DANIEL S. YIP: Maybe a little bit dated, but quite honestly, things haven't changed that much, unfortunately. And we'll talk a little bit about all that. So we'll talk a little bit at least on the epidemiology part of the incidence, prevalence, outcomes, risk factors, and what we could do to maybe modulate some of the risk factors that come about.

So talking a little bit about incidence, really, the incidence-- we have about a million people who have a diagnosis of heart failure-- a new diagnosis of heart failure annually. That really hasn't changed that much. I really wanted to sort of emphasize a couple things and that the incidence is highest in African-American and African-American women and the lowest in Caucasian women.

And that has not changed very much over the years. So our at-risk population certainly is the African-American population. And there are other vulnerable populations, but that's where I think a lot of the primary prevention and secondary prevention is really important to try to stem the tide of heart failure.

If you look at your lifetime risk-- and every time I look at this slide, it really shocks me, for lack of a-- for many reasons. So if you look at-- if you're a 40-year-old person, male or female, a 40-year-old person and really no other history, your risk of developing heart failure sometime during your lifetime is 20%, which is really remarkable to me. And this is, of course, all comers. And some of these people would have infarcts.

But if let's say you said, what's your lifetime risk for heart failure and you've not had a myocardial infarction, at 40 years old, if you're a man, you have a one in nine chance to developing heart failure. And if you're a woman, you have a one in six chance of developing heart failure sometime during your lifetime if you've not had a myocardial infarction in your lifetime starting at age 40, which to me is very, very striking and sobering in many ways as to how prevalent a diagnosis of heart failure is.

Again, even though we live mainly in the world of systolic dysfunction, you have to remember that diastolic dysfunction or heart failure with preserved ejection fraction is a very large problem that, in some ways, is actually more difficult to treat than people with heart failure with reduced ejection fraction.

And later on in this series, we'll spend some time-- there's a very nice talk that's given about heart failure and preserved ejection fraction and surprisingly how the outcome is just as poor with those folks as it is with people with reduced ejection fraction.

So just to sort of wrap up the incidence thing, so trends really haven't changed over time. They're higher in men versus women, the incidence. They are more-- the incidence is higher in African-American population. It does increase with age. It is higher in people with coronary artery disease, which kind of makes a lot of sense.

And again, even though you break down the populations, it's highest in African-American males, lowest in Caucasian females. And if there's any time you guys have any questions, just jump in. It's free-flowing.

Prevalence-- so the prevalence-- we've got 6 and a half million people who carry the diagnosis of heart failure. And it really hasn't-- it hasn't changed a whole lot over time. Particularly in the 2000s, it's pretty steady. But again, about 6 and a half people-- 6 and a half million people in the United States carry the diagnosis of heart failure.

So let's move on to outcomes. So this is Framingham data and a little bit old data, as well as the Mayo Olmstead County data. And it really just shows what the five-year mortality is. And it really hasn't-- you'll see that it has made some improvement over time. But if you carry the diagnosis of heart failure, you have a 50% chance of not surviving five years, which is, again, very sobering.

Many of us have patients who we followed for 10, 15, 20 years. And they're doing fine. And so if those are the people that you're following, then think of all the other people who you're not following who are suffering with the significant mortality. And there's also morbidity.

So the gains that we've made-- it's kind of small if you guys are on the screen. The gains we've made over the years-- so this is 1950 all the way to 2000-- have been early on. So sort of in the first couple-- first, let's say, six months or less, their diagnosis of heart failure, we've made significant improvements there, really resuscitating them early, early diagnosis, and intervening early on.

But beyond that, the curves really are parallel over the decades. It really hasn't changed that much. Again, most of our improvement has been over the early years. But we really haven't made very much improvement on long-term survival. And those of us in heart failure who-- it took a lot of time.

It was early on that we saw successes from, again, initially, hydralazine nitrates. And then ACE inhibitor's been shown to improve survival and the addition of beta blocker and the addition of aldosterone blocker. And then there was a gap of many, many years where there was no significant improvement in survival in this length of time, over a long period of time, until very recently. So this tells you that we've not really uncovered the secret beyond what we can do early on.

So I wanted to also point out from a mortality standpoint, a rehospitalization standpoint, the highest hazard for mortality and rehospitalization are in African-American males. They have a substantially higher risk than Caucasian males and Caucasians as a whole. And it's also the same case for rehospitalization.

