athletes heart- morphological changes?

Question

Is the prolonged conduction a morphological rearrangement of the heart tissue or is it considered a normal adaptation which then leads to uneven depolarisation of the tissue, and how this can result in pauses of the conducting system

Answer 1

The pages listed under this information section contain summaries of relevant topics written by many different experts in the field for the Montgomery Heart Foundation for Cardiomyopathy. The information contained in these summaries was originally collected in 1997 to put together a printed brochure for patients, families and health care professionals. Although these summaries are now 6 or 7 years old, they have been re-reviewed and we believe contain basic and general information that is still helpful to patients and families today.


While the entity of the "athlete's heart" has been recognized for over 100 years, only in the last two decades has the application of echocardiography and other noninvasive imagine techniques permitted definition with some precision of the alterations in cardiac dimensions associated with athletic conditioning. Echocardiography has demonstrated that long-term athletic training leads to an increase in left ventricular (LV) mass due to increases in LV diastolic cavity dimension, wall thickness, or both. These changes in cardiac morphology are relatively mild in absolute terms, and the differences between athlete and non-athlete populations are statistically significant but generally small. Furthermore, cardiac alterations associated with training differ somewhat depending on the particular sporting discipline in which the individual athlete participates. In particular, the changes in LV wall thickness, cavity dimensions, or both associated with long-term athletic training may be more striking in certain sports such as distance running, swimming, cycling and rowing/canoeing. It is in athletes raining in such sports that the differential diagnosis is more likely to be raised.

Differential Diagnosis

Dilated Cardiomyopathy
In an important minority of athletes, the increase in LV end-diastolic cavity dimension that occurs with training overlaps that which is characteristic of certain pathologic entities. While LV cavity dimension is athletes is usually in the range of 53 to 58 mm, in some individuals it may extend into what is regarded as the pathological range of >60 mm (up to 70 mm), and thereby resemble dilated cardiomyopathy. However, the absence of LV systolic dysfunction is usually sufficient to distinguish such physiologic ventricular enlargement induced by training from dilated cardiomyopathy.

Arrhythmogenic Right Ventricular Dysplasia (ARVD)
Because highly trained athletes may demonstrate right ventricular enlargement and a variety of depolarization, repolarization and conduction abnormalities on the ECG, the differential diagnosis between athlete's heart and ARVD may arise. Identification of ARVD by echocardiography may be exceedingly difficult because of technical limitations in imaging right heart morphology (and assessing right ventricular function), and also because the spectrum of disease is broad. Demonstration of right ventricular segmental or global dysfunction or substantial cavity enlargement supports the diagnosis. Magnetic resonance imaging, however, affords a more reliable noninvasive diagnosis of this condition. In ARVD, ECG's frequently show T wave inversion in V1-V3.

Hypertrophic Cardiomyopathy
The dilemma of distinguishing clinically between athlete's heart and structural heart disease most frequently arises with respect to hypetrophic cardiomyopathy (HCM). While at present there is no single approach that will definitively resolve this question in all such athletes, several strategies are described here that alone or in combination offer a large measure of clarification in most instances for this often compelling differential diagnosis. The definition of HCM employed here is that of a patient (or athlete) with evidence of a hypertrophied and nondilated LV in the absence of another cardiac of systemic disease that could itself produce hypetrophy of the magnitude present in that individual.

Wall Thickness
In the vast majority of competitive athletes, absolute left ventricular wall thickness is within normal limits (<12 mm). In some athletes, however, left ventricular wall thickness may be more substantial, 13-15 mm, unavoidably raising the possibility of HCM. In patients with HCM, the increase in LV wall thickness is usually marked; the average wall thickness reported in most echocardiographic studies of this disease is approximately 20 mm, and ranging up to 60 mm. However, an important minority of patients with HCM show relatively mild LV hypertrophy with wall thickness values in the range of 13 to 15 mm, and most of these patients are asymptomatic. Therefore, a diagnostic dilemma may arise in those athletes who fall into this morphological "gray zone" between physiological hypertrophy and HCM with maximal wall thickness of 13 or 14 mm, or possibly 15 mm.

In highly trained athletes, the region of predominant LV wall thickening always involves the anterior septum, although the thickness of other segments of the wall are similar (with differences in the range of 1 to 2 mm). In patients with HCM, the anterior portion of the ventricular septum is also usually the region of maximal wall thickening; however, the pattern of hypertrophy is often heterogeneous, asymmetry is prominent, and occasionally regions other than the anterior septum may show the most marked thickening. In addition, contiguous portions of the LV often show strikingly different wall thicknesses in HCM, and the transition between such areas is often abrupt.

