What next folks!
You definitely should not consider the option of empirical thrombolytic
Look at the ECG of case number 1 in my case presentation series on my
website at http://emguidemaps.homestead.com/JeffMannEMguidemaps.html.
Your description of the ECG sounds nearly identical to the ECG of that
17 year old patient, who was incorrectly treated with thrombolytic
therapy. It turned out to be focal pericarditis! I now always think of
focal pericarditis if there is depression of the ST segment in lead aVR
in a patient who has ECG signs suggestive of an inferior AMI (elevated
ST segments in the inferior leads). A true inferior AMI is associated
with reciprocal ST depression in lead aVL +/- lead I +/- right
precordial leads, but rarely lead aVR.
It is my understanding that patient's with Duchenne's muscular dystrophy
do not have an increased risk of CAD. They have a predisposition to
develop a specific type of dilated cardiomyopathy affecting the
posterobasal LV wall. I have included this excerpt from Braunwald's
"Duchenne dystrophy is an unusual form of heart disease characterized by
a predilection for specific regions of the myocardium: the posterobasal
and posterolateral left ventricular walls.     
Relevant to this
discussion are the scalar electrocardiographic abnormalities in the
dystrophic hamster  and particularly in the canine model of Duchenne
dystrophy.  Dystrophic dogs have deep Q waves and tall right
precordial R waves that develop in animals older than 6 months
corresponding to hyperechoic regions in the posterobasal left
ventricular wall in two-dimensional echocardiograms. 
The following hypothesis has been proposed to explain the posterobasal
localization of myocardial involvement in Duchenne muscular dystrophy.
 Cardiac myocytes are mononuclear and branched, whereas skeletal
myocytes are multinuclear and linear. Skeletal muscle generates force
exclusively along its major axis because of its linear configuration.
Cardiac muscle generates force radially because of its branched
configuration, although the vector of force is principally along its
major axis. The force generated by cardiac myocytes is also distributed
around the cell, owing to its rich sarcolemmal connections to
collagen. Because the forces acting upon skeletal myocytes are directed
almost entirely axially, whereas the forces acting upon cardiac myocytes
are more broadly distributed, strain upon the sarcolemma is more
uniformly directed in skeletal muscle than in cardiac muscle.
In the anterior wall of the left ventricle, the muscle bundles are
"mesh-like," whereas in the posterior wall, the bundles run in a
parallel manner, especially in the epicardial half of the posterior
wall, which is the site of orgin of myocardial involvement in Duchenne
muscular dystrophy. Longitudinal shortening in the posterior wall is far
greater during ventricular systole than in the anterior wall. If the
role of dystrophin is to reinforce the sarcolemma against axial force,
then absence of dystrophin (as in Duchenne muscular dystrophy), would
cause a loss in
structural integrity of those myocytes with the highest degree of axial
forces. It is therefore postulated that the posterior left ventricular
wall is the initial site of cardiac involvement in Duchenne muscular
dystrophy.  ".
Did your patient have any of the classic ECG signs of Duchenne's
muscular dystrophy - tall R waves in the right precordial leads and deep
Q waves in the left precordial leads? It is my understanding that the
ECG in Duchenne's muscular dystrophy can mimic a posterior AMI (tall R
waves +/- tall T waves in the right precordial leads) or an
anterolateral AMI (deep wide Q waves and loss of R waves in left
oriented leads) or an inferior AMI (abnormal wide Q waves and some loss
of R wave amplitude in the inferior leads), but that it does not cause
an elevated ST segment or inverted T waves as is seen in the
injury/ischemia patterns of an AMI.
I therefore think that you have to perform more diagnostic studies to
explain the abnormal ST segments.
I think that your patient requires a stat cardiac catheterisation + stat
echocardiogram to better define the cause of the elevated ST segments in
the inferior leads.
p.s. CK-MB testing is of no value because many patients with Duchenne's
muscular dystrophy have positive levels.
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