Speaking of hospitalizations, it kind of plateaued out with a number of we have about a million hospital discharges with a diagnosis of heart failure in a year. And the readmission rate still is sort of 20% to 25%.

That really hasn't changed a lot, despite all the different processes that we have put in place, all the different time and effort that we've placed, including penalizing hospitals for readmission. That really has not been shown to improve our rehospitalization rate. So maybe-- I'll get off my soapbox here in a second. But maybe that's not the right place to incentivize our readmissions.

So I also wanted-- another sobering fact is the overall mortality. So if you're hospitalized, the one-year mortality is about 30%. And that has not changed. So we still have-- if you're hospitalized, if your heart there was bad enough that you require hospitalization, there is a 30% chance from a population standpoint that you may not survive the year. Again, everyone's an individual.

But sort of in group populations, a third of the people-- almost a third of the people don't survive a year after their index hospitalization for heart failure, which is very sobering. And that's why when we talk about when to refer people, these are sort all risk factors to say, oh, maybe we should think about referring these folks.

So there's been a relative improvement over time. I would argue that this improvement has really been in the early stages, let's say, the first six months of diagnosis, but that it's pretty parallel beyond that over time, that there's a significant five-year mortality. Half the people with a diagnosis of heart failure would not be alive at the end of five years, which is very sobering in my mind.

Mortality increases with age-- worsens with age, which is no surprise and is also very significant in African-American males. And really, we've not made any big changes in post-hospitalization mortality over the years, despite all the efforts that we have. So certainly, anyone who's hospitalized for heart failure, we need to pay special attention to them, because they are at risk for morbidity and mortality. Any questions on that so far?

OK. Talk a little about risk factors. And we'll start that out with a case. In a lot of these things, some of the things I'm going to talk about overlap a little bit with Parak's discussion last week. But the question will open up. Which of the following two conditions represent the highest population attributable risk for developing heart failure?

So which of the two conditions? So is it diabetes and obesity? Is it smoking and chronic kidney disease? Is the hypertension and coronary artery disease? Is it microalbuminuria and left ventricular hypertrophy? Or is it peripheral vascular disease and hypothyroidism?

So I'll let you guys think about that. And I'll give you some data to maybe help us answer that question. And this is a board question. This is a question that is on the heart failure boards. It is a question that is on the cardiology boards.

It is an important question that even though the sexy stuff is new heart failure stuff, cryogenic shock, and that's the kind of stuff that we always like to play in, but unfortunately, there are always these epidemiology questions that sneak on the boards that we have to answer. And that's because it's a tried-and-true question. It's just something we've got to work on.

So let's talk about this. So there are a number of different risk factors. We all know that there are some for development of heart failure. And they're very similar to development of ischemic heart disease, too, if you think about it. So age-- the older you are, the higher the risk. Males tend to have a higher risk factor for heart failure-- for developing heart failure than women.

Hypertension and LVH, certainly myocardial infarction, diabetes, valvular heart disease, obesity-- these are all the major risk factors. Certainly, dyslipidemia, smoking, sleep-disorder breathing, chronic kidney disease, anemia-- these are other things that also contribute to the development of heart failure and also the prognosis.

So there have been over 100 heart failure-associated risk factors that have been described and identified. And so how do you sort them out? So Framingham looked at all the big things that sort of come to mind, the seven or eight big things that come to mind. And certainly, from a hazard ratio, hypertension and myocardial infarction are really way over, with attributable risk in the double digits.

And for hypertension in women, it's attributable risk of almost 60%. So certainly, hypertension and coronary disease or myocardial infarction is of-- plays a significant role in the development of heart failure. And it's been shown multiple times.

And this is in the elderly, where systolic blood pressure greater than 160 and development and presence of coronary disease really increases the attributable risk for developing heart failure. And it also is present in the African-American population, as well as the Caucasian population and perhaps even more so for hypertension, particularly, and coronary disease in the African-American population when compared to the Caucasian population.

So the answer is hypertension and coronary disease. Those are the two biggest risk factors that are attributable to the development of heart failure. And anything we can do to reduce the incidence of hypertension and coronary disease-- and if there's development of hypertension, to mitigate the effect of the hypertension is going to help with decreasing the risk of developing heart failure.

