Athlete’S Heart

The athlete’s heart is mixture of structural and functional changes in the heart of people who are> 1 hour exercise on most days. The lesions are asymptomatic; clinically show bradycardia, systolic heart murmurs and extra heart sounds. ECG changes are common. The diagnosis is made clinically or by echocardiography. A treatment is not required. The athlete’s heart is significant because it has to be distinguished from the serious heart disease.

Intense cardio and strength training lead to veschiedenen physiological adaptation mechanisms. The increased pressure and volume overload in the left ventricle (LV) leads over time to an increase in left ventricular muscle mass, wall thickness and chamber size. Maximum stroke volume and cardiac output increase and lead to a lower resting heart rate and a prolonged duration of diastolic filling. The lower heart rate results primarily from an increase in vagal tone, but a decreased sympathetic Aktiviierung and non-autonomous, the intrinsic activity reducing factors may also play a role. The bradycardia leads to a lesser mykoardialem O2 demand; at the same time an increase in total hemoglobin and blood volume leads to an increased O2 transport. Despite these changes, the systolic and diastolic function remain normal. Structural changes are typically lower than for men of the same / r age, height and training levels in women.

The athlete’s heart is mixture of structural and functional changes in the heart of people who are> 1 hour exercise on most days. The lesions are asymptomatic; clinically show bradycardia, systolic heart murmurs and extra heart sounds. ECG changes are common. The diagnosis is made clinically or by echocardiography. A treatment is not required. The athlete’s heart is significant because it has to be distinguished from the serious heart disease. Intense cardio and strength training lead to veschiedenen physiological adaptation mechanisms. The increased pressure and volume overload in the left ventricle (LV) leads over time to an increase in left ventricular muscle mass, wall thickness and chamber size. Maximum stroke volume and cardiac output increase and lead to a lower resting heart rate and a prolonged duration of diastolic filling. The lower heart rate results primarily from an increase in vagal tone, but a decreased sympathetic Aktiviierung and non-autonomous, the intrinsic activity reducing factors may also play a role. The bradycardia leads to a lesser mykoardialem O2 demand; at the same time an increase in total hemoglobin and blood volume leads to an increased O2 transport. Despite these changes, the systolic and diastolic function remain normal. Structural changes are typically lower than for men of the same / r age, height and training levels in women. Symptoms and complaints For a sports fan, there are no symptoms. The notes are variable, but a bradycardia, a lateralized, broadened, strengthened heart’s impulse, a systolic, river-dependent ejection noise at the left lower sternal, one caused by the rapid early diastolic filling the third heart sound (S3), a diastolic due to the longer filling time can best imposing keep audible in the quiet-Braydkardie 4. heart sound (S4) and an octane carotid pulse. These clinical signs are a result of the adaptive Struktuurveränderungen of the heart during intense athletic training. Diagnosis Clinical assessment Usually ECG Sometimes Rarely echocardiography stress test, the findings are typically collected as part of routine screening or for diagnostic evaluation of nonspecific symptoms. For most athletes, no detailed diagnosis is required, although an ECG is often useful. Exhibit the symptoms of heart disease through (z. B. palpitations, chest pain), should be carried out ECG and echocardiography and stress testing. The diagnosis athlete’s heart is a diagnosis of exclusion: it must be distinguished from other life-threatening diseases that cause similar symptoms (eg, hypertrophic or dilated cardiomyopathy, ischemic heart disease, arrhythmogenic right ventricular dysplasia.). ECG Various changes in rhythm and morphology can occur in the ECG; they correlate poorly with the state of training and cardiovascular fitness. The most common ECG finding is sinus bradycardia Rare is the heart rate <40 beats / min. A sinus arrhythmia accompanied ähufig the slow heart rate. A rest bradycardia may predispose (including couplets and non-sustained ventricular tachycardia) for atrial or ventricular ectopy; Pauses after ectopic beats exceed four seconds not Wech Lener supraventricular rhythm atrial fibrillation Other possible ECG findings AV block include first degree (in up to one third of all athletes) AV block of the second degree (particularly Type I); This finding occurs at rest