Athletic heart syndrome is often mistaken for heart disease. A careful examination will show the difference between the two.
More adults are now participating in athletics, particularly aerobic sports such as cycling and running. This can lead to cardiovascular adaptations that are natural and physiological. But sometimes it may be difficult to distinguish them from disease, particularly demonstrated by certain simple tests like-electrocardiography and 2 D Echocardiography.
Commonly referred to as “athlete's heart”, it's a case of having too much heart. That's the simple explanation for one of medicine's more complex problems: sudden death among athletes.
Like any other muscle, the heart gets stronger with exercise. Athletic Heart Syndrome is a combination of structural and functional changes that occur in the heart of people who train more than an hour on most days.
During intensive, prolonged endurance- and strength-training, the body signals the heart to pump more blood through the body to counteract the oxygen deficit in the skeletal muscles undergoing exercise and in general. Enlargement of the heart and thickening of the ventricular walls are natural physical adaptations to deal with the high pressures and large amounts of blood gushing in and out of the heart. As time passes, these pressures cause the overall muscle mass, wall thickness, and chamber size of the left ventricle to increase progressively.
With the larger volume of blood being pumped at each heart beat, the heart rate when at rest is below normal for non-athletes. So an athlete's resting heart rate may be anywhere between 40 to 60 beats per minute as against 70-100 for a non-athlete.
A similar pathological condition called hypertrophic cardiomyopathy is an abnormal thickening of the muscles in the walls of the heart. Under normal conditions, the heart conforms to a certain size and thickness. In hypertrophic cardiomyopathy, the heart muscle becomes overgrown and the walls of the heart are abnormally thick.
The asymmetric thickening of the heart's wall (chiefly the partition-septum) can lead to an abnormal heart rhythm that can cause sudden and unexpected death after vigorous exercise. This associated condition, which remains undiagnosed in athletes, causes half the sudden death cases involving athletes under age 35.
The athlete's heart syndrome is significant because it must be distinguished from serious cardiac disorders.
The athlete's heart syndrome is asymptomatic; signs include bradycardia (heart rate of 40-60), a systolic murmur (purring sound on heart area heard only by specialists), and extra heart sounds. ECG abnormalities are common. This syndrome is believed to be a benign condition but may be hard to distinguish from other serious medical conditions that cause similar findings but can be life threatening (hypertrophic or dilated cardiomyopathies, ischemic heart disease, arrhythmogenic right ventricular dysplasia). Many changes seen in the athletic heart syndrome mimic those of various heart diseases. Careful examination must be made to distinguish heart disease from athletic heart syndrome.
No adverse effects
Findings are typically detected during routine screening or during evaluation of unrelated symptoms. If symptoms suggest a cardiac disorder (eg, palpitations, chest pain), ECG, echocardiography, and exercise stress testing are done.
Although gross structural changes resemble those in some cardiac disorders, no adverse effects are apparent. In most cases, structural changes and bradycardia regress with detraining, although up to 20 per cent of elite athletes have residual chamber enlargement, raising questions, in the absence of long-term data, about whether athlete's heart is truly benign.
No treatment is required, although three months of deconditioning may be needed to monitor LV regression as a way of distinguishing this syndrome from cardiomyopathy. Such deconditioning can greatly interfere with an athlete's life and may meet with resistance.
The writer is a Consultant Interventional Cardiologist.