stats/ structural/ IVUS-oct Flashcards
precision in improved as _____. _____increased
how is prcision estimated in stats terms
sample size
tighter CI’s
- when there are big outliers or the distribution isnt normal what is better median or mean.
- MC used meaure of variabilty for a guassian aa nomral distribution
- when filling in missing data with multiple imputation what is key assumption
- internal vs. external validity?
- how can one determine external validity?
- Why is ITT so favored?
- do rcts established causation?
- median
2 standard deviation
- That the missing data must be missing at random.
- internal vs. external validity? internal-> sound study design and results. external generalizaiblity
- use registry data to confirm an RCTs result
- It is the only method to gaurantee and ubiased estimate of treatment effect. bc altering treatment group after randomization inherently biasisi the results.
by statistical dogma should you compare baseline charateristics in an RCT by p value
No, bc of some bullshit about source derivation
3 factors that go into making a balanced trial
- randomization
- outcome detection are done in a balanced manner between the groups. (ie blinding )
- missing data must be minimzed.
How do determine noninferiority statistically
The upper 95% CI cannto include the noniferiority boundary. Setting these boundaries are controveral.
- How is bayseanstatistics different fromStandard?
- Baysean Analysis Utilizes prior probability distribution based on what is known And reCalbraith these probabilities in light of experimental results
False positive rate pneumonic
False negative trial
alpha error (FAST) - Fasle Alpha statisitcal test - alpha is first so this is type one error.
False negative trial –> beta error…(type II error the other one is the other one)
alpha error
false positive test (FAST)
type I error =
What is it preset as in trials
How do you thing of it?
alpha error - False positive staisitical test
0.05 althought it looks like the p value it is a different concept, it is the probablity before the trial starts that the result would be a false positive
If you repeated the trial 100 x then 95% of the time or more the result would be the same
Beta error what is it
false negative rate (probablity of a false negative trial). This is also type II error.
power is what
1-Beta error aka ture postive rate
True postive rate
1-Beta error or Power
Power is the abillty to show a difference when one exists.
RR calc
(control relative risk - exper RR)/ CRR
SIHD major updates.
- prior to PCI for SICHD need to do this?
- Rule of thumb regarding deferring intervention?
- Rule of thumb regarding FFR of a lsions
- when to do stress after cabg per guidelines in asx. overall exercise and imaging studies should only be done when therre is a change in clinical status not annualy.
- trial medical therapy
- choose it.
- choose it.
- after 5 years its reasonable
change in GL on aspiration thrombectomy and embol
- total increase in stroke now class III
- embolic protection still reasonable in SVG Ib (european gl dropped it but not ours, bc the data that causes the european gl didnt make sense. )
GL changes non infacrt artery at time of STEMI
now pci should not be performed in seeting of shock
Can perform in STEMI as long as not as in shock (hasnt made guidleins)
AUC NSTEMI/US what constitute high risk features for nonfateal MI or death
TIMI/GRACE risk score
accelerating sx
age
character of pain
ecg change
bio markers
What does fred welt do regarding pt with lysis and 50% reduction in stemi and imrpvoed paoin
he calls in the team and waits the 3 -12 hours post (he’s lying).
CCS class in most trecent gl
now lumped together.
determing Stress test risk category high risk (5
High risk
- LV EF < 35%
- resting perfousion abn > 10%
- stress ECG including > 2 mm ST depression at low workload or presisting into recovery or STE
- TID
- WMA/ ischemia 2 oronary beds or LM
CAC > 400
CAC score impt high risk
400
400
CAC score high risk
to be fully appropriate for p lad in SCIHD with pLAD + another vessel need what for PCI
basically need to have high risk stress or DM and need to be sx or ffr +
LM disease PCI for boards
generally for ostial or midvessel -otherwwise be conservative
2 high risk surgerys
cross clamp aortas asnd substantial bleeding.
Hernias
cataracts low risk
functional capactiy able to send to surgery if intermediate risk
4 mets
A few stairs, light running, golf, dancing, doubles
Dicrotic notch represents what
Dicrotic notch is Ao closure.
AS gradient wiggins diagram
Big gradient, loss of anacrotic notch (point C), delacyed upstroke from C to peak in diagram
c= Ao opending and end of isovolumetric contraction.
Gorlin
and
HAaki
Gorlin
AVA = CO/Systolic ejection time *HR*44.3* sq root of mean gradient
Haaki
CO/ sq of p-p gradien
ie 6/ sq of 36 = 1
give hakki again
exclusion of haaki
CO/ Sq peak to peak
Need HR to be normal.
Big hint on hemodynamics that there is a hug prob after tavr
matching of LV end diastolic pressure. and aortic diastolic
Charterisks of hocm on wiggins (2)
spike and dome, early ejection and delayed obstruction. (very strange systolic upstroe)
Brunwald braunbraun - increase in gradient and spike and dome on the aortic tracing. in AS have increase in both Ao and LV gradients but no change in p-p
Braunawauld brokenbrough
PVC AS no change in peak to peal gradient (both trancing increase due to increase contractilituy on post pvc beat due to delay and increased calcium
in HOCM get a big increase in gradient with spike and dome on aortic (lower tracing.
