2021 Virtual Cardiovascular Evening Symposium: Acute Coronary Syndrome and Women’s Heart Health Updates
Originally Webcast:
We invite you to join your fellow clinicians to learn about cutting-edge best practices in cardiovascular care. Minneapolis Heart Institute® providers discuss topics in prevention, diagnosis, management, and treatment of cardiovascular conditions. Physicians, advanced practice providers, nurses, and clinical support staff are welcome to attend and earn CME.
Host
Speakers
Welcome to the december Minneapolis Heart Institute. Virtual cardiovascular symposium. This is actually the fourth and final symposium of 2021. And as much as I miss and all of us miss the personal interaction, this clearly has been a great um way for us to communicate with all of you through the pandemic and I honestly don't see how this is gonna go away. I think this format is going to be here to stay. But um um certainly we're looking forward to hopefully more in person interaction um as we move forward out of the pandemic, wow, My name is Ryan Abdelhadi. I'm one of the electro physiologist at the Minneapolis Heart Institute. Actually I've been with this practice for almost 13 years and um it's my honor and pleasure to be your host tonight. There will be questions and answers at the end of this uh talk and then this this symposium. So please go ahead and type your questions in the Q. And A. Uh part of the zoom and we will try to answer all of them or most of them at least. Um At the end of the talks um we have two outstanding speakers tonight that will um talk to us about acute coronary syndrome and that's Doctor Jim Kohlberg Turco Beck is one of our interventional cardiologist at United Hospital who also specializes in structural heart disease and valve disease. Uh And also we have dr Ritu Saxena who is in charge and who directs our cardio obstetrics program and she will discuss gender and heart health um with us tonight and all. Most of you are familiar with the Minneapolis Heart Institute and with the programs that we offer. But for those who don't who are not familiar just gonna spend a few minutes minutes introducing the Minneapolis Heart Institute. We're one of the largest comprehensive cardiovascular program in the region and actually in the in the country, um we deliver the entire spectrum of cardiovascular care um from prevention all the way to a heart transplant. And we have unique programs um including our genetic arrhythmia center or cardio obstetrics program, our cardio oncology program and our adult congenital program. Just to name a few with been consistently recognized as the top cardiovascular program in the twin cities and one of the programs in the country by U. S. News and World Report. And this year actually Newsweek came up with their Ranking of the world programs and we were ranked number 20 in the world and number 13 in the country by newsweek. So um uh we uh we feel great about that. Um and I think there are a lot of merits to that. Um We, in addition to delivering care which is really the main mission of the Minneapolis Heart Institute, we do have um um focus in education and and research. We publish around 300 papers every year through our foundation and we have fellowship programs and training programs in almost every sub specialty of cardiology. Um at the Minneapolis Heart Institute, we believe in delivering the highest level of care locally and partnering with primary care providers and uh you can see from the slide. We cover 5 55 locations uh within Minnesota and beyond in the five state region. That's in addition to our Tell a heart program or telehealth program which adds access to some of our patients who are not living close to one of these sites. And we also have uh locations where we have sub specialists, advanced heart failure, electro physiologists. Ct surgeons, vascular surgeons serve these locations again to deliver care locally and partner with primary care providers in the communities. And certainly the merger between the Minneapolis and the same poll group has extended our ability to do so and uh we feel very good about that um cardiology curbside. Um Actually it's a service that was created to support primary care providers and emergency room providers and also hospitalists in the community to deliver the highest level of care locally. There's a cardiologist sitting by the phone um Every day from 7 30 to 5. And that cardiologist is there to answer the phone about any question related to patient care review a test review on E. K. G. Question about medical management or to help facilitate next steps for care including transfer. Um You really don't have to remember that phone number that's on the slide because what you probably should do if you have not done that already is to download the image i mobile app. It's very easy. Um it's been downloaded thousands of times and on that app, you can push a button and that will connect you to our cardiologist uh campsite cardiologist, but also you can access um our transfer center. If you need to transfer a patient, you can access or see the emergency protocols as well as non emergency, the resources such as anti graduation statin therapy And otherwise through that. Uh now curbside I mentioned it's five days away a week, 7:30-5. But we do have a cardiologist in house in the hospital 24 7 that will always respond to any emergent or urgent question by hospital physician or an emergency room doctor. Last year, we partnered with Broadcast, meant to really extend our educational reach. Um and um be able to provide an additional additional tools for for educational purposes. You can through that website, access a lot of educational videos, including these symposiums. All the talks are going to be uploaded on the, on the website. And we partnered with Broadcast Met to bring these uh these cardiovascular symposiums. So they helped create and broadcast these symposiums um which has been again, a wonderful tool for us to stay connected through the pandemic. Um Also last year we started our podcast by creating these cardiovascular conversations. Um just touching on common topics in a light way. It's a 30 minute podcast that you can access through our website or through any really format or any platform you use for to listen to podcasts, you can listen to that when you're driving or exercising or um um you know, you know, just relaxing and uh these are some of the podcast from last year, there will be more coming next year. Um we really have no disclosures, none of the speakers do they have any disclosures um or um conflicts. Uh this is a C. M. E. Event. Um you can get your CMi by filling a survey and this is the website, you can access the service. All you can use this cure code. I'm using your phone camera and I believe this will be also put on the screen at the end um to get your CMi. So without further ado I'm gonna introduce dr jim Kohlberg dr Colbert is one of our fantastic interventional cardiologist at United Hospital. Again, he did most of his training in Minnesota and he has interest also in structural heart disease and he will review acute coronary syndrome. So I will uh dr Colbert take it from here, thank you. Right, and I appreciate you guys all tuning in this evening and uh giving me the opportunity to update you on acute coronary syndrome. Obviously a big topic and a lot to cover in 25 minutes. So we'll kind of go pretty quickly with this but certainly we'll leave time at the end for questions and then move the slides forward here. So today uh we're going to basically do an overview of acute coronary syndrome, uh discuss uh stem the management. And it also ends the not as television of my management guidelines, But then also briefly touched down COVID-19 impact and how that's affected acute coronary syndromes at least across the nation, um and how it's affecting that potential patient population. So first and foremost, it's important to just understand what the path of physiology is for acute coronary syndrome. So obviously it's a progressive process that begins with deposits of lipids within the internal space. But over time it starts to develop into a Fibra fatty stage and vulnerable plaques, which is essentially the mainstay of what but to coronary syndromes and tail. And so as those uh fibra fatty plaques start to become more vulnerable or a thin plaque on the top becomes thinner and vulnerable for disruption. That's essentially what happens in the setting of an acute coronary syndrome. And so, uh number five, what you're seeing is the disruption of the fibrous cap over a development of atherosclerosis, which then essentially leads itself to development from biogenesis. Now, acute coronary syndromes essentially uh encompassed three categories. So there's unstable angina, which obviously is a symptom complex uh, that can be a variant of symptoms, depending on the patient, not everybody presents with the classic elephants sitting on the chest radiating down your left arm. There can be a variety of patients presenting symptoms, which rain. You will obviously talk about a little bit when it comes to the female population. But patients can get a substantial chest pressure radiation down the arm, you can get significant back discomfort, neck discomfort, you can get nausea, you can get dyspepsia, shortness of breath differences. So how they get categorized into those three different subgroups is unstable. Angina is the presenting symptoms without evidence of