TIMI Score Acute Coronary Syndrome

 

Intermediate stress failed. concrete questions why you are calling

22F candidate inpt stress verse cardiac cath.

within 90 minutes

NSTEMI/UA, TIMI intermediate (3-4), high (5-7)

NSTEMI ST elevation

Elevated troponins, chest pain, EKG changes

any 2 of the 3 NSTEMI

Unstable angina

DAPT: asa, statin, heparin, 

oxygen, ace inhibitors, beta blockers, don't give oxygen

give them O2 only for hospitalists via small mechanical fan.

morphine grade 2b.

STEMI: loading DAPT, +/- heparin, go straight to cath lab. 

not in cath lab, thrombolytic. TNK: tenectaplase.

Jama Clinical Reviews

- STEMI cardiac cath w/in 2 hours

STEMI no PCI

- Fibrinolcytics Alteplase, reteplase, tenecteplase, streptokinase

- PCI w/in 24 hours

Cath obstructions STEMI in 2 hours do PCI, if NSTEMI then 24048 hours do cath

NSTEMI

- elevated troponin - NSTEMI

- No elevated troponin Unstable Angina

When to treat w/ PCI

STEMI w/in 2 hours

NSTE-ACS w/in 24-48 hours 

NSTEMI

High sensitivty troponins yes NSTEMI

No Unstable angina

Cause	Type of ACS	Pathophysiology	Characteristics	Percentage of ACS
Plaque rupture	STEMI or NSTEMI	Lipid-laden plaque rupture due to inflammation followed by development of platelet-rich thrombosis	Most common etiology in both sexes<br>	Approximately 60%
Plaque erosion	STEMI or NSTEMI	Plaque erosion occurs with local flow perturbation, resulting in a denuded endothelial surface with formation of neutrophil extracellular traps and propagation of thrombus formation	More common in women than in men	Approximately 25%
Calcific nodule	STEMI, NSTEMI, or UA	A protruding nodular calcification penetrates the lumen surface with subsequent thrombus formation	Patients with chronic kidney disease and those receiving dialysis have a higher prevalence of coronary calcific nodules; calcific nodules are associated with a higher rate of requiring repeated coronary revascularization due to growth of the calcified nodule<br>	Approximately 5%
Coronary spasm	STEMI, NSTEMI, or UA	Extreme vasoconstriction of an epicardial coronary artery, which causes near-total or total vessel occlusion and sometimes superimposed thrombosis; can also occur in the microvasculature	In patients with ACS who do not have obstructive coronary artery disease on angiography, coronary spasm can be evaluated with provocative testing, such as administering acetylcholine, although it is typically treated empirically without such testing	1%-5%
Spontaneous coronary artery dissection	STEMI or NSTEMI	Obstruction to blood flow due to an intimal tear as well as separation of the medial and adventitial vascular walls associated with intramural hematoma protrusion into the lumen; either in single or multiple arteries; more often affects the middle and distal portions of the artery, most commonly the left anterior descending artery	Approximately 90% of patients with SCAD are women (approximately 55% are postmenopausal); emotional stress reported in approximately 50% of patients and physical stress in approximately 30% of patients; fibromuscular dysplasia, systemic inflammatory disorders, peripartum state, and connective tissue disorders predispose; best to reserve PCI or CABG for refractory symptoms	1%-4%
Coronary artery embolism	STEMI or NSTEMI	Conditions such as atrial fibrillation, left ventricular thrombus, valvular thrombus, or paradoxical emboli from the venous system passing through an atrial or ventricular septal defect are associated with coronary artery embolism, which leads to complete obstruction of an epicardial coronary artery or branch and infarction of the myocardium served by that vessel	Evaluation with transesophageal echocardiography and continuous electrocardiographic monitoring are useful to evaluate for several of the causes	1%-3%
Myocardial infarction with nonobstructive coronary arteries	STEMI or NSTEMI	Can occur from a variety of causes, e.g., plaque disruption (plaque rupture or erosion and calcific nodules), epicardial coronary vasospasm, microvascular dysfunction, spontaneous coronary artery dissection, coronary embolism, or coronary thrombosis, which lead to MI despite the absence of any severe obstructive coronary artery stenoses, although the specific cause often remains undiagnosed	More prevalent in women (5 times higher odds) and non-White patients (1.5 times higher odds); less likely to have traditional cardiovascular risk factors<br>	Approximately 5%-6%

