E.J.Lovett, Jr. MD WRAMC

MI in KAWASAKI’S DISEASEMI in KAWASAKI’S DISEASE

E.J.Lovett, Jr. MD WRAMC

Epidemiology of Kawasaki’sEpidemiology 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

E.J.Lovett, Jr. MD WRAMC

CORONARY ARTERY CORONARY ARTERY ANEURYSMSANEURYSMS

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.

E.J.Lovett, Jr. MD WRAMC

CORONARY ARTERY CORONARY ARTERY ANEURYSMSANEURYSMS

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.

E.J.Lovett, Jr. MD WRAMC

Myocardial InfarctionMyocardial 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%

E.J.Lovett, Jr. MD WRAMC

Myocardial InfarctionMyocardial 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.

E.J.Lovett, Jr. MD WRAMC

Myocardial InfarctionMyocardial 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.

E.J.Lovett, Jr. MD WRAMC

EKG and MI: KAWASAKI’sEKG 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.

E.J.Lovett, Jr. MD WRAMC

MI in Congenital Heart DiseaseMI 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)

E.J.Lovett, Jr. MD WRAMC

MI in CHDMI 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

E.J.Lovett, Jr. MD WRAMC

MI in CHDMI 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

E.J.Lovett, Jr. MD WRAMC

THE PEDIATRIC ATHLETETHE 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.

E.J.Lovett, Jr. MD WRAMC

Training EffectsTraining 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.

E.J.Lovett, Jr. MD WRAMC

Training EffectsTraining Effects

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

E.J.Lovett, Jr. MD WRAMC

ATHLETIC HEART ATHLETIC HEART SYNDROMESYNDROME

Clinical Exam:

systolic murmur

bradycardia

audible 3rd and 4th heart sounds

cardiomegaly, globular heart on CXR

E.J.Lovett, Jr. MD WRAMC

ATHLETIC HEART ATHLETIC HEART SYNDROMESYNDROME

Electrocardiographic rhythm changes

sinus bradycardia

sinus arrhythmia

wandering atrial pacemaker

1st degree heart block

Wenkebach

junctional rhythm

E.J.Lovett, Jr. MD WRAMC

Athletic Heart SyndromeAthletic 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.

E.J.Lovett, Jr. MD WRAMC

Athletic Heart SyndromeAthletic 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.

E.J.Lovett, Jr. MD WRAMC

Athletic Heart SyndromeAthletic Heart Syndrome

THE PHYSICAL EXAM,ECG, AND ECHO

OF HIGHLY TRAINED ATHLETES MAY

SIMULATE ISCHEMIC HEART DISEASE

OR HYPERTROPHIC CARDIOMYO-

PATHY.

E.J.Lovett, Jr. MD WRAMC

SUDDEN DEATHSUDDEN 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