MALE SPEAKER: I would have picked smoking.

DANIEL S. YIP: What's that?

MALE SPEAKER: I would have picked smoking. Every time you see smoking, it's always a bad thing. But on a board question, either there or eHarmony, wherever you see smoking, always bad.

DANIEL S. YIP: It's always a bad thing. That's because it's marketing. It's good marketing. There's nobody marketing hypertension.

All the hypertension drugs, no one's pouring any money into hypertensives because they're doing-- it's all the new diabetes medicines. That's what people are spending all their money on. And we'll talk about that in a second.

So risk factor-- risk modulation. So we talked a little bit about hypertension, but we'll also talk about stage A. So ACC/AHA stage A recommendations-- and remember, stage A are people who are at risk but haven't developed any signs or symptoms of heart failure. So it makes sense.

So we're all cardiologists. At one time, we're all internists. So we should be doing these things or treating their hypertension according to guidelines. And again, it's not only systolic hypertension. But especially in the younger population, diastolic hypertension is also a concern.

Treat their diabetes. Treat their lipid disorder. Encourage smoking cessation. Encourage exercise. Mitigate the heavy alcohol use.

And again, certainly, there are populations with hypertension where the use of an ACE inhibitor or ARB could be beneficial for those at risk for heart failure. And perhaps people who have coronary disease, the use of beta blockers would also be very effective, perhaps, in reducing the risk of heart failure. So there is benefit in treating hypertension.

So this is a meta-analysis of a number of randomized trials that looked at the benefit of treatment hypertension. You can see that if you treat hypertension, you have a substantial reduction in the incidence of heart failure, as well as LVH, but sort of more than 50% reduction in this meta-analysis of development of heart failure for those who can treat their hypertension effectively. So there is a plug for getting your blood pressure under control.

But not all classes of drugs are the same. If you look at doxazosin and chlorthalidone, they have a similar benefit for mortality. But if you look at-- just all-cause mortality. But if you look at heart failure, the chlorthalidone group did better than the doxazosin. That's ALLHAT. So that's not a specific heart failure trial, but it's kind of interesting that not all drugs are the same.

Atenolol versus losartan-- and this study showed that losartan had a benefit of decreasing the incidence of heart failure. And so certainly, that led to the recommendation earlier that if you think that you have a patient population at risk, perhaps using the ACE inhibitor and ARB would be beneficial.

Particularly, the ATLAS trial using ramipril has been shown that people with risk factors have been shown to improve their outcomes. So certainly, considering an ACE and an ARB would be powerful. So again, this is JNC 7, but it's really pretty much the same.

So if you're concerned about heart failure using an ACE inhibitor, an ARB, perhaps a beta blocker or diuretic therapy, aldosterone antagonist would be compelling in this population if you have hypertension if you're worried about heart failure. And again, these other drugs have their role.

But certainly, if you have someone and you're worried about heart failure, again, sobering-- half the people at the age of 40 will-- not half. 20% of the people at the age of 40 will develop heart failure sometime in their lifetime. So certainly, leaning towards ACE and an ARB could be very helpful in the population.

So here's a second question. So this is sort of heart failure in the elderly. So you see an 83-year-old male who's not seen a doctor in 30 years. So that happens not infrequently.

And of course, they come to your clinic not because he wants to, but because his daughter, who's probably from out of town, says, dad, you really need to see the doctor. You haven't seen a doctor in a long time. He is very active.

He's asymptomatic. And his blood pressure on exam is 164 over 96. And the rest of his exam is pretty unremarkable. The ECG is normal. The creatinine may be minimally elevated. And so assuming-- and I guess for the boards, you never treat the first blood pressure. But let's say that the blood pressure has been persistently, let's say, in the 160s over 90s.

Which management-- regarding the management of blood pressure, which of the following statements is true; A, there's no evidence of benefit with hypertension management in the elderly greater than 80 years old-- so treating hypertension is no benefit in the elderly; that the systolic blood pressure up to 160 is normal in the elderly; in the elderly, hypertension management does not reduce all-cause mortality but it does reduce fatal strokes and heart failure rates; and then in the elderly, hypertension management reduces all-cause mortality, fatal strokes, and heart failure rates; or the elderly, hypertension management reduces all-cause mortality, fatal stroke rates, but not heart failure rates?