myocardial necrosis or biomarker elevation. Non S. T. Elevation, demise is a different category in the sense that you have elevation of biomarkers but no clear S. T. Elevation on your electrocardiogram and then stem E. Is a clear diagnostic picture based on the electrocardiogram where you have clear E. K. G. Criteria that meet S. T. Elevation. And in those circumstances you're dealing with a complete occlusion of an artery in the non ist elevation arm. It's not generally an included vessel and what you're seeing is a plaque rupture with that combo genesis forming but distal embolization of that trim biotic material which lends itself to the elevation and the biomarker when it comes to the epidemiology or the history and progression of acute coronary syndromes. Fortunately with medical care, we've done a really good job modifying people's risk factors such that stem E. Populations or at least presentations are on the decline. Now that being said we're seeing more significant stable coronary disease that still is progressing as patients risk factors are still present and actually the non S. T. Elevation M. E. And the unstable angina populations are actually on the rise. Which has an intervention a list I can attest to because the complexity of coronary anatomy is definitely becoming more difficult. Now when we talk about S. T. Elevation M. Eyes there's clear diagnostic criteria that the guidelines utilized to classify somebody is meeting it diagnosis and the typical S. T. Elevation of my is generally one millimeter of S. T. Elevation and two contiguous leads in the primordial leads and based on gender, there can be some differences. In addition we can also have circumstances like posteriors mes which are not as frequent but still have to queue in your interest if you're seeing STL or excuse me. SD depression in the uh anti R. Recordable leads occasionally utilizing a posterior lead set which would be the seventh through V. Nine which is on the back can actually be indicative of an S. T. Elevation, posterior lee. You can also have a. D. R. Elevation and global esti depression which frequently can be a sign of either multi vessel disease or in a rare circumstance you can see left main inclusions. He went through T waves are circumstances where you have subtle esti depression and hyper acute T waves. I think a lot of people are familiar with. Well in sign which is usually a deep T. Wave inversion which is oftentimes a progression of an anterior myocardial infarction which generally manifests in patients chest pain free uh moment where the egg is actually demonstrating no longer S. T. Elevation but more of the re profusion T. Wave changes. Left bundle branch is also posed a challenge when it comes to identifying S. T. Elevation. They are no longer considered a criteria consistent with acute coronary syndrome unless it's new. And presenting symptoms are consistent with angina. But there is a criteria known as scar bosie which frequently people are familiar with that do give you some insight in terms of whether or not S. T. Elevation could be pathologic in the setting of those underlying based on U. K. G. Changes. Sorry about that. But when it comes to stem e it's really time is of the essence. And getting somebody to a re perfusion means whether it be pharmacologically or per cutaneous lee is of utmost importance and the reason being is because an ability to salvage mile cardi um and also reduce mortality is directly proportional to the time from symptom onset to re perfusion. And so that really has been the mainstay dictum when it comes to management of acute coronary syndromes is to open up the culprit vessels as soon as possible. And that really is what stemmed the whole level one process. And actually we're fortunate here in the twin cities particularly in Minneapolis Heart Institute. That was one of the pioneers in developing established level one programs. And the idea being is that from patients symptom onset. We want to get them to re profusion as quickly as possible and that depends on patients location. So not everybody is fortuitous fortuitous enough to have one of these events in a metropolitan area where they can get to a PC center quickly. So in those circumstances building in mechanisms within the community to understand additional means to treat an attempt to achieve re profusion prior to getting to a PC. I center specifically with fire analytic therapy is still very much important and germane to our current practice today. And so the idea of door to balloon time is essentially when somebody has symptoms, get them to a cath labs and we can open up their vessel. And the idea is first medical contact to ballooning open the vessel within 90 minutes Not everybody can present to a center. So if it's still within 120 minutes, that's still reasonable. If you're presenting to a non PC. Capable center, as long as you can transfer patients that way, whether it be air ambulance, what have you. But in circumstances where the delay can be over 120 minutes. That's where utilizing something called a pharma co invasive strategy which is frequently a half dose or full dose um uh from politic treatment but then transferred to a PC I capable center for angiography and intervention when came to appropriate. Now as I outlined before. Mh I has been a leader in this particular area and dr tim Henry previous partner at Mh I did develop the level one program with the current partners that are there with essentially establishing a geographic map to identify patients who would benefit from emergent transfer vs considering politic therapy if their distance was over 60 miles and that's still a map that we utilize today when when treating patients with acute coronary syndrome. Specifically studies now let us seem kind of antiquated for us in the twin cities just because we have the ability to intervene with interventions quickly. However, when reviewing the data, Lennox still are used and are actually very effective and the timing one with which you can deliver lyrics is actually critically important in this slide kind of indicates how patients that benefit from a strong politic therapy are generally patients with S. T. Elevation, but also patients who have symptoms onset to treatment and generally the first few hours of their presentation. Older patients obviously tend to have higher comorbidities which then leads them which leads providers to being concerned about utilizing the therapy because of the risk for intracranial hemorrhage or other significant bleeding. And I think that's the biggest worry when it comes to little treatment is the concern of potentially increasing someone's risk of bleeding most catastrophic of which would be intracranial hemorrhage. So currently we do have several um three analytic therapies that are in use. Um streptokinase was the initial one but has now been more or less overtaken by T. P. A. R. Alta place. Um All of the therapy still can be utilized but T. P. A. Is pretty much the main ST treatment for acute coronary syndrome. But like I said, the biggest worry from providers is what is a patient's bleeding risk. And I think understanding the absolute contra indications to utilizing fiber olympic fiber Olynyk therapy is critical but also categorizing patients based on their wrists. And there are various risk models that utilize patients age, um their comorbidities, time of presentation, other medical therapy that they're taking to differentiate folks that may be higher risk to utilize lyrics and in those circumstances you would maybe defer to um invasive strategies regardless of the time frame for transfer. Now, how does lyrics compare to primary PC. I. Well that also has been studied and that's really why getting them to a PC. Capable center is critically important because her cutaneous intervention does pretend a better long term outcomes. And the dynamite trial, which was one of the initial evaluations between these two strategies just came out with his 16 year data this year which continued to show an improvement and composite endpoints mainly as a result of repeat hospitalizations for M. I. And then also cardiac death. So the reaper fusion strategy is essentially getting to a PC center knowing that that timeframe over 120 minutes is where five analytic therapy should be considered and still needs to be understood and considered as a practice as a management for patients with S. T. Elevation lies Once you get politic therapy it frequently still is transferring to a PC. Capable center because oftentimes still proceeding with coronary angiography, with stenting of culprit vessels results in a better long term outcome in terms of mortality and recurrent mace events. So the H. A. Guidelines for primary PC. I. Um include basically proceeding with PC. I within a 90 minute timeframe for PC. I. Capable centers, 120 minutes if you're going to a nine transfer or non PC center as long as you can transfer within that time frame. Still any patients that have symptoms ongoing continued to do invasive strategies. The only circumstance where we would not do an intervention or perceive with angiography is when folks present with over 24 hours of symptoms in our, excuse, me over 24 hours since onset of symptoms but upon arrival are asymptomatic and otherwise stable in those circumstances, there is generally completed and proceeding with any intervention at that point is usually limited uh utility pharma co invasive strategy is what I had