text:
Talk:Clarence Seedorf

Birthplace
Seedorf was born in Suriname, see: http://www.acmilan.com/InfoPage.aspx?id=12622. Stop putting false information on this page. --DR31 (talk) 02:59, 8 August 2005 (UTC)

Lack of detail
This is a very brief article and is written in a poor style, largely because of the bullet points. I've therefore fleshed the article out a bit. If anyone has anything to change then feel free to. --hedpeguyuk 14:27, 11 June 2006 (UTC)

Rahmlee Seedorf
Clarence Seedorf only has two brothers. Jurgen and Chedric. Stefano is their cousin and I don't know Rahmlee, but he's not their brother. Ivo Reemnet (a former professional footballer for Dordrecht '90) is also a relative of the brothers by their mother's side. —The preceding unsigned comment was added by 204.212.126.164 (talk) 14:21, 11 April 2007 (UTC).

Club career
need more info in his stints with Inter Milan and Sampdoria --Xaiver0510 02:42, 10 November 2007 (UTC)

Intercontinental Cup

Seedorf left Ajax in the summer of 1995 for Sampdoria, hence never winning the Intercontinental cup with Ajax, as that match was in December 1995. Please do not alter this! I will try to dig up some info on his Sampdoria stint. Spencer (talk) 15:29, 3 January 2008 (UTC)

There are not just two players that played in both Milan's clubs. There is also Maurizio Ganz for example. Check that out please —Preceding unsigned comment added by 190.247.68.71 (talk) 23:20, 30 April 2009 (UTC)

pic
Although this picture is better than none at all, its probably best to find a picture in which his face is more prominent than his ass. - PietervHuis (talk) 18:58, 22 April 2008 (UTC)

Brazilian wife
It is said that he is married to a Brazilian called Luviana. It doesn't seem a common Brazilian name. Luciana would be a more usual one. But several websites mention Luviana Seedorf. —Preceding unsigned comment added by 200.252.232.240 (talk) 13:47, 11 February 2010 (UTC)

Mersin İdman Yurdu
What is this rubbish? Seedorf has been playing for AC Milan continuously since 2002. He has never played for a Turkish team. And the edits that mention are very poorly done, which leads me to call vandalism. —Preceding unsigned comment added by 199.74.93.92 (talk) 21:35, 22 April 2010 (UTC)

Samuel eto reference
in the article it says Clarence Seedorf is one of the two players who won the champions league with 3 different teams. It says Samuel Eto'o is the other player. I believe Samuel Eto'o has only won the champions league with 2 different teams (Barcelona & Inter Milan) Before Barca he played for Mallorca, they never won the tournament. —Preceding unsigned comment added by 62.108.15.238 (talk) 12:43, 25 May 2010 (UTC)

Eto'o played 3 games with Real Madrid in the UEFA Champions League 1999-2000. —Preceding unsigned comment added by 83.165.244.19 (talk) 17:02, 25 May 2010 (UTC)

Vandalism
Hey, I obviously am not great with doing this but if you read his early career section and the info box this page has been vandalized quite heavily. Nazi cup? Yeah right, and didn't Seedorf play for Sampdoria? His birthdate was changed to 1946 (so I reverted it back to 76) but that was the only part of this I found funny. I don't have the time to fix all of these problems but if someone who knew more about this could fix this, well hey, it would be swell. --BullNiro (talk) 20:58, 16 September 2011 (UTC)

Tragedy of his life, playing for Netherlands.
First thing under the heading International Career: "Due to Surinamese rules against dual citizenship, players who take Dutch citizenship are no longer eligible to represent [Suriname]. Because of this Seedorf, then of Ajax, played international football for the Netherlands national football team. He received his first call up in 1994, at the age of 18."

Man, such a shame. If only he hadn't taken Dutch citizenship, he might have had the enormous honour and privilege of playing for Suriname, instead of having to settle for three times World Cup finalists, the Netherlands.Silas Maxfield (talk) 19:59, 27 May 2012 (UTC)

Winner of Champions League in three teams.
The article states it is the first. Are there others? I couldn't find any. Shouldn't it be corrected from "the first" to "the first and - currently - only"? — Preceding unsigned comment added by Agaved (talk • contribs) 12:57, 17 November 2012 (UTC)

dropped his post-nominal O.O.N.
In the Netherlands, it is not common for recipients of the Order of Orange-Nassau (or any other order of chivalry) to use a post-nominal O.O.N. like people can use O.B.E. in the UK. I removed his O.O.N. post-nominal as it serves no purpose. Mkuyt (talk) 19:28, 19 January 2013 (UTC)

