural Heart Disease
- 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 most commonly involved.7,8
- Linked to infections with certain viruses (coxsackievirus, adenovirus, parvovirus, and herpes virus), bacteria (Borrelia burgdorferi)9, eosinophilic responses after vaccination or pharmacological and environmental toxins (non-infective myocarditis).2, 3
- Athletes are at increased risk of infections, especially elite athletes as usually collectively train, travel, and gather 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 alternated the T cell response, meanwhile increase athlete vulnerability to infections.4,3
- 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.5
- 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 (Marfan syndrome, Ehlers-Danlos syndrome, osteogenesis imperfecta), genetic (fibroelastin deficiency) and degenerative 2ry to infection, autoimmune, vascular disorder.
- MR: caused by MVP, rheumatic heart disease, coronary artery disease, infective endocarditis, or collagen vascular disease.
- MS: caused by rheumatic heart disease.10,11,12
Epidemiology including risk factors and primary prevention
Structural heart disease
- Most common genetic cardiovascular disease.
- Most common cause of sudden cardiac death in young persons, usually between 15-25 years of age.
- In athletes, 40% of SCD were attributable to HCM.13
- Prevalence is 1 per 500 persons (0.2%) in echocardiography-based epidemiologic studies, but even higher – 1 per 200 if genetic, clinical diagnosis and family member are taken in consideration. 8,7
- General population true incidence unknown. 2,3
- Prevalence of 2.3% in college athletes with SARS-CoV14
- In athletes the incidences of SCD after acute myocarditis range from 2-12% of all fatalities.3
- Most common channelopathy
- Prevalence of the disease is 1 in 2000 live births15
- Prevalence is 5 per 10,000 persons.16
- Associated to 4% of all SCD in the general population.17
- Hyperthermia increases risk of arrhythmias. 18
- Prevalence and incidence worldwide is unknown. However, the prevalence of pre-excitation in the general population varies from 0.1 % to 0.3%, which is similar to the athletic population. 19
- Mortality risk in WPW is 0.1 – 0.45% per year. 5
- The risk for SCD in asymptomatic patients is 15%, while 2% in symptomatic. 19
- Official 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. 6,20
- 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 cycline trauma and horse kick due to direct trauma.21,6
- Survival rate increased to > 50% after early CPR and defibrillation protocols improvements and better protection equipment.
Valvular Heart Disease:
- Developed countries: prevalence of rheumatic MS is approximately 1:100,000 worldwide and incidence of 4-10:100,000 in the USA.22
- Developing countries: prevalence is approximate 4-10:1,000 worldwide. 23
- Rheumatic prevalence: 4-10 per 1,000 cases
- Most common valvular disease24
- MVP prevalence is approximately 2-4% of the general population24
- Most cases are benign, MVP-related event of 0.2 % in patients with MVP
- Ratio between women : men is 2 : 1. 10,11,12
- Rheumatic prevalence: 4-10 per 1,000 cases
- Framingham Offspring study reported a prevalence of trivial MR was 88% of men and 92% of women.25
- From mild to severe MR was seen in 19 %25
- Age is associated with the severity of valve damage.
Structural Heart Diseases
- Myocyte disarray, aberrant shapes and chaotic connections combined with fibrosis and abnormal calcium kinetics causing a left ventricular disorganized and hypertrophy myocardium structure. HCM characterized by LV wall thickness greater than 15 mm, impaired LV relaxation and dynamic LV outflow tract obstruction (LVOTO). 26
- Typically, the pathogen is cleared, and immune reaction diminishes without sequelae.
- Cardiac disease occurs when intracellular antigens-specific adaptive immune cells invade the myocardium which provoke an acute myocadiac lesion. Then the healing process (repair subepicardial-midmural myocardial fibrosis) could promote a post-myocardial sequel. 3,2
- Also, new evidence suggested that nonischemic myocardial scar could develop life threatening ventricular arrythmias and arrhythmic cardiac arrest.3
- Type of channelopathy caused by a genetic mutation at LQTS genes that encodes for cardiac ion channel subunits involved in the ionic current modification. This prolongs the duration of the action potential, alternating EKG, especially T wave and prolonging QT interval. 27
- Impaired cardiac sodium, potassium, and calcium channels inducing ventricular arrhythmias causing death.
