I stumbled upon this image from the Heart journal. A good depiction of IAS aneurysm in three dimension.
Image courtesy : Heart 2012;98:79-88 Three dimensional echocardiography in congenital heart disease by Joseph John Vettukattil
Further reading
Posts Tagged ‘asd’
Atrial septal aneurysm : A three dimensional view
Posted in cardiology -congenital heart disease, Echo library and gallery, echocardiography, tagged asd, fossa ovalis, ias aneurysm, real time three dimensional echo on April 15, 2012| Leave a Comment »
Land mark reviews in cardiology :Patent foramen ovale.
Posted in cardaic physiology, cardiac surgery, Cardiology - Clinical, cardiology -congenital heart disease, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged asd, hara virmani pfo jacc article, patent foamen ovale, pfo, pfo and migraine, pfo and stroke on August 12, 2011| Leave a Comment »
Patent foramen ovale (PFO) is the new generation hole in the heart for 21st century cardiologist. Present in about 20% of population , would correspond to 140 crore “man holes” as on 2012 in this planet. PFOs are embryological remnants across the inter atrial septum.
These minute holes measuring few mm are largely a benign finding .In the recent decades , it is being increasingly debated these holes may not be innocent after all .Extensive use of echocardiography in recent times has contributed to the awareness as well as anxiety.
Evidence is mounting linking PFO to
- Migraine,
- Stroke and
- Peripheral embolism.
While the above observation may be true , the fact that >100 crore people have this entity , raises a serious question , as labeling all of them as heart disease will create chaos among the already health obsessed population .
So , the main purpose should be , to identify the high risk subsets* of PFO population .(This will be a <5 % at the most). People with PFO may carry a mental stigma because it is referred to as a hole in the heart by the general public .For many the sense of living with a hole in heart is often more damaging than the hole itself ! (Incidentally , many develop migraine only after reporting about this hole !)In a strict sense PFO is not a hole , rather it is a communication it may be tunnel or slit like .It is argued physician should avoid calling PFO as a hole .
*What is a significant PFO ?
- Large PFOs >5mm
- PFOs that shunt blood
- PFOs with septal aneurysms
- PFOs with documented stroke or embolism
- PFOs with atrial chiary network
- PFO in persons with systemic pro-coagulant states (Except probably in pregnancy )
Final message
PFO is a common residual congenital atrial septal anomaly . Usually benign . One can live with it perfect harmony. Only occasional patients are at risk.
So the prime job of cardiologists is to not diagnose and create panic about this entity. rather reassure them (Is it better do not reveal to them if it is found incidentally ? Patient empowerment group would call this a foul ! I do not support blind empowerment )
At the same time our main aim is to identify the high risk subsets who are prone for events.
Closure of PFO with device is required in a fraction . (*By the way , if PFO is really dangerous , why It is never an indication for surgical closure ? )
Reference
Your search for best information on PFO would end here . Here is a land mark article in JACC by Hara also contributed by Renu Virmani . A US Japan combines initiative : A must read by every cardiologists
http://content.onlinejacc.org/cgi/reprint/46/9/1768.pdf
Landmark articles : New Orleans and the “ASD” connection
Posted in Cardiology -Interventional -PCI, cardiology congenital heart disese, cardiology journals, Cardiology-Land mark studies, tagged asd, ASD device closure, jama on December 6, 2010| Leave a Comment »
It was those great years 1974 -1976. Even before the concept of PTCA was born, few committed cardiologists of New Orleans were on a mission. Closing the ASD in cath lab. They achieved it successfully with a umbrella device.
But 35 years later as on 2010 ,the concept though proven still struggles to prove itself.
Link to related article .
Why there is wide and fixed split of S2 in ASD ?
Posted in Cardiology - Clinical, Uncategorized, tagged asd, ATRIAL SEPTAL DEFECT, fixed split of asd, hang out interval, hangout interval, impedence of pulmonary circulation, puklmonary vascualr resistance, shaver hangout interval, ssytemic vascular ressitance on October 13, 2010| 3 Comments »
- Second heart sound is widely split because the pulmonary hangout interval* is wideFixed because , the RV stroke volume does not show the normal respiratory changes.This is due to dynamic phasic shunting across the IAS ( For example : During inspiration , if RA,RV volume gets augmented by 50ml from IVC inflow , in expiration this IVC augumentation is removed but a 50 ml augmentation from left atrium takes place , this keeps the RV diastolic , as well as systolic volume relatively constant.) This makes the 2nd heart sound fixed .
* Hangout interval is the gap ( in time ) between the arterial pressure curve and the respective pumping chamber pressure curve (RV, LV) at the level of incisura.
