Just
like other muscles; the heart responds to exercise with
increased efficiency. Occasionally the changes can be a
bit unnerving.
The
most important muscle an athlete develops is her heart.
Generally as she becomes more fit, her resting heart rate
slows - a sign that her heart is pumping blood with greater
efficiency. In the first six to 12 weeks of training, resting
heart rate decreases by five to 10 percent.
The
resting pulse of a trained heart is usually less than 70
beats per minute. Many athletes monitor their heart rates
while exercising and while at rest (either immediately
upon awakening or after 10 to 15 minutes of inactivity).
But sometimes the results are unsettling.
For
instance, say you are checking your resting rate after
watching TV for 15 minutes, and you notice a skip between
beats. You continue to monitor your pulse, now rhythmic
and steady; you're not sure if you should dial 911. A while
later, the skip occurs again. All thoughts of getting your
resting heart rate below 70 are out the window; and you
become more concerned with whether you'll survive the night
or not.
Skipped
heartbeats are usually premature heartbeats - one beat
quickly follows another, and the resulting pause in the
rhythm of your normal heartbeat is assumed to be a "skipped" beat.
Occasional premature beats do occur in healthy people and
usually don't indicate a problem unless they're accompanied
by chest pain, light-headedness or other symptoms.
If
you experience a premature beat more than once every 20
to 30 minutes, however; or if you have an irregular heart
rate, palpitations or pauses in your heartbeat, it's extremely
important to see your physician. She can determine whether
you may have a benign condition called athlete's heart
or a more serious problem.
The
term "athlete's heart" describes a collection of changes
that occur as you train. The two most common findings in
trained athletes are bradycardia, or a slow pulse (less
than 70 beats per minute), and phasic sinus arrhythmia,
a pulse that speeds and slows with respiration.
How
common is it to have a pulse that speeds up and slows down
when you breathe?
Up
to 69 percent of aerobically trained athletes demonstrate
phasic sinus arrhythmia. This benign rhythm discrepancy
becomes more common as you become more fit; it temporarily
disappears when you increase your heart rate with exercise.
Physicians
have noted several other changes that reflect the heart's
normal adaptation to training. Besides lowering the resting
pulse rate, training makes the pulse more forceful, producing
a harmless murmur as blood flows through the heart and
blood vessels.
The
athlete's heart may also appear slightly enlarged on a
chest X-ray and an electrocardiogram (EKG) may chart patterns
that would not show on the EKG of an untrained heart. However,
these do not indicate disease.
Aerobics
vs. Anaerobic Training
Like
other muscles, your heart responds in a healthy way to
specific training. if your training is principally aerobic,
your heart must handle a large volume of blood. Its internal
chambers will enlarge slightly and its overall size will
increase.
The
stroke volume - the amount of blood ejected from the chambers
with each beat-will also increase, as your pulse rate decreases.
These adaptations allow your heart to pump blood with maximum
efficiency.
On
the other hand, weight-lifting or resistance training will
cause your heart muscle to thicken without enlargement
of its cavity. This adaptation enables it to generate the
increased blood pressure necessary for anaerobic exercise
but doesn't contribute to a more efficient stroke volume
or a lower pulse rate. If you combine aerobic and resistance
training, your heart will of course show the benefits of
both types of exercise.
Whatever
type of training you do, changes in your heart muscle occur
gradually over the first four to six weeks of consistent
training. Aerobically trained athletes will notice this
adaptation through their lower resting heart rates.
Some
researchers have noted increased resting heart rates with
overtraining. If your resting heart rate suddenly increases
from 60 to 70 beats per minute and you are working harder
than usual, watch out! You may be overtraining and need
to slow down. When you stop training completely your heart
will return to your untrained heart rate within three to
four weeks.
While
there are many benefits to aerobic conditioning of the
heart muscle, a trained heart does not make you immune
from heart problems.
Aerobically
trained people have lower rates of cardiovascular disease,
such as hypertension and coronary artery disease, but a
trained heart is not immune to heart problems. The tragic
deaths of Olympic volleyball player Flo Hyman, collegiate
basketball player Hank Gathers and other young athletes
in their prime are a sobering reminder that no one is invincible.
Still,
sudden death is very rare. In a 20-year study done at the
Air Force Academy on recruit deaths during exercise, the
incidence was 1.7 deaths for 500,000 hours of exercise.
