Sudden death in athletes has been a tragic occurrence in the fields of sports medicine, cardiology, primary care, and pediatrics. By far the most common cause of unexpected death for a younger athlete on the competitive field is cardiac illness; usually that of congenital etiology. However, the use of anabolic steroids, peptide hormones, and stimulants have led to the emergence of acquired heart disease in younger and middle-aged athletes. In contrast, sudden death in an older athlete is typically due to atherosclerotic coronary artery disease.
There are a variety of congenital heart illnesses that occur in the general population. Most of them categorize into structural and non-structural varieties. Congenital structural heart disease will generally affect blood flow within the heart and flow from the heart. Examples include hypertrophic obstructive cardiomyopathy (HOCM), arrhythmogenic right ventricular dysplasia (ARVD), and coronary artery anomalies. Non-structural heart disease involves defects in the electrical system of the heart which may induce unstable and dangerous arrhythmias. Examples include long QT syndrome, Brugada syndrome, Wolff-Parkinson-White (WPW) syndrome and catecholaminergic polymorphic ventricular tachycardia (CPVD). Other congenital structural and non-structural heart diseases exist and have been described previously in the setting physical activity and athletics. Also, drug-induced cardiac effects are of important notice. Anabolic steroids and peptide hormones induce structural changes in the heart. Stimulants can cause dangerous arrhythmias.
These conditions can clinically manifest as syncope/pre-syncope, and in some instances can present as sudden, unexpected death. The associated mortality underscores the importance of early screening and identification of existing heart disease in athletes. Many athletes with pre-existing heart disease are often asymptomatic with a cardiac arrest being the initial manifestation of underlying pathology. The challenging aspect of identifying affected athletes is adequately screening the general population without excessive and unnecessary invasive testing. A thorough sports physical examination including an assessment of personal history, family history, physical exam, and an electrocardiogram can be a useful screening tool in asymptomatic and low-risk athletes. Higher risk athletes, such as those who have abnormal findings or have symptoms, may require more extensive testing.
Upon arriving at a diagnosis, an athlete will undergo risk stratification. Then, a long-term treatment regime is initiated to minimize the risk of sudden cardiac death. Medical management is a common option, while surgical intervention is reserved for specific cases. Inserting an implantable cardioverter-defibrillator (ICD) is appropriate for anyone considered to be at risk for cardiac arrest secondary to a fatal arrhythmia. The decision to continue or abandon the sport of choice results from shared decision making between the physician and patient.
The purpose of this article is to review the causes of sudden death in athletes with a significant focus on the most common etiologies in younger athletes and their presentation and evaluation.
Sudden unexpected death in athletes has been primarily viewed as a disease of cardiac etiology.
Structurally Normal Heart
The frequency of sudden cardiac death in athletes in the current literature is variable depending on the methodology used to gather the data. The general range reported is 1 in 40000 to 1 in 80000. However, there are reports with rates as high as 1 in 3000. The variability is likely due to the applied definition of sudden cardiac death. The various definitions range from those who experienced sudden cardiac death during exertion, rest or survived resuscitation.
The most frequent cause of sudden death in athletes is hypertrophic obstructive cardiomyopathy (HOCM) and severe left ventricular hypertrophy, followed by other structural cardiac defects. HOCM is seen in roughly 1 in 500 people and is more common in men. Coronary artery anomalies are the second most common cause of sudden death in athletes and occur in up to 1.2% of the population. An estimated 20% of coronary artery anomalies may be life-threatening when found in an athlete. Arrhythmogenic right ventricular dysplasia (ARVD) is another known cause of sudden death in athletes and occurs in 1 in 2000 to 1 in 5000 people.
While structural cardiac defects are primarily genetic, anabolic steroid use is a known etiology of severe left ventricular hypertrophy. The prevalence of left ventricular hypertrophy is prominent among steroid users, but its significance varies depending on the specific agents used and various confounding factors.
Non-structural etiologies of sudden cardiac death largely involve ion channelopathies and electrical defects which induce potentially lethal arrhythmias. Congenital long QT syndrome is known to occur in approximately 1 in 2000 births. Wolff-Parkinson-White (WPW) syndrome and preexcitation pathways occur at an approximate rate of 1.5 in 1000. Other illnesses include Brugada syndrome which occurs at a rate of 0.15%; and catecholaminergic polymorphic ventricular tachycardia which occurs in approximately 1 in 10000 people.
