Talk:Atrial septal defect

From Wikipedia, the free encyclopedia
Jump to: navigation, search
WikiProject Genetics  
WikiProject icon This article is within the scope of WikiProject Genetics, a collaborative effort to improve the coverage of Genetics on Wikipedia. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks.
 ???  This article has not yet received a rating on the project's quality scale.
 ???  This article has not yet received a rating on the project's importance scale.
 
WikiProject Medicine / Cardiology (Rated B-class, Mid-importance)
WikiProject icon This article is within the scope of WikiProject Medicine, which recommends that this article follow the Manual of Style for medicine-related articles and use high-quality medical sources. Please visit the project page for details or ask questions at Wikipedia talk:WikiProject Medicine.
B-Class article B  This article has been rated as B-Class on the project's quality scale.
 Mid  This article has been rated as Mid-importance on the project's importance scale.
Taskforce icon
This article is supported by the Cardiology task force (marked as Mid-importance).
 

Decompression sickness?[edit]

I've redirected the article for Patent foramen ovale to this page. At the time, I deleted the following text, because I believe it is untrue:

PFO can cause decompression sickness in divers because a proportion of venous blood carrying inert gases, such as helium or nitrogen does not pass through the lungs. The only way to release the excess inert gases from the body is to pass the blood carrying the inert gases through the lungs to be exhaled. If that inert gas-laden blood passes through the PFO, it avoids the lungs and the inert gas is more likely to form large bubbles in the arterial blood stream causing decompression sickness.

If it is true, someone please re-add it with appropriate links or references. Ksheka 16:01, May 20, 2004 (UTC)

PFO IS a predisposing risk factor in decompression sickness. See [1]

Thanks for the references. Part of the problem is "Why PFO?" The answer, from what I gather is that it's not just PFO. Any ASD can cause this. It's just that PFOs are either more common that secundum ASDs, or their more likely to be underdiagnosed until the individual develops decompression sickness. (I'm not sure which.) Ksheka 10:22, May 21, 2004 (UTC)

Fixed splitting of S2 can also occur in VSD with left-to-right shunt, and in RV failure. Axl 22:32, 8 Nov 2004 (UTC)

References for decompression sickness[edit]

I'll move these into the main article soon... Ksheka

Done.Ksheka 13:24, May 22, 2004 (UTC)

It's all true. As someone who spends her day looking at heart defects... PFO's are common, particularly in females (20-25 % of the population). If you have a known PFO you should avoid scuba diving. If you have an ASD, which is NOT the same a a PFO you should definitely not go scuba diving!! Although you might not have any problems, the likelihood is greater than without atrial septal defects. —Preceding unsigned comment added by 124.19.36.4 (talk) 03:46, 23 June 2008 (UTC)

July 7, 2011: PFO may be a predisposing risk factor in decompression sickness. It is not generally agreed that it is a risk factor of any kind of significance. Theoretically, it is expected that it is. Practically, the risk may be negligible. Divers Alert Network (DAN) is engaged in specific research on the topic now. — Preceding unsigned comment added by 134.223.116.201 (talk) 14:59, 7 July 2011 (UTC)

how common?[edit]

I have both a PFO and an atrial septal aneurysm. My doctor told me that PFO is very common: occuring in 20% of the population. So I can't see how this text could be true? -- "As a group, atrial septal defects occur in 1 child per 1500 live births." please reference. -- 69.195.36.86 16:50, 6 Dec 2004 (UTC)

These are different statistics about different disorders. Atrial septum aneurysm is not an ASD nor a PFO. As for ASD, this is more symptomatic than a PFO, which may be clinically occult (and hence not included in the 1:1500 figure, because they are not being investigated) and often requires no management if the patient is otherwise well.
If come accross any reliable statistics, please post them on Wikipedia with references. JFW | T@lk 17:44, 6 Dec 2004 (UTC)
Note the article for PFO was merged into this one. If we're comparing apples-to-oranges the article should be clarified. Here is a study: in it are 50 control subjects; 18% had PFO, 8% had atrial septal aneurysm [2]. so i still don't know what the figure 1:1500 means.. perhaps this was only easily-detected defects? -- 69.195.36.86 18:25, 6 Dec 2004 (UTC)
That's what I was suggesting. There is no point in trying to detect something if the person with that abnormality is well, and there is no need for intervention. If doctors were to screen the whole population for all sorts of diseases, a lot of false positives would occur, leading to unnecessary and dangerous interventions. If there has been a consequence (e.g. stroke or migraine), then screening for the cause would reveal the ASD/PFO/atrial aneurysm as a cause (warranting treatment).
Good for finding the Cleveland Clinic article. The issue is certainly far from settled! JFW | T@lk 20:09, 6 Dec 2004 (UTC)

