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Re: REGURITATION
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Re: REGURITATION

Posted By dsm on July 07, 1999 at 10:27:11
I HAVE MILD REGURG ON SEVERAL VALVES.  CAN I EXPECT THIS TO BECOME MORE SEVERE AS TIME GOES ON?  AT WHAT POINT IS A VSD BAD ENOUGH TO WARRANT REPAIR VS LEAVING IT ALONE?  WILL A VSD EVENTUALLY CAUSE THE HEART TO GROW IN SIZE?  SEVERAL WEEKS AGO I DID SOMETHINGS THAT WERE NOT TO STRESSFULL AT ALL.  AN HOUR AFTER DOING IT I HAD A BP OF 100/70 AND A PULSE OF 150.  I HAD A BAD HEADACHE AND DIZZINESS ALONG WITH THIS.  THIS IS HAPPENING MORE OFTEN THAN IT USED TO.  COULD THIS BE CAUSED FROM MORE REGURG, VSD  OR WHAT.





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Posted By CCF CARDIO MD - CRC on July 08, 1999 at 10:45:29

Dear DSM,
Thank you for your question.  Both VSD and valve regurgitation may need surgical repair and your doctor can tell you if this is necessary.  I'm not sure what the cause of your symptoms is but I would have it evaluated.  The following is some general information about VSDs and may be somewhat technical so feel free to write back if there are things you don't understand.  
The isolated VSD is the most common congenital defect seen in the pediatric population. For anatomic classification, the interventricular septum can be divided into four regions. Defects of the membranous septum or infracristal VSDs, located in the left ventricular outflow beneath the aortic valve, account for up to 80% of VSDs. The membranous septum itself is small and is located posterior to the conal septum, below the crista supraventricularis. These VSDs typically show a variable degree of extension into the inlet or outlet septum, hence their designation as "perimembranous." Infundibular defects or supracristal outlet VSDs occur in the conal septum above the crista supraventricularis and below the pulmonary valve. Inlet defects are identified at the crux of the heart between the tricuspid and mitral valves and are usually associated with other anomalies of the atrioventricular canal. Defects of the trabecular or muscular septum can be multiple and occur distal to the septal attachment of the tricuspid valve and towards the apex.  
Outcome
The clinical course of ventricular septal defects depend on the size of the defect and the pulmonary vascular bed, both of which can change with time. Unlike atrial septal defects, spontaneous closure of ventricular septal defects can occur and does so as a function of native defect size, anatomy, and patient age. Approximately half of all VSDs are small and up to 75% of those will close spontaneously. Five percent to 10% of moderate or even large VSDs may also undergo some degree of spontaneous closure. Trabecular muscular septal defects may close more frequently than perimembranous defects, while closure of outlet defects is least common. The highest closure rates are observed in the first year of life. Ninety per cent of VSD destined to close will have done so by age 10, while spontaneous closure in adult life is unusual but reported.
The physiologic severity of VSDs takes into account the pulmonary-to-systemic flow ratios (Qp:Qs), the main pulmonary artery pressure (MPAP), and the ratio of pulmonary-to-systemic vascular resistance (Rp:Rs). Ventricular septal defects can be classified based on the criteria used in the First Natural History Study of Congenital Heart Defects. Patients in group I have trivial or mild shunts with a Qp:Qs ratio of <1.5 and a mean MPAP of <20 mm Patients in group II have moderate defects with a Qp:Qs ratio of < 1.2. a mean MPAP  20 mm Hg but an Rp:Rs ratio of <2. Patients in group III have severe defects with an MPAP  20 mm Hg .and Rp:Rs ratio between .2 and .7. Patients in group IV have Eisenmenger's physiology with a systemic or near-systemic MPAP, a pulmonary vascular resistance which is greater than 2/3 systemic resistance, and a right-to-left shunt or a left-to-right shunt with a Qp:Qs of <1.2.
Minimal or mild defects can be expected to cause no significant physiologic abnormality. A moderate or severe defect will cause volume loading of the left heart. Left atrial and ventricular dilatation occur as a function of the degree of left-to-right shunting. Shunting across the ventricular septum occurs predominantly during systole when left ventricular pressure exceeds that on the right. The first intracardiac chamber to sustain a significant diastolic filling abnormality is the left atrium. With moderate or severe defects, the right heart becomes secondarily affected as a function of the rise in pulmonary pressure. Note that this is in contrast to shunting at the atrial level where the right atrium and ventricle tolerate both primary volume and secondary pressure loading. An approximate 10% of