Treatment of pathology at the stage of physiological adaptation is not required. When symptoms appear, the athlete should consult a specialist for a comprehensive examination and correction of the training regimen. Therapy is indicated for the appearance of severe symptoms, unfavorable results of instrumental studies.
The goals of treatment are to slow down the decompensation processes, reduce the severity of clinical symptoms, prevent thromboembolism and sudden death. Therapeutic activities are carried out as an outpatient and inpatient. Indications for hospitalization are the increase in symptoms of heart failure, pronounced arrhythmias, dizziness, fainting and attacks of chest pain.
In clinical practice are used:
- Non-drug therapy. It provides for a reduction in the total loads on the heart and drastic changes in the training regimen, up to their temporary cessation or complete abandonment of sports. It is necessary to revise the diet, include more fresh vegetables, fruits, vitamins, minerals and protein, reduce the proportion of salt and fatty foods, adhere to the principle of fractional nutrition. It is recommended to review the daily regimen, to ensure an 8-hour sleep. Smoking and alcohol are contraindicated.
- Drug therapy. Appointed to patients with severe clinical picture, arrhythmias. Beta-blockers, reducing obstructive effects at rest, reducing cardiac output, blood pressure and myocardial oxygen demand are used. Calcium channel blockers are used, which have a beneficial effect on the myocardium by reducing the severity of diastolic function and ischemic events. In the presence of blockades and atrial fibrillation, antiarrhythmic agents are indicated, often in combination with anticoagulants. In case of severe pain syndrome, the treatment plan is supplemented with nitrates and ACE inhibitors. Diuretics, aldosterone antagonists and cardiac glycosides can be recommended.
- Surgical interventions. Indications for surgical treatment are marked left ventricular myocardial hypertrophy, low efficacy of drug therapy and the final stage of decompensation. Preference is given to myectomy with resection of a part of the enlarged interventricular septum, ensuring normalization of hemodynamics and elimination of symptoms. To reduce the degree of growth of muscle tissue, alcohol septal ablation is performed. In severe cases, a heart transplant is indicated.
The term “sports heart syndrome” was first used in 1899 by the Swedish scientist Salamon Henschen. Pathology is usually diagnosed by sports doctors and cardiologists, in most cases does not pose a danger to life. Less often it masks serious heart diseases or is mistakenly defined as any dangerous disease.
Reliable data on the prevalence among athletes does not exist, does not exclude a hereditary predisposition to decompensation during physical exertion. The average incidence in men is higher. Complications that develop at the final stage of decompensation are the most common cause of death for people under 35 years old who play sports. Usually, bradycardia and structural changes regress after training stops.
Sports Heart Syndrome is the collective name for structural myocardial changes that occur in people who are systematically exposed to intense physical exertion. Most often asymptomatic or with smoothed nonspecific symptoms. With the development of decompensation can cause rhythm disturbances, the development of thromboembolism and heart failure. Diagnostics includes ECG, Echo-KG and stress tests. Treatment is required only for severe structural and functional disorders, including non-drug, drug and surgical methods.
Causes of the sports heart
The sports heart syndrome is an adaptive process in the form of morphological adjustment of the myocardium in response to repeated significant physical exertion. It is more often observed in professional athletes who train for more than one hour every day for several years.
This especially applies to weightlifters and people involved in the development of endurance. Set a limit when the physiological adaptation is transformed into pathology until it succeeds.
Pathogenesis of the sports heart
The basis of myocardial changes, developing in the sports heart syndrome, are several physiological processes that are capable of becoming pathological. With prolonged intense loads, the function of the parasympathetic nervous system and the vagus nerve tone sharply increase.
This helps to slow down the automatic function of the main pacemaker. There is a remodeling of the morphological structure in the form of eccentric or concentric hypertrophy. Observed changes in the volume of the chambers of the heart, the thickness and mass of their walls. Indirectly increased stroke volume and cardiac output.
These two mechanisms together lead to a change in the functionality of the conduction system as a whole, a decrease in the pulse rate at rest and an increase in diastole time.
In proportion to the mass of the myocardium, the number of coronary vessels increases, carrying out its blood supply. Any compensatory process has its limit, after which, while maintaining the same load, new capillaries do not have time to form. This causes the death of cardiomyocytes that are not properly supplied with oxygen and nutrients. Connective tissue scars are formed, conduction along the nerve paths to the muscles from the pacemaker is reduced. The syndrome is complicated by rhythm disturbances, pathological expansion of the heart chambers and the development of chronic heart failure.