- Recent study, identified right anterior ventricular structural abnormalities.28
- Paroxysmal supraventricular tachycardias with ventricular pre-excitation permitting accessory electrical pathways bypass the atrioventricular node.5
- CC is sudden death caused by acquired ventricular fibrillation induced by a blunt blow to the chest overlying the heart.
Valvular Heart Disease
- 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. 10,11,12
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. 26
- Encompasses three phases:
- Acute injury caused by infectious source
- Innate immunologic response
- Recovery or transition to scar and dilated cardiomyopathy
- All types of exercise has to be temporary restricted3, athletes with viral myocarditis are shown to be at higher risk of adverse cardiac events, complications, specially, during intense endurance training. 3
- Clinical reassessment is indicated to return to competition, consisting of 12-lead ECG, echocardiography, exercise testing, 24-h Holter monitoring, and blood sample.3
- Short episodes might be asymptomatic or symptomatic dizziness episodes.
- Long episodes with symptoms of periodic dizziness, syncopal attacks and SCD.
- 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.
- Left-sided thorax severe contusion induces severe cardiac arrhythmia.29
- 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. 30
Specific secondary or associated conditions and complications
- May be associated with other conditions, including Friedrich ataxia or glycogen storage diseases.
- Complications include the following8:
- 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. 7,31
- Nonischemic dilated cardiomyopathy results from prolonged immune system response to endogenous heart antigens.
- Some genotypes are associated with congenital neural deafness.
- May be associated with congenital heart diseases, such as Ebstein anomaly or HCM. 32
Valvular Heart Disease
- 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
- Mostly asymptomatic or only minor symptoms throughout life
- Most common presenting symptoms are the following:
- Exertional dyspnea
- Pre-syncope episodes
- Family history of premature sudden death or syncope is also associated with HCM. 33,31,8, A complete medical and 3 generation family history is recommended.34
- 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. 13
- 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.10,11,12
- 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.
- Other findings include the following:
- Paradoxical S2 split that narrows on inspiration.
- Double-peak pulse.
- 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.
- Midsystolic click, late systolic murmur, accentuated by standing.
- Thoracic bony abnormalities (pectus excavatum, decreased anterior-posterior diameter, scoliosis), low body weight and blood pressure.
- 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 mid-diastolic rumble accentuated by brief exercise. 10
- 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. 31 Genetic testing panels can demonstrate an extensive heterogeneity and multiple molecular pathways ( approximately 2000 sarcomere mutations had been identified). 8
- Elevated troponin I.
- Endomyocardial biopsy
- 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. 35
Echocardiography is the most useful imaging modality for structural or valvular heart disease.
- Transthoracic Echocardiography (TTE)34
- Only left ventricular wall thickness >15mm without a nondilated left ventricle is indispensable for diagnosis
- Diastolic dysfunction
- Left atrium enlargement
- Systolic dysfunction
- Exercise stress testing
- Cardiovascular Magnetic Resonance (CMR) shows in detail the septum, mitral valve, and papillary muscles34
- Useful for the preoperative evaluation before ventricular septal myectomy
- Differentiate HCM from other non-sarcomeric causes that could mimic HCM
- Echocardiography used to rule out other causes of heart failure.
- Cardiac MRI may be used to identify locations for endomyocardial biopsy. 2,3
LQTS, WPW, and BrS
- Echocardiography is normal.
- 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
Supplemental assessment tools
Electrocardiograms (ECGs) are useful for evaluating underlying arrhythmias.
- ECG demonstrates abnormalities up to 90% of patients (do not predict clinical course)34.
- Findings include the following:
- Voltage abnormalities
- ST-segment and T-wave abnormalities
- Prominent Q waves
- Left atrial enlargement
- ECG sensitivity is 40%.
- Findings include nonspecific ST-segment and T-wave abnormalities.
- Findings include the following:
- Abnormal QT interval prolongation.
- Corrected QT interval greater than 470 ms for men and 480 ms for women. 35
- 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.
- 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.
Early predictions of outcomes
- Mortality rates of 0.5% per year (with current treatments strategies and interventions), similar to the general U.S. population overall mortality (0.8 % per year). 7,34
- Incidence of syncope of sudden death by 40 years of age is 20%.