The researchers concluded that "the risk of exercise-related
sudden death is no greater than deaths occurring by chance
alone." Most cases of sudden death in athletes under the
age of 35 are due to pre-existing structural congenital
heart disease.
In
people over the age of 35, exercise-related sudden death
is often caused by underlying coronary artery disease.
Adaptations the heart makes during normal training don't
cause any of these problems. Most of us have healthy hearts,
and appropriate training can reduce one's risk of some
forms of heart disease.
Even
with a healthy heart, exercising with a high fever maybe
risky. You might place undue strain on the heart while
fighting an infection, or you might have a coexisting inflammation
of the heart. Several other factors might indicate that
you are at risk for an exercise-related cardiac problem.
If any of the risk factors listed below apply to you, contact
your doctor and get an evaluation before beginning a program.
Some
cardiac risk factors:
I.
A history of fainting for no apparent reason, especially
if the fainting occurred during or immediately after exercise.
2.
Symptoms of an irregular heartbeat, palpitations, skipped
beats or fluttering heartbeat either when resting or exercising.
3.
A close blood relative who died suddenly before the age
of 55, or a family history of early coronary heart disease,
high cholesterol, Marfan's syndrome or enlarged heart.
4.
A family or personal history of seizures.
5.
You are a male over age 40 or a female over 50, the American
College of Sports Medicine recommends that you have a medical
evaluation before you begin an exercise program.
Aerobically
trained people have lower rates of cardiovascular disease,
such as hypertension and coronary artery disease, but a
trained heart is not immune to heart problems. The tragic
deaths of Olympic volleyball player Flo Hyman, collegiate
basketball player Hank Gathers and other young athletes
in their prime are a sobering reminder that no one is invincible.
Still,
sudden death is very rare. In a 20-year study done at the
Air Force Academy on recruit deaths during exercise, the
incidence was 1.7 deaths for 500,000 hours of exercise.
The researchers concluded that "the risk of exercise-related
sudden death is no greater than deaths occurring by chance
alone." Most cases of sudden death in athletes under the
age of 35 are due to pre-existing structural congenital
heart disease.
In
people over the age of 35, exercise-related sudden death
is often caused by underlying coronary artery disease.
Adaptations the heart makes during normal training don't
cause any of these problems. Most of us have healthy hearts,
and appropriate training can reduce one's risk of some
forms of heart disease.
Even
with a healthy heart, exercising with a high fever maybe
risky. You might place undue strain on the heart while
fighting an infection, or you might have a coexisting inflammation
of the heart. Several other factors might indicate that
you are at risk for an exercise-related cardiac problem.
If any of the risk factors listed below apply to you, contact
your doctor and get an evaluation before beginning a program.
Some
cardiac risk factors:
I.
A history of fainting for no apparent reason, especially
if the fainting occurred during or immediately after exercise.
2.
Symptoms of an irregular heartbeat, palpitations, skipped
beats or fluttering heartbeat either when resting or exercising.
3.
A close blood relative who died suddenly before the age
of 55, or a family history of early coronary heart disease,
high cholesterol, Marfan's syndrome or enlarged heart.
4.
A family or personal history of seizures.
5.
You are a male over age 40 or a female over 50, the American
College of Sports Medicine recommends that you have a medical
evaluation before you begin an exercise program.
The pages listed under
this information section contain summary 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 together a printed brochure for
patients, families and health care professionals. Although
these summaries are now 6 or 7 years ( 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 c years, only in the last
two decades has the application of echocardiography and
other noninvasive imagine techniques permitted definition
wi precision of the alterations in cardiac dimensions associated
with conditioning. Echocardiography has demonstrated that
long-term training leads to an increase in left ventricular
(LV) mass due to i LV diastolic cavity dimension, wall
thickness, or both. These changes of cardiac morphology
are relatively mild in absolute terms, and the between
athlete and non-athlete populations are statistically sign
generally small. Furthermore, cardiac alterations associated
with differ somewhat depending on the particular sporting
discipline in which individual athlete participates.
In particular, the changes in LV wall thickness, cavity
dimensions, or both associated with long-term training
may be more striking in certain sports such as distance
r swimming, cycling and rowing/canoeing. It is in athletes
training in 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-diastc dimension that
occurs with training overlaps that which is characteristic
of certain pathologic entities. While LV cavity dimension
in athletes is in the range of 53 to 58 mm, in some individuals
it may extend in regarded as the pathological range of >60
mm (up to 70 mm), or resemble dilated cardiomyopathy.
