Cath - general

What is the course of the LCx? How is it split into proximal/mid distal?

-          Atrioventricular groove and goes posteriorly 

-          OM 1- 3

-          Proximal: until OM1

-          Mid

-          Distal : Last OM branch until distal (goes to Apex)

What is the course of the LAD and how is it split into proximal/mid/distal?

-          Interventricular groove

-          Diagonals 1-4

-          More septals from diagonals

-          Proximal: until 1^st branch (either septal branch - medial, or diagonal - lateral)

o   There are 10 septal branches!

o   Proximal septal branch supplies bundle of His

-          Mid to end: divide by half

-          Identify by : different movement from rest of vessels, presence of septal perforators

What are the branches of the RCA?

-          Proximal: first RV branch

o   Sinoatrial artery supplies Sinus node in RA > outwards (Supplied by LCx in some)

o   Conus  (supplies RVOT > inwards)

-          Mid

o   First RV branch 

o   Acute marginal after RV branch

-          ?Atrioventricular branch

-          Distal

o   RPDA: Down interventricular septum (acute bend > goes up then goes down)

o   RPL: posterolateral wall

What is barbaeu test?

oboth the radial and ulnar arteries are compressed simultaneously until the plethysmographic wave is lost. Then, the pressure on the radial artery is released, and the shape of the plethysmographic wave is evaluated (check pulse ox)

What are some relative C/i to radial access?

-          Very small radial artery

-          Known pathology in proximal vessel e.g. subclavian stenosis

-          Raynauds/scleroderma/Kawasaki

-          Need to use radial for CABG/used for CABG

o   Left radial is preferred for access post CABG

How is TIMI flow graded?

• Grade 0 No perfusion; no flow beyond the blockage. 

• Grade 1 Penetration without perfusion; contrast agent passes the blockage but doesn't fill the distal vessels. 

• Grade 2 Partial perfusion; contrast agent passes the blockage and opacifies the distal vessels, but slower than normal. 

• Grade 3 Complete perfusion; contrast agent flows as quickly and completely as normal, indicating full reperfusion. 

When is DCB > DES?

Anything less than 2mm cannot put stent

Coronary ectasia/aneurysm

o   If vessels are too huge there is risk of stent thrombosis

o   Slow flow: also aspiration and balloon

Clot

Diffuse disease

High bleeding risk

Ostial disease/bifurcation disease

How is Ca severity graded? (OCT vs IVUS scoring system?)

Ca severity

-          Arc

-          Length

-          Thickness

-          Presence of nodule

OCT calcium scoring system

-          Maximum calcium angle > 180: 2points

-          Maximum calcium thickness > 0.5mm: 1point

-          Calcium length > 5mm: 1point

-          4 or more high risk , need calcium modification therapy

IVUS scoring system

-          Superficial calcium angle > 270spanning longer than 5mm

-          360 superficial circumferential calcium

-          Presence of calcified nodule

-          Vessel reference diameter < 3.5mm

-          Score > /=2high risk of underexpansion

Management of calcified lesions?

-          Cutting balloon

-          Scoring balloon

-          Rotational artherectomy: Rotablation

o   C/I in saphenous venous graft (thrombus and microembolization with no reflow)

-          Orbital artherectomy

-          Intravascular lithrotripsy i.e. shock wave

Causes of coronary ectasia/aneurysm?

o   Previous Kawasaki disease (25%)

o   Artherosclerosis

o   CTD

o   Arteritis (Syphillis, takayatsu, Polyarteritis nodosa)

o   Physiological adaptation

o   Consider sepsis, endocarditis

o   IGG4

Class guideilnes for A) CABG and B) PCI for EF < 35% + multivessel disease?

Class I for CABG

PCI as an alternative (Class IIB ESC)

Class guideilnes for A) CABG and B) PCI for LM disease?

CABG > PCI CLass I if low surgical risk (Lower risk of spontaneous MI And repeat revascularization)

PCI class I if low compleixty (non inferior for survival)

PCI Class IIA if intermediate complexity

Class guideilnes for A) CABG and B) PCI for DM + Multivessel disease?

CABG > PCI CLass I (reduce mortality, reduce repeat revascularizations)

What is classified as multivessel disease?

Involvement of > /=2 vessels with > 70% stenosis

Class guideilnes for A) CABG and B) PCI for Multivessel disease?

CABG Class I

PCI CLass I for low to intermediate complexity

?ischaemia extend

Class guideilnes for A) CABG and B) PCI for proximal LAD stenosis ?

ACC: 2b to improve survival

ESC: Class 1 for CABG or PCI for functionally significant disease, to reduce CV mortality an drisk of spontaneous MI

What is the recommendation for PCI to non infarct artery in STEMI?

