December 2020
December 3, 2020

Facing the reality and fragility of life in sports

8 min read

The Asian Football Confederation (AFC) recently recommended that junior India international Anwar Ali ‘should be restricted from competitive sports activity’ because of a congenital heart condition.

Based on the recommendation, All India Football Federation (AIFF) chose to bar the 20-year-old from playing in any of their sanctioned tournaments.

Anwar has now filed a writ petition in the Delhi High Court against the decision. His legal counsel are now arguing that Anwar’s ‘right to livelihood’ cannot be taken away. They have also cited certain procedural lapses by the AIFF.

The case has been listed for further hearing later this month as Anwar claims the AIFF had violated his fundamental right to earn his livelihood and practice his profession due to the diagnosis of a congenital heart condition called Apcial Hypercardio Myopathy (HCM).

Ali had represented the country at the U-15, U-17, and U-19 levels internationally and was part of India’s squad at the FIFA under-17 World Cup where he started all matches as the main centre back of the team.

AFC medical committee chairman Datuk Gurucharan Singh, said while the decision was drastic with it was an unanimous conclusion made by the numerous medical experts who had looked into Anwar’s prognosis.

Dr Gurucharan Singh

“Though we feel sad and our hearts go out to such an outstanding footballer coming from a humble background yet it is important to face the reality and fragility of life”,” said Dr Gurucharan, who is also the head of the Badminton World Federation (BWF) Medical Committee.

He added that Anwar may have been ill-advised in taking the issue to the courts.

“The MRI done also found some scarring of his heart tissue and that further complicates his case. He can still play social football to keep himself fit, but any high intensity football is totally out,” said Dr Gurucharan.

He added that any viral infection would complicate matters and put Anwar at a higher risk during high-intensity sports.

Both the AIFF and the AFC on their part have offered Anwar alternate path to earn a living through sports.

“It is his fundamental right in wanting to play top level football, but he has to understand that him being alive is of more value to his family and the society,” said Dr Gurucharan.

One player that Anwar should take advise is from former Bolton player Fabrice Ndala Muamba of Zaire. The naturalised British player was also the captain of the English U-19 team.In March 2012, Muamba suffered a cardiac arrest during a televised FA Cup match between Bolton and Tottenham Hotspurs, from which he recovered despite his heart having stopped for 78 minutes.

Following medical advice, he announced his retirement from professional football in August 2012. He even took up a job as a youth coach with Rochdale and also as a sports commentator.

“FIFA’s statistics shows that at least one player per month lose their live due to congenital heart conditions while playing. This is a frightening number and it does not take into account of many others which goes unreported as many national associations do not keep track of such matters,” lamented Dr Gurucharan.

While athletes strive to excel in sports, many do not make it to the top because of their medical conditions.  HCM is a condition that falls in this category and has proven to be deadly for many.

It may make good story telling and inspiring when athletes with pre-existing medical conditions do make it to the top but that is definitely not the reason as to why anyone, even someone with the talent of Anwar Ali, should risk their lives.

Among those, who overcame such adversity to rise to the top is Olympian Wilma Rudolph. Wilma had a tough childhood, suffering paralysis from polio as a young child, scarlet fever and double pneumonia. Doctors were not certain Rudolph would be able to even walk, let alone become an Olympic athlete later in her life.

Her 1956 Melbourne Games Olympic bronze medal debut at the young age of was just the start. She went on to compete at the 1960 Rome games as well. She broke an astounding three world records in her relays, claiming the nickname “The Black Gazelle” for her intense speed, beauty and grace.

Venus Williams has won several Grand Slam titles and an Olympic gold medal in her career. She began breaking records at an early age of 10, receiving her pro card in 1994.

In 2011, Williams was diagnosed with Sjogren’s Syndrome, an autoimmune disease that left her muscles easily fatigued and sore. She converted to eating a vegan diet and transformed her training schedule, which proved successful as she is still competing today in the 2016 Rio Olympics.

Joyner-Kersee at the 1988 Olympic Trials

Jackie Joyner-Kersee is the most decorated female track athlete in history, and a lifelong asthma sufferer. She competed in the heptathlon, winning a silver medal at the 1984 Olympics. In total, Joyner-Kersee earned 3 Olympic gold medals, one silver, and 2 bronze.

Phil Mickelson has won close to 50 PGA events to date, including several majors. He was diagnosed with psoriatic arthritis in 2010, a few years after developing signs of the chronic skin condition psoriasis. His disease causes joint damage and typically affects the wrists, knees, ankles, fingers, and toes—making the rigors of golf extremely difficult. With treatment, he has continued to be a factor on the pro tour and has been able to remain active with his family.

All inspiring a new generation of athletes, but for Anwar it is time for him to inspire others by making the right decision and taking up a different role in sports.

What is Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is the leading cause of sudden cardiac death in athletes in under the age of 35. The genetic disorder is characterised by an abnormally hypertrophied but nondilated left ventricle in the absence of physiological conditions such as physical training or pathological conditions like aortic stenosis or hypertension that would result in left ventricular hypertrophy (Maron, Ackerman, et al. 2005). More than 400 specific mutations within genes have been identified.