However, the absence of LV 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 other abnormalities
on the ECG, the differential diagnosis between athlete's
heart and ARVD may arise. Identification of ARVD by echocardiography
is exceedingly difficult because of technical limitations
in imaging right ventricular morphology (and assessing
right ventricular function), and also because the spectrum
of disease is broad. Demonstration of right ventricular
or global dysfunction or substantial cavity enlargement
supports the diagnosis. Magnetic resonance imaging,
however, affords a more definitive 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 hypertrophic
cardiomyopathy (HCM). While at present there is no single
appropriate test that will definitively resolve this
question in all such athletes, several are described here
that alone or in combination offer a large measure of clarification
in most instances for this often compelling differential.
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 cardiac or 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 thickness is within
normal limits (<12 mm). In some athletes, however, ventricular
wall thickness may be more substantial, 13-15 mm, thus
raising the possibility of HCM. In patients with HCM, the
increase thickness is usually marked; the average wall
thickness reported in echocardiographic studies of this
disease is approximately 20 mm ranging up to 60 mm. However,
an important minority of patients show relatively mild
LV hypertrophy with wall thickness values in the range of
13 to 15 mm, and most of these patients are asymptomatic.
The diagnostic dilemma may arise in those athletes who
fall into this morphological "gray zone" between physiological
hypertrophy and maximal wall thickness of 13 or 14 mm,
or possibly 15 mm.
In highly trained athletes,
the region of predominant LV wall thickness always involves
the anterior septum, although the thickness of other
segments of the wall are similar (with differences in the
range of 1-2mm). In patients with HCM, the anterior portion
of the ventricular wall is also usually the region of maximal
wall thickening; however, the LV hypertrophy is often
heterogeneous, asymmetry is prominent, and occasionally
regions other than the anterior septum may show the marked
thickening. In addition, contiguous portions of the LV
often show strikingly different wall thicknesses in
HCM, and the transition between areas is often abrupt.
Diagnosis of HCM in asymptomatic
athletes is frequently based on echocardiographic assessment
of the magnitude of hypertrophy, on precise quantitative
measurements of wall thickness in a single or region of
the LV wall. It should be emphasized that, in borderline
areas such circumstances present fertile ground for the
overt diagnosis.
Since marked increase in LV
wall thickness often occurs during adolescence in patients
with HCM, young athletes with HCM (<1 may not demonstrate
their maximum expression of hypertrophy until physical
maturation and development is achieved. Therefore, atheletes
with HCM may initially be evaluated with echocardiography
where hypertrophy is still only mild or within the borderline
range; at that time the differential diagnosis with athlete's
heart may be difficult. Such uncertainty can be resolved
by serial echocardiographic examinnations which, in months
or years, may show more definite wall thickeness confirming
the diagnosis of HCM.
Cavity Dimensions
An enlarged LV end-diastolic
cavity dimension (>55 mm) is present in morethan one
third of highly trained, elite male athletes. Conversely,
with HCM, the diastolic cavity dimension is usually small
(<45 mm >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
HC on the basis of LV cavity dimension. However,
when LV cavity size is between the extremes, this dimension
alone will not resolve the correct diagnosis.
Doppler Transmitral Waveform
Abnormalities of LV diastolic
filling have been identified using noninvas pulsed Doppler
echocardiography or radionuclide angiography in 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 indexes of LV filling independent
of whether symptoms or outflow obstruction are present.
Typically, the early peak of transmitral flow ("E," due
to rapid filling) is decreased and deceleration time of
the peak is prolonged; the late peak ("A," due to atrial
contraction) is inverting the normal E/A ratio. On the
other hand, trained athlete demonstrate normal LV filling
patterns. Consequently, in a trained athlete suspected
of having HCM, a distinctly abnormal Doppler transmi velocity
pattern strongly supports this diagnosis, while a normal 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 study of almost
1000 elite Italian athletes, only about 2% had an thickness
of > 13 mm (in the gray zone between physiological hypertrohy
and HCM), and this subset was confined to those in rowing
sports and cycling. Conversely, most other forms of
training, including isometric 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 mass have
been identified in trained athletes. Preliminary findings
that highly trained female athletes rarely show LV wall
thickness( within the aforementioned gray-zone between
athlete's heart and HCM) for example, in a recent
report, none of 600 elite women athletes had thickness
in the range compatible with the diagnosis of HCM (>13).