and during exercise disappears high QRS amplitude inferolateral T wave changes (Note for LV hypertrophy) deep anterolateral T-wave inversion incomplete right bundle branch block A AV-block III. However, the degree is pathologic and should be thoroughly evaluated. This ECG and rhythm changes have not been associated with adverse clinical events, suggesting that various arrhythmias in athletes are not pathological. Arrhythmia usually disappear spontaneously or after ener relatively short period of deconditioning significantly reduziert.Echokardiographie By echocardiography an athlete heart of cardiomyopathies can usually (see table: distinguishing features between athlete's heart and cardiomyopathy) will differ. However, the distinction is not always clear due to the continuum of the physiological to pathological cardiac enlargement. The gray zone between the athlete's heart and the left ventricular septal thickness cardiomyopathy is for: In men, 13-15 mm in women 11-13 mm In this overlap area, the occurrence of a systolic movement of the mitral valve anteriorly heavily on hypertrophic cardiomyopathy out. The diastolic indexes may differ in cardiomyopathy; However, they are normal in an athlete's heart generally. In general, echocardiographic changes correlate poorly with the state of training and cardiovascular performance range. Often a small mitral and tricuspid regurgitation observed. It should be noted that a reduction of physical activity to regression of the heart enlargement in patients leads with athlete's heart, but not in those with Kardiomyopathie.Belastungsuntersuchungen During the stress test remains the heart rate during submaximal exercise below the norm and rises to an appropriate extent and comparable to the heart rate of non-athletes at maximum load on; normalizes quickly after exercise. The behavior of the blood pressure is normal: Systolic blood pressure increases the diastolic blood pressure drops, the mean blood pressure remains relatively constant Many of the changes in the resting ECG go back during exercise or disappear completely; this observation is unique to the athlete's heart and thus a distinctive feature of pathologies. However, the pseudo-normalization of T-wave inversion points may indicate myocardial ischemia and thus requires in older athletes further investigation. However, a normal result of the stress test does not rule out cardiomyopathy. Distinguishing features between athlete's heart and cardiomyopathy property athlete's heart cardiomyopathy left ventricular septal thickness * In men <13 mm in women <11 mm in men> 15 mm in women> 13 mm left ventricular end-diastolic diameter † <60 mm> 70 mm diastolic function Normal (E: A> 1 ) Abn ormal (E: A <1) Symmetrical Asymmetrical septal hypertrophy (in hypertrophic cardiomyopathy) Family history No Can there be blood pressure response during exercise Normal Normal or reduced left ventricular systolic blood pressure deconditioning Hypertrophieregression No left ventricular Hypertrophieregression * A value of 13 to 15 mm in men and 11 to 13 mm in women no decision can be made. † A value between 60 and 70 mm no decision can be made. E: A = ratio of early to late transmitral flow velocity. Prognosis Although the general structural changes which some heart disease are similar, no adverse prognostic implications are known. In most cases, the structural changes and bradycardia have regressed in the detraining, although up to 20% of the athletes an enlargement of the heart chambers is left, raising to prognostic benignity of the athletes heart in the absence of long-term studies question. Treatment Perhaps a period of deconditioning for monitoring the LV regression The athlete's heart syndrome does not require treatment, although a 3-month detraining may be necessary to prove the left ventricular regression and thus to distinguish the syndrome from a cardiomyopathy. The detraining can significantly affect the life of an athlete, and thus may raise hackles. Summary Intense physical training increases the left ventricular muscle mass, wall thickness and chamber size; but the systolic and diastolic function remain normal. The resting heart rate is slow, and there may be a systolic murmur at the left lower sternal border, a third heart sound (S3) and / or a fourth heart sound (S4). The ECG bradycardia, signs of hypertrophy and sometimes other abnormalities such as sinus arrhythmia, atrial or ventricular ectopy and AV block zeigenn I or II. Degree. Structural and ECG changes in athletes heart result in no symptoms; the occurrence of cardiovascular symptoms (eg. B. chest pain, Dyspnow, palpitations), or an AV block III. Grades should prompt a search for an underlying heart disease.

Health Life Media Team

Leave a Reply