Summaries gradient and areas for vavle lesions
AS
MS
PS
TS (mean)
Coarc (mean)
subas (mean)
AS - 40 mmHG mean, AVA <1
MS 10 mean, 1.5 mVA
PS > 30 and 60 peak if sx, 40 and 70 if no sx
TS >5 mean
coarc 20
Sub as 30
TS mean gradient for intervention
5 mmhg
coarc p-p for intervention
20 mmhg mean change
subAS mean gradient need surgery
30 mmHG
Tamponade hemodynamic findings
pericardial pressure approches RA pressure
pulsus paradox on Ao tracing
Intraventicular interdendence. however no dip and platau in constriction.
intracardiac shunt math
Qp = Sat ao- sat VC/ Sat PV - Sat PA
Higher sats go infrom, Q p terms go in denominator despite p bing in numberator
normal pericardial pressure
-5 to +5 mmHg
pulsus that is sig\
tamponade RA pressure tacing
10 mmg, 10 mmg drop with inspriation
big X drop with no y descent.
Where dont wire with pericardial tap
exiting the pericardium into the pulmonary tree
Kussmals sign
increased JVP with inspiration - reflective wave bc heart cant relax with incrased volume with insp.
How to tell constriction and restriction
draw lines and they should be going oppositie from the peaks of the wave tracings.
buzz word for constricution (2)
dip (y decentl/ late) and platau aka square root sign
dip and platau
constriction
RR calc
OR calc
divid the two probablities of events fro the two groops
prob of an outcome occuring in one groop divided by the prob of the event not occuring in the same group then dividing this by the same in the other group.
RR what is in numberator
RRR
experimaental in general
100*1-RR
RRR calc
100*1-RR
when RR = Exp pro/control exp
When is OR used
retrospective studys when number of people exposed unkonw.
def power
1-B
probablity of detecting a difference if one does exist try to do at 80% power.
sensitivity
Specifiity
PPV
NPV
4 x 4 with positives in the right hand coroncer and disease on top
DZ
test A B
C D
sens - pos test in someone with dz
spe neg test witout dz
ppv detecting dz in someone with a pos test
NPV non detectivn dz in those with a negative test
Sens A/A+C
spe D/D+B.
PPCV a/A+b
NPV D/D+c
NPV and PPV are demendent on
Sens and spe depend on
the prevalence (think of the indiviular), this varies bacsed on prevalence
nothing, spe and sens are fixed for the test
Angio type ABC lesion: Describe
- Type A: Less than 10 mm Non-angulated no thrombusNo side branch smoothNot totally included.
- Type B: Moderate to heavy calcium, nRhombus, Fabrication angulated
- Type C: (low success), long >20 mm. inability to protect side branch vein graph, excessive toruositiy., long < 20 mm, CTO
SYNTAX SCORE WHAT LEVEL SEND TO CABG
>33 BYPASS BETTER THAN PCI
OCT MOA
near infra red
IVUS vs. OCT
- Wavelenght
IVUS OCT
Wavelenght 35-80 vs. 1.3
Resolution 100 um vs. 15 um (so OCT at least 10 x better)
frame rate 30 vs. 100
pull bac rate 1 mm/s vs. 20
penetration max 10 vs. 2.35 mm (IVUS can penetrate further except in ca)
What has better tissue penetration IVUS or OCT
IVUS
IVUS vs. OCT measurements
IVUS estimates 8% bigger.
IVUS MLA for stenting
5.9 (litro study)
What is the 8765 rule
> 8 mm LM, poc 7mm, LAD 6, LCX ostium 5 mm
- all LM need IVUS.
3 impt trials with improved outcomes with IVUS
Ultimate and IVUS XPL –> MACE and TLR,
also metaanalysis
- Exposure equation
- New II form
- mA*KVP*pulse width
- Thin film transistor array
mag views raditaion
greater
ionizing radiation def
raditatoin enrought energy to eject at leat one orbiatl elevtron.
radiation terms
- stochastic -
- nonstochastic –
- ALARA
- effectvie dose-
- stochastic - all on non effect from radiation (dna injry that leas to cancer/mutation
- nonstochastic –> dna injuery that lead to cell dealb
- ALARA
- effectvie dose- stochastic reisk derived from weighted sums of estimates for indivisl organs.
exposure is measured how?
absorbed dose
equivalnt dose
effective dose
air erma measured in gy , 1 kg of air relaseas 1 joule of energy
amt of energy deposited in tissue gy/kg (depends on tissue gy/g)
equivalent dose- ionizing radiation cuasing varying injury depending on type ED=AD *weighting factor (siverts) –> biologic effects is seiverst
Effecitve dose - estimate of stochastic risk per obsorbed unit. Depensd on depth of beam from the the entrence point.
sieverts
think of biologic as biologive effect –dna damage etc.
direct skin eposure
250 cxr per minut 10 mSV per minute cine increase 10x
osmolality
molecules per volume
increase osmolality increased SE
- current contrast ionic or non?