from the JAMA Network this is JAMA  clinical reviews interviews and ideas  

about Innovations in Medicine  Science and clinical practice

my name is Dr Gregory Curfman a deputy editor of  JAMA and in this JAMA podcast I'll be speaking  

with Dr Deepak Bhatt Dr Bhatt is executive  director of Interventional cardiovascular  

programs at Brigham and Women's Hospital and  professor of medicine at Harvard Medical School  

he is also a senior physician  at Brigham and Women's Hospital  

Dr Bhatt Dr Renato Lopes and Dr Robert Harrington  have written a review article titled diagnosis  

and treatment of acute coronary syndromes which  appears in the February 15 2022 issue of JAMA  

welcome to the podcast Dr Bhatt  it's great to be with you Dr Curfman  

now acute coronary syndromes are characterized  as sudden reduction in blood supply to the heart  

and the syndromes include SD segment  elevation myocardial infarction or stemi  

non-st segment television myocardial infarction  or nstemi and unstable angina the latter  

two are often grouped together as non-st  segment elevation acute coronary syndromes  

each year an estimated more than 7 million people  in the world are diagnosed with acute coronary  

syndromes including more than one million people  hospitalized in the U.S in this podcast we want  

to bring our listeners up to date on these common  and potentially serious conditions Dr bot to begin  

could you please describe the different mechanisms  and pathophysiology of stemi and stemi and  

unstable angina what is the pathology at the level  of the coronary arteries in the three conditions  

this is a great question that you've asked and  first of all there's a lot of overlap in terms of  

the pathophysiology of acute coronary syndromes  whether we're referring to stemi and stemi or  

unstable angina one differentiator perhaps  between stemi and non-st segment elevation  

acute coronary syndromes is whether the artery is  completely occluded as is typically the case with  

st elevation Mi or incompletely occluded this  is more often the case with a non-st segment  

elevation Mi or unstable angina so even there  there can be potential overlap but let me start  

first with stemi they're typically the underlying  pathophysiology is plaque rupture that is rupture  

of an atherosclerotic plaque in the coronary  artery most often this is a lipid Rich plaque  

a cholesterol-rich plaque with inflammatory  cells and heightened degrees of inflammation  

triggering plaque rupture when that plaque  ruptures and its inner contents are exposed  

to blood a thrombus forms typically a fibrin  rich and platelet-rich thrombus this is the  

underlying pathophysiology of the majority of ST  segment elevation myocardial infarctions however  

a good proportion of non-encity elevation Mi or  enzyme also has a very similar pathophysiology  

perhaps in this setting it's a bit more common  to have thrombus that is predominantly plate rich  

with perhaps a little bit less of a fibrin rich  component but there really is a lot of commonality  

here however plaque erosion is something that's  been recognized in more recent years as a cause  

of acute coronary syndromes though perhaps a  little bit more frequent and end stemi than stemi  

and what plaque erosion refers to is having the  endothelial surface the covering surface of say  

a plaque that gets denuded so plaque erosion often  caused by some sort of perturbation in blood flow  

and then formation of platelet-rich thrombus but  again this could be the cause of stemi but it's a  

little bit more common in nstemi than stemi it's  also a little bit more common in women than men  

now there are other causes as well of acute  coronary syndromes calcified nodules can cause  

stemi or endstemi or unstable angina and here once  more there's lipid Rich plaque encroaching upon  

the coronary artery Lumen where blood would  be flowing but in this case there's a lot of  

calcium that's involved in that plaque and this is  potentially important not only from a mechanistic  

perspective but if this patient were to end up in  the catheterization lab with their acute coronary  

syndrome the presence of that calcific nodule  can pose some particular technical challenges  

there are other etiologies for acute coronary  syndromes as well again plaque ruptures the most  