These observations suggest, therefore, that female athletes
with "borderline" left ventricular wall thicknesses of
13-15 mm (in the normal cavity size) are likely to have
HCM.
Regression of Hypertrophy
with Deconditioning
The observation that increased
LV cavity size or wall thickness is a 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) cooperaton from highly motivated competitive
athletes to interrupt their training to get serial
echocardiographic studies of technical quality.
Familial Transmission and
Genetics
The most definitive evidence
for the presence of HCM in an athlete with increase
in wall thickness probably comes from the demonstration
in a relative of HCM. Therefore, in those athletes in whom
the distinction HCM and athlete's heart cannot otherwise
be achieved definitive 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,which may
be "sporadic" (i.e., absent in relatives other than the
index person.
Recent advances in defining
the genetic alterations responsible for HCM raise
the possibility of DNA diagnosis in athletes suspected
of having the disease. The genetic abnormalities that
cause HCM, however, are heterogeneous. At present, mutations
responsible for HCM have identified in 5 genes; cardiac
troponin T and I, myosin binding proteins such as Beta-myosin
heavy chain and alpha-tropomyosin. This substantiated heterogeneity
has made it extremely difficult and time consuming to use
techniques of molecular biology for the purpose of clinically
resolving differential diagnosis between athlete's heart
and HCM.
Author
Barry J. Maron, M.D., is Director
of the Hypertrophic Cardiomyopathy Center at the Minneapolis
Heart Institute Foundation
Contents of this
site are reviewed by The Montgomery Heart Foundation Cardiomyopathy.
The information expressed in this web site should not be
considered medical advice and individuals should consult
their private physician.
Athlete's Heart
The
changes in the heart produced by long-term, intense training
have been the subject of clinical research for a long
time. As new techniques were developed, the research
methods came to include physical examination, chest radiography
and electrocardiography, as well as Holter monitoring,
cardiac catheterization, and echocardiography. However,
even with all of these techniques, there remain unanswered
questions and problems related to the electrocardiograms
recorded from athletes.
Zeppilli[11,12] has
divided the electrocardiographic abnormalities of athletes into three
categories: physiologic changes, which are clearly due to the effects
of training; borderline abnormalities, which may be due to training
but cannot be distinguished from abnormalities due to heart disease;
and abnormalities not due to training, which can nevertheless be observed
in athletes.
The electrocardiographic abnormalities
observed in athletes are listed in Table 13.7. The differentiation
of training-related electrocardiographic abnormalities from those due
to other causes is described in Table 13.8. An example of an electrocardiogram
of a trained athlete is shown in Figure 13.5, and electrocardiograms
of athletes with two types of hypertrophic cardiomyopathy are shown
in Figures 13.6 and 13.7.
 |
Figure
13.5 (click image to zoom) This electrocardiogram,
showing a large ST segment vector,
was recorded from a normal 27-year-old athlete.
An electrophysiologic
study was normal.
(A-D) Frontal
plane projection and spatial orientations of
the mean QRS, mean ST, and mean T vectors,
respectively. Summary:
Sinus bradycardia is present; there are
46 complexes per minute.
Note that the direction of the large mean ST
vector parallels that of the mean T vector.
This finding, if stable, distinguishes
the mean T vector seen here from that associated
with pericarditis or infarction. Note also
that the ascending
limb of the T wave is more slanted than the descending
limb; this distinguishes the mean ST vector from
the ST vector due to hyperkalemia. This tracing shows
early repolarization which occurs in athletes who develop
diastolic overload of the ventricles.
|
 |
Figure
13.6 (click image to zoom) This electrocardiogram,
showing left anterior-superior division
block and terminal T wave inversion in leads
V1 and
V2, was recorded from a 16-year-old
canoeist. An echocardiogram showed an asymmetric
thickening of the interventricular septum considered
characteristic of hypertrophic cardiomyopathy.
(A-D) Frontal
plane projection and spatial orientations of
the mean QRS, mean ST, and mean T vectors,
respectively.
QRS complex:
The mean QRS vector is directed -60° to the left and 30° posteriorly;
when the QRS duration is 0.10 second or less,
this degree of left axis deviation indicates
the presence of left
anterior-superior division block.
