athletes heart
TRANSCRIPT
HISTORY
Heneschen(1890) used physical
examination to determine increased
cardiac dimensions in elite nordic skiers.
Eugene darling in the same year in
rowers of harvard university.
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Paul dudely white(1900)
studied radial pulse rate
among boston marathon
competitors and was the
first to report marked
resting sinus bradycardia in
long distance runners.2/1/2015 3ATHLETE'S HEART
Earlier it was thought to be beneficial
adaptations to exercise.
But later it was postulated as a form of
overuse pathology and prolonged
participation in sport can lead to
premature cardiovascular system
collapse.
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Athlete’sheart syndrome , a term often
applied to athletic patient who present
with subjective symptoms or abnormal
CVS findings.
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Aerobic /endurance exercises
execises requiring primarily an increase in o2 transpot.
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Resting /strength exercises
exercises primarily stressing the skeletal muscle.
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PHYSIOLOGY
Physical activity acutely increases o2
demand which increases cardiac output
(Q) and arteriovenous difference (A-
V)O2.
1 lit of oxygen consumption (VO2)
produces 5-6 lit increase in Q.
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The CV response to exercise has both
external and internal work rate,
External work rate is VO2 required for
exercise task and is direct determination
of Q.
Internal work rate is MO2 required for
exercise task and is direct determinant
of HR
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Repetitive excercises to increase exercise capacity
Increases VO2
Increased Q(HR and SV)
Increased stroke volume
The increase in SV means that
performing the same exercise task which
requires the same VO2 can be performed
at a slower HR and a lower MO2 or
internal work rate.
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The physiologic mediators of these CV
adaptations may be produced by
increased resting vagal tone and reduced
resting sympathetic tone resulting in
resting sinus bradycardia
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LEFT VENTRICLE
Studies revealed LV hypertrophy and
dilation.
Pellica.et.al showed increased LV end
diastolic diameter and small percentage
had LV wall thickness more than 13mm.
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MORGANROTH HYPOTHESIS
Morganroth.et.el studies demonstrated
concentric LV hypertrophy in strength
training and eccentic LV hypertrophy in
aerobic training.
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Figure 3. Impact of different clinical variables on LV end-diastolic cavity dimensions in a large
population of male and female elite athletes.
Maron B J , and Pelliccia A Circulation. 2006;114:1633-
1644
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On LV systolic function
demonstrated preserved LV ejection
fraction except for one study
On LV diastolic function
improved LV diastolic function is essential
mechanism in preserving stroke volume
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RIGHT VENTRICLE
Cardiac remodelling is not confined to LV
Scharhag et al study demonstrated RV
enlargement parallels LV enlargement
supporting the concept of biventricular
enlargement.
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AORTA
Experiences a significant hemodynamic
load during exercise.
Aerobic exercise- high volume aortic
flow with modest systemic hypertension
Strength exercises-normal volume with
profound systemic hypertension.
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Babee et al studies revealed increased
aortic dimensions in strength exercise
training.
Pellica et al studies revealed incresed
aortic dimensions in aerobic training
exercises.
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LEFT ATRIUM
Studies confirmed high prevalnce of left
atrial enlargement in athletes
SEX AND RACE
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A, An electrocardiogram of a 46-year-old male triathlete who presented after long-standing
palpitations and a recent episode of syncope.
Baggish A L , and Wood M J Circulation. 2011;123:2723-
2735
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ARRHYTHMIAS
Brady arrhythmias such as
Sinus bradycardia
Junctional bradycardia
AV block
The reduced AV conduction velocity may take
accessory pathway such as WPW syndrome.
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Increased vagal tone may be responsible
for early repolarisation and ST
abnormalities.
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VALVE DISEASE IN ATHLETS
AORTIC STENOSIS
Careful evaluation of symptoms and
maximal exercise testing
Warm up dyspnea indicates clinically
important AS
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AORTIC REGURGITATION
Generally tolerate AR,because of
increased HR during exercise, decreases
diastole and regurgitant.
Rarely restrict the patients with AR
unless there is ventricular deterioration.
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AORTIC DISSECTION IN BAV
We do not restrict the patient unless the
patient aortic root dimensions are more
than 45 mm
Annual screening.
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SYNCOPE
Majority of syncope in athlete’s is
attributed to neurocardiogenic syncope.
Manifests in the immediate post exercise
testing owing to sudden reduction in
venous return, which facilitates transient
cerebral hypoperfusion.
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Syncope during exercise, there is a
possibility of malignant arrhythmias,
valvular heart disease and myocardial
ischemia.
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DECREASED EXERCISE CAPACITY
Hyperthyroididm
Exercise induced asthma
Disease of the skeletal muscles
Anemia
AF
Viral illness
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ELEVATED CARDIAC ENZYMES
Increase in cTnT occurs in athletes
following prolonged exertion.
Endurance athletes were documented to
have increased concentrations of CK-MB
and satellite cells in their leg muscles.
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