Classification of the sports heart
The syndrome of the sports heart is currently allocated to a separate nosological unit, which has its own systematization. The classification consists of two forms, which, in fact, are successive stages in the development of morphological and functional changes in the myocardium. The pathology variant is established on the basis of objective and instrumental examination data.
- Physiological sports heart. Resting pulse is less than 60 cuts per minute, a prolongation of the PQ interval is noted, a shift of the ST segment above the isoline by several millimeters in additional leads. The amplitude of the T wave increases, especially in the chest leads. No specific symptoms. The wall thickness of the left ventricle does not exceed 13 mm.
- Pathological sports heart. Symptoms that indicate the development of pathological processes in the myocardium are pronounced decrease or an increase in heart rate, signs of dystrophic changes in the heart muscle, recorded using electrocardiography. The internal volume of the heart increases, as does the thickness of the muscular wall of both ventricles. The T tooth in assignments of V1-V6 becomes even higher, it is sometimes compared to R.
Symptoms of a sports heart
The syndrome is manifested by highly non-specific variable signs that are difficult to differentiate with the normal adaptive response of the myocardium. In the physiological form, symptoms are absent or a decrease in heart rate is observed. In athletes with a pathological form, there is marked bradycardia or unreasonable tachycardia at rest, the appearance of painful sensations behind the sternum during intense cardio training and an overall decrease in physical endurance.
Chronic elevation of blood pressure, frequent dizziness, displacement of the apical impulse to the left, its diffuse nature, increased pulse in the carotid arteries, and rhythm disturbances can worsen if the condition worsens.
Complications of the sports heart
The course of the pathological form of the sports heart syndrome is often accompanied by the development of conditions that complicate the main process. The most common complications include rhythm and conduction disturbances (sinus arrhythmias, blockades, fibrillation), which can be a predisposing factor for thrombosis and thromboembolism.
A significant difficulty in the movement of the impulse through the conduction system can be a causal factor for fainting and cardiac arrest, up to sudden cardiac death. Against the background of massive hypertrophy, infective endocarditis often develops with a lesion of the valve system. Long-term current syndrome in half of cases ends with chronic heart failure.
Diagnosis of the sports heart
Identification of the syndrome in modern conditions is not difficult. Pathology is found in the overwhelming number of athletes, especially athletes. The timely registration of functional and structural changes that may lead to the development of disorders and the appearance of complications comes to the fore.
Diagnosis begins to clarify the patient’s detailed history and establish a possible hereditary predisposition, which can significantly accelerate the onset of severe decompensation. Palpation is determined by a high diffuse apical impulse and rapid pulse. Auscultation can be detected systolic murmur.
From instrumental diagnostic methods are used:
- Electrocardiography. The most typical signs of a pathological sports heart according to ECG studies are overload, left ventricular hypertrophy, high positive or negative T teeth in V1-V6 leads, deep atypical Q in the main and reinforced. Rhythm disturbances are recorded (atrial fibrillation, ventricular arrhythmias, AV block, legs, especially the left, bundle of His, of varying degrees, migration of the pacemaker, atrioventricular dissociation). Holter monitoring is often used to evaluate paroxysmal arrhythmic events and to analyze risk factors for sudden cardiac death.
- Echo-KG. It is considered the key method for the differential diagnosis of sports heart syndrome and cardiomyopathy. When conducting an ultrasound, the structure of the myocardium is assessed, hypertrophy (mainly ventricular) is detected, foci of cardiosclerosis are visualized, their prevalence is described. Obstructed outflow obstruction of the left ventricle.
- Load tests. ECG and Echo-KG are often supplemented by physical exertion, since some cardiac phenomena are observed only with increased patient activity. The occurrence of pain in the heart, a progressive decrease in stamina, persistently high or low blood pressure, dizziness, nausea and rhythm modifications are recorded.
Differential diagnosis is carried out with diseases accompanied by myocardial hypertrophy, especially of the left ventricle: aortic stenosis, an increase in heart mass against the background of arterial hypertension and IHD. In some cases, it is necessary to exclude metabolic diseases that can provoke an increase in cardiac muscle, in particular – amyloidosis.
Forecast and prevention of the sports heart
With complex therapy, the prognosis is usually favorable. In severe hypertrophy, obstruction of the output part of the left ventricle and severe heart failure, the mortality rate reaches 5%. Suspend the process of formation of the sports heart can temporarily stop training for a period of 3 months to 5 years.
Athletes who, having diagnosed syndrome, decide not to interrupt training, it is recommended to review the training program, reduce cardio. It is necessary to regularly use the heart rate monitor to prevent reaching critical heart rate values.