Probe PFO (a very small PFO) occurs in about 20-25% of the population. The difference is the size. So, technically, alot of people have PFO, but saying PFO generally refers to the much larger version of the defect. —Preceding unsigned comment added by 141.106.192.69 (talk) 16:13, 31 October 2008 (UTC)

Genetics[edit]

When I was reading through the article I did not see any mention of the basis of ASD in fetal development, such as how the interventricular septum forms and how defects at different points of its development can lead to the different types of ASD.

I would say this is a relevant point, it sounds like you have some data that hasn't been referenced, please add it. ItalianDeception 09:22, 27 October 2007 (UTC)

Also, does anybody know of a genetic basis for ASD?--Jfurr1981 19:17, 30 October 2005 (UTC)

There is a familiar form, I personally know of two families. I'll try to find a reference. --Ekko 11:41, 31 October 2005 (UTC)

There is definitely a genetic basis for ASD, Dr. Paul Grossfeld of UCSD is a Cardiac Molecular Biologist of note who could provide significant insight into this question. ItalianDeception 09:22, 27 October 2007 (UTC)

TCD[edit]

The claims about trans-cranial doppler ultrasound seems exageratet and unsubstansiated and is made by an anonymous user. Should probably be re-written. --Ekko 13:32, 23 December 2005 (UTC)

The author of this section has not responded, so I will expand: A less invasive protocol; less invasive than what? pioneered in recent years probably means that it's just one group of investigators who uses this technique. Some observers believe the protocol is on the way to becoming the Gold Standard: some believe, is on the way, that comes down to that most don't trust this technique at all yet. At least one clinical study; which publication? 100% accurate; what is the gold standard? Vivisection? Autopsy?
I would hazard a guess that this may be a part of a turf war between radiologists (which would be the ones to perforrm TCD) and cardiologists (who perform trans esophagal and transthoracal echocardiography).
The method might be good, but the article doen't show it. --Ekko 13:02, 25 December 2005 (UTC)
I keep on discussing with myself; here is an interesting german article by Heckman JG et. al. [Detection of patent foramen ovale. Transesophageal echocardiography and transcranial Doppler sonography with ultrasound contrast media are "supplementary, not competing, diagnostic methods"]. Seems the method have merits, but the section is both inaccurate and exagerated. --Ekko 22:19, 25 December 2005 (UTC)

This was covered by a recent review in the NEJM, which mentioned TCD. Frankly it sounds frightening. If I had a PFO I'd rather have bubble echocardiography than transcranial doppler. JFW | T@lk 23:07, 25 December 2005 (UTC)

In a more serious vein: someone should write a small section making people aware that there's a discussion whether one should use time and resources looking for something that's a normal phenomena in at least 25% of the population. What are you going to do with those PFOs you find? Close them? When we lack the resources to take proper care of ther real GUCH-patients? --Ekko 23:50, 25 December 2005 (UTC)

GUCH? JFW | T@lk 02:28, 26 December 2005 (UTC)

Presumably "Grown Up Congenital Heart disease". [3] --Arcadian 03:28, 26 December 2005 (UTC)

Ekko, you are suggesting we should screen the whole word for PFO. That is not what I said. The NEJM review (which I know well because I discussed it at the hospital journal club) is about cryptogenic stroke. If a young patient has a stroke with no apparent cause, PFO is overrepresented when compared to controls. That suggests a causative role or common cause. If you're worried about GUCHies, there should be a funding increase! JFW | T@lk 23:53, 26 December 2005 (UTC)

Ooops! Sorry that my reply came out in a way that seemed aimed at you. It was not. My point was ment to be something like this: rather than a lenghty discussion about small differences in diagnostic tools the "educated layperson" reading wikipedia would probably be better off if we introduced the concept that a PFO is not necessarily something that should be looked for and closed. (I'm aware that there is indications like stroke, migraine and decompression sickness). --Ekko 12:01, 30 December 2005 (UTC)

I see that the anonymous user still can't or won't substantiate his claims. It should be possible, or else the adjectives "less invasive and more sensitive" should be replaced with "other". --Ekko 09:36, 20 April 2007 (UTC)

Prognosis Section[edit]

NOTE:

The following information is opinion/anecdotal (While I can cite references for much of the information provided below, the information is more intended for discussion and consideration amongst referees).