Summary: This
young athlete apparently had hypertrophic cardiomyopathy
unrelated to his athletic exercise. This case
illustrates the problem of distinguishing the
hypertrophy of exercise
from hypertrophic cardiomyopathy. (Reproduced
with permission from the publisher; From Zeppilli
P: The athlete's heart:
differentiation of training effects from organic
disease. Pract Cardiol 14:61, 1988.)
|
 |
Figure
13.7 (click image to zoom) This electrocardiogram,
showing left ventricular hypertrophy
and left ventricular conduction delay was recorded
from
an asymptomatic 31-year-old sprinter.
(A-D) Frontal
plane projection and spatial orientations of
the mean QRS, mean ST, and mean T vectors,
respectively. QRS
complex: The QRS voltage is enormous. The
mean QRS vector
is directed +70° inferiorly, and 15° to 20° posteriorly.
The patient shows left ventricular hypertrophy,
and the absence of
a Q wave in leads I and V6 suggests the presence
of left ventricular conduction delay.
ST
segment: The mean ST vector is directed about
+110° superiorly
and parallel with the frontal plane. The mean
ST vector is
parallel with the mean T vector. T
waves: The mean T vector is directed +115° superiorly
and parallel with the frontal plane. The
T wave abnormality
is due
to left ventricular hypertrophy. Summary:
An echocardiogram taken from this patient
showed apical
hypertrophic cardiomyopathy, unrelated to his
exercise. (Reproduced with permission from
the publisher; From
Zeppilli P: The athlete's heart: differentiation
of training effects from organic disease.
Pract Cardiol 14:61, 1988.)
|
In
athletes, it is not always possible to distinguish the
features of hypertrophic cardiomyopathy from the changes
produced by long-term training. At present, asymmetric
septal hypertrophy and apical hypertrophy identified
by echocardiography are not considered to be consequences
of exercise. Generalized left ventricular hypertrophy
is more likely to be exercise-related.
Ventricular
Electrocardiography 1998. © 1998
Humana Press, Inc.
Athlete's
Heart and Cardiomyopathy
A.
Pelliccia
Istitute of Sport Science,
Department of Medicine
Italian Olympic Committee
Rome, Italy
Long-term
athletic conditioning is associated with
cardiac morphologic changes, including
increased left ventricular (LV) cavity
dimension, wall thickness and mass. The
extent to which LV dimension is increased
in athletes is usually mild: several echocardiographic
studies have shown that absolute left ventricular
dimensions are increased in athletes in
comparison to matched untrained controls
by an average of 10% for cavity dimension
and 15% for wall thickness. These absolute
cardiac dimensions, although increased,
usually remain within the accepted upper
normal limits, and different in most cases
from changes seen in patients with structural
cardiac diseases, such as cardiomyopathies.
In
elite athletes, however, left ventricular
cavity dimensions and, in some instances,
wall thicknesses may be markedly
increased, well above the upper normal limits
predicted
by age and body size. Absolute left
ventricular wall thickness may exceed > 13
mm, in a range compatible with primary
pathologic hypertrophy, i.e. hypertrophic
cardiomyopathy in about 2 % of elite
athletes. Left ventricular cavity dilatation
(end-diastolic
transverse diameter may exceed 60
mm, in a range compatible with idiopathic
dilated
cardiomyopathy in about 15 % of elite
athletes. In such circumstances, the morphologic
features of the athlete's heart raise
the
differential diagnosis between an
extreme physiologic adaptation to athletic
conditioning
and a pathologic cardiac condition.
This differential diagnosis has implicit
ethical,
economic and legal implications,
because the incorrect identification of a
cardiac
disease may lead to unnecessary withdrawal
of an athlete from competition, thereby
depriving that individual of the
varied (including economic) benefits of sport.
On the other hand, the correct diagnosis
of certain cardiovascular diseases
may
be the basis for disqualification
of athlete from competition, in a effort
to minimize
the risk of sudden cardiac death
related to sport activity.
Differential
diagnosis of athlete's heart and hypertrophic
cardiomyopathy.
Hypertrophic
cardiomyopathy is a primary cardiac disease,
for which the most characteristic morphologic
feature is a hypertrophied non-dilated
left ventricle in absence of cardiac or
systemic disease itself capable of producing
left ventricular hypertrophy. The prevalence
of this disease in the general population
is estimated to be 0.2%. The differential
diagnosis of athlete's heart and hypertrophic
cardiomyopathy is of crucial importance,
because sudden death may be the initial
clinical event in young athletes with hypertrophic
cardiomyopathy, often in relation to exertion.
