Sports cardiology is becoming an autonomous subspecialty medical field in the US. Cardiologists are leading the way and defining their role within the space that treats the unique physiology of athletes and the needs of individuals who exercise. The American College of Cardiology has developed a Sports and Exercise Cardiology discipline within their guidelines to address the growing population of these cardiac patients.
Heart Problems Plaguing Athletes
In 2011, sudden cardiac death was a leading cause of death for athletes on the playing field. Sudden cardiac death in sports is rare, and is also often preventable through careful screening. Consequently, sports governing entities highly recommend cardiovascular screenings for all athletes participating in league sports.
Although hypertrophic cardiomyopathy (HCM) is a rarely seen cause of death among active athletes, it continues to garner intense interest because HCM occurs so inexplicably in apparently healthy people and because of the difficulty discerning conditioning hypertrophy from HCM. In addition to producing thickening of the ventricles and heart muscle, HCM also precipitates disarray in heart cells that potentially alters the stability of electrical signals moving through the heart’s lower chambers. Ventricular arrhythmia may occur and cause dizziness, palpitations, and chest pain.
HCM has a genetic component involving abnormalities of genes coding for the heart muscle. It may also be acquired as a result of aging and high blood pressure. The type of HCM suffered by otherwise healthy athletes often develops for reasons that research has yet to discover, because many athletes are young, have normal blood pressure, and test negative for the genes responsible for HCM.
Coronary Artery Anomalies
Coronary artery anomalies (CAAs) are representative of a diversified body of congenital disorders with pathophysiological mechanisms and manifestations that vary. The term “coronary artery anomaly” describes any congenital coronary artery defect but may also refer to the origin of the coronary artery. On occasion, CAA is interchangeable with anomalous coronary artery (ACA).
It is not known what causes CAAs. Abnormal fetal development of coronary arteries may lead to CAA but the disorder itself is mostly attributed to some type of congenital heart disease, such as persistent truncus arteriosus, pulmonary atresia, tetralogy of Fallot, or transposition of the great arteries. Although it is still unknown whether CAA is an inherited disorder, some studies have shown CAA may run in families.
According to the Texas Heart Institute:
“Athletes…are especially at risk of sudden cardiac death if they have a CAA. In fact, CAAs are the second leading cause of death in young athletes. Between 15% and 34% of young people who experience sudden cardiac death are later found to have a CAA. Young athletes who die suddenly are typically found to have suffered HCM or a CAA.”
Diagnostic tests for CAA include MRIs, echocardiographies, magnetic resonance angiograms, angiographies, CTs, nuclear imaging, and transesophageal echocardiographies.
Left Ventricular Hypertrophy of Indeterminate Cause
Left ventricular hypertrophy of indeterminate cause (LVH) affects the left ventricular myocardium when abnormal mass development progresses due to a chronically increased workload on the heart. Aortic stenosis, hypertension, and diastolic overload are often found to be underlying mechanisms provoking instances of LVH. Coronary artery disease may also contribute to the pathogenesis of this disorder as healthy myocardium struggles to compensate for infarcted or ischemic tissue.
In addition to mechanical stress, trophic factors may facilitate development of LVH, and include various neurohormonal substances, specifically, insulin, angiotensin II, norepinephrine, and aldosterone. By stimulating growth factors (insulin GF, fibroblast GF, and transforming GF beta) and cytokines, hypertrophy provoked by synthesis of cardiac proteins is initiated. Restricting sodium intake, controlling arterial pressure, and placing LVH patients on a weight loss program may help regress this disorder. Antihypertensive agents indicated for treating LVH, including angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers followed by calcium channel antagonists, are typically recommended to improve coronary flow reserve and diastolic function.
Myocarditis is an inflammatory disorder affecting the heart muscles that stems from non-infectious and infectious origin. Pathogens responsible for myocarditis in Western countries are typically viruses, whereas people living in developing countries suffer fungal, protozoal, or bacterial forms of myocarditis. Types of viruses responsible for viral myocarditis include (but are not limited to):
- Influenza A/B
- Varicella zoster
(For a complete list of pathogens involved in myocarditis, visit the US National Library of Medicine, National Institutes of Health, at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370379/.)
The onset of myocarditis can occur within days of a pathogen entering the heart muscle and presents with symptoms similar to sudden-onset angina pectoris, myocardial infarction, or arrhythmias. Diagnostic testing methods for myocarditis include laboratory and electrocardiography tests that reveal elevated cardiac enzymes and ST segment changes. Although 60% to 70% of patients improve clinically and hemodynamically, the remaining patients will develop chronic heart failure or dilated cardiomyopathy within months or years.
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