Complete revascularization either during index procedure or within 45 days

What is the recommendation for PCI to non infarct artery in NSTEMI?

complete revascularization during index procedure

Functaionl assessment is Class IIB

How to perform FFR?

1. Intracoronary GTN

2. Introduce pressure wire beyond guide tip

3. Zero pressure within aorta

4. Pass pressure wire distal to lesion

5. Begin IV adenosine 140mcg

6. Return pressure wire to ostium and check for drift (0.03)

</= 0.8 significant

What are the types of hyeraemic agents?

Adenosine (IV or IC): IV hold standard

Papaverine

NTP

Regadenoson

Benefit of iFR over FFR?

No need for hyperaemia

Shorter procedural times

Can be used for ostial lesions

Can assess serial epicardial lesions

What did DEFER show?

No difference between medical treatment vs PCI for FFR > 0.75

What did FAME 1 show?

FFR guided (<0.8) vs angiography guided revascularization in MVD

• ok to defer if > 0.8

What does FAME 2 trial show?

FFR guided (< 0.8) vs OMT for stable angina

• FFR guided a/w reduced risk of future urgent revascularization, but no increase in MI or death (consistent with ischaemia trial)

What are the causes of false negative FFR? (7)

• Guide catheter pressure damping

• No hyperaemia/adenosine inhibited

• STEMI

• LM+ Downstream disease

• Severe AS

• Serial FFR of individual lesion

• Presence of signal drift

What are the causes of false positive FFR?

• CTO receiving collaterals

• Loose pressure connections, air bubbles, transducer connector errors

What are the causes of coronary no reflow?

• epicardial spasm

• Dissection

• Embolis

• If no obvious epicardial mechanism, assume microvascular no reflow

what are the risk factors for no reflow?

• HTN DM HLD

• Delayed presentation to cath lab

• High thrombus burden

• Plaque composition: high lipid

• Lesions longe than 15mm

Prevention strategies for no reflow?

• Avoid aggresive balloon inflation

• COntrolled artherectomy

• Direct stenting

How is coronary dissection classified?

what investigations would you do next?

Dissection

• OCT

• CT aortogram if near ostium

What are the risk factors of coronary dissection?

• over sized balloon

• Calcified lesion

• Deep seating of catheter

What are the prevention strategies of coronary dissection?

-          do not inject contrast if there is dampened pressure waveform

-          achieve coaxial catheter position

-          avoid aggressive wiring strategies

-          avoid use of oversized balloons and high pressure

-          preparation of calcified lesions

Management of coronary dissection?

-          small, non flow limiting dissections do not require treatment

-          proximal edge dissections do not require treatment as stent will prevent forward propogation

-          stenting if wire in true lumen

-          if ostial dissection with aortic dissection> surgery

Causes of SCAD ?

Predisposing

-          Pregnancy/labour and delivery

o   can occur at any time during pregnancy but majority post partum within the first week

-          Fibromuscular dysplasia

-          Connective tissue disease

o   Marfan, ehlers danlos, loey dietz

-          Systemic inflammatory

o   SLE , vasculitis

-          Hormonal  therapy

-          Sarcoidosis

-          Coronary artery spasm

-          Idiopathic

Precipitating factors

-          Intense exercise

-          Intense emotional stress

-          Sympathomimetic use

Investigation for SCAD?

-          CT arterial imaging from head to pelvis (to look for FMD)

o   ?aorta rarely impaired and does not need screening

-          US Carotid/MRA carotids

-          US /CTA renal  

-          Definitive is coronary angiogram but risk of dissection

Management of SCAD

-          Conservative

-          Unless severe presentation with ongoing symptoms, other high risk features

-          SAPT aspirin

o   Some guidelines recommend DAPt

-          Treat hypertension

-          Follow up with CTA 6

o   Guidelines don’t recommend any timing but can do around 6 months

-          Can do regular moderate exercise

o   Avoid extreme or vigorous sports

o   Avoid heavy lifting

perforation

classifcation system for perforation?

Management of coronary perforation?

-          Most can be managed expectantly

-          Place covered stent (downside: hard to maneouvre and may block off branch arteries)

-          Balloon tamponade

-          coil

-          gelfoam embolization

o   sterile, water insoluble, gelatin based sponge

o   thrombosis and inflammation

Causes? Mx?

Causes

•   improper catheter aspiration and flushing

•          loose connection in manifold

•      balloon rupture

Mx

-          100% NRM

-          Aspirate air

-          Intracoronary adenosine (vasodilator)

Intracoronary adrenaline