Al
`
`Date: Wed, 19 Apr 2000 11:06:15 —0500
`From: ovidweb@tioga.lso.missouri.edu
`
`To: hsl_ill@showme.missouri.edu
`Subject: Document Order
`
`Document Order
`
`Date 04/19/00‘_.__._....._‘., .
`
`, ..
`
`Source’Ovid
`
`.
`
`.1-
`
`.1... “MM—flu“- M.
`
`.
`
`UI
`
`Author Journal
`
`,
`
`,
`
`A
`
`Balloon dilatation (valvoplasty) as first line treatment for severe
`Title
`stenosis of the aortic valve in early infancy: median term results and
`
`survival (letter; comment].
`~
`
` determinant_
`
`Volume
`Issue
`
`Page
`ISSN
`
`-1
`0007~0769
`
`Year
`
`1994 Sep
`
`Local Msg Owned by MU HSL
`
`Fullname
`Campus Address
`
`Troy Norred MD
`
`Local Addresg_ *
`Phone
`
`882~7272
`
`Fax
`
`Email
`Comments
`
`norred99@aol.com
`
`Cardiology
`Dept/Major
`Faculty
`Status
`ID
`440807683
`
`
`Department
`Account Number
`
`Cardiology
`c—3—40120—11
`
`Delivery
`
`Mail
`
`_
`
`‘
`
`_
`
`,
`
`-
`
`,
`
`_
`
`,
`
`0
`
`'
`
`'
`
`NORRED EXHIBIT 2007 - Page 1
`
`Medtronic, Inc., Medtronic Vascular, Inc.,
`& Medtronic Corevalve, LLC
`v. Troy R. Norred, M.D.
`CaselPR201400110
`
`

`

`Al
`
`Date: Wed, 19 Apr 2000 11:06:15 —0500
`From: ovidweb@tioga.lso.missouri.edu
`
`To: hsl_ill@showme.missouri.edu
`Subject: Document Order
`
`Document Order
`
`Date 04/19/00‘_.__._....._‘.i .
`
`, ..
`
`Source’Ovid
`
`.
`
`.1-
`
`.1... “MM—flu“- M.
`
`.
`
`UI
`
`Author
`
`Journal
`
`
`
`,
`
`A
`
`,
`
`Balloon dilatation (valvoplasty) as first line treatment for severe
`Title
`stenosis of the aortic valve in early infancy: median term results and
`
` determinant_
`
`Volume
`Issue
`
`Page
`ISSN
`
`survival (letter; comment].
`~
`
`-1
`0007~0769
`
`Year
`
`1994 Sep
`
`Local Msg Owned by MU HSL
`
`Fullname
`Campus Address
`
`Troy Norred MD
`
`Local Addresg_ *
`Phone
`
`882—7272
`
`Fax
`
`Email
`Comments
`
`norred99@aol.com
`
`Cardiology
`Dept/Major
`Faculty
`Status
`ID
`440807683
`
`
`Department
`Account Number
`
`Cardiology
`c—3—40120—11
`
`Delivery
`
`Mail
`
`
`
`NORRED EXHIBIT 2007 - Page 1
`
`