The occurrence of isolated congenital illnesses is relatively low in the general population but in summation is common enough to be a viable health risk given the large number of young athletes.
The function of the heart is to effectively pump blood throughout the body and hence disturbing the blood flow and/or the rhythm of the heart beats negatively impacts the heart's functional goals. Structural defects prevent the heart from effectively pumping blood, especially during times of increased demand. Ion channel defects disturb the regularity of necessary electrolytes which maintain the heart's rate and rhythm. Consequently, untreated structural defects can result in arrhythmia, while a persistent arrhythmia may lead to structural heart changes. An example of this is dilated cardiomyopathy which can develop due to an excessive premature ventricular contraction (PVC) burden.
As the most common cause of sudden cardiac death, hypertrophic obstructive cardiomyopathy involves outflow obstruction of blood flow. The ventricular wall becomes rigid as a result and the left ventricular end diastolic pressure (LVEDP) and left atrial pressures rise contributing to pulmonary congestion. Ultimately, this predisposes patients with HOCM to lethal arrhythmias. A similar process occurs in anabolic steroid-induced left ventricular hypertrophy. ARVD involves fatty infiltration of the right ventricle making the heart susceptible to frequent PVCs and ventricular arrhythmias, particularly during strenuous exercise. Other structural defects such as coronary artery anomalies are considered dangerous depending on the specific anomaly. Left or right coronary arteries originating from the pulmonic artery are considered potentially serious.
Ion channelopathies are due to genetic defects which lead to malformation of the channel proteins. The outcome is electrolyte derangement; specifically potassium, calcium, sodium, and magnesium. Aside from ion channel defects, accessory pathways are another cause of arrhythmias. If a separate electrical pathway, besides the atrioventricular (AV) node, is communicating from the atria to the ventricles, rapid rate and arrhythmias may occur.
Acquired cardiac disease in athletes mostly ties to atherosclerotic coronary artery disease and/or drug-induced cardiac changes. Middle-aged and older athletes are naturally prone to atherosclerosis and hence may be at risk of plaque rupture within the coronary arteries during strenuous exercise. Drug-associated cardiac illness in athletes categorizes into those caused by anabolic agents and those caused by stimulants. Most anabolic steroids and peptide hormones induce left ventricle hypertrophy, often to highly significant degrees increasing the risk of heart failure. In contrast, stimulants may impact the cardiovascular system acutely by inducing arrhythmias with long-term hypertensive and ionotropic effects also inducing cardiac changes.
Younger athletes should undergo a comprehensive physical examination by a physician prior to participating in competitive sports or any intense physical activity.
All athletes should have an assessment for any history of syncope, presyncope, dizziness, palpitations, chest pain, shortness of breath, seizures, severe fatigue and inability to palpate their pulse. The clinician should ask the athlete about whether these symptoms occur during exercise and/or during rest. While presyncope and syncope are most commonly a result of a vasovagal event and/or due to extreme heat, they are often the initial indication of existing cardiac disease in younger age groups. Palpitations will generally be due to benign ectopic ventricular or atrial heartbeats, but a high burden may be a result of existing structural heart disease. Chest pain and dyspnea can be expected in structural heart disease: specifically obstructive cardiomyopathy. Seizures and inability to palpate one's pulse may suggest episodes torsades de pointes, which occurs in those with long QT syndrome. It also points towards the occurrence of an unstable rhythm, such as catecholaminergic polymorphic ventricular tachycardia.
Family history is also essential to assess the existence of genetic heart disorders. Given that these genetic disorders are all inherited and potentially fatal, they may have gone undiagnosed among family members and relatives. Hence, it is vital to ask about any relatives who unexpectedly passed away.
Athletes should be questioned about the usage of performance-enhancing drugs (PEDs), specifically anabolic steroids and stimulants. These agents induce the risk of sudden cardiac death through multiple mechanisms. The most common mechanism is left ventricular hypertrophy in anabolic steroid users, while arrhythmias and vascular injury also occur. High doses of testosterone, use of growth factors, classic agents such as stanozolol, and commonly used injectable drugs like trenbolone; all induce severe left ventricular hypertrophy. Different athletes experience this to variable degrees, and hence knowledge of this history is critical. Also, the usage of stimulants increases the likelihood of arrhythmias, especially in those with existing cardiac illness. Some pre-workout supplements contain potentially dangerous compounds that induce a high burden of ectopic heartbeats, prolong QT and can produce clinical symptoms. Examples of such compounds include 1,3-dimethylamylamine (DMAA) which has been banned in numerous countries. Lastly, blood doping and erythropoietin (EPO) use is of concern, particularly in endurance athletes and has correlated with sudden cardiac arrest.
