Stanford 1
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| name 2 braided and 2 monofil nonabsorb sutures | braided: silk, ethibond; monofil: prolene, nylon
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| name 4 absorb sutures | chromic/plain gut, vicryl (braided), monocryl (monofil), PDS (monofil)
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| name 2 categories of lvls of evidence | size of the effect (I-III), certainty/precision of tx effect (A-C)
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| describe categories for size of effect for EBM | I: benefit >> risk, II: benefit>risk; III: risk> or = benefit
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| describe categories for certainty/precision tx effect for EBM | A=mltpl RCTs or meta analysis (mltpl popul analyzed), B=1 RCT or mltpl nonRCTs, C=consensus opinion, case studies or std of care
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| indications for sx for asympt AS and lvl of evidence (4) | Class IC: if severe AS w other sx or EF 50% or less; Class IIbC: severe AS w abnl response to exercise (can't incrsd SBP 20); Class IIaB: mod AS w other sx
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| periop mortality AVR, incl if also CABG | 3-4% (STS database), 6% if also CABG
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| risk factors for rapid progression in AS | >50yo, severe Ca++, CAD,
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| avg change in severe AS velocity jet and AVA | change in velocity 0.3 m/s/yr, AVA 0.1 cm^2
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| describe Gorlin conundrum | formula for AVA doesn't calculate AVA well in low flow states
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| better ways to assess AS in low flow states | AV resistance and stroke work loss
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| likelihood severe asympt AS will be free of sympt 5y | 50%
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| once sympt present in AS survival | angina 3 yrs, symcope 2y, CHF 1.5y
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| term for pulse in AS | parvus et tardus
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| Gorlin eqn | CO/(HR x ejxn time x 44.3 x mean gradient)
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| describe Moore study on prosthetic pt mismatch in AVR | affects survival if <70yo (although Dartmouth grp showed difft results if use geomet dimensions)
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| describe cutoffs for prosthetic pt mismatch | severe EOA/BSA <0.65, moderate 0.65-0.85
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| cut offs for AS jet velocity, mean gradient, AVA | jet velocity, gradient, AVA: mild= <3, <25, <1.5; severe= >4, >40, <1
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| what is the AVA index for severe AS | <0.6
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| MC BAV | Type I L-R (71% in Stanford study)--also assoc w coarct
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| genetics assoc w BAV | eNOS thgt assoc, NOTCH involved in BAV and Ca++, ACTA2 SMaA famTAAA and dissections and BAV
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| % coarct w BAV | 50-75%
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| Sievers Ross v AVR study | used propensity matching and no diff survival and both same as general population--but Ross had more reoperations, no diff in thromboembol
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| Yacoub Ross v homograft study | at 10yrs homograft did worse and transvalv gradient steadily incrsd; Ross did same as gen population
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| what % severe AS don't undergo surgery | 30%
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| pts enrolled in Ib part of Partner trial | severe AS AVA 0.8, grad 40, velocity 4, inoperable=10% STS risk score or predicted death 15% 30d; exclusion: >3 AR, BAV, no Ca++, EF <20%, CAD needing revasc
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| results Ib Partner | 1 yr mortality 30.7% v 50.7%; 30d TAVI had higher stroke (5% v 1.1%) and vascular cxns (16.2 v 1.1%). 11% mod or severe paravalv regurg
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| which valve used Partner | Sapien
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| cut offs for MS (mean gradient, PA SP, valve area) | mean gradient, PA SP, valve area: mild <5, <30, >1,5; severe >10, >50, <1
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| what's nml MV area | 4-5
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| timeline of MS s/p RhF | 20-40y, once limiting sympt survival 0-15% 10y and once pul HTN mean survival 3yrs
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| indication for sx in MS | Class IB NYHA III-IV mod or severe MS; CLassIC mod or severe MS + mod or severe MR; Class IIaC: severe MS + PASP >60, NYHA I-II
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| how much does MA contract and timing | 20-40%, 89% occurs before LV cxn, which depends on strength and duration of atrial cxn
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| describe MV leaflet open and closure | leaf open starts in ctr w edges still opposed, middle then commissures…leaf closure initiated by LA cxn