`

`
`
`
`élfi“
`
`,.
`
`rK\\
`
`,,..\\1
`
`NORRED EXHIBIT 2007 - Page 2
`
`
`
`

`

`300
`
`Imaging the dissected aorta
`
`SIR,——~I read with interest and sympathy Mr
`Treasure’s editorial on imaging the dis-
`sected aorta.l I agree that it is a difficult to
`achieve a standard approach.
`I have found
`the following guidelines for acute dissection
`clinically reliable:
`(a) Type B dissection is defined as dis-
`section confined to the descending aorta~
`that is, any part of the aorta beyond the
`origin of the left subclavian artery.
`(b) Type A dissection is any dissection
`that involves the ascending aorta, whether
`or not it also affects the descending aorta,
`and irrespective of the site of entry.
`(5) Computed tomography (CT) is a reli-
`able technique for the detection and assess—
`ment of type B dissections. It
`is certainly
`more reliable than angiography. This is
`because the flap in type B dissections is usu—
`ally static and can be reliably imaged by
`CT, despite the fact
`that the true lumen
`may have regained a smooth, circular cross
`section.
`(d) In type A dissection the flap in the
`ascending aorta is often mobile, giving a sig-
`nificant
`incidence of false negative CT
`examinations, but nevertheless .
`.
`.
`(e) the ascending aorta is always dilated
`in type A dissection. If a dissection in the
`descending aorta is accompanied by an
`ascending aorta of normal size it is reason—
`able to exclude type A origin or extension of
`the false lumen.
`In passing,
`I would like to endorse the
`efificacy of transoesophageal sonography in
`the diagnosis of traumatic aortic tear, as
`described by de Belder et al.2 Indeed, I have
`yet to hear of a falsely negative study.
`IB PARTRIDGE
`Harefield Hospital,
`Harefield,
`Middlesex UB9 6]H
`
`1 Treasure T. Imaging the dissected aorta. Br
`Heart] 1993;70:497—8.
`2 de Belder A, Thomas M, Marrinan, M.
`Traumatic rupture of the thoracic aorta
`diagnosed by transoesophageal echocardio-
`graphy. Br Heart] 1993;70:393—411.
`
`This letter was sent to the author, who replies as
`follows:
`
`SIR,——Dr Partridge’s guidelines indicate his
`keen interest in this problem and that he
`has considered it carefully. I will address his
`points item by item.
`(a and b) In the original paper on which
`the Stanford classification is based‘ type B
`is defined as dissection that does not extend
`proximally to the subclavian artery.
`In a
`subsequent paper there was a subtle but
`important
`change
`in
`detail.2 Type A
`includes any dissection that
`involves the
`ascending aorta, just as Dr Partridge writes,
`but type B includes all the rest, thus includ-
`ing some cases with arch involvement.‘ 2
`No classification is perfect but the virtue
`of the current version of the classification is
`that it defines a group (type A) in which a
`challenging but achievable operation on the
`ascending aorta protects the patient from
`three lethal consequences of dissection at
`this site:
`0 Rupture into the pericardium
`0 Severe aorn'c valvar regurgitation
`0 Occlusion of the coronary ostia
`This reduces the risk from near 100% for
`type A to a much lower figure, made up of
`the risk of the operation itself and the risk
`
`associated with any residual uncorrected
`abnormality in the arch and descending
`aorta. Classification is an interesting disci~
`pline. In this instance type A is defined by
`inclusion of the particular characteristic-—
`that
`is,
`involvement of
`the
`ascending
`aorta-and type B is defined by exclusion of
`this characteristic. (5, d, and e) His observa~
`tions on the nuances of the interpretation of
`computed tomograms of the ascending and
`descending aorta are nicely observed and
`ring true.
`Although I had no data or experience on
`which to base a comment,
`I was worried
`when de Belder et al advocated trans—
`oesophageal echocardiography to diagnose a
`traumatic
`aortic
`tear.’ Dissection
`has
`length, so any cross sectional
`image will
`detect it. Traumatic aortic transection is a
`tear with an adjacent haematoma; it is not a
`propagating dissection. Because there are
`other sources of blood (rib and vertebral
`fractures)
`to cause
`the haematoma
`in
`trauma, it is visualisation of aortic wall dis—
`continuity that is critical. High specificity,
`that is confidently excluding the diagnosis
`when it
`is absent,
`is
`required. We have
`argued elsewhere‘ that the cross sectional
`image of CT cannot prove or exclude trau~
`matic
`aortic dissection.
`In a
`critically
`injured patient this makes CT an unneces-
`sary waste of time. The fact
`that
`trans—
`oesophageal echocardiography can be used
`at the bedside makes it attractive, provided
`a negative test is convincing and that any
`induced hypertension and local interference
`do not make the aorta go “pop”.
`TOM TREASURE
`Cardiac Department,
`St George ’5 Hospital,
`Blackshaw Road,
`London SW17 OQT
`