I would like to also note that I am a "Educated Laymen" and nothing more. My daughter has a Secundum type ASD and my motivations are strictly aiding where I may. For a "Laymen" however, I take this subject very seriously and have done some homework, thus has enabled me to make some hopefully worthfile contributions to this article. I have approached my studies as objectively as possible, albeit the emotional connection I have with this condition and my daughter. I have tried to keep things as factual as possible.

PROGNOSIS

A pronosis section is gravely needed that sheds light on the very comforting reality that many children with ASD's undergo "Spontaneous Closure" of their interatrial septal lesion. As a parent of a child with an ASD, I can relate to the vast majority of whom will consume the information presented in this article.

From my exhaustive research, one of the main predictors that a child's ASD may "Close" spontaneously is the significance of the child's shunt and age at initial presentation. A child initially presenting with a moderate sized secundum type ASD (6mm - 8mm), with little to no "Left to Right" shunting, may have a very good chance that the lesion will close on its own without the need for surgical intervention. This of course is not always the case, however, there is a marked trend in this scenario that should not be overlooked. With the exponential growth of the heart in young patients with ASD, there is some data to suggest that even in the presence of a clinically significant shunt, this still may not lower the odds of the child undergoing spontaneous closure of their ASD.

'At a glance: As the heart muscle develops, significant changes within the heart occur that cannot be adequately documented as these changes very from individual to individual. Further, the relavancy and frequency of these changes is difficult to analyze let alone assess (One would need a means of permanently monitoring the heart 24/7/365 with technology not currently available). This mechanism would need to have the capability to visualize the heart's internal growth over time and constantly. This would be to consisently mark internal (Literally constant supervision of the four chambers of the heart and components) physical evolution of a given heart's development and provide a means of measuring and logging hemodynamic characteristics over time. Yes I know this is science fiction today, but I feel something along these lines may indeed one day become a reality, a device like this could lead to a significantly better understanding of the heart (Disease analysis, interpretation, in some cases, prevention).

So getting back on track, while a 99.9% accurate prediction of whether a given ASD will undergo spontaneous closure is not possible, there are some important correlations that can be made to better prepare yourself for the outcome of your case, be it positive or negative.

Focusing on the predominating results from my studies, almost completely positive, what's most reassuring is the existance of trends related to spontaneous closure in ASD. These trends have historically proven to be relatively consistent markers in the likelyhood a child's ASD will in fact undergo spontaneous closure. There are exceptions to these trends so keep in mind that even if your child has a LARGE ASD (>9mm), this does not necessarily rule out spontaneous closure in any way. Alternatively, a small ASD, while statistically more likely to close spontaneously, may also fail to close without surgical intervention.

From my research and sources, shunt significance, lesion size, and age combined, at initial presentation of ASD diagnosis seems to be an even more significant and consistent predictive factor in spontaneous closure of ASD's than lesion size (Though a large ASD will typically be associated with a significant shunt) alone. I have many solid medical references that I have acquired stating rate of incidence of spontaneous closure in secundum type ASD, age to rate of spontaneous closure incidence in various ASDs, lesion size at presentation to spontaneous closure incidence and various other relevant data in various ASDs. A study of progressive Hemodynamic ASD clinical signifigance, at age of presentation over a (3) to (5) year period in children is another likely factor in determining the liklihood of spontaneous closure of ASD. These sorts of studies should be relevantly and suffciently covered in this section.

I have yet to undertake this portion of the article as if I cannot devote the meticulous attention to detail this section would require, I would rather not add it for consideration. Hopefully soon I may find the time to construct this section, or even someone else of similar passion, I highly encourage it, however, if your're going to do it, do it right.

I feel we must be equally responsible in communicating to the masses, not using this Wiki to write a "Medicalese" article that only serves the medical community. It's important to consider the audience and who will benefit most from an article of this nature. With this said, things must also be kept to a strict referential conformity to ensure the validity of the information presented, who best to do this than well-minded Doctors?

