Wikipedia

Athletic heart syndrome

Athletic heart syndrome(AHS) is a non-pathologicalcondition commonly seen insports medicinein which the humanheartisenlarged,and the restingheart rateislowerthan normal.

Athlete's heart
Other namesAthlete's heart,[1][2]Athletic bradycardia,orExercise-induced cardi Omega ly
Thehuman heart
4 chamber cine view of a healthy male athlete's heart, demonstrating dramatic enlargement of all chambers (LVOT at 69mm) and thickening of the heart walls.
SpecialtySports cardiology

The athlete's heart is associated with physiologicalcardiac remodelingas a consequence of repetitive cardiac loading.[3]Athlete's heart is common in athletes who routinely exercise more than an hour a day, and occurs primarily inenduranceathletes, though it can occasionally arise in heavyweight trainers.The condition is generally considered benign, but may occasionally hide a serious medical condition, or may even be mistaken for one.[4]

Signs and symptoms

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Example ultrasound of an athlete

Athlete's heart most often does not have any physicalsymptoms,although an indicator would be a consistently low resting heart rate. Athletes with AHS often do not realize they have the condition unless they undergo specific medical tests, because athlete's heart is a normal,physiologicaladaptation of the body to the stresses of physical conditioning and aerobic exercise.[5]People diagnosed with athlete's heart commonly display threesignsthat would usually indicate a heart condition when seen in a regular person:bradycardia,cardi Omega ly,andcardiac hypertrophy.

Resting heart rate recorded in an elite athlete demonstrating bradycardia at 42 bpm

Bradycardia is a slower than normal heartbeat, at around 40–60 beats per minute. Cardi Omega ly is the state of an enlarged heart, and cardiac hypertrophy the thickening of the muscular wall of the heart, specifically theleft ventricle,which pumps oxygenated blood to theaorta.Especially during an intensive workout, more blood and oxygen are required to the peripheral tissues of the arms and legs in highly trained athletes' bodies. A larger heart results in highercardiac output,which may allow it to beat more slowly at rest, as more blood is pumped out with each beat.[medical citation needed]

Another sign of athlete's heart syndrome is anS3 gallop,which can be heard through astethoscope.This sound can be heard as thediastolic pressureof the irregularly shaped heart creates a disordered blood flow. However, if anS4 gallopis heard, the patient should be given immediate attention. An S4 gallop is a stronger and louder sound created by the heart, if diseased in any way, and is typically a sign of a serious medical condition.[6]

Cause

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Aerobic/EnduranceandResistance/Strength exerciseimpact oncardiac remodelingand growth[7]

Athlete's heart is a result of dynamic physical activity, such as aerobic training more than 5 hours a week rather than static training such as weightlifting. During intensive prolongedenduranceorstrength training,the body signals the heart to pump more blood through the body to counteract theoxygen deficitbuilding in theskeletal muscles.Enlargement of the heart is a natural physical adaptation of the body to deal with the high pressures and large amounts of blood that can affect the heart during these periods of time. Over time, the body will increase both the chamber size of theleft ventricle,and themuscle massand wall thickness of the heart.[8]

Cardiac output,the amount of blood that leaves the heart in a given time period (i.e. liters per minute), is proportional to both the chamber sizes of the heart and the rate at which the heart beats. With a larger left ventricle, the heart rate can decrease and still maintain a level of cardiac output necessary for the body. Therefore, athletes with AHS commonly have lowerresting heart ratesthan nonathletes.[medical citation needed]

The heart becomes enlarged, or hypertrophic, due to intense cardiovascular workouts, creating an increase instroke volume,an enlarged left ventricle (andright ventricle), and a decrease in resting heart rate along with irregular rhythms. The wall of the left ventricle increases in size by about 15–20% of its normal capacity. No decrease of thediastolic functionof the left ventricle occurs.[9]The athlete may also experience an irregularheartbeatand a restingpulse ratebetween 40 and 60 beats per minute (bradycardia).[10]