`1 Daily PO, Trueblood HW, Stinson EB,
`Wuerflein RD, Shumway NE. Management
`of acute aortic dissections. Ann Thorac Surg
`1970;10:237—47.
`.,
`,
`2 Miller DC, Stimson EB, Oyer PE, Rossiter S],
`Reitz BA, Griepp RB, Shumway NE.
`Operative treatment of aortic dissections. ]
`Thorac Cardiovasc Surg 1979;78:365—82.
`3 de Belder A, Thomas M, Marrinan M.
`Traumatic rupture of the thoracic aorta
`diagnosed by transoesophageal echocardio»
`graphy. Br Heart] 1993;70:393—4.
`4 Unsworth—White M], Buckenham T, Treasure
`T. Traumatic
`rupture of
`the
`thoracic
`aorta——computed tomography may be a
`dangerous waste of time. Ann R Coll Surg
`Engl (in press).
`
`Anthracyclines and the heart
`
`SIR,—I thank Dr Rhoden, Dr Hasleton, and
`Dr Brooks for an excellent review of anthra-
`cyclines and the heart.1
`I would like to point out an error. The
`evidence for doxorubicin—related cardiotoxi—
`city
`involving myocardial
`adrenergic
`derangement comes
`from mI-meta~iodo—
`benzylaguanidine (MIBG) rather than from
`mI»methoxy-isobutyl
`isonitrile
`(MIBI).2
`These radiopharrnaceuticals are quite dis-
`‘ similar. MIBG shares similar uptake mecha-
`nisms into sympathetic nerve endings as
`noradrenaline. It is therefore ideally suited
`to imaging both the distribution of sympa—
`thetic nerve endings in the heart as well as
`neuroendocrine tumours such as pheochro—
`mocytomas.“ MIBI is a myocardial perfu-
`sion agent available in cold kit form that is
`labelled with technetium~99m rather than
`with iodine-123. MIBI is a lipophilic agent
`taken up into myocytes independently of
`
`Letters
`
`the sympathetic nerve endings but roughly
`proportionally to myocardial blood flow.
`MIBI is therefore used to assess the patency
`of coronary arteries rather than the status of
`the sympathetic nervous system.’
`PAUL THOMAS
`Department of Nuclear Medicine,
`]ohn Hunter Hospital,
`Locked Bag 1,
`Newcastle [Mail Centry,
`NSW 2310,
`Australia
`
`We thank Dr Thomas for drawing attention to this
`error and we apologise to the authors of the review for
`introducing this mistake when the technical editor
`mistook the abbreviation [MIBG for MIBI. Authors
`can help us to avoid such mistakes by spelling out
`all
`abbretn'att‘ons
`and
`acronyms
`at
`the
`first
`mention—EDITOR
`
`Brooks N.
`P,
`l Rhoden. W, Hasleton
`Anthracyclines and the heart. Br Heart ]
`l993;70:499—502.
`2 Valdes—Olmos RA, Ten Bokkel—Huinuk WW,
`Greve IC, Hoefnagel CA. ml—MIBG and
`serial
`radionuclide
`angiocardiography in
`doxorubicin—related cardiotoxicity. Clt'n Nucl
`Med I992;I7:l63—7.
`3 Dae M. Scintigraphic assessment of cardiac
`innervation using iodinev123 metaiodoben—
`zylguanidine.
`In: Ernst E van der Wall,
`Sochor I-I, Righetti A, Niemeyer MG, eds.
`What’s new in cardiac imaging? Dordrecht:
`Kluwer Academic Publishers, 1992;377—85.
`4 Gross MD, Shapiro B, Thrall JH. Adrenal
`scintigraphy. In: Gottschalk A, Hofi‘er PB,
`Potchen E], eds. Diagnostic nuclear medi-
`cine, Baltimore William and Wilkins,
`1988;826—7.
`5 Rigo P, Larock M, Braat SI-I. Myocardial per-
`fusion imaging with teclmetium«99m isoni~
`triles: Attractive thallium substitutes? In:
`Ernst E van der Wall, et al eds. What’s new
`in cardiac
`imaging? Dordrecht: Kluwer
`Academic Publishers, 1992;69—85.
`
`Balloon dilatation (valvoplasty) as first
`line treatment for severe stenosis of the
`aortic valve in early infancy: median
`term results and determinants of sur-
`vrval
`
`SIR,—~In their otherwise excellent article
`Bu’Lock and her colleagues‘ do not give
`any details of the morphology of the aortic
`valve
`itself,
`specifically the number of
`leaflets. This matter
`is of
`importance
`because in the so—called unicommissural
`and unicuspid variant of aortic valvar steno-
`sis recent studies have shown that the leaflet
`tissue is attached within the aortic root in a
`circular rather than a semilunar fashion.2
`This arrangement would seem, on morpho-
`logical grounds, to militate against success-
`ful balloon dilatation: but morphologists are
`constantly wary of predicting outcomes in
`life from their observations on cadaveric
`hearts. For this reason it would be invalu—
`able to know whether Bu’Lock and her col‘
`leagues had information on the number of
`leaflets present in the valves dilated in their
`patients?
`ROBERT H ANDERSON
`Department of Paediatrics,
`Royal Brompton National Heart and
`Lung Institute, Dovehouse Street,
`London S W3 6LY
`
`l Bu’Lock FA, Joflfe HS, Jordan SC, Martin RP.
`Balloon dilatation (valvoplasty) as first
`line
`treatment for severe stenosis of the aortic
`valve in early infancy: medium term results
`and determinants of survival. Br Heart ]
`l993;70:546—53.
`2 McKay R, Smith A, Leung MP, Arnold R,
`Anderson RH, Morphology of the venu’icu»
`loaortic junction in critical aortic stenosis. ]
`Thorac Cardiovasc Sarg 1992;104:434—42.
`NORRED EXHIBIT 2007 - Page 3
`
`