common followed by plaque erosion than coronary  spasm is a cause of acute coronary syndromes  

this is where the smooth muscle that is in  the artery constricts it can be focal it  

can be multifocal it can be multi-vessel it can  involve the epicardial arteries it can involve  

the microvasculature and it does appear that  coronary spasm if we give provocative agents say  

in the catheterization Labs such as acetylcholine  is maybe a little more common than we used to  

think it was on the other hand most of the time  when it's suspected it's treated empirically but  

still it's important to understand that it can be  a part of the pathophysiology of acute coronary  

syndromes either the primary player or sort of a  secondary phenomenon say when the endothelium has  

been damaged and secondarily there may be spasm  and then there may secondarily also be thrombosis  

spontaneous dissection is another cause of acute  coronary syndromes it may manifest as stemi or  

even nstemi but a proportion in particular Rusty  elevation am I we now know is due to scad or  

spontaneous coronary artery dissection there's  certain situations such as in the peripartum  

state where it might come up a little more  frequently than otherwise and this involves an  

intimal tear that is a terror of the inner layer  of the coronary artery and that can obstruct the  

coronary artery in fact we're still learning a lot  about scad including the pathophysiology of scad  

there are some that believe that the mechanism  is predominantly what I mentioned at tear in the  

intima and the creation of a true Lumen where  blood is Flowing as it should in a false Lumen  

that can then fill with blood and compress or  obliterate the artery lumen there's also a line of  

thinking that some proportion of the spontaneous  coriary dissections are from blood forming from  

the adventitial side of things and forming within  the adventition media of the artery again leading  

to a compressive phenomenon and obliteration of  blood flow so we're still learning a lot about the  

biology of scad and it's likely the case there's  several different forms with different specific  

pathophysiologies behind them another cause I'll  mention is coronary embolism such as when someone  

has atrial fibrillation or a left ventricular  thrombus that decides to move and obstruct a  

coronary artery so this can cause stemi or nstemi  and then finally there's a category called minoka  

or Mi with non-obstructive coronary arteries  it accounts for about five to six percent of  

myocardial infarctions and that basically means in  those patients who have a coronary angiogram there  

there's no obstructive plaque there might be some  mod plaque but no severe plaque and then we assume  

that one of the causes I mentioned or some other  causes on a rather long list of potential causes  

is the etiology of the acute coronary syndrome  and sometimes more advanced imaging things like  

MRI can help us get it with the pathophysiology  might have been what the reason for that Mi with  

non-obstructive coronary arteries from Anoka  might have been so as you can see there really   a variety of different etiologies well that's  a great summary thank you very much for that  

and just to be clear about the distinction between  plaque rupture and plaque erosion do you consider  

these to be different degrees of disruption of  a plaque or does plaque rupture actually involve  

Hemorrhage out of the plaque itself and does  that Hemorrhage contribute to coronary thrombosis  

so it's a great question plaque rupture more  often results in complete arterial occlusion  

as with a stemi whereas plaque erosion may be more  likely to lead to non-obstructive acute coronary  

syndrome such as a non-state segment elevation  Mi and for reasons that aren't totally clear it  

appears that plaque erosions a bit more common in  women than men with the reason for that is I think  

is something that will need to be elucidated in  the earth to come that might provide some insights  

into why there may be some subtle differences  in ACS presentations and trajectories after  

presentation men versus women the biology is a  little bit different in as much as plaque erosion  

is more a response to the endothelium being  disrupted or denuded whereas plaque rupture as  

you said is more a matter of exposure of the inner  contents of the plaque to the flowing blood and  

can include such things as enter plaque Hemorrhage  as well so there are some differences if one looks  

at autopsy specimens for example between these  two there's also some potential implications for  

management in general plaque rupture that presents  clinically is going to be treated if it's a stemi  

with a stent in most regions of the world or in  regions of the world whether that's not possible  

with fibrinolytic therapy therapy directed towards  breaking down the fibrin rich thrombus whereas for  

plaque erosion say in an end stemi they're in  fact fibrinolytic therapy has been found to be  