The level of physical activity in a person determines what physiological changes the heart makes. The two types of exercise are static (strength-training) and dynamic (endurance-training). Static exercise consists of weight lifting and is mostlyanaerobic,meaning the body does not rely onoxygenfor performance. It also moderately increases heart rate and stroke volume (oxygen debt). Dynamic exercises include running, swimming, skiing, rowing, and cycling, which rely on oxygen from the body. This type of exercise also increases both heart rate and stroke volume of the heart. Both static and dynamic exercises involve the thickening of the left ventricular wall due to increased cardiac output, which leads to physiologic hypertrophy of the heart. Once athletes stop training, the heart returns to its normal size.[10][11]

Diagnosis

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Athlete's heart is usually anincidental findingduring a routine screening or during tests for other medical issues. An enlarged heart can be seen atechocardiographyor sometimes on achest X-ray.Similarities at presentation between athlete's heart and clinically relevant cardiac problems may promptelectrocardiography(ECG) and exercisecardiac stress tests.The ECG can detectsinus bradycardia,a resting heart rate of fewer than 60 beats per minute. This is often accompanied bysinus arrhythmia.The pulse of a person with athlete's heart can sometimes be irregular while at rest, but usually returns to normal after exercise begins.[12][13][14]

Regardingdifferential diagnosis,left ventricular hypertrophyis usually indistinguishable from athlete's heart and at ECG, but can usually be discounted in the young and fit.[15][16]

It is important to distinguish between athlete's heart andhypertrophic cardiomyopathy(HCM), a serious cardiovascular disease characterized by thickening of the heart's walls, which produces a similar ECG pattern at rest. This genetic disorder is found in one of 500 Americans and is a leading cause ofsudden cardiac deathin young athletes (although only about 8% of all cases of sudden death are actually exercise-related).[17][18]The following table shows some key distinguishing characteristics of the two conditions.[19]

Athlete's heart should not be confused with bradycardia that occurs secondary torelative energy deficiency in sportoranorexia nervosa,which involve slowing of metabolic rate and sometimes shrinkage of the heart muscle and reduced heart volume.[20][21]

Feature Athletic heart syndrome Cardiomyopathy
Leftventricular hypertrophy < 13 mm > 15 mm
Left ventricular end-diastolic diameter < 60 mm > 70 mm
Diastolicfunction Normal (E/A ratio > 1) Abnormal (E/A ratio < 1; orpseudonormal E/A)
Septal hypertrophy Symmetric Asymmetric (in hypertrophic cardiomyopathy)
Family history None May be present
BPresponse to exercise Normal Normal or reduced systolic BP response
Deconditioning Left ventricular hypertrophy regression No left ventricular hypertrophy regression

Themedical historyof the patient (endurance sports) andphysical examination(bradycardia, and maybe athirdorfourth heart sound), can give important hints.

  • ECG– typical findings in resting position are, for example, sinus bradycardia,atrioventricular block(primary and secondary) and incomplete (IRBBB) or completeright bundle branch block(RBBB) – all those findings normalize during exercise.[9][22]
  • Echocardiography– differentiation between physiological and pathological increases of the heart's size is possible, especially by estimating the mass of the wall (not over 130 g/m2) and its end diastolic diameter (not much less 60 mm) of the left ventricle.[9][23]
  • X-ray examination of the chest may showincreased heart size(mimicking other possible causes ofenlargement).[24]
  • Cardiac MRI - In athlete's heart, there is balanced atrioventricular remodeling, reduced thickening of the heart after detraining, nolate gadolinium enhancement,low to normalT1 signal,and normal extracellular volume.[25]
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See also:Hypertrophic cardiomyopathy screening

Because of several well-known and high-profile cases of athletes experiencing sudden unexpected death due to cardiac arrest, such asReggie WhiteandMarc-Vivien Foé,a growing movement is making an effort to have both professional and school-based athletes screened for cardiac and other related conditions, usually through a careful medical and health history, a good family history, a comprehensive physical examination includingauscultationof heart and lung sounds and recording ofvital signssuch asheart rateandblood pressure,and increasingly, for better efforts at detection, such as an electrocardiogram.[citation needed]