A physical examination is necessary for all young athletes. A general full body exam should be done, including a neurological assessment, a musculoskeletal examination, and a thorough cardiovascular assessment. A thorough cardiac exam consists of listening to rate and rhythm, S1 and S2, the presence of S3 or S4, and/or any palpable heaves, lifts or thrills. The existence of any murmurs should be noted and evaluated while increasing or decreasing the preload and afterload using physical maneuvers.
The initial diagnostic assessment of any athlete who is undergoing screening for cardiac diseases, and/or an athlete undergoing assessment for syncope is an ECG. The ECG will provide information on the rate and rhythm of the heart, and can indicate structural abnormalities. Assessment of the ECG should include the following:
Other significant findings that can present on an ECG include pathological Q waves, significant ST-segment changes, and third-degree atrioventricular blocks.
Normal Physiologic Findings On ECGs
Athletes may have findings on their ECG that would otherwise be considered abnormal in the general population. Sinus bradycardia (under 60 beats per minute) is among the most common benign abnormal ECG findings, but very low heart rates should not be ignored. Infrequent PVCs and premature atrial contractions (PACs) are also considered normal among both the general population and physically active people. However, specific findings on ECGs considered normal among athletes but abnormal in other populations include:
Left and right axis deviation and left or right atrial enlargement may or may not be considered abnormal depending on other findings and the clinical context. If present in isolation, they are generally not considered abnormal. However, co-existence with other borderline or abnormal findings warrants further investigation.
Two types of athletes will qualify for a 24 or 48-hour Holter monitor: athletes with abnormal ECG findings and/or athletes with symptoms caused by potential cardiac pathology. The Holter monitor will provide greater insight into the athlete's electrophysiology over a greater period compared to an ECG. Arrhythmias will be detected on the Holter monitor and the etiology of symptoms, such as palpitations, can potentially be uncovered. The Holter monitor is especially useful for assessing the burden of PVCs given that their frequency of occurrence largely points to their significance. People with ARVD will generally have a high PVC burden and may also experience non-sustained ventricular tachycardia (NSVT).
A stress test allows for the reproduction of potentially dangerous arrhythmias that may occur during exercise but are infrequent at rest.
An echocardiogram allows for a general overview of the heart's structure. Evaluating the four cardiac chambers, valvular structures, and the heart's ejection fraction can be made using an echocardiogram.
Multiple criteria exist that combine clinical evaluation, ECGs, and echocardiograms. They carry variable levels of evidence, and hence their utility is subject to use within a clinical context. An example of well-established criteria is the Schwartz scoring scale for evaluating long QT syndrome.
Long QT syndrome is a known cause of syncope and sudden death among both the general population and athletes. The most common cause of prolonged QT on an ECG is secondary to medication use. The absence of medication-induced QT prolongation warrants further investigation into a possible congenital etiology. A normal QTc in men is less than 440ms, and in women, it is less than 460ms.
The following represents a scoring system to assess the probability of long QT syndrome in a patient.
Physiologic versus Pathologic Left Ventricular Hypertrophy
Left ventricular hypertrophy is a common occurrence among athletes. A mild to moderate degree of hypertrophy occurs as a natural response to exercise, particularly endurance-based and isometric exercise. Large levels of hypertrophy are generally noted to be pathological and are known to be induced either genetically and/or as a result of anabolic steroid or peptide hormone use. One differentiating factor between physiological and pathological left ventricular hypertrophy is the wall thickness itself. On an echocardiogram, a normal ventricle will be 6 mm to 11 mm. Under 13 mm is generally not considered to be hypertrophic from a clinical perspective, although 11-13 mm is borderline thickened. Over 16-18 mm is considered significantly enlarged and crosses over into the territory of hypertrophic obstructive cardiomyopathy.
The grey area of 13 mm to 16 mm requires clinical evaluation to differentiate between physiological adaptations to exercise and cardiomyopathy.
Symptomatically, athletes may experience syncope, dizziness, and dyspnea during exercise. They will also generally be younger.
ECGs will be done to assess athletes for the voltage criteria for left ventricular hypertrophy; of which three criteria exist. Although positive voltage findings are often normal in athletes, the degree of their elevation provides information to be used within a clinical context.