not useful in fact harmful in terms of causing  bleeding complications with no benefit and it  

does appear that a higher proportion of patients  with plaque erosion may end up doing fine managed  

medically without stenting as opposed to those  with plaque rupture where stenting does seem to  

be particularly useful so there are some definite  differences in the pathophysiology and they do  

have implications for the treatment some of which  has been fully worked out some of which really  

does need more research all right thank you for  that now I wonder if we could turn to the clinical  

presentation of acute Corner syndromes and are  there differences in the clinical presentations  

among the three types of acute coronary syndromes  I wonder if you can discuss that for a moment  

this is really a key point that you've raised  for anyone directly involved with patient care  

understanding the pathophysiology is important for  present care it's important for future research  

but understanding the differentiation among  these acute coronary syndromes that's critical  

for right now for today in managing the care of  patients with ACS so the first step in a patient  

with suspected ACS assuming that they're in an  emergency setting if they're calling from home  

or somewhere else they need to call Emergency  Medical Services 9-1-1 in the U.S and be brought  

immediately to an emergency department but then  within 10 minutes of arrival the standard of   care is to get an ECG or electrocardiogram and  there are the key thing to look for is whether  

ST segment elevation is present or is not present  on the ECG if it is present on the ECG that is a  

stemi rst segment elevation myocardial infarction  that means everything needs to kick into high gear  

the system needs to move quickly that is a medical  emergency and time is muscle as they say it really  

matters to move quickly here so that's a very  important diagnosis to make and we'll talk about  

the treatment later but that ECG is key for that  differentiation if SD segment elevation is not  

present well then it is a non-st segment elevation  ACS and that broadly speaking is then divided into  

n stemi non-st segmentation Mi or unstable angina  again the key differentiator here between stemi  

and non-stemi type ACS is the ECG and whether St  elevation is or is not present so now here for the  

non-sd segmentation ACS there's no SD simulation  present the next step is to check a troponin level  

preferably a high sensitivity troponin level and  if that is elevated initially or on subsequent  

testing then the diagnosis of nstemi is made if  on the other hand that troponin level is negative  

and remains negative on subsequent testing then  the diagnosis of unstable angina is made so it  

really matters a lot what that electrocardiogram  shows and then in the case of non-sd segmentation  

ACS with that initial triple opponent shows or  subsequent requirement and in terms of subsequent  

troponin most algorithms would say within three  hours is when that subsequent troponin should be  

drawn the most recent data actually suggests an  algorithm of checking again in one or two hours  

is probably even more efficient with no loss  of sensitivity or specificity so I think the  

way to get to stemi and stemi-unstable angina is  quite clear with use of the electrocardiogram and  

with use of the troponin now of course this is  all in patients who've presented with a clinical  

syndrome that's consistent with ACS and we should  talk about that a bit in terms of the symptoms  

but in terms of the broad classifications this is  how to classify patients into the different types  

of acute coronary syndromes excellent well you  brought up symptoms so why don't we talk about  

symptoms which sometimes can be very classic but  other times maybe not so much can you comment  

about that absolutely so chest discomfort at rest  is the most common presenting symptom of acute  

coronary syndromes there's no question about it  and everything that I was talking about in terms  

of the categorization of ACS applies to patients  presenting with a high pre-test probability of  

having an ACS so they're presenting with chest  discomfort I'm not referring to say troponin  

measurements that are done in the hospital for  a variety of other reasons where the presenting  

symptom is something else or there's no symptom  even in that circumstance troponin elevation  

is a bad prognostic sign but that isn't really  what we're talking about today in terms of ACS  

and how to manage acute coronary syndrome so  chest discomfort in both men and women is the  

most common presenting symptom but it's important  to realize that a significant number of patients  

will have other less specific symptoms such as  dyspnea which can occur in isolation although more  

commonly still occurs with there being some sort  of chest pain I think in Prior years there's been  

lots of talk about atypical chest pain the most  recent American College of Cardiology American  

