The heart undergoes profound changes in response to athletic training, producing in well-conditioned athletes morphologic, functional, and electrophysiologic alterations. But a perplexing situation for the clinician is the athlete whose problem cannot be attributed to the athletic heart syndrome. The usual clinical situation is one in which exercise-associated collapse, near-syncope, or syncope is the presenting complaint, and a carefully taken history and physical examination reveal little. Further workup will usually include an electrocardiogram (ECG) and/or an echocardiogram. If the ECG demonst

Another diagnostic measure that can be taken is to have a competitive athlete undergo a period of deconditioning. Left ventricular cavity size or wall thickness can be shown to be a physiologic consequence of athletic training by serial ECG exams. After a short period of reconditioning, decreases in cardiac dimensions and mass are evident.(37) Detraining produces a rapid and progressive decrement in morphology.(43) For example, elite athletes with left ventricular hypertrophy may show reduction in wall thickness of about 2 to 5 mm within 3 months of deconditioning.(32) Therefore, repeat echocardiography following this deconditioning will show normalized wall thickness in athletes, but not in individuals with HCM.

The prognostic importance of syncope in HCM is not completely understood, and the diversity of the mechanisms potentially responsible for this symptom makes management particularly complex. Since it is usually impossible to determine the mechanism responsible for a single episode of syncope, these patients should be evaluated conservatively using non-invasive testing.(31)

The most definitive evidence for the presence of HCM in an athlete with increased wall thickness comes from the demonstration of the disease in a relative.(37) The estimated prevalence of HCM in the general population is about 1 in 500. HCM has a familial transmission as an autosomal-dominant trait, with variable expression, so not all people with the gene trait will have the disease. Over the past 15 years the genetics of HCM have been elucidated in great detail and new mutations continue to be discovered. These mutations can lead to significant changes in protein structure, configuration, and electrical charge.(42) In athletes whom the distinction between HCM and athlete’s heart syndrome cannot be distinctly made by other methods, ECG of family members may resolve the diagnosis. Absence of HCM in a family, however, does not necessarily exclude the diagnosis since HCM may be sporadic.(37)

In the vast majority of competitive athletes, absolute left ventricular wall thickness is normal or only mildly increased, around 12 mm. In some athletes, however, the increase in left ventricular wall thickness may be more substantial, up to 16 mm, unavoidably raising the possibility of HCM. In patients with HCM, the increase in left ventricular wall thickness is usually marked, and the average wall thickness reported in most echocardiographic studies of this disease ranges from 20 mm to greater than 50 mm.(32)

While HCM may be suspected during pre participation sports evaluations by prior occurrence of syncope, family history of the disease, or by a loud heart murmur, such clinical features are relatively uncommon among affected individuals. One study showed that potentially lethal cardiovascular abnormalities, including HCM, were suspected by the standard pre participation exam in only 3% of 115 high school and college athletes who ultimately died suddenly of such di

Some topics in this essay:
College Cardiology, Absence HCM, , ECG’s Depending, ECG Rhythm, left ventricular, wall thickness, heart syndrome, left ventricular wall, ventricular wall, ventricular wall thickness, physical examination, history physical examination, left ventricular hypertrophy, ventricular hypertrophy, history physical, female athletes, patients hcm, athletic training, athletic heart syndrome,