64 SLICE CT ANGIOGRAPHY A BOON

FOR PATIENTS WITH SEVERE LV

DYSFUNCTION

R ARUNKUMAR MOHANAMURUGAN
PRATAP KUMAR S VENKATESAN B
RAMAMURTHY SOMASUNDARAM
ARUNACHALAM V E DHANDAPANI R dilated cardiomyopathy.Remaining 33 patients
SUBRAMANIAN GEETHA SUBRAMANIAN have 60% TVD 40% DVD) None had single
DEPT OF CARDIOLOGY MMC CHENNAI
vessel disease suggesting that more severe the
CAG is the gold standard for assessing the
LV dysfunctionmore severe the extent of
severity and extent of CAD. 64 SLICE CT
CADIn 33 patients 13 had ischaemic LV
angiograph is a recent innovation . In patients
dysfunction 20 had post infarct failure. Of
with suspectedischaemic cardiomyopathy or
which 1 had moderate to severe Mitral
post infarct severe LV dysfunction,CAG
regurgitation due topapillay muscle
carries higher risk. 45 consecutive patients
dysfunction.ThoughCABG could not be taken
(M36 F9) in age group 36 -67 with mean age of
based on CT ANGIO findings at present still it
57 yrs who presented with severe LV
is a very goodtool & a boon to di-fferentiate
dysfunction with angina .64SLICE CT
accurately Non ischaemic DCM from
angiography was suggested in these patients as
Ischaemic DCM. In these patients it is possible
it needs only peripheralvenous access & patient
to correct failure & suggest conventional CAG
needs to be in the lying posture for very less
at a later date and plan revascularusation
time compared to conventional
procedures.Thus 64 SLICE CT helps us to
angiography.After assessing the renal function
define dignosis & buy time to control failure &
and adequate heart rate control patients
improve the outcome after revascularization &
underwent CT angio.In 12 patientcoronary
to avoid unnecessary CAG in patients with
were normal suggesting
normal coronaries
A UNUSUSAL PRESENTATION OF IVEMARK SYNDROME IN THE ERA OF 64 SLICE CT
ANGIOGRAPHY
R ARUNKUMAR MOHANAMURUGAN PRATAP KUMAR G GNANAVELU B RAMAMURTHY
GEETHA SUBRAMANIAN
DEPT OF CARDIOLOGY MMC CHENNAI
Asplenia syndrome is a rare syndrome of
visceral heterotaxy occurring in 1:1,50,000
general population and in 1 :10000 congenital
Heart disease patients.With the addition of 64
Slice CT angiography to noninvasive cardiac
diagnostic modalities the evaluation of this
syndrome has become easier and more number
of affected patients are going to be diagnosed
in future.This case is presented to highlight the
same.13 year old girl born of
nonconsanguinous parents presented with
progressive cyanosis since birth and class II
breathlessness.Clinical examination revealed
cyanosis, clubbing,Marfanoid habitus 3/6
systolic murmur over LSB CXR showed
cardiomegaly with reduced pulmonary blood
flowECG – sinus rhythm, RAD RVH ,RAE
Echocardiogram- Levocardia, common AV
canal defect , Double outlet right ventricle,
mild common AVvalve regurgitation ,
moderate valvular Pulmonary stenosis
Persistent LSVC , total anomalous pulmonary
venous drainage supracardiac type but
termination of vertical vein could not be traced,
D MGA ,Right sided Aortic arch with mirror
image branching ,both Aorta and IVC on
right side of midline in abdomen Conventional
Cath study OPD, large inletVSD ,common AV
valve with moderate regurgitation ,goose neck
deformity, Double outlet right ventricle,
moderate valvular Pulmonary stenosis
Persistent LSVC draining into Right atrium viz
coronary sinus, right sided aortic arch with
mirror image branching pattern.
64 SLICE CT ANGIOGRAPHY OF HEART ,LUNGs
AND CORONARIES (TRIPLE) angiography
SitusAmbiguus/MesocardiaRight atrial
isomerism/ Common AV canal defect/ Double
outlet Right VentricleModerate AV valve
regurgitation\ Moderate valvular pulmonary
stenosis D-MGA /Total anomalous pulmonary
venous connection joining R SVC Common
origin ofcoronaries from LCC Right sided
aortic Arch Bilateral eparterial Bronchi/