Heart Association chest pain guidelines that just  came out at the end of 2021 actively discourage  

the use of that term atypical chest pain and the  reason is not just to be the workplace but to make  

sure that treating Physicians realize that that  nomenclature can sort of lead us down Pathways  

that aren't useful the historical thinking perhaps  being that women are more likely to have atypical  

chest pain for example but it turns out that's  really not true Studies have shown I'll quote one  

particular study but there are several now that  approximately 79 percent of men and 74 percent  

of women presenting with acute coronary syndromes  have chest discomfort at rest as their predominant  

presenting symptom so yes you could say oh that's  more common in men than women but 79 versus 74 to  

me is a relatively small difference not clinically  actionable so again the majority of men and women  

with ACS are presenting with chest discomfort at  rest now what about the what used to be called a  

typical symptoms such as dyspnea well it turns  out that in the particular study I was quoting  

for example 48 of women did have non-specific  symptoms but guess what so did 40 of men so again  

these so-called non-specific previously perhaps  called atypical symptoms are occurring in women  

that's true but they're also occurring in men  but more importantly in both the women and men  

even if they are having these non-specific  symptoms still a lot of them are also having  

chest discomfort they might lead by saying  oh yes I'm having really bad shortness of   breath but then it turns out they are also having  chest discomfort so the history is in all things  

remains very important when such a history that's  concerning of these sorts of symptoms of chest  

discomfort chest pain chest pressure uh dysmia Etc  are occurring at rest and are significant well ACS  

should be suspected and then we need to launch  into the algorithm that you and I just reviewed   in terms of ECG within 10 minutes and then High  sensitivity troponin testing shortly thereafter  

so let's say we now have a diagnosis and  we want to move quickly on to treatment  

and the treatment of the three types of acute  coronary syndromes has advanced substantially  

in recent years and there is overlap among  therapies for the three categories of acute  

coronary syndromes treatment might be broadly  categorized into reperfusion therapies on the  

One Hand In Medical therapies on the  other and if we could begin with stemi  

I wonder if you could please discuss the  recommended steps in the management of stemi  

absolutely this is really important to know  because time matters as I alluded to before   so all the patients presenting with ACs of all  three types should be treated with anti-platelet  

and anticoagulant therapy on presentation in  a minimum this is typically off an aspirin  

and unfractionated heparin but there could be  more in terms of antiplatelet or anticoagulant  

therapy but then the key sort of determination  as I mentioned is the ECG and if there's St  

elevation it's time to activate that is called  the cardiac catheterization lab if there is a  

catheterization lab that's available within two  hours data show that's the way to go take that  

patient of the cath lab with the stemi and more  often than not there's an obstructed epicardial  

coronary artery open it up typically with a stent  and that is the treatment of choice now if there  

isn't a catheterization lab available within two  hours because there's a blizzard or because it's  

a part of the world where there aren't cath Labs  that are as commonly placed well then the best  

thing to do is to treat promptly with fibrinolytic  therapy or thrombolytic therapies it used to be  

called and there are altar plays where the plays  or connected plays or the Agents of choice but  

if cost is an issue in that particular region of  the world streptokinase remains an option as well  

for fibrinolytic therapy even in those patients  treated with Linux they should then be transferred  

to a facility that can perform percutaneous corn  intervention within the next six to 24 hours or so  

great now in terms of end stemi are there any  important differences between the management of  

nstemi and stemi it's a terrific question  in general it's felt that the timing is  

urgent but not quite as emergent as with stemi but  that can sometimes be misleading because sometimes  

nstemi's or stemmies in Disguise so for example  the left circumflex artery and occlusions that  

are notorious for not presenting with ST segment  elevation same sort of situation with a large  

diagonal Branch off the left anterior descending  artery where there may not be SD segment elevation   on the 12 lead surface ECG but in fact there is an  occluded artery so in patients that are having an  

nstemi that appear to be high risk such as those  with ongoing chest pain despite initial medical  

therapy marked ST segment depression that is new  and persists if an echocardiogram is done in the  

emergency department a patient with a presumed new  wall motion abnormality those patients should be  

treated just like an st signal Ovation Mi patient  in terms of going to the cath lab emergently  