At present time there is no single approach
that will definitively resolve this differential
diagnosis in all instances, although several
criteria appear useful in this regard,
as summarized in Figure 1.
|
|
| Fig
1: Flow-chart showing criteria
used to distinguishing
hypertrophic cardiomyopathy (HCM)
from athlete's
heart when the left ventricular
(LV) wall thickness is
within the shaded gray zone of
overlap,
consistent with both diagnoses. |
Left
ventricular morphology (Figure
2):
 |
Fig.
2. Comparative echocardiographic
images of left ventricular hypertrophy
characteristics of hypertrophic
cardiomyopathy (A, B) and athlete's
heart (C, D). Parasternal long
axis (A) and short axis (B) views
and respective schematic drawings
of the left ventricle, at the
same calibration, from a 18-year-old
with hypertrophic volleyball
player with cardiomyopathy. In
comparison, the same views and
schematic drawings (C, D) from
a 25-year-old elite rower with
physiologic left ventricular
hypertrophy. In the subject with
hypertrophic cardiomyopathy,
the maximum thickness is 18 mm
in the anterior ventricular septum,
but the posterior free wall is
8 mm, resulting in a markedly
asymmmetric distribution of hypertrophy.
In the rower, the maximum ventricular
septal thickness is 15 mm, and
there is a more symmetric distribution
of hypertrophy. The left ventricular
cavity is within normal limits
(48 mm) in the patient, but is
enlarged (58 mm) in the rower.
Abbreviations: ALFW = antero-lateral
free wall; AVS = anterior ventricular
septum; MV = mitral valve; PFW
/ PW = posterior free wall; PVS
= posterior ventricular septum;
VS = ventricular septum. |
1) Wall thickening. The
maximum wall thickness found in
highly trained athletes is 15-16 mm, that
likely
represents the upper limit of physiologic
left ventricular wall thickening.
Instead, in patients with hypertrophic
cardiomyopathy,
including those who are asymptomatic
and involved in athletic activities,
the maximum wall thickness shows
a broad range of values, 15 to 60 mm, and
averages
22 mm. A minority of patients with
hypertrophic cardiomyopathy, however, show
relatively
mild hypertrophy (wall thickness
13 to 15 mm) and, therefore, this single
criterion
may not differentiate physiologic
from pathologic hypertrophy in all instances.
2) Distribution
of hypertrophy. The distribution
of hypertrophy in athlete's heart
is sustantially symmetric and regular.
Although
the different segments of left
ventricular wall may not be thickened
to an identical
degree (maximum wall is usually
in the anterior ventricular septum),
differences
between contiguous segments of
left ventricle are generally very
small (< 2
mm) and the overall pattern of
myocardial hypertrophy appears
homogeneous. In patients
with hypertrophic cardiomyopathy
the distribution of hypertrophy
is, in contrast,
characteristically asymmetric and heterogeneous.
3) Left
ventricular cavity. In athletes
with physiologic wall thickening,
left ventricular
cavity is also consistently enlarged
(end-diastolic cavity diameter > 55
mm). The left ventricular cavity
shape appears normal, with the
mitral valve
normally positioned within the
cavity and no evidence of left
ventricular outflow
tract obstruction. In patients
with hypertrophic cardiomyopathy,
including those who are
asymptomatic, left ventricular
cavity dimension is small or within
normal limits
(end-diastolic cavity diameter
often < 45
mm. Therefore, in some cases, it
is possible to resolve the diagnostic
ambiguity of
borderline wall thickening in athletes
on the basis of left ventricular
cavity dimension, when either < 45
or > 55 mm. However, when absolute
cavity dimension falls between
these two extremes, this criterion
does not
reliably discriminate between physiologic
and pathologic hypertrophy.
4) Dynamic
changes in left ventricular hypertrophy.
Serial echocardiographic studies have shown
dynamic changes in left ventricular
wall
thickness associated with variations
in intensity of training. Of note,
in elite and highly-trained rowers examined
both at the peak conditioning (when
maximum
wall thickness averaged 13-15 mm)
and after 3 months of deconditioning, was
documented a significant reduction
in
wall thickness (by 2 to 5 mm, mean
3). In hypertrophic cardiomyopathy, no
substantial
changes in wall thickness would
be expected to occur in response to changes
in the
level of physical activity. Consequently,
a brief period of forced deconditioning
combined with serial echocardiographic
studies may be a useful diagnostic
to distinguish physiologic from primary
pathologic hypertrophy.