Anelectrocardiogram(ECG) is a relatively straightforward procedure to administer and interpret, compared to more invasive or sophisticated tests; it can reveal or hint at many circulatory disorders and arrhythmias. Part of the cost of an ECG may be covered by some insurance companies, though routine use of ECGs or other similar procedures such asechocardiography(ECHO) are still not considered routine in these contexts. Widespread routine ECGs for all potential athletes during initial screening and then during the yearly physical assessment could well be too expensive to implement on a wide scale, especially in the face of the potentially very large demand. In some places, a shortage of funds, portable ECG machines, or qualified personnel to administer and interpret them (medical technicians, paramedics, nurses trained in cardiac monitoring, advanced practice nurses or nurse practitioners, physician assistants, and physicians in internal orfamily medicineor in some area of cardiopulmonary medicine) exist.[citation needed]

If sudden cardiac death occurs, it is usually because of pathological hypertrophic enlargement of the heart that went undetected or was incorrectly attributed to the benign "athletic" cases. Among the many alternative causes are episodes of isolated arrhythmias which degenerated into lethal VF and asystole, and various unnoticed, possibly asymptomatic cardiac congenital defects of the vessels, chambers, or valves of the heart. Other causes includecarditis,endocarditis,myocarditis,andpericarditiswhose symptoms were slight or ignored, or were asymptomatic.[citation needed]

The normal treatments for episodes due to the pathological look-alikes are the same mainstays for any other episode ofcardiac arrest:cardiopulmonary resuscitation,defibrillation torestore normal sinus rhythm,and if initial defibrillation fails, administration ofintravenousepinephrineoramiodarone.The goal is avoidance of infarction, heart failure, and/or lethal arrhythmias (ventricular tachycardia,ventricular fibrillation,asystole,orpulseless electrical activity), so ultimately to restore normalsinus rhythm.[citation needed]

Management

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Athlete's heart is not dangerous for athletes (though if a nonathlete has symptoms of bradycardia, cardi Omega ly, and cardiac hypertrophy, another illness may be present). Athlete's heart is not the cause of sudden cardiac death during or shortly after a workout, which mainly occurs due tohypertrophic cardiomyopathyandarrhythmogenic cardiomyopathy(ARVC), two genetic disorders. Although a link between intensive exercise and exercise-induced arrhythmogenic right ventricular cardiomyopathy exists.[3][6]

No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that theventricular remodelingmight conceivably predispose for serious arrhythmias,[26]no evidence has been found of any increased risk of long-term events.[27]Athletes should see a physician and receive a clearance to be sure their symptoms are due to athlete's heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athlete's heart or if a differential diagnosis is difficult,deconditioningfrom exercise for a period of three months allows the heart to return to its regular size. However, one long-term study of elite-trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning.[28]This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athlete's heart is if athletes or nonathletes simply assume they have the condition, instead of making sure they do not have a life-threatening heart illness.[29]

History

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The athlete's heart syndrome was first described in 1899 bySalomon Henschen.He compared the heart size of cross-country skiers to those who livedsedentarylives. He noticed that those who participated in competitive sports displayed symptoms of athlete's heart syndrome. Henschen believed the symptoms were a normal adjustment to exercise, and felt concern was not needed.[9]Henschen believed that the entire heart became enlarged. He also believed athletes with AHS lived shorter lives than those who did not acquire the syndrome. Because his research occurred throughout the 19th century, technology was limited, and it became difficult to devise appropriate ways to measure the hearts of athletes. Few believed in Henschen's theory about athletes having larger hearts than those who did not participate in sports. The latter, however, in addition to Henschen's belief of an enlargement of the entire heart among athletes is in agreement with the four-chamber dilation seen with modern imaging modalities in individuals with athlete's heart.[30]

See also

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References

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