The benefits of sport, both to the individual and the community, greatly outweigh the risks to participants. No pathological conditions are caused by exercise.

    This article will review briefly the physiologic changes that occur with cardiac conditioning, clinical findings and sudden cardiac death occurring in athletes as well as discuss the issues of screening prior to participation in sporting activities and the provision of defibrillators at sporting venues.


Athlete’s Heart


   In 1892, Sir William Osler wrote: “In the process of training, the getting wind as it is called, is largely a gradual increase in the capability of the heart . . . The large heart of athletes maybe due to the prolonged use of their muscles, but no man becomes a great runner or oarsman who has not naturally a capable if not a large heart”(1). Indeed, the entity of “athlete’s heart” has been recognized for over 100 years. However, only in the past two decades has the application of echocardiography and other noninvasive imaging techniques permitted definition with some precision of the alterations in cardiac dimensions associated with athletic conditioning.

   The athlete’s heart reflects a normal physiologic response to exercise. However, the constellation of findings on physical examination, in the resting electrocardiogram (ECG), stress test, Holter monitor, and echocardiogram of a well trained athlete can occur in certain pathological cardiac conditions, which may result in misdiagnosis and mislabeling of otherwise healthy individuals. Athletes can certainly have cardiovascular disease. Distinguishing between non-pathological changes in cardiac morphology associated with training (athlete’s heart) and certain cardiac diseases with the potential for sudden death is an important and not uncommon clinical problem.


Physiologic Changes


   Physiologically, the heart maintains its ability to function adequately as a pump by altering heart rate and contractility when a sudden demand is placed on it. However, when a long-term demand is imposed on the heart, pump function is maintained by means of cardiac adaptive responses. Chronic demand can be related either to pressure overload or volume overload. When pressure overload is chronic, the heart responds by increasing septal and free-wall thickness to normalize myocardial wall stress (La Place’s law). When chronic volume overload occurs, left ventricular end-diastolic diameter increases, with a proportional increase in septal and free-wall thickness to normalize wall stress. The increase in the diameter and in ventricular wall thickness can be considered appropriate compensation for the chronic volume overload placed on the hearts of athletes, who require sustained increases in cardiac output during competition.

  In a well-trained athlete, the constraints due to La Place’s law may be compensated for by increasing myocardial mass. A larger myocardial mass reduces the cardiac wall tension required for cardiac ejection. An athlete in need of a high capacity for oxygen transport benefits from a large stroke volume, a low heart rate, and a thickened ventricular wall. Thus, the changes in cardiac dimensions that occur with training result in an increased efficiency of cardiac performance.
 

Table 1. Resting ECG Abnormalities in athletes

 

Table 2. Ambulatory Echocardiographic findings in athletes

 

Table 3. Causes of Sudden Cardiac Death (Athletes and non-Athletes)

 

Clinical Findings


    Athletes often have a slow resting heart rate, a third and fourth heart sound may be present as well as a systolic murmur. The resting ECG more frequently shows variations from the accepted normal (Table 1) and Holter monitoring more frequently picks up various rhythm disturbances than in age matched controls (Table 2).

    When athletes undergo stress testing there is a higher rate of false positive results both because of the low prevalence of coronary disease in this population (Bayes Theorem) and because of the higher incidence of resting ECG changes.

   Echocardiographic changes with exercise vary with the degree of dynamic (isotonic) and static (isometric) training. With dynamic or isotonic training the heart size increases due to chamber dilatation and left ventricular wall thickness increases proportionally (2). From La Place’s Law, wall stress remains normal. With static or isometric training, echocardiographic findings are somewhat controversial. Some studies show that when corrected for lean body mass there is no difference from normal controls, but other studies show that heart size increases mainly due to an increase in left ventricular wall thickness with a minimal increase in left ventricular end diastolic dimension.

  The hearts of elite athletes involved in such training can be distinguished from pathological conditions such as hypertension and hypertrophic cardiomyopathy because in these disease states there is often a decrease in left ventricular end diastolic dimensions. In elite athletes the inter-ventricular septum may be differentially thickened, suggesting the possibility of hypertrophic cardiomyopathy, but in athletes the septal wall thickness to left ventricular end diastolic dimension ratio is usually less than 0.48 and septal wall thickness is unlikely to be more than 16mm. These measurements are often exceeded in patients with hypertrophic cardiomyopathy. Furthermore, the presence of systolic anterior motion of the mitral valve (SAM) usually indicates the presence of hypertrophic cardiomyopathy, even in a trained athlete. With cessation of training the hypertrophy of athletic conditioning resolves, often within a matter of some weeks.