`

`
`
`
`
`
`
`
`
`
`
`NORRED EXHIBIT 2007 - Page 4
`
`

`

`Letters
`
`This letter was shown to the authors, who reply
`as follows:
`
`Familial atrioventricular septal defect:
`possible genetic mechanism
`
`Sim—«We thank Professor Anderson for his
`pertinent
`reminder of the importance of
`morphological
`factors in congenital heart
`disease and their potential relevance to the
`treatment of patients with aortic stenosis.
`The reason that data on valve morphology
`were not included in our report is that we
`believe it is often difficult to be certain of
`leaflet morphology based solely on echocar—
`diography in neonates with severe aortic
`stenosis. The poor correlation between
`echocardiographic predictions and observed
`morphology at the time of surgery was well
`described in the paper by Leung and
`Anderson.‘
`In
`their
`study,
`echocardio—
`graphic examination of 20 infants with criti-
`cal
`aortic
`stenosis
`identified
`16 with
`bicuspid valves, four with tricuspid valves,
`and no unicuspid valves. This contrasts
`with the surgical
`findings
`in the same
`infants where six valves were described as
`unicuspid, 13 bicuspid, and 1 tricuspid.
`In the patients we studied,2 the aortic
`valve was considered to be bicuspid in six,
`tricuspid in five, and one may have had a
`unicuspid valve. Because
`few of
`these'
`patients had visual inspection of the aortic
`valve (either surgically or at necropsy) we
`are unable to comment on the validity of
`the echocardiographic findings. There did
`not seem to be any correlation between
`echocardiographieally
`determined
`valve
`morphology and outcome. The principal
`determinants of survival being left ventricu— .
`lar
`(rather than aortic valve) dimensions
`and presence and severity of associated
`lesions. The patient with the apparently
`unicuspid valve had an excellent response to
`balloon valvoplasty.
`It does, however, seem logical to believe
`that aortic valve morphology may have an
`important influence on the degree of relief
`of valve obstruction obtained,
`on
`the
`propensity for early re—stenosis, and on the
`maintenance of longer term valve compe-
`tence. Studies of the relation between valve
`morphology and the outcome of balloon
`dilatation might be of considerable interest.
`Precordial echocardiography may not be
`adequate
`for
`such cases, where
`trans-
`oesophageal echocardiography or intravas—
`cular ultrasound may be of additional value.
`F A BU’LOCK
`on behalf of
`H S jofle
`S C jordan
`R 1’ Martin
`Bristol Royal Hospital
`for Sick Children,
`St Michael’s Hill,
`Bristol 332 83]
`
`1 Leung MP, McKay R, Smith A, Anderson
`RH, Arnold R. Critical aortic stenosis in
`early infancy. ] Thorac Cardiovaxc Surg
`1991;101:526—35,
`2 Bu’Lock FA, Joffe HS, Jordan SC, Matin RP.
`Balloon dilatation (valvoplasty) as first line
`treatment for severe stenosis of the aortic
`valve in early infancy: medium term results
`and determinants of survival Br Heart I
`1993;70:546v53.
`
`the report of
`S1R,—We read with interest
`Kumar et al describing a family in which the
`mother and her two daughters by different
`fathers had atrioventricular septal defects
`not associated with trisomy 21.1 They sug-
`gest that an autosomal dominant pattern of
`inheritance may be involved in this pedi-
`gree, although a multifactorial or cytoplas~
`mic mechanism cannot be ruled out.
`in
`We recently described five families
`which two or more members had isolated
`atrioventricular septal defect. Parent-to—son
`transmission of concordant cardiac defect
`was documented in four cases. The mother
`was affected in three cases and the father in
`one.2
`Lately we found an additional example of
`atrioventricular septal defect in four mem-
`bers in two generations of the same family
`(figure). None of
`the
`family members
`showed phenotypic anomalies and all had a
`normal karyotype. They were examined by
`electrocardiography and echocardiography.
`A partial atrioventricular septal defect was
`diagnosed in one case (11 5) and a complete
`defect in two cases (111 1 and III 2). The