alluded to before. And so patients who do get limits. You still transfer to a PC capable center almost universally. We're still capping those patients whether it's class one or Class two indications just depending on the symptom complex that they have upon arrival. If they are asymptomatic, it does not have to be done urgently, but anybody with signs of failed re profusion get directly taken to the Castle, any patient asymptomatic upon transfer. Those generally patients are not necessarily needing angiography emergent lee and if they've already completed their infarct again it's usually not indicated to proceed with any coronary angiography is usually there in fact has been completed now. Despite Pushing towards a aggressive door to balloon time, we've made incredible strides to achieve that within that 90 minute timeframe. But we've kind of plateaus in terms of the overall mortality was stemming. So now we've been able to achieve those really aggressive door to balloon times. But still mortality tends to stay about the same whether you're within that 90 minutes or over that 90 minute time frame. And so P. C. I. Is just one component of management for S. T. Elevation of my pharma. Co therapy is obviously a huge adjunctive treatment and this in and of itself could be its own talk. But obviously the main ST treatment for folks who come in with S. T. Elevation eyes is an aspirin treatment which has continued to be proven to be beneficial. Anti coagulation which is most frequently being utilized with um fractionated heparin and then also our final purity in treatment or P two Y 12 inhibitors. Initially it started with clopidogrel but that has since more or less been replaced by both procedural and taika galore which are newer agents that block the P two Y 12 inhibitors, but the reason why they have more or less exchange for Plavix is because of their quicker onset of action action. And in comparative trials showing a greater reduction mortality. With a CS trials, Demi's across the board are folks that are going to be preloaded prior to them arriving in the cath lab. We want to have the most aggressive anti platelet inhibition as possible and that's generally why all of these patients are going to get pre treated when patients are transferred as chronicle invasive strategies. We still load them with anti platelet therapies but the timing of which is just dependent in terms of when they arrive and when the PC is plant pass a grille in and of itself does have a black box warning for certain patients because of an increased risk of bleeding. Specifically patients generally over age 75 or low BMI patients or any patient with a previous stroke, there is a black box warning and it's used because of an increased risk of bleeding. Both stemming therapy essentially is a commonplace across most centers. I think most people are probably familiar with the cocktail of medications that patients get. Dual anti platelet therapy is still a mainstay treatment for post pC patients with stents, still to date. The H. A. C. C. Requires 12 months of dual anti platelet therapy unless utilizing a bare metal stent which is infrequently used given the newer generation drug eluting stents and the significant reduction in re narrowing within stents. With the contemporary stent technology, beta blockers have universally shown reduction in myocardial infarction when utilized acutely in the setting of an S. T. Elevation of my and are still maintaining a mainstay of treatment as long as piece of human dynamics tolerate. Ace inhibitors and arbs also used frequently, particularly most benefit in patients with LV dysfunction and large anti Ramiz statin treatment. Obviously still a mainstay in terms of preventing secondary events but also stabilization of plaque. That is there. We evaluate all of our steamy patients with comprehensive TTS to get a better understanding of the LV function. In addition to utilize more goal directed therapy based on what the LV function necessitates cardiac rehabilitation is critically important. And in addition nutritional consultations understanding the importance of a cardiac healthy diet in terms of reducing patients long term effects and recurrent cardiovascular events. Complete revascularization has also become a hot topic within the interventional world. And mainly the question is, You know, should patients who have other non culprit related severe blockages be intervened upon. And the answer is yes. And what we're finding is a lot of that plaque that's there is actually also unstable plaque. And so several trials from 2013 of the current date are demonstrating that during the index hospitalization or even the index procedure, it may be beneficial to complete patients revascularization. The historical dictum was to discharge patients and have them return for stage intervention but based on these trials and compelling data. We are changing our practice in terms of managing that. Hey guys, I'm a little forward there. And so another important thing from an interventional perspective is does access matter. And radio versus ephemeral access has also been a hot topic of debate. And at present we are generally seeing in radio versus ephemeral access sites uh in stemming populations of reduction in all cars mortality. In addition to bleeding with a radio access, which is another paradigm shift in terms of how we're managing these patients with a more frequent attempt at radio access for patients with these acute coronary syndromes. But still there are challenges with them. Cardiogenic shock still continues to be an issue. 8-12% of all patients presenting with Demi do develop some form of shock, which increases mortality considerably. In addition, out of hospital cardiac arrest is a big issue. Again, increasing mortality 10fold. This has led itself to developing shock if not cardiogenic shock or out of hospital arrest centers so that we have dedicated specialists not only in the Cath lab but also dedicated advanced cardiologist, specifically in heart failure that can help manage these critically ill patient. But in addition, there is always going to be delayed presentations, patients still in rural communities have a difficulty getting into hospitals understanding symptoms. People should be worried about there's discrepancies in both racial and gender inequality when it comes to managing the queue coronary syndromes that still have yet to be mitigated, interesting too is in hospital access events actually portend higher mortality for similar reasons, patients frequently are not identified quickly. In addition they maybe not on telemetry and for various reasons there's frequently delays for patients to get optimal profusion strategy out of hospital cardiac arrest also is a whole different issue in and of itself not very common but yet it is still seen and portends it tremendously. Poor prognosis in patients who suffer from this disorder. Obviously if patients are resuscitated and have steady, they go directly to the Cath lab but there's been a lot of debate whether or not patients who do not have an S. T. Elevation upon their kg. With rusk. Do you take them to the Cath lab? And the data to date is suggesting that generally you treat these patients optimally in an iCU let them recover and then once neurologically stable you can then electively return for angiography Unless s chemically driven need to perform revascularization sooner dictates that management, now known as the elevation of my is different. So like I had mentioned before that the elevation of my trauma genic conclusion the vessel is totally closed. E. K. G. Evidence of S. T. Elevation known as the elevation of my is generally thought to be an acute plaque rupture but the vessel's not closed and what you're seeing biomarker elevation as a result of thrombosis. Embolism of that trauma genic milieu. Now not as the elevation of mai's essentially treated similarly to uh the elevation of knives. But the difference being is when do you want to implement a re profusion strategy? And that's been the biggest debate and non ist elevation on my management is When do you take these patients to the cat file? Generally speaking, the kind of universally adopted management strategy is folks who have evidence of high risk features. They're unstable, shock persistent symptoms. Despite addition medicinal treatment, patients generally are going to be taken to the cath lab immediately. Otherwise patients can be categorized into high risk or low risk based on E. K. G. Changes, intermittent persistent symptoms. Also risk tools to evaluate people's risk stratification To a early invasive strategy which is generally within 24 hours. But those patients that are lower risk despite biomarker elevations don't necessarily have to go to the Cath lab immediately. And that's called a delayed interventional strategy which is generally between 24-72 hours. Now, those um risk model or excuse me, risk stratification tools we frequently use are things called the timmy or thrombosis and myocardial infarction score or a great score and essentially no one's really calculating this at the bedside but it's more or less a clinical intuition in terms of how sick these patients are and it usually incorporates their age, How bad is there a K. G changes, What are their human dynamic present presenting vitals? Are they unstable? Congestive heart failure. Obviously the more you accumulate, the higher risk these patients are and the more