Incisura is the notch on the descending limb of arterial pressure curve , when the pulmonary or aortic valve closure occurs . When we analyse the simultaneous pressure recordings of RV ,LV/Pulmonary artery/Aorta , the arterial pressure curves faithfully accompanies the chamber pressure curve along the dome of the chamber pressure curve till it descends , where it dissociates , from the chamber pressure curve and hangs out for a certain milliseconds. This time interval is called as hang out interval (Named by Shaver et all )
What is the normal pulmonary hangout interval and systemic hangout interval /
Pulmonary hangout interval is 60-80ms
Aortic hang out interval is 20 ms
Why does it happen ? What does it signify
It happens because , even as the chamber pressure falls below the arterial pressure ( Note: Semi lunar valves close at this cross over point ) blood continues to rush forward , with momentum in to the pulmonary and systemic circulation, in spite of the pressure cross over has happened, the semilunar valve doesn’t get closed exactly at the cross over point .It gets closed little later than true cross over point.This gap in time is the hangout interval. This Interval keeps the arterial pressure not only to be sustained little longer but also slightly higher .
This interval is an indirect( inverse) marker for vascular impedance of the distal draining circulation .The impedance is same as vascular resistance for all practical purposes.Since pulmonary circulation is a low impedance circulation , it has a wide hangout interval and the systemic circulation vice versa.
How much of S2 widening is contributed by RBBB in ASD ?
This is not known .But it has a minor role in prolonging S2 split. This is because , the RBBB in ASD is most often incomplete and peripheral one .( Pesudo RBBB due to RVOT dilatation )
What happens to S2 when pulmonary arterial hypertension develops in ASD ?
It is often narrow and fixed . Pulmonary arterial hypertension makes the pulmonary circulation to behave like systemic , hence the impedance becomes high and the hang out interval is significantly lost and second sound is narrowly split. (But fixity may be maintained.)It also depend upon the RV function and associated RBBB. RV dysfunction and RBBB both tend to widen the split.*Mild PAH usually does not alter the S 2 splittingIs there any other cause for wide and fixed splitting of second heart sound ?
Having known the reasons for widening and fixity it is easy to understand , a patient with right heart failure and RBBB can have a wide and fixed split .
Widening is due to RBBB (Delayed activation of RV ) . Fixity is due to severe right heart failure makes the RV out put relatively constant .(As RV inotropism is not good enough to handle the inspiratory augmentation of RV end diastolic volume.)
Why in VSD the second heart sound is not wide and fixed split even though hemo- dynamically it fulfills the same hemodynamic scenario ?
* Hangout interval is the gap ( in time ) between the arterial pressure curve and the respective pumping chamber pressure curve (RV, LV) at the level of incisura.
Incisura is the notch on the descending limb of arterial pressure curve , when the pulmonary or aortic valve closure occurs . When we analyse the simultaneous pressure recordings of RV ,LV/Pulmonary artery/Aorta , the arterial pressure curves faithfully accompanies the chamber pressure curve along the dome of the chamber pressure curve till it descends , where it dissociates , from the chamber pressure curve and hangs out for a certain milliseconds. This time interval is called as hang out interval (Named by Shaver et all )
What is the normal pulmonary hangout interval and systemic hangout interval /
Pulmonary hangout interval is 60-80ms
Aortic hang out interval is 20 ms
Why does it happen ? What does it signify
It happens because , even as the chamber pressure falls below the arterial pressure ( Note: Semi lunar valves close at this cross over point ) blood continues to rush forward , with momentum in to the pulmonary and systemic circulation, in spite of the pressure cross over has happened, the semilunar valve doesn’t get closed exactly at the cross over point .It gets closed little later than true cross over point.This gap in time is the hangout interval. This Interval keeps the arterial pressure not only to be sustained little longer but also slightly higher .
This interval is an indirect( inverse) marker for vascular impedance of the distal draining circulation .The impedance is same as vascular resistance for all practical purposes.Since pulmonary circulation is a low impedance circulation , it has a wide hangout interval and the systemic circulation vice versa.
How much of S2 widening is contributed by RBBB in ASD ?
This is not known .But it has a minor role in prolonging S2 split. This is because , the RBBB in ASD is most often incomplete and peripheral one .( Pesudo RBBB due to RVOT dilatation )
What happens to S2 when pulmonary arterial hypertension develops in ASD ?