`daughter of a patient with atrioventricular
`septal defect had an isolated cleft of the
`mitral valve (111 3).
`Anatomical differences between isolated
`mitral' clefts and clefts associated with an
`atrioventricular
`septal defect have been
`described.3 The high frequency of isolated
`mitral cleft in families with atrioventricular
`septal defects,” including our family, and
`its prevalence in patients with Down’s syn—
`drome (4/420 1; 3/5200 in our experience),
`however, suggests that
`this malformation
`should be included in the spectrum of atrio-
`ventricular septal defects.
`Monogenic autosomal dominant inheri-
`tance with incomplete penetrance could
`explain the atrioventricular septal defects in
`the families we studied and those reported
`by other workers. Normal parents of
`affected children could be obligate caniers
`of the gene involved in familial atrioventric-
`ular septal defects. The father-to-daughter
`transmission of cardiac malformation in two
`cases excludes cytoplasmic inheritance in
`these families. Moreover, atrioventricular
`septal defects in patients with and without
`Down’s syndrome differ not only in terms
`of the prevalence of partial or complete
`forms"7 but also in terms of the distribution
`of
`associated
`cardiac malformations.”
`These
`anatomical
`differences
`and
`the
`absence of linkage in the molecular analysis
`of chromosome 21 in families with atrioven—
`tricular septal defect”‘° suggest
`that
`the
`gene or genes involved in the pathogenesis
`of atrioventricular septal defect in “normal”
`children are different from those in patients
`with Down’s syndrome.
`MARIA CRISTINA DIGILIO
`BRUNO MARINO
`ALDO GIANNOTTH
`BRUNO DALLAPICCOLA
`Paediatric Cardiology and Genetics,
`Otpedale Bambino Gert),
`00165 Rome, Italy
`
`
`
`
`
`
`
`O Female
`
`1:] Male a Dead
`
`m Atrioventricular septal defect
`
`0 Isolated cleft mitral valve
`
`Pedigree
`
`1 Kumar A, Williams CA, Victorica BE.
`Familial atrioventricular septal defect: possi-
`ble genetic mechanisms. Br Heart I 1994;
`71:79—81.
`2 Digilio MC, Marino B, Cicini MP, Giannotti
`A, Formigari R, Dallapiccola B. Risk of con—
`genital heart defects in relatives of patients
`with atrioventricular canal. Am 7 Di: Child
`1993;147:1295—7.
`3 Smallhorn IF, DeLeval M, Stark J, Somerville
`J, Tylor JFN, Anderson RH, et al. Isolated
`anterior mitral
`cleft:
`two
`dimensional
`echocardiographic assessment and differen-
`tiation from “clefts” associated with atrio-
`ventricular
`septal
`defect. Br Heart I
`1982;48:109‘16.
`4 Disegni E, Pierpont MEM, Bass IL, Kaplinksy
`E. Two dimensional echocardiography in
`detection of endocardial cushion defect
`in
`families. Am ] Cardiol 1985;55:1649—52.
`5 Cousineau AJ, Lauer RM, Pierpont ME,
`Bums TL, Ardinger RH,
`21 al. Linkage
`analysis of autosomal dominant atrioventric—
`ular canal defects: exclusion of chromosome
`21. Hum Genet 1994;93:103—8.
`6 Marino B, Vairo U, Como A, Nava S,
`Guccione P, Calabro R, Marcelletti C.
`Atrioventricular canal in Down’s syndrome.
`Am 7 Dis Child 1990;144:1120—2.
`JA.
`7 Carmi
`R1
`Ferencz C, Boughman
`Endocardial cushion defect: further studies
`of “Isolated" versus “syndromic” occur-
`rence. Aijed Genet 1992;43:569~75.
`8 De Biase L, Di Ciommo L, Ballerini L,
`Bevilacqua M, Marcelletti C, Man'no B.
`Prevalence of left-sided obstruction lesion in
`patient with atrioventricular canal without
`Down’s syndrome. 7 Thorac Cardiovasc Surg
`1986;91:467—70.
`9 Wilson 1., Curtis A, Korenberg JR, Schipper
`RD, Allan L, Chenevix~Trench G, er al. A
`large, dominant pedigree of atrioventricular
`septal defect (AVSD): exclusion from the
`Down’s syndrome critical region on chro-
`mosome 21, Am ] Hum Genet 1994;53:
`1262—8.
`S, Digilio MC, Marino B,
`10 Melchionda
`Giannotti A, Mingarelli R, Dallapiccola B.
`Analisi di linkage con marcatori de11e regioni
`Zlq ed 8p in una famiglia con canale atrio-
`ventricolare. G Ital Cardiol 1993;23:7.
`
`NORRED EXHIBIT 2007 - Page 5
`
`

`

`
`
`
`
`
`
`
`
`
`
`NORRED EXHIBIT 2007 - Page 6
`
`