likely you're going to be moving towards an invasive strategy. Earlier this has been studied at nauseam in terms of all and non S. T. Elevation in my patients. When should we be taking them to the cath lab? And if you group them all in one cohort there's a statistical trend towards taking in the cath lab earlier. However, there really is not a difference between the standard 72-hour management versus early meaning within 24 hours. The only exception is in those patients who have high risk features. And so those people with high timmy scores or high GRE scores, there is clear statistical evidence for an early invasive strategy in terms of intervention. Now when it comes to treating these vessels generally treat the culprit vessel mm. However they also do frequently have multi vessel disease and the incidents of three vessel disease with non S. T. Elevation demise in unstable angina can be as high as 30%. And so really it depends on kind of the complexity of patients, coronary anatomy and in these particular populations were more frequently having this heart team approach between cardiothoracic surgery and interventional ist to determine based on their coronary anatomy which revascularization, revascularization strategy would be better. And coronary bypass is still very frequently utilized, particularly patients with LV. Dysfunction, diabetes. And we use something called a syntax score which is generally a classification of the complexity of people's anatomy. Now the pharmacologic therapy for an honest elevation allies essentially the same as it is for stemming. The only real difference is when are we giving these patients that diana perdon or P two Y 12 inhibitors And honestly you can justify your bias pretty much whichever way you want to go because there is conflicting data on this matter. But generally speaking with the contemporary P two Y 12 inhibitors were finding that the onset of action is so quick that we're able to actually load patients with these medications in the Cath lab after we define their anatomy. And that actually was proven in a recent trial, particularly with prasugrel where we're able to actually load these patients in the Cath lab without having it preloaded with still very good outcomes in terms of recurrent mace abouts and reduction of mortality. So the general treatment when it comes to and steamy is obviously um fractionated heparin but then anti platelet therapy with aspirin when it comes to anti coagulation. Like I said, most of the time it's an fractionated heparin heparin. Occasionally we use direct from and inhibitors in the form of bivalve rudin. However, um fractionated heparin tends to be the main ST treatment, mainly because data has shown some increased incidence of stent thrombosis with by val Rudan anoxic parent or low molecular weight heparin has also been utilized particularly in transferring centers but generally in a hospital setting during pC. We will be using impression it'd happen aspirin mainstay treatment and then obviously our P two Y 12 inhibitors whether it's press a grill, taika galore or planet, interesting new therapies, particularly our kang galore and candle or is a very attractive agent, particularly for patients who are really unstable intubated, unable to take oral therapy. It's an ivy P two Y 12 inhibitor and the attractive quality of this medicine is it acts quickly. Um but then it also can be turned off quickly within about 60 minutes. And so for those folks we do utilize it. It's incredibly expensive therapy but it does have uh an attractive use within the A. C. S. Population. Two B three a inhibitors are not used as frequently just because of their increased risk of bleeding and they are more often used in the time of the Catholic procedure when there's a significant high cloud burden. The invasive strategy as we have talked about before tends to be emergent when those patients have emergent needs to be evaluated. Alternatively, we then categorize patients based on their clinical risk to an early meeting within 24 hours strategy of invasive in evaluation versus a delayed strategy. If they're in the lower risk category. The post and semi treatment again very similar again 12 months duration for drug eluting stents. We do refer these patients for cardiac rehabilitation and then appropriate age related risk factor modification with lipid control, blood pressure, diabetes control, tobacco cessation, diet control, etc. Now, one group that I think is of specific interest is we frequently are seeing patients who developed uh a CS syndromes but are also an anti coagulation because of Except and this does pose a significant challenge with what we call Triple therapy. And what we have shown in recurrent trials is that Triple therapy does not bode well in terms of patients uh adverse event rates, essentially there is a tremendous increase in bleeding risk when patients are on prolonged triple therapy with aspirin. A sign appeared in or take a galore and then some form of oral anti coagulation. Generally speaking, it still can be used but in a very brief time frame generally for the duration of patients, hospitalization seems reasonable or At most within one month after their index procedure. After that point, there does not appear to be any clinical benefit for continued Triple therapy. And in fact there is a adverse event rate because of the increased risk of bleeding. Generally speaking, the victim is the final period in RPG Y 12 inhibitor. More often than not Plavix with oral anti coagulation, either warfarin or one of the direct oral anticoagulants therapies. Now, obviously COVID-19 has thrown a huge wrench in how we're managing acute coronary syndromes within the last two years um we've obviously had to change the way we manage people just because of the need for PPE and lack thereof. But for the most part, what we've seen surprisingly is there's been a reduction in a CS presentations since the advent of the pandemic and that actually is worldwide. Not only here in the United States. With that said what we're also seeing is folks that do come in with S. T. Elevation, demise. They have a kind of variant of presentations And in about 20-30% of patients who fit the criteria of annex are actually not having any culprit related vessels. So they're frequently falling into categories of myocarditis, potentially coronary beso spasms, michael from biotic disease or potentially um taco suba or stress cardiomyopathy. But the folks that do actually have clear cut acute coronary syndromes either and stem ease or S. T. Elevation of eyes tend to be sicker with higher mortality rates and I also have a tremendously high clot burden that we've noticed in the settings. The other thing we're also noticing is people are neglecting their symptom complex and they're presenting late and as a result the sicker patient comes in which is a much more complicated intervention but in addition a much more complicated post interventional hospital stay. The COVID-19 has definitely posed a challenge for all individuals. But we are certainly seeing it within the cardiology field, particularly an intervention. The one more slide here. Just a few pearls I know this is a ton of information that's hard to kind of condense this and I apologize for talking pretty quickly but you know A. C. S. S. Stayed pretty standard in terms of pharmacologic treatment Invasive strategies being number one. with a few contemporary pearls that I wanted to add in there with regards to at least contemporary practice today. But a few other things to think about obviously when patients present with any chest pain syndrome or vague symptoms that may not fit the criteria. Repeating EKGs are important because we can frequently find clear cut dynamic changes that would lend itself to being more aggressive for an A. C. S. Management V. One through V. Three SD depression continued to think about potential post. Um I guess considering uh post um I or excuse me post your leaves which are beef 7 39 on the back with inferior mes are frequently pre load dependent. So be cognizant of that basil dill laters which drop your pre load can get those patients somewhat unstable. There are oftentimes needing fluids frequently berated Kartik as a result of heart block. Um And oftentimes can also have in farce of their RV which lend itself to evidence of clinical pre load dependence Demi complications are still important If somebody's presenting early it's really going to be a rhythm disturbance or arrhythmias. So defib relating those folks quickly is what we're looking for when they're presenting. That's why calling E. M. S. Or 911 is what we always need to tell our patients because a rhythm a genic death is the most common reason people have a fatal result as a result of the next elevation of mine. Late presentations can result in late complications. three wall rupture, pericardial tamponade, the SDS, papillary muscle ruptures which result in acute mitral regurgitation, significant de compensated heart failure or peripheral embolization as a result of a L. V. Thrombosis. A few other interesting tidbits morphine, although it is still considered part of the initial treatment strategy, there has been some emerging data with the fact that it may block gut absorption, particularly RPG Y 12 inhibitors. So in those circumstances we may use more aggressive anti platelet therapy in the Cath lab, cocaine induced Bezos, spasms or am I still occur And in those circumstances