It is often narrow and fixed . Pulmonary arterial hypertension makes the pulmonary circulation to behave like systemic , hence the impedance becomes high and the hang out interval is significantly lost and second sound is narrowly split. (But fixity may be maintained.)It also depend upon the RV function and associated RBBB. RV dysfunction and RBBB both tend to widen the split.*Mild PAH usually does not alter the S 2 splitting
Is there any other cause for wide and fixed splitting of second heart sound ?
Having known the reasons for widening and fixity it is easy to understand , a patient with right heart failure and RBBB can have a wide and fixed split .
Widening is due to RBBB (Delayed activation of RV ) . Fixity is due to severe right heart failure makes the RV out put relatively constant .(As RV inotropism is not good enough to handle the inspiratory augmentation of RV end diastolic volume.)
Why in VSD the second heart sound is not wide and fixed split even though hemo- dynamically it fulfills the same hemodynamic scenario ?
Guess the answer .It will be posted soon.
How do you locate the level of the lesion in Right bundle branch block ?
Posted in Cardiology - Clinical, cardiology -ECG, Uncategorized, tagged asd, central rbbb, distal rbbb, ebstein anomaly, fixed split s2, incomplete rbbb, peripheral rbbb, proximal rbbb, proximal vs dital rbbb, rsr' in v1, si vs s2, split s1 in rbbb, split s2, t1 vs m1, wide spilt of s1, wide splitting of s2 on April 25, 2010| 1 Comment »
Like in neurological disease, one can locate the site of block in bundle branch blocks. Though it has never been thought , to be clinically important to localise a BBB . (Unlike coronary lesions)
Generally , RBBB can be proximal or distal peripheral type.The commonest site could be the distal type.
It should be realised , for over 100 years in electrocardiology , we have been using some inaccurate terminologies just because it is easy to understand or being traditional .It is difficult to assimilate a fact , even today that “An electrical delay in conduction and block are one and the same ”
In fact, bulk of the RBBB is nothing but delayed conduction over this bundle. So whenever we say RBBB , we imply an incomplete block ie conduction still occurring over the so called blocked bundle.(This dogma applies for LBBB and AV blocks also to a lesser extent)
Examples of delayed RV /RVOT conduction
- Any disease where RVOT dilatation occur can cause a RBBB
- Atrial septal defect
- Many cases of RVH
- Pulmonary arterial hypertension
What is the benign rSr’ pattern in V1 ?
This is nothing but a relatively late depolarisation of RV outflow or conus that produce a terminal RV activity .
Many of the ostium secundum ASD may show just this rSr’ pattern confirming there is no organic damage to RBB in ASD .
Calling rSr’ pattern as incomplete RBBB is not advisable (As many ECG books may suggest ) .This is because , even full blown RBBB pattern may actually be an incomplete one .Further , the degree of terminal r’ in V1 or s in lead 1 does not always determine the completeness of RBBB.
Is there a totally blocked right bundle branch block ?
Yes , it is not common .
- It can occur in extensive anterior MI .
- Some cases of Ebstein anomaly.
It can be an working rule , complete RBBBs locate the lesion proximally and incomplete ones distally .
What is the other evidence for RBBB in ASD is only a simple delay in conduction ?
After ASD closure in many of the patients the RBBB pattern may disappear.This indicate RVOT regression .
Can you clinically differentiate the proximal from distal RBBB ?
Ironically ,what is difficult in ECG may some times be possible clinically.The classical description of wide splitting S2 occur often in peripheral RBBB.
It represents a delay in the closure of pulmonary valve due to delayed electrical activation or increased hangout interval as in ASD .Logically S1 should also be split in RBBB. But this is not often discussed.
This is because , the split in S1 is lesser in magnitude and is not influenced by the hangout interval .(Hang out interval is the time taken for the blood ejected from RV to fill the pulmonary circulation. Due to the low impedence of pulmonary circulation the the blood that is ejected into the MPA continue to run off for about 100milli seconds even after the RV/PA pressure crossover .)
S1(T 1) occurs immediately with the onset of RV contraction . Similarly M1 occur with LV contraction.It should be recalled it requires hardly 5mmhg of RV pressure to close the tricuspid valve and about 10mmhg for LV to close the mitral valve.
If for some reason if there is a delay in RV contraction , as in very proximal RBBB the T1 is delayed and hence S 1 split.
Note in most of the peripheral or distal RBBB the bulk of the RV free wall contraction is not interfered with . So , in distal RBBB it is highly unlikely the S1 will be delayed or split while S2 will be delayed.
What happens to S2 in proximal RBBB ?
Logic would dictate both S1 and S2 should be wide split.
Final message
There is a simple way (Some would call this an futile academic excercise !)to differntiate proximal from distal RBBB.If the first heart sound is split wide , it fixes the lesion proximally. This may indicate a more adverse outcome than a simple peripheral delay in conduction.