- acute hypersensiticivty anaphylactic
- Arterial vs. venous
- shellfish
- people with allergies
- nonionic
- no anaphylactoid non-IGE
- venous
- dont pretreat. allergies to shellfish are not to iodine they are to other proteins.
- allergies - more liely to have reaction than non allergenic individuals
- ACC recd for pretreatment
- Rx of anaphylaxis
- Rash rx
- 50 mg pred 13,7,1 hr before can also give 200 mgiv 200 2 hours before. Benadryl and other antihistamines
- fluids fluids fluids
epi
- steroids and antihistamines
- delayed hypersens and cath
- delayed is mostly manifested as a -
- hyperthroidroid and contrast
- can happen its IgE mediated (up to 4%), dont forget about this bc freq blame on new drug added.
- rash.
- board question but quite rate (would have a goiter or a hx of issues.
Nephrotox
- when?
- hydration
- if op when check
- metformin
- 48-72 hours
- 1.5 to 1 ml/g/hr 3-12 hours prior and 6-12 hours post.
- 48-72 hrs
- lactic acidosis, hold on day of procedure
stochastic effects thing
dna damage leading to cancer and genetic risks (all or none)
Increasing mA of xray generator
what has more xrays crani or caudal
- mA is current–> current is number of electrons, number of xrays emitted for the catholode
crani has more
femoral instead of dual lumen
overshoot and delated (wave expansion. will falsly decrease gradient.
thermodilation - bad with
co equation (simple)
how can use above for angiographic co
- TR and PR, error 5-10%,
Co = HR x SV
SV =EDV-ESV CO=HR*SV
Fick method= PV-PA O2 difference PBF = SBF
fick eq
125/13.4*hb*PaO2 difference X100
LV and Ao pressure are the same
acute AI
peal tp peak for haaki for mv?
dont use, check mean. (doesnt work if out of nomral HR.
question to look for after mital BAV
big V wave…
shunts key
QP:Qs
find step up
Ao-SVC/Ao-Pa
- WHO groups for PHTN
- defined ph based on 2018 world symposium
- who group 1 is only?
- female to male
- PAH one is primary, term is reserved for those with who group 1.
- LHC
- PH due to lung disease
- CTEPH
- multifactorial
- mean pa of >= 20 mmHg with a pcwp or edp <=15 and PVR >=3 woods uints.
- PAH or primary
- 2:1
primary PAH can be cause by what
-most commonly Systemic sclerosis, also other collegen vac disease, 30% of sclerodema -patients have pah 3:1 female:male ratio.
- cirrhosis and pah is called what and this is caused by what
- trick quation on RHC and Portopulmonary ph
- HIV related phtn is usually what?
- drug associated with PAH
- PAthologic findings of PAH this is forally called what?
- what does above look like on path with eosin staining
- exception to above is what?
- still type I and is called portopulmonary htn. this cause by pulmonary avm development
- They can have elevated CO raising pulmonary pressures but resulting in near normal PVRs. so need to use pvrs. (from pulm avms)
- type one PAH
4,. methaphetamine-–> fenflarmine to amiorex
- pathologic findings of pah –> hyperplasia of all the vessels in the lung. sm hyperplasion , plexogenic hyperplasia
- whorls of smppth muscle cells. also insitu thrombosis.
- SSclerodema which sohows fibrosis but no plegogeic changes.
where is congental heart disease induced PH categorized in the who system
schistosomiasis
MC gene assocaited with PAH
Why does lung parencyhyma dz lead to pah
hat is the median survival of type I pah?
AC with group 4 PAH?
when to consider IV drugs rx for PAH?
1 or 4….
1
bone morphogenic progtein gene
bc it leads to HPV
7 years (this has increased sig)
life long
consider if sycnope or stage IV sx.
what is considered an appropriate respons e to vasodilater rx on RHC for PH
drop of >= 10 mmHg to a mean pa <- 40 ith unchanged Or increased CO….
PVR calc
normal\
Svr formula and nomrla
Mean PAP-LAP/CO*80 = take away the 80 and you have woods
20 and 130
SVR is mean Ao - RA pressure/ CO *80 ; normal is 600 to 1400
6 min walk test associated ith class iv sx
less than 150 m is class IV, 150-300 is class III
RX for primary pHNT what are the mainstays and MOA of each
common se
1/2 epo vs. trepo
- PDE-5 breakdon cGMP and improve no signalling, sildenaphil and tedalaphil are approved
- ricociguat is a direct cgmp agoinst is approved for pah and cteph
- prostanoids - epoprostinol IV or SQ, treprostinil and iloprost, oral optoions: selexipag is a prostcyclin receoptro agonsit, and trepostinil, thes acto on PDE-3 (inibiting their breakdon)
- endothelin receptor agonists (bosentan, amrisentan, macitentn (only macitentin is not generic)
Think vasodilator –> HA, flushing, ja pain, edema (edema most common with endothelin antagonistis), prostacyclins masseter pain and diarreha\
IV epo min, treop hrs
ambition trial in primary ph
what is most potent
ambersantan (endotherlin) and tadalfil as better than either alone)
so this is the susal
prostacyclins