obviously isolating to one particular therapy like a beta blocker can cause unopposed alpha organism. So it's things to always consider to avoid in those circumstances. But again, the really reiterated point is primary PC continues to be the preferred method. But we still are living in a community with multiple patients that are not living close to PC capable centers. So we still need to be aware of our fiber analytic option as well as our farm ical invasive strategy. But as Ryan had said, you know cardiologist, we're always making ourselves available and we are always here to answer any questions when they come up. So please do not hesitate to give us a call. Um so quick overview. I know it was a lot. So I apologize for talking super fast but I appreciate you guys taking the time and look forward to any questions that come up. Thanks rita and thanks jim. So um Dr Saxena is uh one of our cardiologists at the Minneapolis campus and she runs our new obstetrics program. Um She actually explained in both critical care and cardiology and she did her training in new Mexico and Oregon. So Um No one is better to give us an update on gender and heart health. So go ahead direct well. So I'm re too sexy and I have the great honor of being the co director of our cardio obstetrics program at um the at Abbott here on the um west side of the twin cities. Um we're gonna talk actually about gender and heart health. My other great passion in life other than thinking about pregnant women, which is what I was doing earlier today. Um I also like to think about gender differences in ischemic heart disease and just how heart disease is different in women. But I will talk about cardio obstetrics because I can't resist in any talk I give, even if I was talking about my kid's soccer team, I probably would still bring up my cardio obstetrics flight 19 oh eight. Heart disease became the official number one killer of women. And since 19 oh eight heart disease has remained the number one killer of women In 2018, which is the last set of statistics That we have from the CDC cardiovascular disease was responsible for about 420,000 deaths. Women represent about 49% of all deaths in cardiovascular disease, about one minute one death every one minute and 16 seconds. Um, so you guys will be on this for a little bit more than an hour and a half. I'll let you guys do the math. Not only is cardiovascular disease responsible uh, for being the number one killer of women, it's also Quite expensive to the health care system. In 2016, cardiovascular disease was the first list of diagnosis and about 2.2 million women discharged from short stay hospital. And despite women being about 50% of patients in cardio, in cardiology, only about a quarter of bypass. And about a third of for continuous coronary interventions occur in women. So, as you can see here between 19 Um, and about 2013, actually more women died uh, than men did in about 2013. We reached equipos with men for the rates of death and that's due to things like the Go red for women and heart campaign and the Wise Women campaign. But unfortunately since 2010 heart disease have been up tick, including for young women. So we know that it's the number one killer of women are mortality is different in women. 23% of women who are over the age of 45 who have a first heart attack die within a year, compared to 18% of men. The five year mortality is about 47% in women and 36% in men, wow, we're just moving ahead. Apparently, my slides are going up. The five year incidents of heart failure after the first m. I. Is definitely increased in white women. But as you can see here, black women um kind of Have the highest prevalence of heart failure. Regardless of whether you're 45-64 or 65-74, they fall off over 75 just because they're more mortality rate. Uh there's not that many black women alive simply because they hit their mortality rates earlier. So, again, I direct co direct the cardio obstetrics program at Abbott. And it's really hard for me to talk about really anything without showing the slide, which for those of you who have not seen it, this is the maternal mortality rates in the United States. Um, my slides are just taking off for some reason. Any ideas, guys. Nevertheless, um, the maternal mortality rate was about 17.4/100,000 live births in 2018. Uh we beat every developed country um in the decades between 1990 and 2015, there was a worldwide decline of maternal mortality about 44% in the decades between 2000 and 2014. The United States had an increase in maternal mortality by about 27%, certain states like Texas, they're pushing about a 50% increase. We know that when we look at pregnancy related ducks And we think about the reason that these women die, the majority of it is actually things that general cardiologists deal with day in and day out, cardiovascular conditions, coronary condition, cardiomyopathy, or we can't muscle preeclampsia, eclampsia. What I like to refer to as hypertension of pregnancy. Um, this is when you pull them all, about 40% of these deaths in the United States and elsewhere could be related to things. I see day in and day out in a cardiology um clinic, we know that there is some variation by uh ethnicity, um racial and ethnic gaps clearly existing. Um, maternal mortality statistics, if you happen to be a black woman in the United States, that's pregnant, your 3 to 4 times more likely to die than a white woman more often do things like pre eclampsia and eclampsia and pulmonary or amniotic embolism versus a white woman that tends to Have more issues with mental health problems. And most of these deaths occur within uh, 42 days in the postpartum period. The sad thing is, most of these deaths are actually preventable. This is from the California medical collaborative, that actually is one of the few states in the country that actually have decreased their maternal mortality rates. And what they found was that most of these deaths, about 90% of them could have been prevented and prevented, probably by paying attention to the warning clinical symptoms and signs. And so really if we thought about the signs and symptoms, I asked my 96 year old patient in General Medicine clinic, do you have chest pain? Are you short of breath? Do you have P. And G. Or thought mia do you have lower extremity swelling? Are is your heart racing? Do you have issues with headaches, high blood pressure and or low blood pressure? If we actually asked women these same questions, we would probably be able to prevent about 80% of the maternal mortality deaths that we see because maternal mortality is so high and these women are so complicated. Those of us who practice cardio obstetrics truly believe it needs to be multidisciplinary and how we manage these patients. I spent my um the majority of my day at Mother Baby today, working with my great colleague dr Bigelow, seeing patients with everything from severe mental stenosis to palpitations, We manage them multidisciplinary, where we actually see patients together. There's a cardio obstetrics dr, a maternal fetal medicine doctor uh nurse coordinator. We have our pharmacists to see patients with a social record patients with all of our patients are discussed in a multidisciplinary format prior to delivery planning. We have electro physiologists that we work with adult congenital doctors that we work with as well as a tv surgeon that comes to the we take care of patients from preconception all the way through what's aptly named the fourth trimester and then identify those women that actually are increased risk for cardiovascular disease later in life really quickly. How does our program do? Well we actually looked at this. This is actually data that we just presented at the american heart association from our program Adelina, where we looked at how a cardiovascular obstructive program does compared to just general cardio care and pregnant women which is just referring a patient to general cardiology that happens to be pregnant. We looked at our patient population between 2018 and 2019 being married to a historical court and found that oddly enough we saw much sicker patients. So this is what's called a modified World Health Organization classification. The higher the number the more sick the patient is. And we saw across the board more sick patients in the C. B. O. B. Program. And there wasn't really much difference in how they did. We. We did have more um longer length of stay after vaginal delivery. But again remember these women primarily died within 3-7 days after delivery. So we kind of purposefully set it up to watch them longer. We had no doubts in either in our program which knock on wood continues. But what we did learn is that in the six months postpartum We had about half the readmission rate and er visits that those individuals just seen by general cardiology um in the 2016, Cohort. So we did better um in terms of readmission in Edie visits and these women had a better outcome. So pregnancy is a huge difference in how women do with heart disease. But women's outcomes, as I just said, are worse than men. We have pregnancy complication as dr cole beck noted, there is evidence of a gender bias. Women have smaller blood vessels and really at the end of the day, women are just not small men, we absolutely present differently than men. We have. We do have chest pain, although that chest pain may be more back shoulder arm discomfort. Women are more likely to complain of