Sokolow-Lyon index: S in V1 + R in V5 or V6 greater than or equal to 35 mm or R in aVL greater than or equal to 11 mm
Cornell Voltage criteria: Men = S in V3 + R in aVL greater than 28 mm / Women = S in V3 + R in aVL greater than 20 mm
The Romhilt-Estes point score system may also be useful, which looks at similar voltage criteria as well as ST-T abnormalities, left axis deviation and QRS duration. Other indications of HOCM on an ECG are pathological Q waves, ST-segment depressions, LBBBs and T wave inversions.
Aside from measuring left ventricular wall thickness on an echocardiogram, asymmetrical septal hypertrophy and a small left ventricular cavity diameter are additional indicators of cardiomyopathy. As well, evidence of outflow obstruction is a key factor in assessing the risk of sudden cardiac death.
Additional diagnostic tools will generally be used if there exists significant suspicion of cardiomyopathy in a young athlete; this includes cardiac magnetic resonance imaging (MRI) which will give detailed insight into differentiating physiological and pathological hypertrophy, allow for visualization of fatty infiltration in ARVD, and also reveal many potential congenital abnormalities. Angiography is another available tool and is the gold standard for the diagnosis of coronary anomalies and ARVD. Electrophysiology studies are an option for the evaluation of arrhythmias, particularly when the etiology remains unidentified.
Outside of cardiac testing, the use of genetic testing is quite prevalent in assessing for any congenital issues. An extensive range of congenital illnesses may undergo evaluation with genetic testing, but definite answers will not always be apparent.
Heart disease in athletes involves a combination of general treatments and specific treatments. From a lifestyle standpoint, many athletes may be asked to avoid strenuous exercise and other aggravating factors for a brief period. Physical and/or mental stress increases cardiac demand but also may trigger potentially fatal arrhythmias. Upon establishing a long-term treatment regime, there should be a process of shared decision making in regards to the athlete returning to their sport of choice. The athlete will undergo a phase of risk stratification, and many variables will play a role in determining their risk of sudden death and the appropriate treatment regime. Aside from the athlete's physiology, their specific sport also can significantly affect the long-term risk. Although earlier views in literature were that many forms of heart disease in athletes should end their athletic careers; the literature in 2019 holds the view that many athletes can safely return to their sport of choice if they undergo a correct treatment process.
Medical management generally involves the goal of increasing blood flow and lowering the risk of arrhythmias. Hence, beta-blockers are a commonly used medication in these patients. Calcium channel blockers may also be an option. Surgical and percutaneous choices also exist for certain structural defects, such as surgical septal myomectomy or alcohol septal ablation in HOCM. In the case of congenital arrhythmias, ablation may be performed to eradicate the electrical source of the arrhythmia. When the risk of sudden death is appreciated, an implantable cardioverter defibrillator (ICD) may be placed in case the patient goes into cardiac arrest. ICD placement has dramatically improved the prognosis in all athletes with congenital heart defects and has even allowed for continued sports participation. The last option in certain defects is a heart transplant.
In all patients affected with congenital heart disease, it is also essential to maintain adequate hydration, electrolyte levels and to routinely follow up with a physician. Unfortunately, a specific diagnosis may warrant abstaining from sports, but this should always be a result of a shared decision-making process between the physician and the patient.
The evaluation of sudden death in athletes must include non-cardiac etiologies.
Given that syncope in athletes a key alarming symptom, other probable etiologies should be considered in evaluating syncope.
The prognosis for athletes diagnosed with cardiac disease depends on the specific illness, the degree of pathology and the treatment regime.
Hypertrophic obstructive cardiomyopathy: Near normal life expectancy, often asymptomatic. ICDs are highly effective in those at risk of sudden cardiac death.
Coronary artery anomaly: Pathological anomalies have an unknown risk of sudden death. Other anomalies are benign, and no evidence exists to show a shorter than normal life expectancy.
Arrhythmogenic right ventricular dysplasia: Good long-term outcome in those who are treated and do not have left ventricular involvement. ICD can drastically improve the prognosis. Many athletes may be forced to abstain from sports.
Congenital long QT syndrome: Low-risk of sudden cardiac death if adequately treated. Risk drops lower after the age of 40.
Wolff-Parkinson-White syndrome: Sudden cardiac death is a rare occurrence if treated.
