67 yrs male HTN DCMP Severe LV systolic dysfunction Ef 35 % Atrial fibrillation Recurrent TIA Drowsiness Altered sensorium breathlessness h/o doe class 2 from few days P=130 AF FVR Bp 110/60 MMHG Chest B/L basal crepts CVS –irregular heart sounds CNS --intact Mild facial +pedal edema noted His Trop i was negative and BNP was > 1000 Case of DCMP, severe LV systolic dysfunction CHF AF -FVR CVA ? Patients drowsiness and altered sensorium improved with overnight BiPAP and diuretic, Amiodarone and other drug supports
Patient still needed bipap support
Echocardiography revealed strange findings It ischemic Cardiomyopathy with RWMA in lad and LCX territory , LVEF was 35% A continuous FLOW noted in RA origination from some chamber situated just besides the SUPERIOR wall of RA, near IAS attachment to RA It was continous fow-- eccentic jet ORIGINATING near IAS swirling towards anterolateral spect of ra WHAT COULD BE THE REASON OF THE FLOW ? FROM WHERE UNUSUAL CHAMBER APPEARED? WHY PATIENT TAKING TIME TI RECOVER ? PSEUDOENURYSM FORMATION AT LATERAL WALL OF RV SOMEHOW LEAKING IN RA FROM RV ---NO EVIDENCE IN ECHO
SUPRACARDIAC PAPVC – NO CLINIACVL
EVIDENCE
COR TRIATRIUM – ANATOMY UNLIKELY
LEAKING OF SOME CARDIAC VEIN
AFTER FURTHER ASSESMENT 1. IN PLEX , 4 C VIEW OR SHORT AXIS VIEW IT WAS HARD TO DETECT THE JET AS WELL AS THE ANUYRYSM
2. IN 5 CHEMBAR ANEYURM WAS NOTED BUT
RUPTURE WAS NOR SEEN
3. USUALLY SINUS OF VALSALVA ANEUYRYSM
CAN BE EASILY SEEN IN SHORT AXIS VIEW OR 5 CHAMBER VIEW AS WELL RUPTURE CAN BE DETECTED ON HIGH INDEX OF SUSUSPECION
4. FLOW USUSALLY DETECTED IN RV
IF WE HAVE SUSPECTED AS CASE OF RUPTURE OF SINUS OF VALSAVA WHERE IS THE ORIGIN OF JET TO CLEAR THIS DILEEMMA WE DID CARDAIC MRI …BUT TO NO AVAIL AORTOGRAM DONE IN CATH LAB
SHOWS THE ANBNORMAL ANEURYSM OF
SINUS OF VALSAVA AS WELL IT JET GOING TO RA RSOV is a rare cardiac anomaly with the reported incidence of (0.5%-1.5%) in western and (1.2%-4.94%) in Asian population.
Most frequently it is congenital in origin due
to either a congenital absence of continuity between the aortic media and the annulus fibrosus, or a developmental structural defect in the aortic annulus itself which can gradually give way under aortic pressure to form an aneurysm. can rupture into a low pressure cardiac chamber.
The other causes include trauma, bacterial endocarditis,
syphilis, cystic medial necrosis and atherosclerosis. It commonly originates in the right coronary sinus followed by non-coronary sinus and ruptures into the right ventricle followed by right atrium
left coronary cusp does not usually arise from the bulbar septum as do the right and noncoronary cusps, thus explaining the rarity of ruptured left sinus of Valsalva aneurysm.
In most of the patients diagnosis is generally made in the
third decade and out of them 51-88% are males. As the reported mean survival of these patients with untreated RSOV is 3.9 years
and in view of dramatic clinical presentations of sudden
onset biventricular failure, reported low perioperative mortality and high long term survival after surgery, an early surgical intervention is indicated as soon as the diagnosis is made.
The most common coexisting cardiac anomaly with RSOV is
VSD with an incidence ranging from 09- 78%. ADIVSED AVR THANK YOU