Left
ventricular filling
Indexes
of left ventricular filling may be useful
in distinguishing athlete's heart from
hypertrophic cardiomyopathy. Trained athletes
with phisiologic LV hypertrophy consistently
show normal left ventricular filling pattern
In contrast, abnormalities in relaxation
and filling have been described as characteristic
features of hypertrophic cardiomyopathy,
and are present in up to 80% of patient.
In hypertrophic cardiomyopathy, diastolic
dysfunction is not strictly related to
the severity of left ventricular hypertrophy,
and may be present in cases with only mild
hypertrophy and no symptoms, that most
likely require differential diagnosis form
athlete's heart. The most frequent abnormalities
are a slowed deceleration of early diastolic
flow velocity associated with increased
late (atrial) peak flow velocity and reversed
ratio of early-to-late diastolic peak flow
velocity.
Type
of sport
Knowledge
of the characteristics of athletic
training may be helpful in identifying
physiologic
and pathologic hypertrophy. Marked
left ventricular wall thickening is virtually
limited to elite, highly-trained
athletes
engaged in endurance disciplines
(primarily rowing, canoeing and cycling).
Consequently,
absolute increase of left ventricular
wall thickness (> 13 mm) in an athlete
training in most other sporting disciplines
is unlikely
to represent the effect of conditioning
alone.
Gender
Gender
itself may be a useful criterion
for discriminating physiologic from pathologic
hypertrophy.
Physiologic left ventricular wall
thickening (>13 mm) is virtually confined
to male athletes. On the other hand,
men and women with hypertrophic cardiomyopathy
do not differ with regard to morphologic
expression of the disease, either
in terms
of maximum wall thickness (mean:
22 mm in both sexes), distribution of left
ventricular
hypertrophy and number of hypertrophied
segments involved. This feature largely
reflects the fact that hypertrophic
cardiomyopathy is a primary, genetically
determined, myocardial
disease. Therefore, the finding of
borderline wall thickness (i.e., 13-15 mm)
in a female
athlete is unlikely to be the consequence
of athletic conditioning itself and
is more likely the expression of pathologic
cardiac condition.
Electrocardiogram
In
athletes with physiologic left ventricular
hypertrophy, a variety of electrocardiographic
abnormalities can be found, not uncommonly
mimicking those seen in patients
with hypertrophic cardiomyopathy, such as
markedly increased
QRS voltage, T wave inversion and
abnormal Q waves. In hypertrophic cardiomyopathy,
the 12-lead electrocardiogram is
abnormal
in the vast majority of patients
(> 90
% of cases), showing a wide variety
of patterns, which are often bizarre. However,
no particular electrocardiographic
pattern
is specific for the hypertrophic
cardiomyopathy and in the individual subject
the 12-lead
electrocardiogram may not consistently
discriminate between athlete's heart
and pathologic hypertrophy.
Familial
transmission and genetic screening
The
most definitive evidence for the presence
of hypertrophic cardiomyopathy in an athlete
with an increase in wall thickness comes
from the demonstration of this disease
in a relative. Therefore, echocardiographic
screening for affected family members represent
a potential method for resolving this diagnostic
uncertainty. However, absence of echocardiographic
evidence for hypertrophic cardiomyopathy
in family members does not exclude occurrence
of the sporadic form.
In
recent years, a variety of genetic defects
have been found in association with familial
hypertrophic cardiomyopathy and have raised
the possibility of DNA-diagnosis in athletes
with borderline hypertrophy. Most of the
disease-causing mutations have been identified
in genes located on chromosomes 1, 11,
14 and 15; these genes encode the sarcomere
proteins cardiac troponin-T, myosin binding
protein-C, beta-myosin heavy chain and
alfa-tropomyosin, respectively. Furthermore,
a large number of mutations for each of
these abnormal genes have been described.
In most cases, different families have
been shown to have different mutations,
and some of these have been associated
with an unfavourable natural history and
clinical course In consideration of the
substantial genetic heterogeneity of hypertrophic
cardiomyopathy and the relatively complex,
time-consuming and expensive techniques
necessary for the genetic screening, identification
of the disease-causing mutations is, at
present, quite laborious and not routinely
available for clinical practice.
Differential
diagnosis of athlete's heart and idiopathic
dilated cardiomyopathy
Idiopathic
dilated cardiomyopathy is a primary myocardial
disease characterized by left ventricular
dilatation and systolic dysfunction. The
prevalence of this cardiac disorder has
been estimated to be 0.4 % in the general
population. Left ventricular cavity dimensions
show a broad range of absolute values and
in a few instances the degree of dilatation
may be minimal. The magnitude of impairment
in left ventricular systolic function is
also broad, and in the early stages of
the disease may be minimal.