The bottom line guys:

ASD in this article is portrayed for it's potentially devastating effects and not the more common scenario that many ASD's either close spontaneously to entirety or result in the Patent Foramen Ovale (PFO). According to a very credible source of mine (I know, a statement like this is always subjective without granular analysis of the source's credibility and contributions), it is not at all unheard of to hear of a person living into their 80's or beyond with an ASD. While this is nothing more than anecdotal, my source happens to be a well known cardiac molecular biologist who has stated that this is actually quite common. The common presentation I'm told is typically that of an elderly female suffering from Congestive Heart Failure (CHF) that gets referred to a pediatric cardiologist for treatment considerations. I have also been told by this biologist, quite remarkably regarding one case, upon further investigation of the patient's symptoms, an ASD the size of a "Golf Ball" was found and of course the underlying origin for the CHF in the patient. An ASD CAN be a very serious condition and it also be very BENIGN, I believe this should be illustrated more clearly in this article. Surgical intervention, be it transthoracic or minimally invasive transcatheterization is often NOT required and this should be more clearly conveyed to the public.

ItalianDeception 09:16, 27 October 2007 (UTC)

I agree completely. --Ekko (talk) 09:35, 29 April 2008 (UTC)

I agree with you completely.I am a medical student and one of my friends aged 22 has just been diagnosed with an ASD.this guy is 6 feet 3 inches tall,plays soccer,cricket and is a boxing champion.the defect was diagnosed in an attempt to find the reason his blood pressure never rose above 90/60mmHg.and even at this blood pressure he was fine and the body had no signs of weakness or easy fatiguability.now the doctors have referred him for an ASO implantation but he is not willing to get it because it is apparently a benign ASD.Surgeon Mary (talk) 13:14, 22 July 2011 (UTC)

Symptoms?[edit]

The article says the patient is often found to be notably symptomatic, but what are the symptoms? Una Smith 21:08, 14 June 2007 (UTC)

Children: failure to thrive, recurrent bouts of respiratory problems. Adults: as the article states: Adults with an uncorrected ASD will present with symptoms of dyspnea on exertion (shortness of breath with minimal exercise), congestive heart failure, or cerebrovascular accident (stroke). They may be noted on routine testing to have an abnormal chest x-ray or an abnormal EKG and may have atrial fibrillation. --Ekko 20:13, 15 June 2007 (UTC)

PFO and cryptogenic stroke in older people[edit]

Still worth looking at JFW | T@lk 01:39, 29 November 2007 (UTC)

Transcranial ultrasound[edit]

Gene Hobbs repeatedly inserts a sentence regarding transcranial detection of PFOs that is not based on the reference given (I've read the ""Letter to the editor"). In adition the reference is a letter to the editor, in a journal marginal to this kind of medicine. This is bogus science! --Ekko (talk) 15:21, 26 April 2008 (UTC)

Rather than search for primary source to support or refute the statement in the letter, Ekko's professional bias is to discount the professional opinion of letter's author. It is my understanding that the gold standard for PFO diagnosis is TEE as it has been repeatedly proven to be more specific than TTE.[1][2] TCD has a growing body of evidence showing that it is less risky and has similar accuracy to TEE.[3] No worries, I will not edit this again as I do bow to Ekko's professional opinion.
  1. ^ Belkin RN, Pollack BD, Ruggiero ML, Alas LL, Tatini U (September 1994). "Comparison of transesophageal and transthoracic echocardiography with contrast and color flow Doppler in the detection of patent foramen ovale". Am. Heart J. 128 (3): 520–5. PMID 8074014. 
  2. ^ Saary, MJ and Gray, GW (1999). "The Possible Relationship Between Patent Foramen Ovale and Decompression Sickness". Defence R&D Canada (DRDC) Technical Report. DCIEM-TR-1999-001. Retrieved 2008-04-27. 
  3. ^ Belvís R, Leta RG, Martí-Fàbregas J, et al (April 2006). "Almost perfect concordance between simultaneous transcranial Doppler and transesophageal echocardiography in the quantification of right-to-left shunts". J Neuroimaging 16 (2): 133–8. doi:10.1111/j.1552-6569.2006.00021.x. PMID 16629735. 
Gene Hobbs (talk) 23:08, 27 April 2008 (UTC)
But why didn't you cite those references, instead of a «letter to the editor», with much less value? I have often discussed the use of transcranial ultrasound with the radiologists performing it, both in relation to PFO and PDA, and do not doubt that this method have it's use. But I think that you should specify which age groups you are talking about. A 60 year old person is something quite else than a five year old child. And that you should cite good sources, which you have now (a primary source), but not then (secondary). Ekko (talk) 07:43, 28 April 2008 (UTC)
I am not familiar enough with the cardiac literature or authors. I posted the opinion of someone in a journal that I am comfortable with. Thank you for your time. —Preceding unsigned comment added by Gene Hobbs (talkcontribs) 17:13, 28 April 2008 (UTC)

