Subtle Test Results Distinguish Athlete's Heart


AUSTIN, TEX. — Subtle clues in test results will help to differentiate athlete's heart from hypertrophic or dilated cardiomyopathy, Christine E. Lawless, M.D., reported at the annual meeting of the American Medical Society for Sports Medicine.

It's tough to distinguish athlete's heart from hypertrophic cardiomyopathy (HCM) when an athlete's left ventricular wall is thickened in a nondilated, normally contractile left ventricle with no systolic anterior motion of the mitral valve, said Dr. Lawless, a cardiologist in group practice in Winfield, Ill.

About 20% of highly trained athletes have what looks like left ventricular hypertrophy, with a left ventricular wall thickness between 1.3 cm and 1.5 cm; normal thickness is 1 cm.

Physicians should suspect HCM rather than athlete's heart if the patient has an unusual pattern of left ventricular hypertrophy, a small left ventricular cavity, left atrial enlargement, an unusual ECG pattern, or abnormal left ventricular filling. Other risk factors for HCM include female gender and a family history of hypertrophy (Circulation 1995;91:1596–601).

“If the thickness decreases with deconditioning, then you know that would be athletic adaptation to exercise,” she advised.

In one case, a 48-year-old man who had run 18 marathons over a period of 25 years was referred to Dr. Lawless after an irregular heartbeat was found during a physical for a new job.

He had a normal cardiovascular examination but showed atrial fibrillation on an ECG, which can be seen both in athletes as they age and in patients with a cardiomyopathy, she said. An echocardiogram showed asymmetric septal hypertrophy, systolic anterior motion of the mitral valve, and moderate mitral valve regurgitation.

At that point, Dr. Lawless was going to err on the side of diagnosing the runner with HCM, but a later echocardiogram showed that his abnormalities had normalized after deconditioning.

“He was one of these folks who fell in the gray zone,” Dr. Lawless said.

Genetic testing for 11 mutant genes in HCM will help to detect about 65% of HCMs, she added, but insurance may not cover testing, which can cost up to $4,500.

A slightly dilated left ventricle may also be the result of athletic conditioning, and not an early manifestation of dilated cardiomyopathy, if the left ventricular ejection fraction (LVEF) is normal, Dr. Lawless said.

Close to 15% of highly trained athletes appear to have a dilated ventricle with an end-diastolic dimension of about 6.0 cm, compared with a normal value of 5.6 cm.

Several years ago, Dr. Lawless saw a 39-year-old male cyclist whose father had had a cardiac arrest as a result of dilated cardiomyopathy.

The cyclist had a normal cardiac exam besides premature ventricular contractions. Although his left ventricular septal thickness was within the normal range, he had a lower than normal LVEF and larger than normal left ventricular end-systolic and end-diastolic dimensions.

Cyclists are known to have a smaller left ventricular end-systolic dimension than patients with dilated cardiomyopathy.

After deconditioning did not improve the cyclist's LVEF or end-diastolic dimension, she placed him on an ACE inhibitor and a β-blocker.

After a course of these medications, he underwent “reverse remodeling” and showed an increase in LVEF and no change in end-diastolic dimension.

Dr. Lawless allowed the man to return to cycling following the reverse remodeling, but cardiologists vary in their opinion on whether patients who normalize their left ventricular ejection fraction can return to sports participation.

“I think a lot of us look at the intensity of the sport, the triggers for sudden death in that particular sport, and we use our best judgment,” she said.

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