Copyright problem removed
Prior content in this article duplicated one or more previously published sources. The material was copied from: www.insideworldsoccer.com/2013/03/clarence-seedorf-red-card-botafogo-madureira.html. Copied or closely paraphrased material has been rewritten or removed and must not be restored, unless it is duly released under a compatible license. (For more information, please see "using copyrighted works from others" if you are not the copyright holder of this material, or "donating copyrighted materials" if you are.) For legal reasons, we cannot accept copyrighted text or images borrowed from other web sites or published material; such additions will be deleted. Contributors may use copyrighted publications as a source of information, but not as a source of sentences or phrases. Accordingly, the material may be rewritten, but only if it does not infringe on the copyright of the original or plagiarize from that source. Please see our guideline on non-free text for how to properly implement limited quotations of copyrighted text. Wikipedia takes copyright violations very seriously, and persistent violators will be blocked from editing. While we appreciate contributions, we must require all contributors to understand and comply with these policies. Thank you. Struway2 (talk) 17:33, 13 May 2014 (UTC)

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title: Talk:Clarence Seedorf


text:
Ventricular septal defect

A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. The extent of the opening may vary from pin size to complete absence of the ventricular septum, creating one common ventricle. The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes.

The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children in the United States. It is also the type that will most commonly require surgical intervention, comprising over 80% of cases.

Membranous ventricular septal defects are more common than muscular ventricular septal defects, and are the most common congenital cardiac anomaly.

Signs and symptoms
Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.

VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis.
 * Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.

The restrictive ventricular septal defects (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger's syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.

Cause
Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome. Congenital heart disease, particularly VSDs, is the number one cause of death for children with Down syndrome ages birth to two.

A VSD can also form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.

A congenital VSD can result from a disturbance in the morphogenesis of the heart in its embryonic stages. In the fifth week of gestation, the heart undergoes multiple processes of septation and forming a dextral loop. Interfering with the latter leads to insufficient leftward movement of the ventricular outflow tract over the atrioventricular canal, which in turn can result in a VSD or, in the most extreme cases, a double outlet right ventricle with one.

A ventricular septal defect arises when the superior part of the interventricular septum, which separates the right and left ventricles of the heart, fails to fully develop. The right ventricle pumps blood to the lungs to get oxygen, while the left ventricle pumps blood to the rest of the body to provide oxygen to tissues. A ventricular septal defect results in the mixing of oxygen-rich blood with oxygen-poor blood, increasing strain on the heart and lungs.

Pathophysiology
During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium. This has two net effects. First, the circuitous refluxing of blood causes volume overload on the left ventricle. Second, because the left ventricle normally has a much higher systolic pressure (~120 mmHg) than the right ventricle (~20 mmHg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms.

In serious cases, the pulmonary arterial pressure can reach levels that equal the systemic pressure. This reverses the left to right shunt, so that blood then flows from the right ventricle into the left ventricle, resulting in cyanosis, as blood is by-passing the lungs for oxygenation.

This effect is more noticeable in patients with larger defects, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller defects may be asymptomatic. Four different septal defects exist, with perimembranous most common, outlet, atrioventricular, and muscular less commonly.

Diagnosis
A VSD can be detected by cardiac auscultation. Classically, a VSD causes a pathognomonic holo- or pansystolic murmur. Auscultation is generally considered sufficient for detecting a significant VSD. The murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle. If there is not much difference in pressure between the left and right ventricles, then the flow of blood through the VSD will not be very great and the VSD may be silent. This situation occurs a) in the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired VSD. Confirmation of cardiac auscultation can be obtained by non-invasive cardiac ultrasound (echocardiography).  To more accurately measure ventricular pressures, cardiac catheterization, can be performed.

Classification
Although there are several classifications for VSD, the most accepted and unified classification is that of Congenital Heart Surgery Nomenclature and Database Project. The classification is based on the location of the VSD on the right ventricular surface of the inter ventricular septum and is as follows:

Type 1
Type 1 is sub aortic

Type 2

 * Type 2 also known as perimembranous, paramembranous, conoventricular, membranous septal defect, and subaortic.
 * Most common variety found in 70%

Type 3
Type 3 also known as inlet (or AV canal type).
 * Commonly associated with atrioventricular septal defect, found in about 5%

Type 4
Type 4 also known as muscular (trabecular)
 * Located in the muscular septum, found in 20%. Can be sub classified again based on the location into anterior, apical, posterior and mid

Type: Gerbode
Type: Gerbode also known as left ventricular to right atrial communication
 * Due to absence of Atrioventricular septum.