Diagnosis of HCM in asymptomatic athletes is frequently based solely on echocardiographic assessment of the magnitude of hypertrophy, and often on precise quantitative measurements of wall thickness in a single segment or region of the LV wall. It should be emphasized that, in borderline cases, such circumstances present fertile ground for the over diagnosis.

Since marked increase in LV wall thickness often occurs during adolescence in patients with HCM, young athletes with HCM (<16 years old) may not demonstrate their maximum expression of hypertrophy until full physical maturation and development is achieved. Therefore, an athlete with HCM may initially be evaluated with echocardiography when hypertrophy is still only mild or within the borderline range; at that point in time the differential diagnosis with athlete's heart may be difficult. However, such uncertainty can be resolved by serial echocardiographic examinations which, in months or years, may show more definite wall thickening, confirming the diagnosis of HCM.

Cavity Dimensions
An enlarged LV end-diastolic cavity dimension (>55 mm) is present in more than one third of highly trained, elite male athletes. Conversely, the patients with HCM, the diastolic cavity dimension is usually small (<45 mm), and is >55 mm only in those who evolve to the end-stage phase of the disease with progressive heart failure and systolic dysfunction. Therefore, in some instances, it is possible to distinguish the athlete's heart from HCM solely on the basis of LV cavity dimension. However, when LV cavity size falls between the extremes, this dimension alone will not resolve the differential diagnosis.

Doppler Transmitral Waveform
Abnormalities of LV diastolic filling have been identified noninvasively with pulsed Doppler echocardiography or radionuclide angiography in many patients with a variety of cardiac diseases associated with LV hypertrophy. Most patients with HCM, including those with relatively mild hypertrophy (i.e., that could be confused with athlete's heart), show abnormal Doppler indexes of LV filling independent of whether symptoms or outflow obstruction are present. Typically, the early peak of transmitral flow-velocity ("E," due to rapid filling) is decreased and deceleration time of the early peak is prolonged; the late peak ("A," due to atrial contraction) is increased, inverting the normal E/A ratio. On the other hand, trained athletes invariably demonstrate normal LV filling patterns. Consequently, in a trained athlete suspected of having HCM, a distinctly abnormal Doppler transmitral flow-velocity pattern strongly supports this diagnosis, while a normal Doppler pattern is compatible with either HCM or athlete's heart.

Type of Sports Training

The specific nature of athletic training itself has a major influence on the type and magnitude of the changes in LV dimensions. For example, in a study of almost 1000 elite Italian athletes, only about 2% had an LV wall thickness of > 13 mm (in the gray zone between physiological hypertrophy and HCM), and this subset was confined to those in rowing sports and cycling. Conversely, most other forms of training, including isometric (or power) sports such as weight-lifting or wrestling, were not associated with absolute increases in wall thickness beyond 12 mm.

Gender

Gender differences with regard to alterations in cardiac dimensions and LV mass have been identified in trained athletes. Preliminary findings indicate that highly trained female athletes rarely show LV wall thicknesses that are within the aforementioned gray-zone between athlete's heart and HCM. For example, in a recent report, none of 600 elite women athletes had LV wall thickness in the range compatible with the diagnosis of HCM (>13 mm). These observations suggest, therefore, that female athletes with "borderline" left ventricular wall thicknesses of 13-15 mm (in the presence of normal cavity size) are likely to have HCM.

Regression of Hypertrophy with Deconditioning

The observation that increased LV cavity size or wall thickness are physiological consequences of athletic training may be substantiated by serial echocardiographic examinations showing a decrease in cardiac dimensions and mass with deconditioning. Decrease in wall thickness associated with deconditioning is inconsistent with HCM. Identification of such changes in wall thickness with deconditioning, require: (1) compliance from highly motivated competitive athletes to interrupt their training; and (2) serial echocardiographic studies of technical quality.

Familial Transmission and Genetics

The most definitive evidence for the presence of HCM in an athlete with an increase in wall thickness probably comes from the demonstration of HCM in a relative. Therefore, in those athletes in whom the distinction between HCM and athlete's heart cannot otherwise be achieved definitively, echocardiographic screening for affected family members represents a potential method for resolving this diagnostic uncertainty. The absence of HCM in family members, however, does not exclude this disease since it may be "sporadic" (i.e., absent in relatives other than the index case).

Recent advances in defining the genetic alterations responsible for HCM raise the possibility of DNA diagnosis in athletes suspected of having this disease. The genetic abnormalities that cause HCM, however, are greatly heterogeneous. At present, mutations responsible for HCM have been identified in 5 genes; cardiac troponin T and I, myosin binding protein-C, Beta-myosin heavy chain and alpha-tropomyosin. This substantial genetic heterogeneity has made it extremely difficult and time consuming to use techniques of molecular biology for the purpose of clinically resolving the differential diagnosis between athlete's heart and HCM.

Answer 2

You have got best answer already