Which is the Best Reperfusion Therapy in STEMI? (Sanjay Kunapuli, MD)


everyone good afternoon I hope lunch has

sold you well was the morning session

boring or what I thought it was fabulous

and we thank all our faculty and you're

gonna move on to our afternoon sessions

by the way we love your questions keep

on rolling we may not be able to answer

each and every one of them and I

apologize but due to time constraints

but we will try and catch get to all of

them if possible

so we load those so keep on keep on keep

on sending those the next speaker I have

a pleasure of introducing is one of my

friend and my colleague is a fellow

international cardiologist dr. ku Nepali

he runs our cath lab program out in


Willowbrook Methodist and is one of the

busiest interventional cardiology

sign-off so welcome dr. ku Nepali who's

gonna talk to about what is the best

reperfusion stare therapy in STEMI

patients Thank You dr. Shaw and thank

you dr. Zagreb for having me here I hope

none of us are gonna need reperfusion

after nice barbecue so the topic I'm

going to talk about is reperfusion an ST

elevation myocardial infarction it is

rather an expansive topic but it's also

quite important because it is

life-saving if I have to sum it up in

two slides the entire talk it's this

everyone needs to be Reaper fused and

currently PCI is the best option for

reperfusion so that's my disclosures

roughly half a million people have

coronary artery disease every year this

is the heat map right now we are hot in

Texas for our heart disease

dr. Jones probably talked to you guys

this morning about evolution of plaque

this is these are our arteries starting

at the right when we are born and to

endure 40 years of age there's two kinds

of plaque there's vulnerable plaque and

there's stable plaque vulnerable plaque

is I I call it it's like creme Bowl a

very thin layer on the top and very bad

stuff inside you don't want vulnerable

plaque why is it important to know these

plaques because that what that's what

forms the basis of the entire spectrum

of the acute coronary syndrome plaque

rupture then leads to either non-st

elevation myocardial infarction or st

elevation myocardial infarction which is

complete occlusion of an epicardial

coronary artery resulting in cessation

of blood flow

this little pictorial will show what

happens plaque ruptures the everything

inside the plaque is exposed you get

platelet aggregation which then forms a

thrombus why is it important to know

this it's because this is where

therapies act either fibrinolysis or the

medic the anticoagulants that we use so

once again for all groups of patients

that present with stemming coronary

artery perfusion is the basis and needs

to be performed either with primary PCI

or fibrinolysis why because it improves

myocardial cell which and reduces

mortality PCI is preferred

compared to fibrinolysis if it can be

performed by and tie in a timely fashion

by an experienced expert operator when

it's not available you need fibrinolysis

some of the things that you may

encounter these are more emergency room

terms door to needle door to balloon and

PCI related delay so most cause most

cases of stem ease are caused by plaque

rupture of plaque ruptures so you get a


epicardial coronary artery patients with

STEMI should receive reperfusion either

with PCI or fibrinolysis and this is

true for all patients that present

within the first 12 hours so what do we

have do you have either fibrinolytics or

mechanical some key items regarding

thrombolytics or fibrinolytics

even though PCI remains the reprovision

strategy off choice it's not available

everywhere there's a lot of hospitals in

the United States and elsewhere these

hospitals may not have PCI capability or

may not have backup surgeries so what do

you do in such cases you need to know

about fibrinolytics fibrinolytics are

plasminogen activators they are serine

proteases that participate in the lysis

of fibrin by converting plasminogen to

plasmin so there are three kinds there's

fibrin specific agents

there's intermediate fibrin specific

agents and then there's non fibrin

specific agents you've probably heard

this term before time is muscle it comes

from time is my accordion meaning that

the earlier you can get to open an

artery the better it is with every hour

that progresses the myocardium is

progressively dying and the first 2 to 3

hours are considered the most critical

time this pictorial shows you what

happens when an epicardial coronary

artery on the top here is open and it's

not open as so subsequently the

myocardium ends up dying a little bit of

a historical perspective 1933 first

paper those published Tillet and Gardner

they described the fibrinolytic activity

of beta hemolytic streptococcal oral

fusion that's the first paper they

published effect of patients with step

Takako for religion

so once again they are serine proteases

they participate in the lysis of

converting of fibrin by converting

plasminogen to plasmin there are fibrin

specific agents intermediate fibrin

specific agents in non fibrin specific

agents this is a slide you should

probably know and get asked what are the

absolute and what are the relative

contraindications for giving

fibrinolytics most of the time that your

physicians or are the ones that

encounter patients that they need to

give final access basically the

take-home message for this is anyone

that has had an intracranial bleed

anyone that has had a good stroke anyone

that has had an aneurysms intracranial

ii there's one caveat to this is that if

you've had a acute ischemic stroke

within the last three hours you can get

TPA so that is the caveat streptokinase

was the original fibrinolytic agent it's

a single chain polypeptide it's derived

from beta hemolytic strap it binds to

plasminogen makes a complex for acute MI

streptokinase is administered 1.5

million units over 60 minutes and all

