Athletes with arrhythmias constitute a potentially high-risk group that may need special attention and evaluation in addition to care that might be required for nonathletes, especially if these athletes have symptoms. Athletes with arrhythmias may have syncope, palpitations, or even cardiac arrest. Some athletes with arrhythmias require restriction of their athletic activities or at least aggressive therapy due to their underlying heart problems and/or their arrhythmias, but others can return to full activity if the arrhythmia is corrected (e.g., with ablation) and there are no other significant risks due to the presence of other heart disease.
Athletes are different from nonathletes because of their high visibility; their drive, which can push them beyond normal physiologic stresses; specific physiologic stresses that result in major changes in the sympathetic/parasympathetic innervation of the heart and vasculature; metabolic changes such as hypokalemia, hyponatremia, acidosis, and other electrolyte abnormalities; and alterations in carbon dioxide and oxygen saturation. There can be fluctuations in body temperature and other physical and psychological influences. There can be changes in circulating mediators such as angiotensin-converting enzymes, steroids, serotonin, and histamine. In addition, during sports activities, there can be extreme changes in heat and cold exposure, further stressing the physiologic milieu.
The type of exercise (static, dynamic, anaerobic, or aerobic) may have a significant impact on the outcome for that individual. Arrhythmias can start with extreme initial stress, during prolonged activity, and sometimes at abrupt termination of activity.
It can be difficult to determine if heart disease is present or if cardiac abnormalities represent adaptation to exercise; for example, increased left ventricular wall thickness may be due to “athlete’s heart,” and deconditioning might reverse the effects. This type of adaptation may be specific to both the type and amount of training. Furthermore, there can be bradycardia and other arrhythmias that are typical for a highly trained athlete. The difference between hypertrophic cardiomyopathy and athlete’s heart may be related to the electrocardiographic patterns of left ventricular hypertrophy, the size of the left ventricular cavity, the presence or absence of left atrial enlargement, the presence or absence of bizarre electrocardiographic patterns, the change in wall thickness with deconditioning, a family history of channelopathies such as long QT interval syndrome (LQTS), hypertrophic cardiomyopathy, catecholaminergic polymorphic ventricular tachycardia (CPVT), or similar high-risk conditions.
Sudden death in the United States occurs only rarely in young athletes; the most common causes include hypertrophic cardiomyopathy, commotio cordis, coronary artery anomalies, ventricular hypertrophy from an undetermined cause, myocarditis, ruptured aortic aneurysm, arrhythmogenic right ventricular cardiomyopathy, coronary artery obstruction or anomalies, aortic valve stenosis, atherosclerotic coronary disease, dilated cardiomyopathy, myxomatous mitral valve degeneration, asthma and other lung conditions, heatstroke, drug abuse, and cardiac channelopathies.
The most common sports in which sudden death tends to occur are basketball, football, track, soccer, and swimming.
There are now new recommendations and guidelines on eligibility for competitive athletics and sports based on underlying cardiovascular conditions. Additionally, there have been revisions in evaluation, management, and restriction of athletes at risk for arrhythmias.
Evaluation of the athlete with palpitations or syncope is a challenge because athletes tend to have conditions that do not necessarily lend themselves to easy testing and testing tends to have a low sensitivity and specificity. Neurocardiogenic syncope is the diagnosis of exclusion.
Supplements of concern regarding induction of arrhythmias and even sudden death include stimulants such as amphetamines and cocaine, androstenedione, dehydroepiandrosterone (DHEA), growth hormone, erythropoietin, alcohol, narcotics, ephedra, and many other drugs. Drug testing may be required.
The electrocardiogram is often abnormal in trained athletes and therefore is not predictive of development of arrhythmias. These abnormalities include prominent QRS voltage, tall T waves, and early repolarization waves. Early repolarization is a notch on the down stroke of the R wave and is actually a prominent J wave ( Fig. 10.1 ). It can occur several millimeters above the isoelectric line and may be mistaken for ST elevation, as in myocardial infarction or pericarditis. Recently, a form of early repolarization unassociated with high QRS voltage, and especially prominent in the inferior leads, has been associated with sudden death due to primary ventricular fibrillation (VF) but its occurrence is thought to be rare. Other ECG abnormalities include ECGs suggesting right ventricular cardiomyopathy, LQTS, Brugada syndrome, and hypertrophic cardiomyopathy.