The prevalence of HCM is estimated at 1 in 500 in the general population and is more prevalent in males of African-American descent.

The walls of the left ventricle thicken in a variable pattern in HCM. As often as 28% of the time, physical obstruction of blood flow occurs during systole. Up to 80% of individuals with HCM have abnormally small coronary arteries that may cause myocardial ischemia (Maron, Ackerman, et al. 2005). Cellular abnormalities include myofibrillar disorganisation and death with resultant fibrotic scarring.

Although outflow obstruction can occur, the presence of left ventricular diastolic dysfunction is more common. Either outflow obstruction or diastolic dysfunction can impair exercise performance even in the least symptomatic person (Maron, Ackerman, et al. 2005). Both decreased wall distensibility and incomplete myocardial relaxation contribute to altered left ventricular filling (Maron et al. 1987), which leads to left atrial dilation and potential development of emboli.

Regional myocardial ischemia likely occurs because of the abnormally small coronary arteries and inadequate capillary density (Maron et al. 1987). Adding random fibrosis of the cardiac musculature produces a combination of ischemia, fibrosis and impaired vasodilator reserve that can lead to arrhythmia and sudden death.

Signs and Symptoms

Symptoms of HCM are fatigue, dyspnea, exertional angina and syncope or near syncope. These symptoms may not correlate with the degree of ventricular hypertrophy or be predictive for sudden death (Maron, Shirani, and Poliac 1996). Physical examination can provide valuable information, but the findings are not consistent. On palpation, an increased left ventricular impulse may be felt. Pulses may be bifid in character and exhibit a brisk upstroke. On cardiac auscultation, a classic, harsh precordial ejection murmur may be heard at the left lower sternal border toward the apex. The murmur increases with standing or Valsalva manoeuvre and diminishes with squatting; however, a murmur is not always present.

It is important to consider differential diagnoses before determining clinical HCM. The clinical symptoms alone of exertional angina, syncope, and near syncope point to many conditions that could cause sudden death. They also can be related to benign conditions, such as dehydration or vasovagal syncope, or noncardiac conditions, such as asthma or gastroesophageal reflux disease. The potential for a serious, life-threatening condition, however, warrants an immediate referral.

Referral and Diagnostic Tests

Athletes with symptoms of exertional angina, syncope, or near syncope should be referred immediately to a physician who specialises in cardiology for evaluation. Fatigue and dyspnea uncharacteristic for a particular athlete warrant concern and certainly physician referral when accompanied by a heart murmur.

Standard laboratory tests, such as a resting 12-lead ECG or chest radiograph, have limited utility in screening for HCM. The most useful diagnostic test is echocardiography, or magnetic resonance imaging (MRI) with gadolinium contrast (Maron, Douglas, et al. 2005; Maron 2015b). Increased left ventricular wall thickness (>15 mm) is the most helpful diagnostic parameter. The majority of male athletes and all female athletes have a ventricular wall thickness of 12 mm or less (Pelliccia et al. 1991). Therefore, the range from 13 to 15 mm may pose a diagnostic dilemma because it is possible to have physiological hypertrophy in this wall thickness range; however, this hypertrophy has been reported only in male cyclists and rowers (Pelliccia et al. 1991).

Another sign of HCM that can be seen on an echocardiogram is a ventricular septum or free wall thickness ratio greater than 1:3. Asymmetric wall thickening and decreased left ventricular diastolic cavity dimension (<45 mm) may also be present. In addition, the echo may reveal abnormal diastolic filling with decreased early filling and increased late filling and abnormal ultrasonic myocardial reflex activity in the athlete with HCM (Maron et al. 1993).

Discontinuing athletic activities for a few weeks to 1 mo for the athlete with these symptoms may help clinicians to determine whether the problem is HCM or simply athlete’s heart (Maron et al. 1993). Hypertrophy of the ventricular wall will not resolve with detraining in a person with HCM.

As a diagnostic tool for HCM, echocardiography is the gold standard. People with HMC are limited to low-intensity sports, but there is a suggestion that those with a family history of sudden death at a young age due to HCM are strong candidates for an implantable cardioverter defibrillator to allow for a more normal life (Maron 2015a).

Treatment and Return to Participation

On the basis of the 36th Bethesda Conference recommendations, athletes with hypertrophic cardiomyopathy should be restricted from participation in all competitive sports with the possible exception of low-intensity (class IA) sports such as golf, bowling and billiards (Mitchell et al. 2005). Furthermore, the placement of an implantable cardioverter defibrillator (ICD) in a patient with HCM does not change the competitive sports recommendations for this disease.

Although the clinical significance and natural history of genotype positive–phenotype negative individuals remain unresolved, no compelling data are available at present with which to preclude these patients from competitive sports, particularly in the absence of cardiac symptoms or a family history of sudden death.


Detection of HCM can be difficult, but the patient’s medical history is invaluable. A comprehensive medical history can reveal an autosomal dominant transmission pattern, a family history of cardiac disease, or a record of other premature sudden death in family members. Unfortunately, medical histories have not been as useful as expected because of the variability of expression of the trait.

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