n1 Male/female= 1.5
n2 80% 0f patients are under 5 yrs of age
n 3 U.S. attack rate 1/10,000
n 4 Attack rate for Asians 6/10,000
n 5 Attack rate for African American 1.5/10K
n 6 2%die during subacute or conval. stage from acute thrombosis of aneurys. CA’s
CORONARY ARTERY ANEURYSMS
Diffuse dilation of CA’s during the acute phase in 30-50% of patients.
2 Aneurysms persist in 15-20%, reduced to < 5% if gammaglobulin used in the acute phase
3 Most commonly in LCA>LAD>RCA
4 50% regress to no observable lesion
Onset: 40% within 3 months
73% within first yr.
20% occur more than 2 yrs out
5% greater than 6 yrs
Symptoms:63% had symptomatic MI
54% presented in shock
1 Activity: Only 14% had MI during play or exercise. 63% during sleep or at rest
2 Mortality: 22% died during the first MI
Infants<1yr, 43% died
Prognosis: 41% asymptomatic. Cardiac symptoms due to MR, decreased LV EF, LV aneurysm,angina. 16% of survivors had second MI, 63% died.
Distribution of coronary stenotic lesions( >75% narrowing):
fatal cases: 80% had 2 or 3 vessel disease.40% involved LCA
5 survivors: 85% had 1 vessel disease( 50% RCA). None had involvement of left main
EKG and MI: KAWASAKI’s
nFatal cases: 87% had abn Q waves at presentation, Q waves in in precordial leads in 1/2. Deep Q’s in II,III and AVF in 1/3.
MI in Congenital Heart Disease
n1 Usually ass. with a pressure overloaded ventricle(AS,PS,TAPVR)
n 2 Most commonly subendocardial or papillary muscle infarction
n 3 Infarcts occur in the ventricle with the pressure overload
n 4 Not ass. with CA anamolies( excluding pulmonary atresia VSD)
MI in CHD
n1 Represents a myocardial supply demand imbalance
n2 Subendocardium at risk due to pressure
load and nature of blood supply
n3 Papillary infarction of either ventricle may be associated with a Q wave and diminishing R wave in lead V3R
n4 80% of hearts with TAPVR
n 5 90% of hearts with severe PS
n 6 100% of hearts with severe AS
n7 most hearts had acute and old infarcts
n 8 incidence of infarcts appeared independent of surgery
THE PEDIATRIC ATHLETE
Exercise and Training:
Exercise - Bodily exertion for the purpose of restoring the the and functions to a healthy state or keeping them healthy
1.Dynamic:changes in muscle length and joint movement with small force.
2.Static: large force with little or no change in muscle length or joint move
nDynamic training: increased LVED diam., The more conditioned, the greater the increase. May begin as early as one week into training.There is an increase in LV wall thickness. Also resting and exercise stroke vol increase. Kids less than 10 yrs seem to show the increase inLV thickness but not in diameter or stroke vol.
nStatic exercise leads to increased wall thickness without increased LV diameter. There is also no significant increase in stroke volume.
ATHLETIC HEART SYNDROME
audible 3rd and 4th heart sounds
cardiomegaly, globular heart on CXR
nElectrocardiographic rhythm changes
wandering atrial pacemaker
1st degree heart block
nElectrocardiogram: Changes in Repol.
ST segment elevation in precordial
ST segment elevation normalizes with
Tall T waves ass with ST elevation
Isolated T wave inversion.
Increased LV end diastolic dimension
Increased LV wall thickness
IVS thickness may increase out of
proportion to LVPW
IVS/LVFM may be 2/1, this is reversed
Athletic Heart Syndrome
THE PHYSICAL EXAM,ECG, AND ECHO
OF HIGHLY TRAINED ATHLETES MAY
SIMULATE ISCHEMIC HEART DISEASE
OR HYPERTROPHIC CARDIOMYO-
A witnessed or unwitnessed natural
death resulting from sudden cardiac
arrest occurring unexpectedly within 6
hours of a previously witnessed usual
normal state of health.
Barry Maron 1980