patients with ventricular septal defects develop Eisenmenger's complex, typically during the first decade when pulmonary vascular resistance rises progressively to exceed systemic levels resulting in shunt reversal. The majority of patients with Eisenmenger's physiology are said to have nonrestrictive defects. By definition this means that there is no resistance to flow at the level of the defect per se. Typically the defect is as large as the aorta, pressures in both ventricles are equal, and the degree of shunting is determined by the ratio of pulmonary to vascular resistances. This has two major implications: the first is that the pulmonary vascular bed is exposed directly to systemic pressures in the left ventricle, resulting in an accelerated rise in pulmonary pressure and resistance; the second is that, likewise, the right ventricle is directly exposed to pressure overload early in life. In the simplest terms a restrictive VSD is one through which there exists a systolic pressure gradient between both ventricles in the absence of right ventricular outflow tract obstruction. In physiologic terms this is useful insofar as it indicates that there is a resistance to left-to-right shunting at the ventricular septal level and that the size of the defect is less than that of the aorta. It follows that in terms of physiologic severity a "restrictive" defect is often trivial, mild, or moderate but can also be severe as long as the pressure between both ventricles has not equalized.
Management
The First Natural History Study of Congenital Heart Defects enrolled 1,280 patients with ventricular septal defects from 1958 to 1969. The overall 25-year survival rate for all patients managed with medical or surgical therapy is 87%, with mortality rates increasing with the severity of the VSD. Adult presentation is most frequently that of a small restrictive VSD, native or post-surgical, or that of a large unoperated VSD with Eisenmenger's complex.
Patients with Eisenmenger's complex can survive into the fourth decade. The focus of management for patients with Eisenmenger's complex will center around the medical complications of cyanosis . These include death due to intracardiac or pulmonary complications, prevention of infective endocarditis   , and systemic complications related to the neurological, hematological, and renal systems. These issues are discussed in this chapter as part of a discussion of the medical complications of cyanosis applicable to all patients with Eisenmenger's syndrome. Excluding those with Eisenmenger's physiology, the majority of unoperated patients will have had a mild VSD in infancy or childhood and therefore have a favorable long-term prognosis. Late results following operative closure of isolated ventricular septal defects show residual patency in up to 20% of cases but with only a 5% incidence of need for reoperation, indicating that most residual surgical defects are small. For small residual defects-native or surgical-the management revolves around endocarditis prophylaxis and complications related to secondary valvular anomalies. Perimembranous defects may regress in size through aneurysm formation by engaging part of the septal tricuspid leaflet, resulting in secondary tricuspid insufficiency. Prolapse of the right or noncoronary cusp results in acquired aortic valve disease in about 2% of patients, regardless of surgical status. This occurs most frequently with subarterial outlet VSDs but also with perimembranous and inlet defects. The surgical management of this group of patients is controversial and needs to take into account the location of the VSD, the degree of aortic regurgitation, and the patient's age. Hence, for a substrate of patients with small VSDs, the potential for progressive valvular insufficiency necessitates careful consideration and follow-up even after the defect is closed.
In general, and taking into account that patients with VSDs constitute one of the first groups to undergo complete intracardiac repair, the overall status of this patient population is good to excellent. Clearly this is encouraging but does not obviate the need for regular supervision and follow-up.
I hope you find this information useful.  Information provided in the heart forum is for general purposes only.  Only your physician can provide specific diagnoses and therapies.  Please feel free to write back with additional questions.
If you would like to make an appointment at the Cleveland Clinic Heart Center, please call 1-800-CCF-CARE or inquire online by using the Heart Center website at www.ccf.org/heartcenter.  The Heart Center website contains a directory of the cardiology staff that can be used to select the physician best suited to address your cardiac problem.











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