On
the other hand, left ventricular
cavity dimension may be markedly enlarged
(end-diastolic
transverse diameter > 60 mm)
in a sizeable proportion of highly-trained
athletes (about 15%). In these individuals,
therefore the differential diagnosis
between idiopathic dilated cardiomyopathy
and physiological
left ventricular enlargement of athlete's
heart may raise.
Left
ventricular morphology (Figure
3)
 |
Fig.
3. Comparative echocardiographic
images of left ventricular dilatation
in idiopathic dilated cardiomyopathy
(a) and athlete's heart (b).
Parasternal, short axis and M-mode
tracing of the left ventricle
from a 20-year-old asymptomatic
patient with idiopatic dilated
cardiomyoapthy (a). In comparison,
the same views at the same calibration,
from a 26-year-old elite rower,
who was a participant at the
Olympic Games (b). In both the
patient and the elite athlete,
the left ventricular cavity is
dilated to the same extent (67
mm); however, the ventricular
septum and free wall are relatively
thin (8 mm) and show a reduced
systolic motion in the patient,
but are increased (up to 13 mm)
and show a normal systolic motion
in the rower. In the patient,
the mitral valve and papillary
muscles are superiorly located;
in the athlete, the mitral valve
is normally located within the
left ventricular cavity. |
In
athletes, physiologic left ventricular
cavity enlargement is associated with enlargement
of the right ventricular and atrial chambers,
as an expression of a global cardiac remodeling.
In elite athletes, the maximum left ventricular
end-diastolic cavity dimension does not
exceed 70 mm, that likely represents the
upper limit of physiologic left ventricular
enlargement. In patients with dilated cardiomyopathy,
on the other hand, dilatation of both ventricles
is common, but left ventricular enlargement
usually predominates and may be substantial,
as an expression of primary myocardial
disease. The enlarged left ventricular
cavity in athletes maintains the normal
ellipsoid shape, while LV cavity in patients
with dilated cardiomyopathy usually achieves
a more spherical shape, in association
with impaired contractility and deterioration
of the clinical status. Indeed, in dilated
cardiomyopathy, mitral regurgitation is
common, due to dilatation and distortion
of the mitral ring. Left ventricular wall
thickness may be within normal range in
both instances, but relative wall thickness
is usually (mildly) increased only in the
athlete’s heart.
Left
ventricular function
In
athletes with physiological left ventricular
dilatation, global systolic function is
normal, and regional wall motion abnormalities
are absent. Therefore, in an athlete with
left ventricular cavity dilatation, evidence
of systolic dysfunction is the most reliable
criterion for differentiating athlete's
heart from primary pathologic condition,
such as idiopathic dilated cardiomyopathy.
Type
of sport
In
assessing whether an enlarged left ventricular
cavity in an athlete represents a physiological
or pathologic condition, knowledge of the
athlete's training may also be useful.
Long-term, intensive training in largely
aerobic disciplines (primarily cycling,
cross-country skiing, canoeing, rowing
and soccer) has been shown to represent
the strongest determinant for p hysiologic
enlargement of left ventricular cavity.
Electrocardiogram
A
wide range of electrocardiographic alterations
have been described in association with
both physiologic left ventricular dilatation
and idiopathic dilated cardiomyopathy.
However, no particular pattern is specific
for idiopathic dilated cardiomyopathy and,
in the individual athlete, the analysis
of 12-lead electrocardiogram may not reliably
discriminate between athlete's heart and
this pathologic condition.
*
Assumed to be the nonobstructive form of
HCM in this discussion, since the presence
of substantial mitral valve systolic motion
would confirm, per se, the diagnosis of
HCM.
+ May
involve a variety of abnormalities, including
heterogeneous distribution of left ventricular
hypertrophy (LVH) in which the asymmetry
is prominent, and adjacent regions may
be of greatly different thicknesses,
with sharp transition evident between
segments; also, patterns in which the
anterior ventricular septum is spared
from the hypertrophic process and the
region of predominant thickening may
be in the posterior portion of the septum
or anterolateral or posterior free wall.
Co-Authors:
F.M. Di Paolo
R. De Luca
Istitute of Sport Science, Department of
Medicine
Italian Olympic Committee, Rome, Italy
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