shortness of breath, were more likely to complete complain of weakness and fatigue. If you happen to be a young woman, you're more likely to have atypical chest pain or chest pain than older women, which are more likely to have shortness of breath. Yeah, because our symptoms are definitely often minimize them. We often are too busy to seek care because while we're busy taking care of our kids, giving talks, doing work, taking care of her husband's taking care of our house. We really have what's called the Wonder Woman phenomenon were just too busy to seek care, too busy to take care of ourselves. And then we often attribute symptoms to something else. There's also an under appreciation or lack of awareness when it comes to heart disease. Um Being the number one killer and women In 2009 about 65% of women and those are white women were aware heart disease was the number one killer of women told me about a third of black and hispanic women. It is the number one killer of black and hispanic women as well. In the United States. They redid this survey and in 2019 it dropped from a 65% awareness to about a 44% awareness that heart disease was the number one killer of women. More women felt that cancer was the number one killer of women and breast cancer in particular had increased. Now breast cancer no pun intended is near and dear to my heart that a family member just diagnosed with it and thank goodness for her. She does not die from breast cancer but women do die from heart disease. So we minimize our symptoms are symptoms are often different. But then we do show up to the emergency room were less likely to get work up, we're less likely to get invasive procedures. As I mentioned we're actually less likely to leave the emergency room with that. Very important. E. K. G. That dr Colbert talked about turns out I thought this was something of the past but recently in May of 2021 there was an A. C. C. Presentation by a resident when they looked at their E. R. And it turned out women were 11% more likely to leave the er without in kg. For similar cardiac symptoms compared to men were absolutely less likely to get referred to cardiology and were less likely to get struck. So we have different symptoms. We have a different evaluation. We have different risk factors. There are absolutely the traditional risk factors absolutely impact women. Some of them have the same risk as it meant. Such as cholesterol, obesity, our family history of cardiovascular disease. Sedentary lifestyle but certain risk factors are actually more um uh impactful in women than they are in men such as hypertension, diabetes tobacco actually confers a greater risk in women than it does in men. There are female predominant risk factors such as rheumatology disorders, lupus, rheumatoid arthritis, lupus actually increases our risk of ischemic heart disease by threefold rheumatoid arthritis increases our risk of heart disease but about a similar to diabetes. Depression plays a much larger role as the psychological stress in women. If you happen to be a young woman with depression and suffer a heart attack like dr Colbert spoke about you're actually much more likely to die than if you don't have depression. Then there are the female specific risk factors which all the labor in a minute when it comes to pregnancy. But early monarchy. If you had your period less than the age of 11. Your increased risk If you've had early menopause you lose your period before the age of 40. You're actually at significant increased risk. We know that adverse pregnancy outcomes hugely impacts our risk for not just hypertension later in life, but cardiovascular disease. Ischemic heart disease stroke, heart failure, diabetes. This is UK bio bank data that was published in 2019. Looking at women who had hypertensive disorders of pregnancy, Not only are the disease processes of coronary artery disease, heart failure, aortic stenosis and mitral regurgitation more prevalent, but they actually occur at a younger age compared to those women that don't have hypertensive disorders of pregnancy also turns out that about anywhere from half to two thirds of the excess risk that these disorders um lead to later in life could be abated by treating our hypertension to just guideline accepted um values. Unfortunately in this country, women are about a third a third of women with hypertension get treated appropriately to guideline accepted values. So are risk factors are different. What happens to us in pregnancy impact us later than in life, but our arteries are different. Um We have smaller diameter arteries. We actually see less vocal stenosis. We have more diffused pattern of after sclerosis. We have more soft plaque. We have more vascular dysfunction. And despite um the fact that we don't have this focal stenosis. Our prognosis is not any better. So, I always love to show this picture. Yes, I carried around in my pocket. I show it to patients. This is what dr Colbert likes to put stents in the big juicy red vessel but what really feeds the heart are these small vessels. And women tend to have more small vessels and please don't leave this toxic dr saxena said women don't get after sclerotic disease. That is absolutely not true. Everything Dr Colbert said applies to women and we should be applying guideline directed medical therapy to all women with acute coronary syndrome. Non stem ease and stem ease. Women absolutely get after sporadic disease, both stable and vulnerable plaques. But women are more apt um than men to have issues with Bezos. Spastic angina micro vessel dysfunction. We tend to see things like spontaneous coronary artery dissection in Takatsu both much more commonly in women than we do. And then and because women tend to have more um myocardial infarction without obstructive coronary artery disease, we actually have coined a term called Manaka which is my cardio infection. Or am I know coronary artery disease or Anoka which is ischemia. No coronary artery disease, diagnostic criteria for an M. A. Is exactly what dr Colbert said. Troponin E. K. G. Changes. Um No obstructive coronary artery disease on an angiogram. And really no other reasons such as to Kosovo's or myocarditis for having um these uh this presentation likely could be due to coronary micro vessel dysfunction could be based on spastic could be black disruption sometimes scad is missed and called Madoka. Although the mortality rates are lower compared to myocardial infarction with obstructive coronary artery disease. These women have similar rates of persistent angina, nonfatal cardiac events um compared to obstructive coronary artery disease. And they usually have a worse quality of life in that spontaneous coronary artery dissection is much more prevalent in women Across Angiogram series, it's about 4%. But in women, especially younger women, it can be up to about 35% of women who present with acute coronary syndrome. For those of you who don't know what uh spontaneous coronary dissection is. It is a caring of the blood vessel um where the blood vessel actually pulls the intimate lining pulls away from the media and advent tisha. Um and that leads to either a tear or an intramural hematoma most commonly. This is seen in young women below the age of 60. These individuals don't have traditional or even risk enhancing risk factors for cardiovascular disease. More often than not, they actually in series up to 80% or more have what's called fiber muscular dysplasia. Most of these women, if they present with acute coronary syndrome or non stem ease, We actually recommend a medical management approach because catheter-induced complications are quite common in 2019. Researchers at the Minneapolis Heart Institute Foundation actually showed those individuals who present with me have ongoing no flow in the coronary actually can be well treated with stents If you get a stent, you should be on dual anti platelet therapy. Otherwise, the recommendation for medical therapy is lifelong aspirin indefinitely and beta blocker therapy as much as possibly tolerated. And then of course, if your pump function is reduced, guideline driven left ventricular systolic dysfunction therapy. And even though the scad-related mortality is low, there's actually a high rate of adverse events. And about 10-20% of these women have recurrence. It does occur during pregnancy and we actually have a term for it. It's called Peace Cat and it can actually complicate pregnancies and lead to increased morbidity and mortality. The other side of the coin for women who are in the menopausal or postmenopausal phase is that women are more uh postmenopausal women are more often to present with something called broken heart syndrome or Taka Sudo cardiomyopathy. Otherwise known as stress cardiomyopathy. Where the stress of whatever it may be being a surprise party. Physical trauma, emotional stress exerts an acute impact on the heart where we think that overwhelming cata column in surge actually leads to acute micro vessel dysfunction and perhaps actually my reversible maya site damage at the level of the cellular level. Um leading to what looks like a heart attack. But when we look, there's no obstructive coronary artery disease. We're actually in the process of researching broken heart syndrome at Elita at Abbott Northwestern. We're actually using FmRI to actually look at coronary microvascular flow to see if the micro vessel dysfunctions. Just a cute or if it remains chronically keep, keep