So which one do you think? So one of all-- first of all, do you think it's important to treat hypertension in the elderly? The answer's yes because we wouldn't be talking about this if the answer was no. And so then the question is, in the elderly-- if you do treat hypertension, does it reduce all-cause mortality, fatal strokes, and heart failure risks or just some of these? And so we'll talk about that next.

Oh, sorry. The answer is-- I'm sorry. I moved this slide around. So the answer is it does improve all-cause mortality, fatal strokes, and heart failure rates. And this is the data here.

So the data shows that this is in patients greater than 80 years old, that those who are treated for hypertension have a reduction in fatal or non-fatal strokes, all-cause mortality, and mortality from cardiovascular causes, as well as death from stroke, as well as death from heart failure. So again, treatment of hypertension in the elderly is valuable in all sides, in all places.

And they are most effectively treated with-- in this study, they used diuretics with or without ACE inhibitors-- so again, another plug for ACE inhibitors with a little bit of diuretic. And frequently, the elderly's hypertension is volume-dependent. So judicious use of diuretics sometimes is very effective in this population.

So moving on from hypertension to dyslipidemia, certainly, the higher your blood sugar is or the development of diabetes increases your risk for developing heart failure over time. So again, treatment of diabetes is effective. And this is showing that the higher your A1C is, the higher your rate of development of heart failure. So again, people with poor glycemic control are at increased risk for developing heart failure.

And with the new SGLT2 inhibitors showing improvement in mortality, I think that's one of our newer tools in our toolbox to see what can we do for people with diabetes to try to improve their outcome. So there's more to be learned about the SGLT2 inhibitors.

And perhaps in one of the journal clubs coming up during the series, we can maybe spend a little bit of time talking about the SGLT2 inhibitors, because it's relatively new and not all the heart failure docs I think are very adept at using that, because we live in the heart failure world. And even though at one time, we were internists, sometimes with all the new changes in diabetes, sometimes we're a little bit uncomfortable treating that.

So metabolic syndrome-- certainly, that goes hand-in-hand with diabetes. If you have metabolic syndrome, you're going to be increased risk for developing heart failure.

Obesity is a significant risk factor. It's not as strong as hypertension and coronary disease, but there is an increased incidence of development of heart failure if you're obese. And we're not going to talk about this later, but there's a difference between risk factors of developing heart failure and risk factors for survival.

So interestingly, there's a paradox. If you're overweight-- if you have the diagnosis of heart failure and you're overweight, your prognosis is actually better than if your weight was underweight. That probably has to do with the cardiac cachexia that's associated with advanced heart failure. So again, we're talking about the risk factors of development of heart failure. A little bit later on, we'll talk about risk factors for survival.

But anyway, just I diverged a little bit. But certainly, obesity places you at increased risk for the development of heart failure. So now, we're going to talk about, again, the risk factors and prognosis. And we're going to shift a little bit from what are the risk factors that we associate with the development with heart failure with, OK, you already have heart failure.

What can we do with the risk factors that you have to modulate that? Or is there anything in the risk factors that you have that would perhaps give us the idea from a prognosis standpoint? So that's kind of what we're going to talk about. And I touched a little bit about quality of life assessment or also known as "patient-reported outcomes," which is another fancy word for "quality of life assessment."

So again, it's really important. If you have the diagnosis of heart failure, many times, people come to us. And when they're in the office, they say, well, I know I have heart failure. Someone's told me I have heart failure. I've been referred here because they told me if I don't get a heart transplant in-- pick a time-- six months, a year, two years, five years, whatever it is, I'm going to die.

And so I have a house payment. I have young kids. We're thinking about moving out of town. I need to know what my prognosis is. I need to know, am I going to be alive a year from now? Or do I need to start making plans?

Or am I going to-- do I need to retire? Do I need to stop working? I'm a physician. Do I need to-- I'm a physician. I'm 55 years old with heart failure.

Do I say, you know what? I'm going to retire early because I only have five years to survive and I want to spend that time with my family? Or do you guys think that I have 15, 20-year prognosis and maybe I can work a little bit longer for my family?

So I think prognosis is really an important question. And sometimes, we have really great tools. And sometimes, we don't have really good tools to help answer that question. Again, all the questions we answer for the patient are based on population studies. And every individual is different.