Brugada syndrome: Risk stratification is done to assess the need for interventional treatment. Asymptomatic patients have a near normal life expectancy whereas symptomatic patients can have a life expectancy as low as 40 years old. No strong and direct association to athletics.
Catecholaminergic polymorphic ventricular tachycardia: Poor prognosis if it is not diagnosed early as it often presents in childhood. ICDs and beta blockers drastically improve outcomes.
Other conditions may either have an unknown prognosis or have a highly variable prognosis dependent on response to treatment. Lastly, compliance with treatment is also a concern, especially in younger athletes. Many athletes may need to abstain from sports for some time until they receive a thorough evaluation and a treatment regime is finalized. Compliance with the period of abstinence, adherence to the treatment regime and avoidance of other aggravating factors are all instrumental in the prognosis.
The most serious complication in athletes with cardiac illness is sudden cardiac death. Syncope, presyncope, and dizziness are frequently experienced, particularly during exertion. Dyspnea and chest pain are common complaints.
Consultation with a cardiologist with specialized knowledge in managing athletes is the recommendation when high-risk pathology is suspected.
Evaluation of an athlete at risk for sudden death should be performed with a multidisciplinary team that includes the primary care provider, nurse practitioner, cardiologist, pediatrician, and an internist. Patients should receive education about their diagnosis, its prognosis and how it is affected by physical exertion. Certain conditions require the patient to avoid any and all physical exertion until the establishment of a treatment regime. Patients should also avoid other potentially dangerous triggers. It is critical to provide all of the relevant information to the patient so that the healthcare provider and patient can engage in shared decision making about whether or not to continue the chosen sport.
The prognosis depends on the type of heart pathology, the age of the patient, other comorbidities, and level of physical activity.
We are looking for contributors to author, edit, and peer review our vast library of review articles and multiple choice questions. In as little as 2-3 hours you can make a significant contribution to your specialty. In return for a small amount of your time, you will receive free access to all content and you will be published as an author or editor in eBooks, apps, online CME/CE activities, and an online Learning Management System for students, teachers, and program directors that allows access to review materials in over 500 specialties.
This is an academic project designed to provide inexpensive peer-reviewed Apps, eBooks, and very soon an online CME/CE system to help students identify weaknesses and improve knowledge. We would like you to consider being an author or editor. Please click here to learn more. Thank you for you for your interest, the StatPearls Publishing Editorial Team.
Click Your Answer Below
Would you like to access teaching points and more information on this topic?
Click Your Answer Below
Would you like to access teaching points and more information on this topic?
|Musso P,Carballo S, [Current practice for the prevention of sudden death in young athletes]. Revue medicale suisse. 2018 Oct 17; [PubMed]|
|Modaff DS,Hegde SM,Wyman RA,Rahko PS, Usefulness of Focused Screening Echocardiography for Collegiate Athletes. The American journal of cardiology. 2019 Jan 1; [PubMed]|
|Al-Khatib SM,Stevenson WG,Ackerman MJ,Bryant WJ,Callans DJ,Curtis AB,Deal BJ,Dickfeld T,Field ME,Fonarow GC,Gillis AM,Granger CB,Hammill SC,Hlatky MA,Joglar JA,Kay GN,Matlock DD,Myerburg RJ,Page RL, 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: Executive summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart rhythm. 2018 Oct; [PubMed]|
|Chistiakov DA,Myasoedova VA,Melnichenko AA,Grechko AV,Orekhov AN, Role of androgens in cardiovascular pathology. Vascular health and risk management. 2018; [PubMed]|
|Wasfy MM,Hutter AM,Weiner RB, Sudden Cardiac Death in Athletes. Methodist DeBakey cardiovascular journal. 2016 Apr-Jun; [PubMed]|