I'll keep you all posted, come back in a year and report out our data at that time. So this is kind of hispanic heart disease. Um as an overview, you know, again, women do get obstructive heart disease but they also get non obstructive heart disease. There's acute findings and chronic finding and across the board applying guideline directed medical therapy and guideline based therapy for revascularization. Um cardiac rehab, which women probably benefit for more but are less likely to go to uh makes a huge difference. Things like coronary micro vessel dysfunction, spontaneous coronary artery dissection, stress cardiomyopathy may also benefit for things like mindfulness based stress reduction. Again, women's brains, much like women's hearts work just a little bit differently. Um We're more often to have a fear response to things um instead of having blood pressure and heart rate response. So, as I've alluded to through the whole evening, we have significant disparities in treatment. We have delay in onset when we do present and get stents were less likely to be given aspirin for acute coronary syndrome were less likely to go home with a guideline directed statin therapy were also less likely to be adherent to medicines as we know that these medicines were not studied in women and we're likely to have more higher side effects. We have less revascularization, The one that stymies. Me is we're less often referred to cardiac rehab. Despite the fact that women have probably have better outcomes from cardiac rehab, we're more likely to die um out of hospital and we have an increased risk of rehospitalization. Absolutely. Our quality of life is poorer um after myocardial infraction and were much more likely to have angina. So I like to pause and think about the positive. I try to be as positive as possible and I tell patients that 80% of what I do, actually, both in my cardio obstetrics practice and my um general cardiology practice is preventable for those of you who have not seen the wheel of prevention or Had her doctor medium to speak about the wheel of prevention. This is from the 2019 American College of Cardiology Guidelines for Primary Prevention. I really do like the wheel of prevention. It really talks about how to keep people's hearts happy healthy and well, the things that I would add to the wheel of prevention is ask women about their menopause risk factors. There men are key risk factors in their pregnancy risk factors if you happen to take care of pregnant women and they've had hypertensive disorders of pregnancy or other adverse pregnancy outcomes, encourage them to breastfeed. It actually does decrease their cardiovascular disease later in life. And I honestly think everybody should have their tenure risks or calculated, it's probably much more powerful in predicting who needs prevention aggressively. Um compared to and applying risk enhancing factors compared to just looking at the cholesterol, saying the cholesterol's okay, So a long time ago now, it's been a long time. I graduated medical school. It was a long time ago and we were taught that something magic happened at menopause in women's life. Um, for those of you who've experienced menopause, I understand it's not so magical, but um, nothing magical happens at menopause. There isn't a light switch that turns off and all of a sudden we're at risk for cardiovascular disease, I truly believe. And I think the more we think about it, the better we'll do as a country that we should start thinking about cardiovascular disease. Younger women um, and thinking about those risk factors even prior to pregnancy because they do impact our adverse pregnancy care. And as I am a researcher at the Minneapolis Heart Institute Foundation, this is probably one of my favorite, most poignant cartoons is that we have studies of fruit flies, mice, hamsters, frogs, monkeys. Men with this research. But medical research using women as subjects trust never occurred to anybody. We've been behind in about 37 to 40 years for cardiovascular disease research in this country. Women only make up about 30% of cardiovascular research trials right now. And very recently this summer actually, in july, the land set had a commission that reported out cardiovascular disease worldwide and women. So it turns out that heart disease is not only the number one killer in the United States, it's actually the number one killer of women worldwide. About almost nine million women died in 2019 from heart disease worldwide by my slides. Um 275 million women were diagnosed with cardiovascular disease in 2019. About 35% of all deaths are due to cardiovascular disease. What we do know is that women are understudied, as I said, under recognized, underdiagnosed, undertreated and absolutely underrepresented in clinical trials. If you want a little light reading, it is pretty much a compendium. I have. I would have you look it up. It actually does talk about solutions for how to add more women to research and do a better job of uh treating us and raising awareness. I think raising awareness is the first step to any problem, improved guidance on prevention strategies and then absolutely refer women for symptoms, diagnostic testing, treatment, cardiac rehabilitation, as we're saying, cardio obstetrics clinic, it's your heart's fault until we tell you otherwise. Um and then really those guidelines that dr Colbert, so um uh beautifully laid out. We should apply them across genders equally because they do benefit women just as much as they do men. And with that, I'll turn it back to Dr Abdel Hadi. Thank you. Thanks rita and Jim. And um, you know, for everyone, there is a Q. And a um app that you can type your questions if you have any. I'm just gonna um asked me to first after saxena about aspirin. I know there has been a lot of questions that came regarding the use of aspirin and primary prevention and secondary prevention. And traditionally if you go back a decade ago there was a lot of talk about how women and men might respond differently to aspirin. Can you comment in general about aspirin use and how is that different between primary and secondary prevention and whether women should be looked at different. So yes, absolutely. There the women, especially at an older age had an increased risk of bleeding as we do with any of our blood dinners. Just again, drugs were not tested in women. Um but I think applying aspirin across the board for primary prevention has fallen out of favor as the US preventive task force came out with that actually just this fall um that aspirin for primary prevention, if you do not have plaque, you do not have a high increased risk score. Aspirin may not be right for you in women, just like in men, if you have risk enhancing factors and an elevated risk, Your um of greater than 7.5%, especially if you're pushing 15% for your ten-year risk score. The recommendation is aspirin. If you have coronary artery calcium score usually I think about 100 or greater, we do recommend aspirin therapy and then just because I have to bring it back to pregnancy riot if you happen to be a woman at risk for adverse pregnancy outcomes such as pre eclampsia. Aspirin actually decreases the risk of preeclampsia by about 30 to 40%. So a lot of cardio obstetrics patients are an aspirin to help prevent preeclampsia. So it does have utilization in different places. But aspirin across the board is not correct for everybody. Thanks rita. Um And almost every patient that I see now ask about aspirin um There was a there are a lot of questions about how we can obtain copies of the presentation and um I know that all these presentations will be available through the website of broadcast Met. Um So on the entire presentation. So um you know I think I don't know if we can put that um if we can type in the chat maybe the website for that so people can have access to that as well. Um All right I'm gonna ask a question to dr Covic dr kovac. You mentioned the use of anti platelet with either warfarin or dual anti regulation. Is that zero perception different. Um If someone has had an acute coronary syndrome versus just elective pc i if there's anything like that or the um um And uh do you have any comment on using a lower dose of direct oral anticoagulants potentially? And finally along the same line you feel comfortable and stable coronary disease using only the uh only direct oral anticoagulants, oral Torah picks Evan without anti plate that yeah. You know great question. Red. So you know, I mean this is always an evolving topic and obviously germane to your your specialty as well. What they've said is, you know, we we we are always changing how we're managing folks with both coronary disease and risk for thrombosis bolic. That's what they said. So, you know, with acute coronary syndromes, you know, we're usually still staying with the anti platelet therapy. Um and generally I think the most universal treatment strategy is a final purity in plus oral anti coagulation and frequently implemented almost immediately in the hospital. And so the triple therapy is a pretty rare exception. Um and just for probably that one week, if not a month, complete duration. There is uh discussions with regards to stable coronary disease, particularly with monotherapy with the direct oral anticoagulants. So I think as you and and raining are aware about River rocks band or Xarelto has actually been shown to be effective in mono therapy for treatment of stable