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MI in KAWASAKI’S DISEASE

MI in KAWASAKI’S DISEASE. Epidemiology of Kawasaki’s. 80% 0f patients are under 5 yrs of age Male/female= 1.5 U.S. attack rate 1/10,000 Attack rate for Asians 6/10,000 Attack rate for African American 1.5/10K 2%die during subacute or conval. stage from acute thrombosis of aneurys. CA’s.

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MI in KAWASAKI’S DISEASE

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  1. MI in KAWASAKI’S DISEASE

  2. Epidemiology of Kawasaki’s • 80% 0f patients are under 5 yrs of age • Male/female= 1.5 • U.S. attack rate 1/10,000 • Attack rate for Asians 6/10,000 • Attack rate for African American 1.5/10K • 2%die during subacute or conval. stage from acute thrombosis of aneurys. CA’s

  3. CORONARY ARTERY ANEURYSMS • Diffuse dilation of CA’s during the acute phase in 30-50% of patients. • 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.

  4. CORONARY ARTERY ANEURYSMS • In 25%, aneurysms persist but reduced in size. • In 25%, aneurysmy heal to severe stenosis or complete occlusion. • Of all pats. with aneurysms, 7-10% have MI. • Giant aneurysms(> 8mm) during the acute phase at highest risk for MI.

  5. 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%

  6. Myocardial Infarction • Activity: Only 14% had MI during play or exercise. 63% during sleep or at rest. • 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.

  7. Myocardial Infarction Distribution of coronary stenotic lesions( >75% narrowing): • 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.

  8. EKG and MI: KAWASAKI’s • Fatal 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.

  9. MI in Congenital Heart Disease • Usually ass. with a pressure overloaded ventricle(AS,PS,TAPVR) • Most commonly subendocardial or papillary muscle infarction • Infarcts occur in the ventricle with the pressure overload • Not ass. with CA anamolies( excluding pulmonary atresia VSD)

  10. MI in CHD • Represents a myocardial supply demand imbalance • Subendocardium at risk due to pressure load and nature of blood supply • Papillary infarction of either ventricle may be associated with a Q wave and diminishing R wave in lead V3R

  11. MI in CHD • 80% of hearts with TAPVR • 90% of hearts with severe PS • 100% of hearts with severe AS • most hearts had acute and old infarcts • incidence of infarcts appeared independent of surgery

  12. 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.

  13. Training Effects • Dynamic 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.

  14. Training Effects • Static exercise leads to increased wall thickness without increased LV diameter. There is also no significant increase in stroke volume.

  15. ATHLETIC HEART SYNDROME • Clinical Exam: systolic murmur bradycardia audible 3rd and 4th heart sounds cardiomegaly, globular heart on CXR

  16. ATHLETIC HEART SYNDROME • Electrocardiographic rhythm changes sinus bradycardia sinus arrhythmia wandering atrial pacemaker 1st degree heart block Wenkebach junctional rhythm

  17. Athletic Heart Syndrome • Electrocardiogram: 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.

  18. Athletic Heart Syndrome • ECHO: 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.

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

  20. 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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