GHUCJOFSJB;BVKVS0VIGVYFK.[edit]

Italic text —Preceding unsigned comment added by 70.26.72.63 (talk) 01:50, 15 November 2008 (UTC)

162 8th INTERNATIONAL PEDIATRIC CARDIOLOGY AND HEART VEIN SURGERY CONGRESS (ASD DEVİCE CARDİ-O-FİX)[edit]

162 8th INTERNATIONAL PEDIATRIC CARDIOLOGY AND HEART VEIN SURGERY CONGRESS P-100 A (New) Device Without Reported Results: Middle Term Results; Transcatheter Atrial Septal Defect Closure with Cardi-O-Fix Ahmet Celebi, Celal Akdeniz, Ender Odemis, Abdullah Erdem, Turkay Saritas, Elnur Imanov, Halil Demir, Fadli Demir Dr. Siyami Ersek Breast Heart Vein Surgery Training and Research Hospital Pediatric Cardiology Clinic, Istanbul Purpose: Transcatheter treatment method in Atrial Septal Defect (ASD) closure has become the number one treatment choice today. For this reason many different devices are being used. In this study, our experiences for children and teenagers regarding ASD closure with Cardio-O-Fix device which does not have any reported results in the literature and the middle term results are being presented. The cardiofix device is a known device that has been used in the past for things such as male enhancement surgery and for scientists to be able to bust a nut at work while their colleagues are none the wiser. Without this device intercourse in the rectum would not be possible. Method and Rationale: Secundum ASD cases showing right ventricle volume load symptoms with transthoracic echocardiography have been taken to the catheter laboratory for closure purposes. In patients who had planned ASD closure with Cardi-O-Fix device, taking into consideration the device trial period at the beginning, device diameter to be 􀂔20 mm has been seen as appropriate. In all these cases, the process has been carried out using transthoracic echocardiography (TTE). Closure attempts have been carried out on patients who had sufficient septal rims outside aortic rims and with the measured Qp/Qs>1.5. Right after the implantation, residue shunt has been administered with echocardiography and angiography. Echocardiographic analysis has been carried out on all cases the next day and aspirin has been recommended for six months. Findings: Catheterization has been applied in our clinic on 185 cases for the purpose of ASD closure, the operation has been aborted for 4 cases due to various reasons. In 27 of 181 cases with successful attempts, ASD closure attempt has been carried out with Cardi-O-Fix device. While the device diameter has been 􀂔20 mm for 22 of the cases, later on, closure has been administered on 5 cases with larger defects using a device diameter 􀂕20 mm. Attempts have been successfully completed in all cases. In cases where Cardi-O-Fix is used the average age is 7.52±5.37 (3.5-29 years), TTE defect diameter 12.5±1.6 (9.7-19.5 mm), Qp/Qs 1.83±0.33 (1.5-3.1), stretched balloon diameter 17.3±3.29 (12.5-24 mm), average device diameter 17.12±3.65 (12-26 mm), average device/total septum rate 0.48±0.1 (0.3-0.76). The operation time has been 66±30.4 (30-150 minutes), analysis time 19.8±12.1 (9-67 minutes). No Major complication has been observed in any of the cases where COF has been used. Results: It has been demonstrated that in medium width, in defects where device with diameter up to 20 mm has to be used, the use of Cardi-O-Fix was safe and effective. Progressing from the working strategy in 5 cases where device with diameter >20 mm is used, the fact that attempt success is 100% and that there are no complications shows that it may be used safely in bigger defects. The fact that cost is relatively lower when compared to other devices might be a reason for preference. —Preceding unsigned comment added by 85.99.4.95 (talk) 07:21, 26 May 2009 (UTC)

"Current" clinical trials[edit]

The subsection on Patent Foramen Ovale states that several clinical trials are currently underway. This could use a time reference, since "current" is a temporary condition. --Chris Noe (talk) 19:39, 13 August 2009 (UTC)

Patent foramen ovale and Migraine[edit]

There's a little bit in the article that links PFO to Migraine, and has already been tagged "citation needed". As a migraineur I followed this through. The data I could find seems to say that while there's a link between the two conditions, it's not proved as a causal link; and that treating the PFO doesn't help migraines. In fact in some patients it even causes them to have migraines where they never had them before. As I don't have a relevant degree I don't feel I should remove the link; but I've tagged it disputed.Number774 (talk) 21:45, 15 January 2012 (UTC)