coronary disease with no anti platelet therapy. And eloquence is also being studied at reduced dozing um with published data that supports similar outcomes as River rocks man. So yes, I think, you know, in patients that are on the anti coagulation. I think we're going to see a trend moving towards monotherapy with the direct oral anticoagulants. Um but in the two coronary syndrome, I think they're still very clear data uh to support use of final puritans or Taika galore for generally speaking 12 months. Um And in those folks that are on oral anticoagulants were probably using Plavix or at least switching to Plavix generally after about a month just because of a positive data with prasugrel and taika galore with you know the newer oral anti quake. Thank you. I'm jim question that came actually uh is with the ers with emergency rooms full. Is that affecting where ambulances are taking patients and you know when it comes to the you know appropriate time to balloon and so forth. Is that affecting how we're caring for patients with covid? And um E. R. Is being full. Yeah great question. So you know to be honest, no it hasn't. You know I think there are exceptions where we're still transferring patients um um to pC. I. Capable centers and or excuse me transferring patients um urgently to you know tertiary care centers. And I think most capable centers are still getting stem ease. Initial strategies with Covid was looking really aggressively at cyber analytic therapy and thinking should we be listening more of these patients to reduce exposure in the hospital. And so far that really hasn't panned out as being as effective because as I alluded to previously these folks are actually really sick in the Truax cohorts of covid positive patients that come in benefit much much more from interventional or pc therapies. And so you know we're still pretty much resorting to invasive strategies for all of these folks. And most ers are still accepting them in tertiary centers regardless of the bed capacity in the E. D. Thanks jim. And I just want to add as well there, you know we're all going through the challenges of you know full um ers and hospitals and hospital beds. But I hope and I believe probably every health system but definitely at the Minneapolis Heart Institute um there are certain situations where um certain emergencies will almost always be accepted. Um And uh patients with S. T. Elevation M. R. Is one of them where um even if that patient comes to the cath lab and is held somewhere until there's a bed. Um We put every effort to bring these patients and there's a list of patients where we believe that obviously delaying care is inappropriate and we um tend to find a way to accept them. So I just want to make sure that that that unfortunately doesn't apply to other patients uh as the hospitals are full and the others are full and where we are sometimes unable to accept these patients and they wait in the E. R. S. Which is um you know not the ideal but that doesn't apply for a lot of things that dr cole beck discussed today. Um So there is a question for you dr Kolberg along the same line about managing anti coagulation in patients with acute coronary syndrome who are already on therapeutic anti calculation for another indication. And the question specifically is would you use happen uh if the patient is already on anti coagulation and I'm assuming there might be a difference if there you know, if there are concomitant with therapeutic i in our versus there on Doha. And when was the last, does can you comment on that for hospitalists to deal with these patients and admit them to their hospitals and have to deal with them medically? Yeah, I mean these are tough cases, you know, I think it's hard to standardize the management for the reasons you just alluded to rab is, you know, a lot of these patients we got to figure out when their last dose was. You know, obviously if you have the ability to check and iron are and their therapeutic, you know um you may not necessarily need to utilize infraction. It had burned right up front. Remember a lot of these patients are getting treatment emergent li you know, and obviously the non ist television in my patients that have maybe a more about delayed invasive strategy, you would have the opportunity to allow that anti coagulation aware off and then institute and um fractionated variety of heparin. What's there Einar becomes uh you know, below therapeutic. So I would say for the most part if they're adequately anti coagulated iron are therapeutic or given a dose of the dock um um you know, prior to their presentation still therapeutic, I don't feel there has to be an urgent need to implement a um fractionated heparin. Um And if they're going to the cath lab we're going to do that at much higher levels. That would be treated systemically in the hospital. Great. Um and uh you know at the end of uh at the end of this uh presentation um if we can just put again that Q. R. For the survey so people can fill the survey to get their cmi. So one last question and then hopefully we'll be able to put that up. The question is for patients who present with medical illness and they end up having what is described as troponin leak. Right? I mean it's not an acute traumatic event or secondary am I? Um It has a different name everywhere for every day for someone like me who is a it was a heart electrician. But do you how do you treat them from an anti platelet standpoint? Are these patients that you put on Plavix uh for how long? Um do they you know, do you do the same approach when it comes to medical therapy or not? Yeah. Great question. You know I mean that's a number difficult definition. Right? So the idea of the type to M. I. Or the myocardial auction demand mismatch. You know remember it's not truly in acute coronary syndrome and so frequently it's the demand of their medical illness that drives some mild cardio necrosis just because of that mismatch and in the auction supply. And so those patients, I don't think necessitate uh the similar dual anti platelet strategy that a true path of physiologic acute coronary syndrome has. And so do they necessitate further evaluation? Absolutely. And so I think for the most part, when we get consulted on folks who leak a troponin and have have a clinical scenario consistent with a type. To me, those patients are usually going to get further risk stratified once optimist from their medical condition with generally either an in or out patient, non invasive stress imaging. We often to actually use trans thoracic echo while hospitalist and have that guide our acuity in terms of how we would manage patients. In other words, if they have they'll be dysfunction that would be knew that we would potentially want to consider doing some form of a ischemic evaluation while they're in the hospital, yes. Found to have coronary disease intervened with stents or we are really certain that they are falling into criteria for that acute coronary syndrome, like a wall motion abnormality that we're going to manage medically. Those are the circumstances were dual anti platelet therapy for the recommended duration would be able, right and there um two questions, one of them was dr saxena about how can women advocate for themselves. I know dr saxena had to leave. So I I think I don't think she's she's on the symposium anymore. Um She has a recruitment dinner actually she's going to meet one of our future partners. Um But uh last question here is for your vision is um somebody referred to the host exam study where um you know they're talking about potential benefit from long term Plavix as opposed to aspirin post pC. I. As a maintenance therapy. And um do you see that potentially changing our approach where we might use products instead of aspirin as a long term maintenance after B. C. I. Yeah. You know I think there's actually historical data to support science purity and treatment for um you know just after sclerosis in general and there's a trial I think in the two thousands called the Capri trial that actually looked at medically managing coronary disease. But it also included patients with stroke and particularly peripheral vascular disease. And actually those patients pretended a better benefit with monotherapy with clopidogrel. And so you know. Yes I do think there can be a I think there is room to potentially utilize those therapies and going to be more clinical trials to indicate the efficacy um probably to a greater advantage than a baby aspirin. And so I do think it might be something there are circumstances where empirically we do use the final beer gene treatment for patients post intervention where it was a complex Pc. I that we would prefer them to be on that as opposed to dual anti platelet therapy or just aspirin alone. So I do think there's stuff coming down the pike that would probably guide our treatment but at present I don't think that's necessarily universally accepted practice as of yet. Alright, well thanks everyone for joining us. Uh I learned a lot. I know that and hopefully we all did. Uh I think we will again we will post the QR code for the survey next. So if you wanna have your phone ready and and post it then that's that's great. Um Thank you everyone. Thank you mm hmm. Yeah. And um. Mhm. Mhm. Yes, mm hmm mm mm hmm. Yeah. Mhm. Mhm. Yeah. Yeah. Mhm mm. Mhm. Yeah. Mhm. I'm full. Mhm mm. Okay. Mhm. Mhm. Sure. Yeah. Mhm. Yeah. Yeah. Mhm. Oh. Oh. Oh okay. Yes. Mhm. Yeah. Dad.