patients that get streptokinase get

aspirin 325 problems with streptokinase

you develop an allergic reaction you can

either develop that first time or you

can develop a I G Mei mediated allergic

reaction the second time around patients

are known to have hypotension during

streptokinase administration and then

the third is bleeding with all federal

litigations the first trial that showed

a mortality benefit with fibrinolytics

was the gissy trial

it was a large trial about 12,000

patients and it showed remarkable degree

of benefit when criminal it exposed in

acute MI patients second thermal it ik

is Ulta place or TPA

something that is used more commonly now

it's a recombinant type of plasminogen

activator it it's a naturally occurring

enzyme there's a serine protease and

it's produced by a lot of cells in our

body in contrast to streptokinase it's

fibrin specific so that performs an

important key point and it's also

front-loaded and has a short half-life

all patients receiving TPA should

receive heparin and when studied in the

gussto trial

it showed a mortality benefit compared

to streptokinase problem with TPA

patients can develop edema or lingual

edema and this can be rare but when it

happens it can be severe

Retta place is our PA a recombinant

plasmid is an activator it's less

vibrance selective than TPA that's

pretty much it's not used much so you

don't see it often you don't hear about

it very often

the one that's used nowadays and the is

the drug of choice for acute MI patients

in the United States and Canada it's

tenecteplase tnk TPA is genetically

engineered it's a multiple point mutant

of recombinant TPA

it's got a long plasma half-life so why

is that important you can give one dose

and it's it acts it's 14 times more

fibrin specific than streptokinase the

timi 10 a and T V 10 B trials were the

ones that basically showed significant

mortality benefit however when looked at

higher doses really is no benefit for

connector plays at higher doses and then

the last one

Leno took place it's not even used

anymore because of increased risk of

strokes in patients

so fibrinolytic agents if you have to

summarize it says that the if someone

presents with a STEMI

the choice is primary PCI if you don't

have primary PCI fibrinolytic agents

currently the paralytic agent of choice

is tenecteplase the absolute

contraindications are intracranial

bleeds intracranial hemorrhage

intracranial aneurysms and there's

relative contraindications this is the

dosing chart for patients that get

problematic agents so moving on if not

fibrinolytic agents what is the other

option it's the option of choice primary

PCI what is primary PCI mean primary PCI

is when you take someone to the cardiac

catheterization lab do a coronary

angiogram cross the lesion with the wire

and inflate a balloon that is

percutaneous coronary intervention so

percutaneous coronary intervention

refers to either ptc a pci drug lu

placement of either bare metal stent or

drug-eluting stent it passes the whole

thing the current treatment of choice

ACC ESEA guidelines recommend primary

PCI to be performed in all acute MI

patients within 120 minutes or first

medical contact ideally within the first

90 minutes when they come so that is

what you call the door-to-balloon time

and they come into the emergency room

and you're rushing them and the way that

you record or the balloon time they can

hit the door in the emergency room you

take them up to the cath lab you cross

the lesion you burr you open you restore

blood flow that's your door-to-balloon

time that in 90 minutes is a number you

want to be because that's where you get

your greatest benefit for myocardial

Salvage a lot of trials about 23 of them

that showed PCI versus fibrinolytic

agents what is better PCI significantly

better primary PCI versus with balloon

angioplasty versus fibrinolysis

significantly lower mortality of 30 days

lower rate of death and read

fortune with PCI ie PTC a versus

terminal I have problematic agents this

was first in the pammi one trial then

the denominator is a couple of other

times when you have patients that

present with pericarditis left bundle

branch block diagnosis that is not very

clear you can't give them their analytic

agents PCI is the preferred route of

choice whereas fibrinolysis preferred

it's preferred in patients that show up

after the 120 minutes or if you don't

have a PCI performing center that's

pretty much the only time the one thing

that I wanted to emphasize something

that you may see is what's called

facilitated PCI meaning that you're

transporting someone to a PCI facility

and what do you do there isn't really no

data that supports that give them five

medications then go for a planned PCI if

it's a rescue PCI yes but not for a

planned PC on the third option is

cabbage coronary artery bypass grafting


not very often and patients that do need

it are often very sick these are

patients that have either had a

complicated or unsuccessful pci either

they're very complication with acute MI

or they present with STEMI and continue

to have recurrent cardiogenic shock or

ischemia how long do you wait for these

patients usually wait till they cool

down can be anywhere from six hours to a

couple of days who do you not reap

refuse obviously people that don't want

to be a Reaper fused number one that

have serious severe end-of-life issues

or hospice or you know patients that you

have bleeding risk so once again the

take-home message patient presents with

STEMI you have to recruit fusion

strategies programmatic agents or PCI if

they can be taken to the cath lab within

the first 120 minutes ideally within the

first 90 minutes

call the interventional cardiologist if

not and if you can give them

fibrinolysis if there's going to be a

delay that's the only time that you

should be getting terminal lyrics anyone

with intracranial bleeds or active leads

is not a candidate