Cardiovascular Causes of Sudden Death


   Sudden death in athletes is uncommon, with an annual incidence of about 1:200,000 high school athletes in the USA, resulting in about 100 exercise related deaths per year.

   In athletes who are >35 years, sudden death is most commonly due to underlying coronary artery disease. A variety of cardiovascular diseases have been identified as potential causes of sudden death in young competitive athletes, i.e., <35 years old, and are listed in Table 3. The vast majority of these deaths occur on the athletic field during severe exertion in the context of training or competition. Each of the responsible diseases is also known to cause sudden death in non-athletes. The most common cause of sudden death in young athletes appears to be HCM.3 Although there are a number of athletes who have died with this condition, there is a suggestion that its importance has been over-emphasized by repeated reporting of the same cases in the literature.

   Concussion of the heart or commotio cordis has been the subject of recent research.4 There have been several case reports where a blow to the precordial area, often without undue force, has resulted in the sudden death of an athlete. Hockey, baseball and lacrosse players are particularly susceptible to such injuries. Link et al 4 demonstrated in a swine model that a blow to the chest wall, which coincides with the T wave results in ventricular fibrillation 90% of the time. If the blow falls on the QRS complex, heart block or asystole occurs 30% of the time. A blow timed elsewhere in the cardiac cycle causes ST segment elevation on the subsequent ECG complex; the significance of this is unclear. If ventricular fibrillation occurs and lasts for more than four minutes without defibrillation, successful resuscitation is unlikely. This raises the question as to whether defibrillators should be available at sporting venues and if so, who should be trained in their use.


Medical Assessment of Athletes


   There is no uniform agreement about whether screening should be performed prior to participation in sport. Screening is a requirement in most states of the USA and in Italy. In Australia, elite athletes have to undergo medical assessment prior to participation in scuba diving, boxing, motor racing, gliding and hockey. The American Heart Association has issued guidelines for screening prior to participation in sport.5 It is suggested that specific inquiry regarding a family history of sudden death or heart disease be made. The issues of a heart murmur, hypertension, fatigability, syncope, exertional dyspnea, and exertional chest pain should be raised with participants. The examination should include auscultation for a heart murmur, examination of the femoral pulses, measurement of the blood pressure, and an assessment of possible features of Marfan’s Syndrome.

   Screening of athletes prior to participation in sport may provide an opportunity for primary care physicians to raise other issues with teenagers and young adults. This age group does not often attend for medical consultation and it may be opportune to also discuss issues such as vaccination, smoking, alcohol and other substance abuse.


CONCLUSIONS


   It is accepted that the benefits of sport far outweigh the relatively small risks involved. In highly trained athletes with substantial left ventricular hypertrophy, it is of critical importance to clarify whether the increased left ventricular wall thickness represents the expression of the physiological adaptation of the heart to athletic training or a pathological condition such as HCM. While at present there is no single approach that will definitively resolve this question in all such athletes, several strategies exist that, alone or in combination, help the physician to distinguish between these two entities.

   Physician awareness of this compelling diagnostic dilemma, as well as the parallel consideration of pre-participation athletic screening and the provision of defibrillators at sporting venues may reduce the already low incidence of sudden cardiac death occurring in athletes, to even lower levels. By familiarizing themselves with the nuances of the athletic heart, physicians can both reassure athletes and help avoid costly and anxiety provoking evaluations that too frequently result in invasive procedures and premature cessation of an athlete’s career.


References


1. Osler W. The principles and practice of medicine. New York: Appleton, 1892;635.

2. Pellicia A et al. Physiologic left ventricular cavity dilatation in elite athletes. Ann Intern Med. 1999. Jan 5; 130:23-31.

3. Mann BJ et al. Sudden death in young competitive athletes. JAMA. 1996; 76:199-204.

4. Link MS et al. An experimental model of sudden death due to low energy chest-wall inpact (Commotio Cordis). N Engl J Med.1998; 338(25): 1805-1811.

5. Mann BJ et al. Cardiovascular preparticipation screening of competitive athletes: a statement for health professionals from the Sudden Death Committee (Clinical Cardiology) and Congenital Cardiac Defects Committee (Cardiovascular Disease in the Young) American Heart Association. Circulation.1996; 94: 850-856.



 

MICROCHIP TECHNOLOGY             The Present

Ant size = 6 mm long; chip size = 1 mm square width; size of smallest circuit on the chip in picture is 300 nanometers or 300 billionths of a meter                                               The Future                                      INVISIBLE CHIPS Chip size will be equivalent to size of human cells. One application of the future technology will be in pharmaceuticals. Scientists aim to develop cell-sized capsules, which will be able chemically to recognized diseased cells and deliver the appropriate drugs.