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| cut offs for AR (angio grade, vena contracta width, regurg vol, regurg %, ERO) | (grade, VC width, regurg vol, regurg %, ERO): mild: 1+, <0.3, <30, <30, <0.1; severe= 3/4+, >0.6, 60, 50, 0.3
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| how does heart compensate for AR at sarcomere lvl | sarcomere added in series so nml preload at sarcomere lvl, but incrsd wall stress (incrsd chamber size), also incrsd afterload leads to hypertrophy…so both P and vol overload
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| indications sx for AR | Class I: sympt, chronic severe; chronic severe asympt if EF<50 (Class I) or ES >50 (Class IIb); if moderate AR and sx on asc Ao or CABG (Class IIb)
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| what's the name of bobbing head sign in AR | de Musset sign
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| name of pulse in AR | Corrigans pulse or water hammer P (bounding pulse)
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| name of murmur in AR | Austin Flint (1836-1915, president of AMA 1884)
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| med tx for AR | afterload reduction w ACEI/nifedipine to reduce SBP, but don't use if no HTN
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| describe what happens in IVC in AV fxn | just before AV opens Ao root expansion helps leaflets open, NC (connected to fibrous part MVAC) expands least, also longitudinal expansion of root
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| describe what happens AV during ejxn | ann cxn (NC least), while commissures continue to expand (Lansac found base cont'd to expand), LC and NC clockwise torsion, RC CC. amt of torsion predict dP/dt while EF predicted ann cxn
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| describe what happens AV during IVR | ann cxn asymm, commissures symm, longitudinal compression, when min LVP decrses work shifted to L base
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| describe what happens AV during diastole | just recoil
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| what's the diff dynamics and kinematics | kinematics is 3D location, by understanding dynamics (constitutive eqns) given boundary conditions can solve for kinematics
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| types of MR by Carpentier classif | I=nml leaflet motion , annular dilation or endocarditis; II=prolapse, floppy MV w chord elong/rupture; III=restricted motion, A=diastole, B=systole, in rheum A+B, IMR=B, DCM=B + annular dilation
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| % of CHF w FMR. % FMR s/p inferior MI | 40% of CHF and 40% inferior infarct (bc PM pap displaced laterally)
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| causes of MR in W Countries | 70% degen w prolapse, 20% ischemic w tenting, 2-5% ea endocarditis and rheym
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| cut off to consider MVP | 2mm above annulus
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| cut offs MR (angio, VC width, MR vol, MR %, ERO) | (grade, VC width, regurg vol, regurg %, ERO): mild: 1+, <0.3, <30, <30, <0.2; severe= 3/4+, >0.7, 60, 50, 0.4…same as AR exc upper end of VC width and ERO
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| indications sx for MR | ClassIB: acute severe sympt, chronic severe sympt NYHA II-IV EF>30% and/or ES >55, asympt chronic severe EF 30-60% and/or ES >40; ClassIIaB: asympt chronic severe EF>60%, ES <40 if repair >90%
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| how much EF change s/p surgery | decrs 10%
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| recurrence of MR after surgery | IMR annuloplasty (95% + CABG) in Cleveland incrs 3/4+ MR from 13 to 28% at 6mos…similar for difft ring types and smaller rings don't help
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| LA and LV measurements that predict outcome | LA vol >40 means severe MR and predicts A fib; LVESVI >30ml/m^2 poor outcome
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| how does MVP murmur change w loading | midsys click w late sys murmur, incrsd w standing and valsalva, decrs w squatting (same as HOCM and opposite of MR), handgrip incrses MVP murmur and decrses HOCM
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| describe Crawford classif aneur | I=desc thoracic, II=desc and infrarenal **highest risk paraplegia, III=distal desc and infrarenal, IV=infrarenal
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| describe deBakey classif | I=asc and desc, MC and worst px, II=asc, III=desc (b if also infrarenal)
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| indication surgery TAAA | TAV asc 5.5, desc 6.5; MFS/BAV asc 5, desc 6; LDS: 4.5…4.5 if AV surgery, >1cm/yr grwth, dissection
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| indications AAA surgery | 5.5cm or 2x nml, >0.5cm/6mo, any sympt
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| types of endoleak | I=seal (prox or distal), II=bw branch vessel and sneur sac, ie IMA or intercostal, III=through graft, IV=incrs size aneur sac endotension
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| preop mgmt of aneur/dissxn | MAP 60-80, HR 60, metoprolol, no SNP (decrsd afterload incrses shear and dP/dt)…decrsd SBP is to prevent rupture and anti impulse (decrs dP/dt)
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| % dissxn w/o tear, how occurs | 13% no tear, thgt intramural hematoma from bleeding of vasa vasorum