We can say to somebody, if you have 100 people just like you, only 10 people-- only 10 out of the 100 really need a transplant. But are you one of the 10? Or are you one of the 90 who don't need transplant? So we really don't know very well, other than population idea, of where people are from a prognosis standpoint.

So there are lots of risk factors that are associated with outcomes that have been described. And I'm just going to go over a couple of them. So physical exam-- Parak talked a little bit about this last time-- is a powerful indicator from a prognosis standpoint. Again, this is mainly short-term prognosis.

So somebody who's got elevated jugular venous pressure or someone who has a third heart sound, certainly, their survival is going to be not as good as someone who does not have elevated jugular venous pressure or presents with no S3.

So again, this is data that shows from hospitalization survival, death from all causes-- again, the presence of a third heart sound or presence of JVP increases your risk for mortality. So again, those signs are significant signs. And I think if someone presents to you with increased jugular venous pressure or a third heart sound, you need to really pay attention to them because they're at increased risk.

Certainly, ejection fraction is significant. So if your ejection fraction is greater than 45%, your prognosis is different than someone whose ejection fraction is less than 25%. So there are other tools that help us figure out the-- differentiate those who are going to survive or not survive in these lower ejection fractions. And we'll talk a little bit about that later on.

But please note that many of these deaths are sudden deaths that happen. And that's why it's really important. That's why all of our data would show that if your EF is less than 35%, you really need to have an ICD implanted for primary prevention of sudden cardiac death, that if you're class two and your EF is low, you're more likely to die from an arrhythmia than you are to die from pump failure.

So that's where that conversation-- sometimes, it's difficult with patients that we have and your EF is less than 35%. And maybe they've never been hospitalized for heart failure. And they feel great. They are very active. They're playing basketball, if they are young enough to do that. They're working. They're doing all sorts of things. They have extreme workouts.

And you tell them, hey, you know what? You really need to have a defibrillator implanted. That's a difficult discussion with them, particularly if they're active, particularly if they use their arms, because you're talking about putting a defibrillator that impacts their lifestyle somewhat. But you're really doing them a favor, because those are the folks that die from sudden death. Those are the people who come in at sudden death. It happens time over time.

So right ventricular dysfunction is also a significant risk factor for mortality. Every one that we see with diastolic dysfunction and-- I don't really pay attention to the ejection fraction, because everyone's got an EF of 20, 25 at best, maybe 30%. And that's just the population that we deal with.

What I really focus on is what's the right ventricle like? What's the right ventricle like? I look at what the-- and there's other things I look on the echo. But certainly, the presence of right ventricular dysfunction is a risk factor for mortality and certainly for symptoms, as well, too. So when I start seeing the right ventricular function starts to decrease over serial echo, I'm concerned.

The second thing I look at on an echo is the left ventricular end-diastolic diameter. In this one study, it showed that if your left ventricular end-diastolic diameter is less than 7.5 centimeters, then your prognosis is significantly lower than if it's smaller. So I look at what's the size of the left ventricular end-diastolic diameter. Is it increasing over time? Is it staying the same? Is it decreasing?

To me, that's the other thing I look at on the echo. I don't spend as much time, but it has been shown that people on the echo who have a restrictive filling pattern have decreased survival. I think that that is a sign of a sick heart when they start having a more restrictive filling than not. So that's sort of-- many people look at that as one of the echo findings.

Left atrial size has been also used as a surrogate of looking for prognosis. And I'll just tell you what I do on the echo is I look at what's the left ventricular end-diastolic diameter. I look to see what the right ventricular function is like. And I look to see the severity of mitral regurgitation.

It's really impressive to see someone who maybe has a dilated left ventricle but very little mitral regurgitation who really feels well. And for whatever reason, when the mitral regurgitation starts to get worse, they start to become more symptomatic. So those are the things I pay attention to. I pay attention to the left ventricular end-diastolic diameter, the right ventricular function, and the severity of mitral regurgitation.

So I'll pause there. Does anyone-- what else does the group-- are there are any other factors or anything else on the echo that you guys sort of spend time on looking at or trending? No?

PARAK: Just valvulopathy, as you mentioned, size of the ventricle, size of both ventricles, functioning of both tentacles, and then progression in TR, MR. Especially after a biv placement and that's not markedly improved, that also provides information. But these are the methods.