Treatment
Most cases do not need treatment and heal during the first years of life. Treatment is either conservative or surgical. Smaller congenital VSDs often close on their own, as the heart grows, and in such cases may be treated conservatively. Some cases may necessitate surgical intervention, i.e. with the following indications:

 * 1) Failure of congestive cardiac failure to respond to medications
 * 2)  VSD with pulmonic stenosis
 * 3) Large VSD with pulmonary hypertension
 * 4) VSD with aortic regurgitation

For the surgical procedure, a heart-lung machine is required and a median sternotomy is performed. Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only suitable for certain patients. Repair of most VSDs is complicated by the fact that the conducting system of the heart is in the immediate vicinity.

Ventricular septum defect in infants is initially treated medically with cardiac glycosides (e.g., digoxin 10-20 μg/kg per day), loop diuretics (e.g., furosemide 1–3 mg/kg per day) and ACE inhibitors (e.g., captopril 0.5–2 mg/kg per day).

Transcatheter closure
A device, known as the Amplatzer muscular VSD occluder, may be used to close certain VSDs. It was initially approved in 2009. It appears to work well and be safe. The cost is also lower than having open heart surgery. The device is placed through a small incision in the groin.

The Amplatzer septal occluder was shown to have full closure of the ventricular defect within the 24 hours of placement. It has a low risk of embolism after implantation. Some tricuspid valve regurgitation was shown after the procedure that could possibly be from the right ventricular disc. There have been some reports that the Amplatzer septal occluder may cause life-threatening erosion of the tissue inside the heart. This occurs in one percent of people implanted with the device and requires immediate open-heart surgery. This erosion occurs due to improper sizing of the device resulting with it being too large for the defect, causing rubbing of the septal tissue and erosion.

Surgery
Surgical closure of a Perimembranous VSD is performed on cardiopulmonary bypass with ischemic arrest. Patients are usually cooled to 28 degrees. Percutaneous Device closure of these defects is rarely performed in the United States because of the reported incidence of both early and late onset complete heart block after device closure, presumably secondary to device trauma to the AV node.

Surgical exposure is achieved through the right atrium. The tricuspid valve septal leaflet is retracted or incised to expose the defect margins.

Several patch materials are available, including native pericardium, bovine pericardium, PTFE (Gore-Tex or Impra), or Dacron.

Suture techniques include horizontal pledgeted mattress sutures, and running polypropylene suture.

Critical attention is necessary to avoid injury to the conduction system located on the left ventricular side of the interventricular septum near the papillary muscle of the conus. Care is taken to avoid injury to the aortic valve with sutures.

Once the repair is complete, the heart is extensively deaired by venting blood through the aortic cardioplegia site, and by infusing Carbon Dioxide into the operative field to displace air.

Intraoperative transesophageal echocardiography is used to confirm secure closure of the VSD, normal function of the aortic and tricuspid valves, good ventricular function, and the elimination of all air from the left side of the heart.

The sternum, fascia and skin are closed, with potential placement of a local anesthetic infusion catheter under the fascia, to enhance postoperative pain control.

Multiple muscular VSDs are a challenge to close, achieving a complete closure can be aided by the use of fluorescein dye.

Epidemiology
VSDs are the most common congenital cardiac abnormalities. They are found in 30-60% of all newborns with a congenital heart defect, or about 2-6 per 1000 births. During heart formation, when the heart begins life as a hollow tube, it begins to partition, forming septa. If this does not occur properly it can lead to an opening being left within the ventricular septum. It is debatable whether all those defects are true heart defects, or if some of them are normal phenomena, since most of the trabecular VSDs close spontaneously. Prospective studies give a prevalence of 2-5 per 100 births of trabecular VSDs that close shortly after birth in 80-90% of the cases.

Famous people who had ventricular septal defect

 * Madhubala (1933–69), Indian actress. Died at age 36.
 * XXXTentacion (1998–2018), American rapper and singer-songwriter. Murdered aged 20
 * Asa Hartford (born 1950), still alive

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Ventricular septal defect