|Udelson JE, Evaluating and Reducing the Risk of Sudden Death in Hypertrophic Cardiomyopathy. Circulation. 2019 Feb 5; [PubMed]|
|Datta J,White CS,Gilkeson RC,Meyer CA,Kansal S,Jani ML,Arildsen RC,Read K, Anomalous coronary arteries in adults: depiction at multi-detector row CT angiography. Radiology. 2005 Jun; [PubMed]|
|Engel HJ,Torres C,Page HL Jr, Major variations in anatomical origin of the coronary arteries: angiographic observations in 4,250 patients without associated congenital heart disease. Catheterization and cardiovascular diagnosis. 1975; [PubMed]|
|Elias Neto J,Tonet J,Frank R,Fontaine G, Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) - What We Have Learned after 40 Years of the Diagnosis of This Clinical Entity. Arquivos brasileiros de cardiologia. 2019 Jan; [PubMed]|
|Barbosa Neto O,da Mota GR,De Sordi CC,Resende EAMR,Resende LAPR,Vieira da Silva MA,Marocolo M,Côrtes RS,de Oliveira LF,Dias da Silva VJ, Long-term anabolic steroids in male bodybuilders induce cardiovascular structural and autonomic abnormalities. Clinical autonomic research : official journal of the Clinical Autonomic Research Society. 2018 Apr; [PubMed]|
|Pourmand A,Mazer-Amirshahi M,Chistov S,Sabha Y,Vukomanovic D,Almulhim M, Emergency department approach to QTc prolongation. The American journal of emergency medicine. 2017 Dec; [PubMed]|
|Itoh H,Crotti L,Aiba T,Spazzolini C,Denjoy I,Fressart V,Hayashi K,Nakajima T,Ohno S,Makiyama T,Wu J,Hasegawa K,Mastantuono E,Dagradi F,Pedrazzini M,Yamagishi M,Berthet M,Murakami Y,Shimizu W,Guicheney P,Schwartz PJ,Horie M, The genetics underlying acquired long QT syndrome: impact for genetic screening. European heart journal. 2016 May 7; [PubMed]|
|Ostby SA,Bos JM,Owen HJ,Wackel PL,Cannon BC,Ackerman MJ, Competitive Sports Participation in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia: A Single Center's Early Experience. JACC. Clinical electrophysiology. 2016 Jun; [PubMed]|
|Yadav S,Sitbon YH,Kazmierczak K,Szczesna-Cordary D, Hereditary heart disease: pathophysiology, clinical presentation, and animal models of HCM, RCM, and DCM associated with mutations in cardiac myosin light chains. Pflugers Archiv : European journal of physiology. 2019 Jan 31; [PubMed]|
|Gervasi SF,Palumbo L,Cammarano M,Orvieto S,Di Rocco A,Vestri A,Marano R,Savino G,Bianco M,Zeppilli P,Palmieri V, Coronary atherosclerosis in apparently healthy master athletes discovered during pre-PARTECIPATION screening. Role of coronary CT angiography (CCTA). International journal of cardiology. 2018 Nov 20; [PubMed]|
|Vorona E,Nieschlag E, Adverse effects of doping with anabolic androgenic steroids in competitive athletics, recreational sports and bodybuilding. Minerva endocrinologica. 2018 Dec; [PubMed]|
|Carbone A,D'Andrea A,Riegler L,Scarafile R,Pezzullo E,Martone F,America R,Liccardo B,Galderisi M,Bossone E,Calabrò R, Cardiac damage in athlete's heart: When the [PubMed]|
|Laszlo R,Scharhag J,Burgstahler C,Striegel H,Steinacker JM, [Sports cardiology : Overview of relevant clinical topics]. Herz. 2018 Feb; [PubMed]|
|Abu Bakar NA,Luqman N,Shaaban E,Abdul Rahman H, Prevalence and predictors of electrocardiogram abnormalities among athletes. Asian cardiovascular [PubMed]|
|Ben Halima A,Kobaa D,Ben Halima M,Ayachi S,Belkhiria M,Addala H, Assessment of premature ventricular beats in athletes. Annales de cardiologie et d'angeiologie. 2019 Jan 22; [PubMed]|
|McClean G,Riding NR,Pieles G,Watt V,Adamuz C,Sharma S,George KP,Oxborough D,Wilson MG, Diagnostic accuracy and Bayesian analysis of new international ECG recommendations in paediatric athletes. Heart (British Cardiac Society). 2019 Jan; [PubMed]|
|Parisi A,Tranchita E,Minganti C,Sperandii F,Guerra E,Calò L,Borrione P,Pigozzi F, Young athletes with ventricular premature beats: Continuing or not intense training and competition? Scandinavian journal of medicine [PubMed]|
|Cay S,Ozeke O,Ozcan F,Topaloglu S,Aras D, All the things that we should think about if we want to diagnose the long QT accurately. Pacing and clinical electrophysiology : PACE. 2019 Feb; [PubMed]|
|Farzam K,Richards JR, Rhythm, Premature Ventricular Contraction (PVC) 2018 Jan; [PubMed]|