but in the majority event stemi cases where  that's probably not going to be the case there  

you still want to move quickly typically the  guidelines would say within 24 to at most 48  

hours or so to get that patient to the cardiac  catheterization lab assuming that they don't  

have any contraindications and then based on the  coronary Anatomy undergoing revascularization  

about 60 or so patients will end up getting a  coronary stent about 10 or so will get coronary  

bypass surgery during that index hospitalization  and the remainder will be treated with medical  

therapy only of course all the patients  will be treated with medical therapy and   be given lifestyle modification recommendations  on discharge but specifically the ones who have  

severe blockages will be treated percutaneously  or with surgery so that's the management of  

nstemi in general though low risk and stemi or  unstable angina can be managed medically as well  

as the the initial therapy where the medicines  I mentioned are given but additionally medicines  

directed towards controlling ischemia things like  beta blockers but also other risk factor control  

medicines lipid lowering therapy Etc employed  and if the patient continues to have symptoms  

then they would go on to the catheterization  lab in that more so-called conservative strategy  

where initial medical therapy only is utilized or  there it would make sense to also do early on some  

sort of non-invasive evaluation historically  that's been stress testing but more recently  

in areas where it's available non-invasive  computed tomography angiography or CT angio  

has really caught on as a quick way to exclude  severe coronary disease that is if that comes  

back looking pretty normal it's unlikely that  the patient has an ACS whereas if that comes  

back looking like there's severe coronary artery  disease or it's a bit ambiguous then the patient   will likely undergo cardiac catheterization anyway  so there is I think a lot more subtlety to the  

management of non-sd segmentation ACS than there  is of stemi with a few different Pathways that are  

possible but in general patients that are higher  risk even those that have unstable angina with  

negative troponins if they've got things such as  heart failure Dynamic ECG changes ongoing chest  

discomfort any sign of hemodynamic instability  there again prompt catheterization and if  

appropriate based on the anatomy revascularization  would be indicated great thank you very much now  

I wonder if there's any specific guidance that  you'd offer Physicians as they provide longer term  

care and follow-up for their patients with acute  coronary syndromes what potential complications  

should Physicians be especially mindful of during  that longer term follow-up period this is really  

an important aspect of the care of the patient  with ACS so far we focused in this conversation  

on the early care that's critically important  of course what the long-term care is as well  

data such as from the reach registry published in  Jama some years ago showed that in patients with  

atherosclerosis if they had a history of Prior  Mi and I'll generalize here to say prior ACS  

they have a substantial rate of recurrent ischemic  events about 20 percent or so at least will have  

an ischemic event such as cardiovascular death  the my stroke in the next four years or so so  

these are high risk patients even if they've done  well initially it's important to recognize that  

it's important to provide counseling regarding  lifestyle modification including things such as  

smoking cessation or vaping cessation or cessation  of use of any sorts of tobacco products important  

to council against drug abuse or proportion of Mis  are due to things like cocaine or amphetamine or  

opioid use or even marijuana that many Physicians  actually don't know of that relationship between  

marijuana use and myocardial infarction so  important to counsel patients against using  

all those different substances for those that are  overweight weight loss would be important a diet I  

would say in particular diet that is plant-based  I would generally recommend and daily exercise  

is another important part so all of this I think  is easiest to Institute by referral to a formal  

cardiac rehabilitation program that remains quite  under utilized in the United States and worldwide  

but I think every patient with ACS should at  least be offered that possibility of cardiac  

Rehabilitation where all the different lifestyle  measures and more can be implemented beyond the  

lifestyle aspect then there's medical therapy  so the majority of patients being discharged   with acute coronary syndromes should be discharged  on Dual anti-platelet therapy that means aspirin  

typically low dose aspirin in the range of 75  to 100 milligrams a day and also an ADP receptor  

antagonist and the choices are Clopidogrel  project girl or tycagorn probably goes beyond  

the amount of time we have to discuss all the  issues pertaining to choice of agent there but  

the review article does touch upon some of those  considerations so dual antiplatelet therapy for  

the majority of patients with ACS irrespective  of whether that treatment was with a stent or  