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| where dissxn tear in acute A | R anterior and sprials
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| preop malperf acute A, how relates to mortality | Mohr 2009, if preop malperf 30% early mortality (v 14%), cor malperf and visceral worst; 48% cor resolve incl 60% paraplegia
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| outcome for visceral malperf in acute A | 75% in hospital mortality
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| overall mortality Acute A dissxn | 1-2%/hr, used to be 50% 48h, now if make 24hr, 10-20% 2d-5d, then 1%/d
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| how many Acute A present w CP | 15-20%
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| how many Acute A present w AI | 75% but in 85% can save native AV
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| when take acute B dissxn to surgery | if rupture or intractable pain. Rupture actually did not incrs risk cxns or mortality
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| op mortality Acute B Coselli | 22% and 6% paraplegia
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| mgmt desc thoracic asympt and inoperable | no TEVAR, Demers Stanford study 2004, 5yr TEVAR 31% v 78% if operable (no comparison no tx v TEVAR)
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| % aneur undiagnosed | 85%
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| when is risk death highest s/p dissxn | first 2 yrs
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| how many ppl get new aneury s/p dissxn | 20% get new aneur from dilation of residual false lumen
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| who used cellophane to wrap aneur | Abott and Paulin in 1949
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| name for cystic medial degen | Erdheim dystic medial degen
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| BAV and types of arches | I=Ao root (13%), II=incl tubular asc Ao (14%), III=tubular and trvrs (28%), IV=root, asc, trvrs (45%)
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| should BAV Ao be replaced sooner | Class C, know BAV Ao abnl, grow more quickly, dissxn younger, but Yale study showed similar rate rupture, dissxn + better longterm survival (younger, healthier)…cxns not at smaller dia
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| endovascular v med tx for uncomplicated B dissxn | INSTEAD trial showed no diff 2yr
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| how much do Ao expand s/p TEVAR | 0.1cm/y asc, 0.3cm/yr desc and exacerbated by patent intercostals…tendency to dilate bc applies radial force
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| what % dissxn have MFS | 5-9%
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| % of MFS sporadic mutation, overall incidence MFS | up to 25%, overall incidence 1:5,000
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| who MFS named after, and when gene discovered | Antoine Marfan Fr pediatrician in 1896 who noticed in little girl, gene discovered 1991
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| systemic features MFS | arachnodactyly, high palate, jt hypermobility, flat feet, ectopia lentis, hernias, MVP, PTX, pectus, scoliosis
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| role of fibrillin in eye | ciliary zonules
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| key diff Loeys Dietz and MFS | hypertelorism, cleft palate/bifid uvula, aterial tortuosity, club feet, thin velvety skin w easy bruising, more diffuse medial degen
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| mutation in LDS and how relates to TGFb signaling | TGFbR1,2 but increasd pSMAD2 suggests TGFb signalling is upregulated
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| what rescues phenotype LDS in mice | losartan by blocking TGFb
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| how freq famTAA in TAA, genetics | 19% TAA have 1st degree relative w TAA, present younger, assoc w TGFbR1,2; ACTA2, if also PDA assoc w MVHII
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| what's arterial tortuosity syn? Genetics | AR glu transporter mutated (SLC2A10) and incrsd TGFb; they have facial dysmorphism
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| mutation in Ehlers Danlos IV | vascular type of Ehlers Danlos, mutation Col III have pale translucent skin
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| decsribe kyphoscoliosis type of Ehlers Danlos | type VI, due to lysyl hydroxylase mutation, fragile eyes and mscl wknss, very rare
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| name 3 other syndromes w FBN mutations | 1) Shprintezene Goldberg (craniostenosis, MR; FBN1 and others); 2) Weille Marchesani (spherophakia round eyes, brachydactyly, stiff jt; FBN1); 3) Congen contractural arachno (crumpled ears, contractures; FBN2)
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| describe features and genetics of homocystinuria | AR defect cystathionine synthase defic, Marfanoid w/o arachnodactyly, dwnwrd subluxation, hypercoag, MV/AV regurg w/o Ao dilation, MR, scoliosis, large stiff jts, often blond, blue eyed
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| dx and tx homocystinuria | dx: decrsd methionine in urine and blood, tx B6 cofactor helps convert homocysteine to cystathionine, diet restrict methionine, ASA
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