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गुरुवार, 6 जनवरी 2011

MI in KAWASAKI’S DISEASE

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
1 n
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

Most commonly in LCA>LAD>RCA

50% regress to no observable lesion

Myocardial Infarction
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
                  chest pain:<4yr20%,
                                   >4yr 80%
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


3  
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):
 

4  
fatal cases: 80% had 2 or 3 vessel disease.40% involved LCA


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

Training Effects

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

nClinical Exam:
   systolic murmur
   bradycardia
  audible 3rd and 4th heart sounds
  cardiomegaly, globular heart on CXR

nElectrocardiographic rhythm changes
   sinus bradycardia
   sinus arrhythmia
   wandering atrial pacemaker
   1st degree heart block
   Wenkebach
   junctional rhythm

nElectrocardiogram: Changes in Repol.
    ST segment elevation in precordial
    leads.
        ST segment elevation normalizes with
    exercise.
       Tall T waves ass with ST elevation
    Isolated T wave inversion.



nECHO:
     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
           with deconditioning

Athletic Heart Syndrome
THE PHYSICAL EXAM,ECG, AND ECHO
OF HIGHLY TRAINED ATHLETES MAY
SIMULATE ISCHEMIC HEART DISEASE
OR HYPERTROPHIC CARDIOMYO-
PATHY.
SUDDEN  DEATH

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

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