How will you diagnose ostium primum ASD clinically in the bed side ?
Posted in Uncategorized, tagged asd, av canal defect, ostim primum, ostium secundum on January 29, 2010| Leave a Comment »
ASD is the most common acyanotic heart disease. Clinically distinguishing ostium primum (OP-ASD ) from ostium secundum (OS- ASD) is not an easy task . A Wide fixed split pf S2 , a short systolic murmur and PA pulsations in left second space, a loud P2 and a hyperdyanmic RV occur in both . The following features might give a clue for OP -ASD .
- While OS-ASD is often an isolated anomaly , isolated OP- ASD is very rare.It usually occur as a part of partial or complete AV canal .
- Early onset of symptoms
- Early onset of pulmonary arterial hypertension( PAH )
- Extra murmur of 1.VSD 2.MR (Cleft mitral valve ) may be present
- Biventricular enlargement (MR/VSD)
- ECG -Left axis deviation -Structural defect in left bundle ?
Confirmation is by Echocardiography and angiogram is rarely required today . Documentation of classical goose neck deformity of LV outflow confirms the diagnosis.
Pulmonary artery pulse pressure : A simple parameter to predict reversible PAH In Eisenmenger syndrome
Posted in cardiac surgery, Cardiology -Interventional -PCI, Hemodynamics, Uncategorized, tagged 100% oxygen, asd, bi directional shunt, bosentan, cyantoic heart disease, eisenmenger syndrome, heath edwards, irreversible pulmonary hypertension, left to right shunt, mean pulmonary arterial pressure, mean pulmonary artery pressure, oximetry, pah, papp, pda, pht, prostocyclin, pulmonary artery diastolic pressure, pulmonary artery pulse pressure, pulmonary hypertension, pvr vs svr, reversible pulmonary, right to left shunt, sildanefil, tolazoline, vsd on December 20, 2009| Leave a Comment »
PAH is the major determinant of surgical outcome of left to right shunts. In this modern era of cardiac care allowing a child with left to right shunt to progress to a stage of Eisenmenger syndrome is considered as a huge medical failure . But , this is still rampant in many of the developing countries .
Cardiologists are divided over the issue of operability of Eisenmenger syndrome .The confusion is largely due to the conflicting data of outcome in these patients. While there is strong data when PVR exceeds SVR , the death is imminent in the post operative period .
What has complicated the issue is there are many case reports where severe PAH patients have been successfully operated. Most would think it is a statistical exception and one can not alter the traditional criteria based on few case reports.
But ,it remains an irony as on 2009 , we do not have a proper methodology to assess reversibility of PAH in Eisenmenger syndrome . Further , there is a significant number of patients with high PVR , who continue to experience an unabated left to right shunting . We do not have an answer for either the mechanism of such shunts and how to manage these patients.
Click over the slide to view full PPT presentation in PDF format .
This short paper was presented in the Annual scientific sessions of cardiological society of India 2009 regarding the usefulness of a new parameter to assess reversibility of PAH. This may not be called as a study rather a report of our experience in five patients with eisenmenger syndrome
Download the full PPT presentation in PDF format.
Unusual Atrial septal defects : Sinus venosus type of ASD .
Posted in Uncategorized, tagged asd, ATRIAL SEPTAL DEFECT, chd, congenital heart disease, coronary sinus asd, left to right shunt, os asd, ostium primum, septum primum, SINUS VENOSUS ASD, SVC TYPE OF ASD on August 5, 2009| 1 Comment »
Atrial septal defects are one of the commonest forms of congenital heart disease.
- The commonest being the ositum secundum ASD ( Which is in fact is a defect in the development of septum primum)
- The next common is ostium primum defect which is a part of AV canal or atrio ventricular septal defect.
Other forms of ASD include
- SVC type /Also called sinus venosus type of ASD .
- IVC type
- Coronary sinus defect -Also called partial or complete forms of unroofed coronary sinus
SVC type ASDs
They are in the strict sense can not be called as ASD. This is because there is no defect in any of the embryological inter atrial septal component.
There is no direct communication between RA and LA, instead a window or passage of communication between pulmonary vein and SVC. Right upper lobe pulmonary vein is usually the culprit .Some times more than one PV communicates with SVC.
The exact area of this PV-SVC window occur between anterior surface of right upper lobe PV with postero lateral surface of SVC.
PAPVC partial anomalous pulmonary venous drainage can be considered an integral part of this defect as RUPV is linked with SVC.
Can we have a combination of SVC ASD and OS ASD ?