Asplenia/ Midline liver USG abdomen Situs
ambiguous Midline liver with bilateral right
lobes Both IVC and Aorta on the right side.
Absent Uterus and upper vaginaChromosomal
study done.xray spine spina bifida.Barium
meal series shows nonrotation of GUT Reason
for reporting this patient is Postpaediatric
presentation in the IVEMARK syndromeis
quite unusual despite the major cardiac
anomalies.One main reason for survival
adolesence age is the presence of moderate
pulmonarystenosis which acts like a pulmonary
banding preventing the pulmonary vascular
disease.All systemic findings in the same
patient is also uncommon as we can see in
these patientIn this pt of asplenic syndrome but
for 64 SLICE CT such comprehensive
unraveling of findings in pulmonary
vasculature,venous anomaly bronchial situs,
cardiac defects, coronary anomalies, aortic
anomalies, visceral heterotaxy could not have
been possible
BETTER LATE THAN NEVER—DELAYED THROMBOLYTIC THERAPY IN SUBACUTE
SUBMASSIVE PULMONARY THROMBOEMBOLISM
GEETHA SUBRAMANIAN , MOHANAMURUGAN , ARUNKKUMAR
DEPT OF CARDIOLOGY MADRAS MEDICAL COLLEGE, CHENNAI.
Thrombolytic therapy is sheet anchor in
subacute sub massive PTE presenting within
2 weeks with RV dysfunction . In our
institution 3 patients 2 males 1 female
presented at the mean age of 54 years with
3-4 weeks h/o class 4 symptoms fatigue and
lightheadedness. Clinical ECG, X-rays,
chest echo evaluation showed unexplained
severe PHT with dilated MPA RV RA TR
PR.Thrombus could not be picked up in
echo.CT chest with contrast revealed large
thrombus in distal RPA with multiple
emboli in segmental pulmonary arteries in
both lungs. Interestingly all of them had
normal Doppler study of lower limb veins .
The female patient had mildly calcified
coronary sinus thrombosis which probably
was the source for PTE ‘ protein P S
antithrombin levels were normal. All patients
were severe diabetic detected for the first
time suggesting acquired resistance to
activated protein and S .Cardiolipin negative
since the patients did not opt for surgery
and continued to in class 4 despite
conventional anticoagulants and drugs for
PHT .Since PHT was severe around 65-75
mm we opt to give a trial of thrombolytic
therapy though it was late presentation as a
life saving grace streptokinase was given
in the dose of 100000 units/hrs for 48 hours
with periodic echo. At the end of 48 hours
since there was no fall of PHT by echo we
extended the therapy up to 72 hours . It had
definite fall of PHT by 15 mm improved
to class 2. 6 minute walking improved , pts
were able to climb stairs without
difficulty. This dramatic improvement can
be explained by 1.reduction in the size of
large embolus and dissolution of multiple
small emboli improving perfusion reducing
ventilation perfusion mismatch 2 reduced
release of vasoactive substances due to
dissolution of emboli preventing
bronchospasm and improving ventilation 3
reduction in formation of fresh thrombi in
deep veins and in situ thrombus in
pulmonary circulation 4 since PA pressure
fell by nearly 20% and since surgical
results are variable we continued the patients
on anticoagulants and drugs including
sildenafil,.
In short if this benefit could be proven in
more number of other patients also with
PTE who come late after 3-4 weeks after
the onset there will be a paradigm shift in
“time window: for thrombolytic therapy in
PTE which could be life saving cost
effective,prevent further deterioration and
improve survival to help us to buy time to
plan the pulmonary embolectomy surgery.
Proof of pudding is in eating it .In short
delayed thrombolytic therapy given over a
longer period of 72 hours stresses the concept
of BETTER LATE THAN NEVER should
be followed in treatment of PTE with delayed
Presentation.