|Farzam K,Tivakaran VS, QT Prolonging Drugs 2018 Jan; [PubMed]|
|Schwartz PJ,Ackerman MJ,Wilde AAM, Channelopathies as Causes of Sudden Cardiac Death. Cardiac electrophysiology clinics. 2017 Dec; [PubMed]|
|Rawlins J,Bhan A,Sharma S, Left ventricular hypertrophy in athletes. European journal of echocardiography : the journal of the Working Group on Echocardiography of the European Society of Cardiology. 2009 May; [PubMed]|
|Lee H,Song HJ,Paek YJ,Park KH,Noh HM,Kim G,Seo YG, Clinical Characteristics Associated with Electrocardiographic Left Ventricular Hypertrophy in Clinical Normotensives without a History of Hypertension: a Cross-Sectional Study. Korean journal of family medicine. 2019 Feb 7; [PubMed]|
|Nomsawadi V,Krittayaphong R, Diagnostic performance of electrocardiographic criteria for left ventricular hypertrophy among various body mass index groups compared to diagnosis by cardiac magnetic resonance imaging. Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc. 2019 Feb 5; [PubMed]|
|Pelliccia A,Solberg EE,Papadakis M,Adami PE,Biffi A,Caselli S,La Gerche A,Niebauer J,Pressler A,Schmied CM,Serratosa L,Halle M,Van Buuren F,Borjesson M,Carrè F,Panhuyzen-Goedkoop NM,Heidbuchel H,Olivotto I,Corrado D,Sinagra G,Sharma S, Recommendations for participation in competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and pericarditis: position statement of the Sport Cardiology Section of the European Association of Preventive Cardiology (EAPC). European heart journal. 2019 Jan 1; [PubMed]|
|Saarel EV,Law I,Berul CI,Ackerman MJ,Kanter RJ,Sanatani S,Cohen MI,Berger S,Fischbach PS,Burton DA,Dziura J,Brandt C,Simone L,Li F,Olshansky B,Cannom DS,Lampert RJ, Safety of Sports for Young Patients With Implantable Cardioverter-Defibrillators. Circulation. Arrhythmia and electrophysiology. 2018 Nov; [PubMed]|
|van Driel B,Asselbergs FW,de Boer RA,van Rossum AC,van Tintelen JP,van der Velden J,Michels M, [Hypertrophic cardiomyopathy]. Nederlands tijdschrift voor geneeskunde. 2019 Feb 7; [PubMed]|
|Blusztein DI,Zentner D,Thompson T,Jayadeva P,Liang D,Wang R,Winship I,James PA,Trainer AH,Kalman JM,Vohra J, Arrhythmogenic Right Ventricular Cardiomyopathy: A Review of Living and Deceased Probands. Heart, lung [PubMed]|
|Castro Hevia J,Dorantes Sanchez M,Martinez Lopez F,Castañeda Chirino O,Falcon Rodriguez R,Puga Bravo M,de Zayas Galguera J,Antzelevitch C, Multiple serial ECGs aid with the diagnosis and prognosis of Brugada syndrome. International journal of cardiology. 2019 Feb 15; [PubMed]|
The intent of StatPearls is to provide practice questions and explanations to assist you in identifying and resolving knowledge deficits. These questions and explanations are not intended to be a source of the knowledge base of all of medicine, nor is it intended to be a board or certification review of Pathology-Forensics. The authors or editors do not warrant the information is complete or accurate. The reader is encouraged to verify each answer and explanation in several references. All drug indications and dosages should be verified before administration.
StatPearls offers the most comprehensive database of free multiple-choice questions with explanations and short review chapters ever developed. This system helps physicians, medical students, dentists, nurses, pharmacists, and allied health professionals identify education deficits and learn new concepts. StatPearls is not a board or certification review system for Pathology-Forensics, it is a learning system that you can use to help improve your knowledge base of medicine for life-long learning. StatPearls will help you identify your weaknesses so that when you are ready to study for a board or certification exam in Pathology-Forensics, you will already be prepared.
Our content is updated continuously through a multi-step peer review process that will help you be prepared and review for a thorough knowledge of Pathology-Forensics. When it is time for the Pathology-Forensics board and certification exam, you will already be ready. Besides online study quizzes, we also publish our peer-reviewed content in eBooks and mobile Apps. We also offer inexpensive CME/CE, so our content can be used to attain education credits while you study Pathology-Forensics.