- Usually fatal with only 25% of resuscitations successful. 6
- 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. 36
Rehabilitation Management and Treatments
Available or current treatment guidelines
Structural Heart Disease
- Athletes with HCM, mild- to moderate-intensity recreational exercise should be recommended to improve general health follwoign the guidliness of general population.34
- The use prophylactic ICDs is not recommended for the purpose of allowing participation in high-intensity sports.34
- Asymptomatic patients (genotype-positive, phenotype-negative for HCM), participation in competitive sports of any intensity is reasonable. 34
- 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”.34
- 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.37
- Athletes with probable or definite myocarditis should not participate in competitive sports while active inflammation is present.
- Patients may return to play if left ventricular function and markers of inflammation are normalized and no presence of relevant arrhythmias are identified. 3839 Also, a general consensus exists that suggested restriction of exercises programs for a time frame of 3-6 month depending of the severity of the condition.40
- COVID-19 patients should follow a return to physical activity protocol of 5 phases once the patient is asymptomatic for at least 7 days. 41
- 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. 42
- Treatment includes the following:
- Long-acting beta²-antagonists.
- Implantable cardioverter-defibrillators can be considered in patients at high risk of sudden death.
- Left cardiac sympathetic denervation (LCSD) is recommended if a patient fails to B-blockers or ICD is contraindicated.43,44
- Competitive sports may be considered once asymptomatic on treatments for at least three months. 42
- Athletes with WPW and without structural heart disease, tachycardia, or those athletes who have undergone ablation can participate in all competitive sports.
- Young athletes with evidence of high-risk features of the action potential will be disqualified from competitive activities.45
- Radiofrequency ablation of the aberrant pathway in WPW has potential for a definitive treatment.
- Recurrence rates between 10 – 23%.5
- Primary prevention includes softer-core balls, but improved chest protection has not shown to protect against CC.
- If a Commotio cordis victim does not have an underlying cardiac disease, implantable cardioverter are not recommended. 42
- Secondary prevention includes wider access to automated external defibrillators.
Valvular Heart Disease
- 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.
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.42,46
- 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:
- Repair or replacement of the mitral valve.
- Percutaneous mitral balloon valvotomy
- Mitral commissurotomy
- Mitral valve replacement30,12
- Individuals that required surgical valve replacement with mechanical prosthesis plus anticoagulation are recommended to avoid contact sports or sports associated with trauma.47
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.48
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.49
- 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. 33,49,50
- ECG is included in European guidelines while American guidelines suggest that ECG should only be considered in relatively small cohorts.49
- Multimodality imaging (Echocardiography or MRI) is not recently recommended for universal pre-participation cardiac screening.49
Cutting Edge/Emerging and Unique Concepts and Practice
Alcohol septal ablation and Myectomy decreases septal thickness and motion, enlarging the LV outflow tract and improving cardiac muscle function in persons with HCM.7,51 Both technics are superior to medication in drug-refractory HCM, but in the absence of a randomize control trial on both methods a cardiomyopathy team is suggested to choose the best option depending on patient morbidity.51
Minimally invasive cardiac valve-replacement and sutureless valve replacement may allow patients a faster return to daily activities with fewer cost related to rehabilitation resources, but return to play is still based upon anticoagulant use, valvular function, and ventricular systolic function.52,53,54
The new molecule mavacamten, which is an allosteric inhibitor of cardiac myosin ATPase, improves the exercise capacity among other factors in patients with Obstructive HCM in the clinical trial EXPLORER-HCM perhaps reducing the risk of sudden death.55
Novel coronavirus infection-COVID-19 creates concerns about myocarditis in athletes. New protocols for these patients have been created to detect the prevalence and future complications of the virus infection to myocardial tissue, these protocols should include cardiac magnetic resonances (CMR) to detect myocarditis prevalence in college athletes after COVID-19 infection. However, more studies will be done to standardize these protocols and to follow long term complications.56
Gaps in the Evidence-Based Knowledge
Gaps in the evidence-based knowledge
The American Heart Association/American College of Cardiology do not recommends universal ECG screening in healthy young athletes.42,49 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.49,57 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).58
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.59
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.59
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.
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.59
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.59
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.4
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- Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients with Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Vol 135.; 2017. doi:10.1161/CIR.0000000000000503
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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. 8/3/2017
Odrick R Rosas, MD, PhD
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Victor Rosado, MD
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Daniel Almodovar-Frau, MD
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Martin Roldan-Auffant, MD
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