This is possible .But two embryological errors need to occur. This is often seen as a large OS ASD with deficient or absent superior rim. So whenever superior rim of IAS is deficient a PAPVC and a SVC ASD should be looked for.
Clinical features
- SVC type ASDs generally shunt lesser blood than OS ASDs. (Often<2:1) .This is because it is not the LA that is communicating with RA instead only a
- It is usually a single PV (some times 2) that shunts from left to right.
There is a distinct possibility of missing this lesion in routine echo.Minimal RA,RV enlargement may give us a clue.The classical subcostal or 4 chamber view in echocardiography may not visualise these defects.
So, whenever one encounters mild dilatation of RA and RV and the IAS appears intact, a meticulous search and a focused echo in the superior aspect of IAS is warranted. Angled superior views may pick up this defect.A transesophageal echocardiogram (TEE) is often required to confirm it.
Therapeutic issues
- Device closure is not possible
- Surgery involves little more technicality than ASD OS.
- Small defects can be patch closed.
- Some times the SVC has to be disconnected from the PV and anastamosed separately on right atrial appendage. SVC resection will aid the surgeon in proper patch closure.
- Post operative follow up is necessary as SVC obstruction or PV obstruction may be a delayed consequence
References
http://asianannals.ctsnetjournals.org/cgi/content/full/10/3/231
Management of Atrial septal defect : Device closure lagging behind surgical closure !
Posted in cardiac surgery, tagged amplatzer asd device, asd, asd surgery, asdos, device closure, ostium primum, ostium secundum, pfo, starflex on May 11, 2009| 8 Comments »
Atrial septal defect is one among the commonest congenital heart disease .After years of controversy, there is consensus now , all significant ASDs need to be closed , at whatever age it is detected.
This rule does not apply to small ASDs without chamber right atrial and right ventricular dilatation. These defects and PFOs need not be closed .
Over the years , the controversy has shifted from Should we close ? to How to close ?
There are two options available : Device closure , Surgical closure
The following table compares the both treatment modalities
( Personal perspective )
Final message
Device closure is a complex, costly, often difficult and error prone cardiac procedure .It needs long term follow up and may carry a life long risk of major cardiac complication.It is useful only in selected subset of ASD patients. Surgical closure prevails over device closure in most situations.
Is this article has biased view against this emerging pediatric interventional procedure of ASD closure ?
It may appear so . But that is the reality as on 2009 !.May we hope technology evolves further and take our surgeons head on .
2012 update on ASD device closure .
The hard-ware as well as the expertise has improved a lot and it is on right track to become a real challenge to surgery.
The only issue again is the availability of rims to mount the device . Another realistic and sensitive issue which have I come across is , many interventionist cardiologist do feel awkward when they experience unexpected rim shortage on table. They should realise it is not their fault.
Always be ready to abandon the procedure and refer to the surgeon , according to your true conscience
After all , improperly delivered device is a life long pain for the patient .He has come to you with a great belief isn’t !
2014 update
Device closure for most ASDs in both children and adult is now possible with high degree of success. We have crossed about 50 patient experience. And I am truly amazed , how within a short period the device closure is about to conquer the crown from the surgeons ! (Exciting new data are coming from my colleague Dr Gnanavelu from the new Super specialty hospital of Government of Tamil Nadu Chennai. )
Reference
Aortic erosion following ASD closure
And now , a biochemical diagnosis for pulmonary hypertension !
Posted in cardiology -congenital heart disease, tagged 100% oxygen, asd, bi directional shunt, biochemical diagnosi of pulmonary hypertension, eisenmengersyndrome, heath edwards, nitric oxide, pd, pht, reversibility of pulmonary hypertension, right to left shunt, severe pulmonary hypertenison, tolazoline, vsd on March 27, 2009| Leave a Comment »
Biochemical diagnosis for PHT and Eisenmenger syndrome
Identifying reversibility of pulmonary arterial hypertension remains a difficult clinical problem.Heath edwards grading of pulmonary hypertension is based on lung pathology .Grade 4 and 5 constitute severe obstructive vascular pathology including pulmonary vascular necrosis.
Lung biopsy is an invasive procedure and has a huge risk in patients with elevated pulmonary artery pressure.
Do we have an alternative ?
Does the pulmonary artery sheds necrosed endothelial cells into the circulation ?
Yes it seems so , This month’s Nature cardiology reveals a breakthrough concept
The CEC (Circulating endothelial cells count ) can be used as marker and may be considered a non invasive equivalent of lung biopsy
http://www.nature.com/nrcardio/journal/v6/n4/full/nrcardio.2009.18.html
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