DANIEL S. YIP: Yeah. And it's also actually-- tagging on to what Parak said, it's very remarkable how if you optimally treated someone medically with ACE inhibitor, beta blocker, or Entresto plus aldosterone blocker, how many of these factors do improve, that the MR gets better.

The RV becomes smaller. The left ventricular end-diastolic diameter starts to decrease in size, particularly with the beta blockers. It's quite remarkable how much improvement you'll see over time. I'll spend a little bit of time with functional capacity.

Certainly, the New York Heart Association classification, all of us know this by heart. It does play a role in prognosis. We know that-- this is SOLVD data. But regardless of whether you receive beta blocker-- sorry, ACE inhibitor trial-- didn't receive ACE inhibitor, there is a significant difference in mortality if you're class IV versus class I.

So the more severe your symptoms are, the worse your prognosis is. And certainly, people move from one class to the other. But certainly, people persistently in class III, class IV are going to have a higher mortality than people who, let's say, were class III at one time but we were able to get them to class I or II.

This is a really busy slide. Really, what I wanted to say is let's say if you just do a simple six-minute walk-- you do a simple six-minute walk and you're able to get more than four and a half meters-- I'm sorry-- 450 meters. So if you do a six-minute walk and they can accomplish or they can travel more than 450 meters in the six minutes, their prognosis is very good.

These are the people, they don't need transplants. They don't need advanced heart failure therapies. They just need good evidence-based therapies. And doing a six-minute walk annually if you don't have access to a cardiopulmonary exercise study is a very valuable tool in trying to assess what prognosis is.

When I see somebody for the first time, I do try to get an idea of what their functional capacity is. Can they vacuum? Can they make the bed without stopping? Could they put the dishes away? Could they put things above their head?

Things like that, simple things like that, certainly sometimes will give you an idea of what their functional capacity is. Parak, you were going to say something.

PARAK: Yeah, I completely agree. I can't tell you how many times you see somebody in the clinic. And the patient themselves says, oh, yeah. I exercise X, Y, and Z and I can do X, Y, and Z. And then you put them either on a six-minute walk test or a cardiopulmonary stress test and they bomb it or they don't do well.

And so I think doing a six-minute walk test gives you an idea as to, number one, what their functional status is, number two, whether you can trust what they're saying in clinic. And it may kind of give you a year to year kind of delta. It may give you an idea as to whether somebody is declining. And so I think it's a very useful tool. Sorry for interrupting there.

DANIEL S. YIP: Yeah. But for us in advanced heart failure and transplant, we use the VO2 stress test. And there will be a talk later on in the series all about that.

For those of you who are aware, we use a cut point-- it's an old cut point of 14 milliliters per kilogram per minute-- as a prognosis. And this is sort of the inflection point. Or if you're 13, 14 milliliters per kilogram per minute or less, your prognosis is poor compared to if it's greater than 14 milliliters per kilogram per minute.

But beta blockers-- the [INAUDIBLE] data from the use of 14 milliliters per kilogram per minute or the more recent-- and after that, people use 50% predicted as a cut point for mortality. People with beta blockers, those are-- those studies were done in the pre-beta blocker era or beta blockers were not used very much.

Certainly, we know that the standard of care right now is people with decreased left ventricular dystolic function should be receiving beta blockers. We also know that beta blockers decrease oxygen consumption by decreasing heart rate. So maybe that 14 milliliters per kilogram per minute is not the same as someone who's on a beta blocker.

And so it turns out that if you are on a beta blocker, maybe it's not 14 milliliters per kilogram per minute that is your cut point. It may be less than that. So again, we all sort of mix that up with-- so maybe someone with a VO2 max of 12 or 13 milliliters per kilogram per minute is OK if you're on a beta blocker. But if you're not on a beta blocker, maybe 14 is the better cut point. So there are a number of studies that sort of try to talk about that.

Hemodynamics-- I'm not going to spend a lot of time, other than certainly from all-cause mortality, doing the hemodynamics-- again, mitral regurgitation plays a significant role in predicting survival. So the presence of mitral regurgitation, a low cardiac index, and a high mean pulmonary artery pressure are all risk factors for the development of-- prognosis for survival.