bypass surgery or medications alone in addition  to dual antiplatelet therapy then we want to make  

sure that the patients are on potent LDL reducing  therapy so by that I mean high intensity statins  

for all patients barring true contraindications or  intolerances acetamide for many patients is a way  

to further lower their LDL cholesterol potentially  if the triglycerides are elevated consideration  

of lycosapentethyl and then medicines that have  been used historically in ACS patients such as  

beta blockers and ACE inhibitors or Angiotensin  receptor blockers and mineral corticoid receptor  

antagonists now there it sort of depends on  different things beta blockers are strongly  

indicated if there's left ventricular dysfunction  or if there's significant residual coronary artery  

disease with angina it's not so clear what their  utility is if the left ventricular function is  

totally normal and the patient has been fully  revascularized our ACE inhibitors or arbs are  

strongly indicated if there's left ventricular  dysfunction or diabetes or if there's just   hypertension that needs to be treated and mineral  corticoid receptor antagonists specifically for  

patients with left ventricular dysfunction so  it's a rather long list of things to consider the   patient especially the de Nova ACS patient might  have come in with no medicines but now they're  

going to go out on a lot so we have to consider  pill burden and cost and a number of other issues   as well but that's the basic list of medications  and one should consider Beyond just good control  

of hypertension good control in those that have it  of diabetes and other cardiovascular risk factors  

so there are a lot of therapeutic interventions  that need to be considered in patients with acute  

coronary syndromes and before we wrap up I  just wanted to ask you if you foresee any  

new developments in the management of  acute Corner syndromes on the horizon  

do you anticipate novel advances that  Physicians should be watching for  

I'm glad you asked in this review article  hopefully your readers will see that ACS and  

the study of ACS is very Dynamic there's a lot  that's already been going on in the field over   the past few years over the past several years  it's not ACS like it used to be say a decade ago  

similarly I think in the next decade we'll  see tremendous advances in the field of acute   coronary syndromes in terms of what's going on  in the catheterization lab further advances in  

stent technology further advances in assessing  whether coronary lesions are significant and  

should or should not be stented further advances  in cardiac surgery as well further advances in  

medical therapy that would apply to the vast  majority of ACS patients were I hope will have  

antith thrombotic agents that are not only  potent but perhaps less bleeding risk than  

what we have available today as well in terms of  the lipid axis I think will have even more potent  

ways of lowering LDL cholesterol and Associated  lipid related and inflammatory biomarkers there  

are a number of randomized clinical trials that  are going on that are looking at a variety of   different agents that Target the lipid axis the  inflammatory axis drugs that are diabetes drugs  

such as sglt2 Inhibitors that are being studied  in post-acs patients so really it's a long list  

of medicines that are being studied some are  drugs that are being used for other indications  

I mentioned the sglt2 Inhibitors others are being  developed specifically as novel agents and find  

finally I'll just say there's also work going  on in terms of remote monitoring of patients so  

potentially in the future we'll have a situation  maybe using wearables where patients who are at  

high risk for ACS such as ones who are already  had an ACS are monitored remotely and there's  

a trigger that goes off with their wearable their  their smartphone or whatever that lets them know  

or lets their physician know or lets Emergency  Medical Services know that there might be trouble   Brewing so I see a lot of advances coming in the  next decade in ACS well Dr butt you are a Fountain  

of Knowledge on this topic and other topics too so  thank you very much for your insightful commentary  

on these important clinical conditions thank  you very much and thanks to all our listeners  

and I want to remind listeners that further  details about acute Corner syndromes may be  

found in the review article by Dr spot Lopes and  Harrington in the February 15 2022 issue of Gemma  

this episode was produced by Daniel morrow at the  JAMA Network the audio team here also includes  

Jesse mccorders Shelly stefans Lisa Hardin Audrey  Foreman Marilyn frickle luck and Dr Robert golub  

is the Gemma executive Deputy editor to follow  this and other Gemma Network podcasts please visit  

us online at Gemma networkaudio.com once again  I'm Dr Gregory kerfman a deputy editor of Chama