Again, this is not only baseline cardiac output, but what's your cardiac output in response to exercise. So people who are able to increase their-- who have a normal heart rate or more of a cardiac output response to exercise, their survival's significantly better than people who have not been able to increase their cardiac output in response to exercise.

I'm not going to spend a lot of time on biomarkers. But certainly, we know the higher your BNP level, the higher your norepinephrine level. And it's a sign of poor prognosis.

What you may not realize is uric acid level is also-- high uric acid is also a risk factor from a prognosis standpoint. It's probably a surrogate or is a surrogate for reduced renal function. So certainly, that goes hand in hand. And certainly, low sodium is a poor prognostic factor when looking at mortality.

Hemoglobin-- also, anemia has been shown to-- the presence of anemia has been shown to portend higher mortality. However, like many of the other things, treatment of anemia has not been shown to reverse that mortality risk. But certainly, someone who comes who is anemic, you really are concerned because they're at higher risk and probably are the ones that you're more concerned about, rather than people who come seeing you with a normal hemoglobin.

Talked about renal dysfunction-- certainly, people with elevated creatinine are at increased risk for all-cause mortality and heart failure death. But not all creatinines are the same. These are different examples when someone has a serum creatinine at 1.2, what it means.

Certainly, a GFR is a better reflection of what the renal function is like. And so the lower the GFR, the worse the prognosis. So if your GFR is less than 45%-- less than 45, then your prognosis is much poorer than people with better GFR. So anybody with chronic kidney disease stage III is what in my mind would be considered increased risk. And that's pretty much our whole population in the Mayo Heart Failure program, unfortunately.

From an electrophysiology standpoint, we all know this. The wider your QRS is, the higher your mortality. And that's why people with a QRS duration of greater than 150, we recommend that re-synchronization therapy be considered, because that's been shown to improve mortality. In the last couple of minutes, we'll talk a little bit about patient-reported-- some about patient-reported outcomes, but also some of these other heart failure scores. Parak touched on that a little bit earlier.

So the question is there's a 56-year-old male with a history of anterior myocardial infarction and severe left ventricular dysfunction that's referred to you for consideration for transplantation. So with respect to the prognosis determination, which of the following is true?

SHFM is the Seattle Heart Failure Model-- incorporates the use of medical therapy and can be used to list patients for transplant. B, peak VO2 provides the same prognostic information as Heart Failure Survival Score. HFSS is Heart Failure Society Score. HFSS, but not SHFM, includes the KCCQ.

So this is sort of a number of abbreviations. So just remember, KCCQ is the Kansas City Cardiomyopathy Questionnaire score. SHFM-- Society of Heart Failure Models-- was developed for outcomes among hospitalized heart failure patients. HFSS-- Heart Failure Survival Score-- was developed in patients with advanced heart failure to aid listing decision, but does not include the impact of medical therapy.

So I don't think that there is-- this is sort of esoteric. I don't think it's really that important, other than to understand what are the factors that go into these different scoring models. So Parak yesterday-- last week said who uses these scoring models. And we don't use them very often. But we do have in our minds what are components to the scoring models and what are important when we have that discussion with our patients regarding survival.

So it turns out let's look at the Heart Failure Survival Score. So it looks like a number of different variables. The ones that came out were ischemic heart disease, left ventricular ejection fraction, mean blood pressure, peak VO2, wide QRS, serum sodium, and resting heart rate. So these are the seven variables that go into the survival score.

Again, does it matter what the score is? Yes, it matters, because we do know that people with low risk have improved survival. But I would say that the biggest take-away is these are the things that if your patient has, you have to pay attention to it. If they have ischemic heart disease, if their EF is low, if their VO2 is low, if their blood pressure is low, if they have a wide QRS complex, if their serum sodium is low, and they have an increased heart rate, you know that these people are increased risk.

You need to pay attention to those folks. You don't have to know the actual score, but you know that people who have these are at increased risk. But it does not take into effect treatment. It does not go-- it just says, do you have these risk factors? What's your prognosis? It doesn't talk about what medications you are and things like that.

But the Seattle Heart Failure Model does include medication. So if you're using this tool, it does include lab data. So here's a uric acid here. So that's part of the Seattle Heart Failure Model. It looks to see what drugs you're on, what medications you're on, and is there improvement in survival if you check these different medication treatments.

Also, are you using a device? So those are all criteria that you use-- again, this does take into effect lab data. It does take into effect-- into consideration what medications. But it does not take into include-- into account what their VO2 stress test result is or six-minute walk or anything like that.

The one thing just to remember in the Seattle Heart Failure Model is that these are outpatients that were used to do the model, that it's not for inpatient-- patients who are inpatient. And the data would suggest that it underestimates the risks. So that means it overestimates survival, again, because these are all outpatient folks, not patients who are in the hospital.

So if you're looking at that, it may be-- it's a good starting point. I think Parak has used-- uses in his practice, where if you check off this is the benefit if you take your ACE inhibitor. This is the benefit if you take your beta blocker. So I think there's value in that. But I think to actually use the numbers, I would be a little bit cautious, because everyone's an individual and may be a little bit different. And we do know that it probably underestimates the risk. So that means it overestimates survival.

So the answer to this question was the Heart Failure Survival Score was developed in advanced heart failure patients, but does not include medical therapy. Remember, it's just the seven risk factors associated with heart failure developing.

So just a little bit about quality of life assessment in the last couple of minutes-- so the patient-reported outcomes. And so it's important to get the patient's perspective. What can you do? How much fatigue and dyspnea do you have? And certainly, that plays a role in their psychosocial interactions with others and with complying with medications.

And sometimes, there's a disparity between what patients report how they're feeling, what they tell you, and really how they really are. And sometimes, these different models or these different surveys are very effective in sort of getting at the truth of patient-reported outcomes.

So this is sort of the alphabet soup of KCCQ-- so Kansas City Cardiomyopathy Questionnaire. And the MLWHF is the Minnesota Living With Heart Failure score. So these are two different tools that are used many, many times. And you see that in many papers.

There's a difference between the Kansas City Cardiomyopathy Questionnaire versus the Minnesota Living With Heart Failure. In both cases, they are patient-reported outcomes, where the patient will let you know how they're feeling. And here's kind of a silly question, which one it is. We'll talk about that in a second.

But this is the Minnesota Living With Heart Failure score. It is 23 questions-- 22 or 23 questions. It's in the 20s. It is the higher your score is-- sorry. The lower the score is, the worse it is. So it's the opposite as the Kansas City Questionnaire, whereas the higher the score is, the better you are.

So it's the actual opposite. That's why the question is the lower the Minnesota score is, the better the outcomes. And so that's the score. So you want to see a low score for the Minnesota Living With Heart Failure score. You want to see a high score for the Kansas City Questionnaire if you want to look at that.

And I guarantee you if you're taking heart failure boards, this question will be on here because, one, nobody really cares. And two, it's an easy question to ask. It's been validated. But I say that in jest, but there is value to this, because this is the way that you can really get at how people are really feeling. And there is the validity in that if there is an improvement in the Kansas City Cardiomyopathy Questionnaire or an improvement in the Minnesota Living With Heart Failure score, there is actually improvement in survival.

In our bad patients, we do that routinely. And I would suggest in probably selected populations, there may be value in measuring that on an ongoing basis just to see where things are. And so if you were to just look at your patients and say, what do we want to do to-- let me show you that. Let me give you that so you can write that down.

So you say, well, so what can we do to follow our patients on a regular basis and not spend a lot of money to see how they're doing? And I would suggest doing a six-minute walk on a regular basis and doing one of the patient-reported outcomes surveys, like either the Kansas City or the Minnesota Living With Heart Failure questionnaires.

If you did that on a regular basis, especially if you're in a really busy practice, you may be able to sort of follow how people are doing without spending a lot of money. Your staff can-- you can-- your staff can administer the survey and give you the results. Someone can do the six-minute walk and give you the results.

I think there's value in getting an echo periodically. I know that goes against the use criteria. But I think if you feel that there's perhaps been a change in patient's condition, it's worthwhile doing echo. We always get an echo of what's been optimized medically when we think that we have them on the optimal medical therapy with beta blockers or an RME or ACE inhibitor and ARB or aldosterone blocker.

And we've had the chance for them to exercise and maybe get through cardiac rehab. To me, that's the optimal time to get the echo. And we do-- in our practice, we'll do a cardiopulmonary exercise test at the same time. In your practice, if you don't have that available to you, doing a six-minute walk at that time would be-- I think that's the most valuable time to do those things. So I'll stop there.