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Acid Reflux causes and Treatment

How to Prevent a Heart Attack in Those with Heart Disease

How to Prevent a Heart Attack in Those with Heart Disease

(audience applauding) – Thank you for that kind introduction. So I’m gonna go against
my instincts and talk. And I wish that I had
heard the introduction about what this series is all about before right now, (chuckles) but we’ll do the best we can, and then when it’s time
for me to stop talking just give me the sign. I hear a little bit of an echo, but if it doesn’t bother anybody else, okay, we’re fine. So this is what I plan to discuss. What are the causes of a heart attack. What do the guidelines recommend to do for what’s called secondary prevention, which is the prevention
of a second heart attack, or once you’re diagnosed
with heart disease, what can you do to prevent
bad things from happening? And then some on the latest evidence if time permits. So here is a schematic
of a coronary artery. When we are born, I guess I can use this as a pointer, no. So when we’re born, we have
these beautiful clean arteries. You’re looking down the pipe and blood’s flowing through it. Over time, in other
words, as we get older, if we’re exposed to certain factors, things change in the lining of the artery and those people who
develop atherosclerosis get plaque formation. This is a core of lipid
particles, cholesterol, mixed in with some inflammatory cells, and sometimes with calcium,
oftentimes with calcium, and if the person who develops these, because of their exposure to risk factors, changes those risk factors,
there can be shrinkage, thickening of this cap, and
shrinkage of the lipid core. But often, usually it
expands, and this structure, called the fibrous cap, which is a barrier between this lipid core and
the blood, can get thinner as it’s exposed to certain
chemicals that are secreted as the body is trying to
eat up this cholesterol and get rid of it, it
actually can cause weakening of this fibrous cap, and
there could be a rupture where it’s weakest. And when the fibrous cap ruptures, then blood mixes with
this necrotic lipid pool and a blood clot forms. And if that blood clot
occupies all of this space, and occludes the artery,
it closes off the artery, that causes a heart attack, also known in medical terms
as a myocardial infarction, represented by this bluish area of heart muscle that’s dying. If it’s not totally occlusive,
maybe it’s a small clot, maybe it’s not as big a
clot as it would’ve been because the person is taking aspirin. This can heal without
causing a heart attack, and you end up with a
narrowing in the artery where that plaque ruptured,
and symptoms may develop, typical symptoms of what’s called angina, often pronounced, for some reason, angina, for people who don’t have
the MD after their name. And that typical symptom
is feel fine at rest, go up a flight of stairs, and tightness, or squeezing, or heaviness, no
doctor it’s not really pain, I don’t get pain, but
I get this heaviness, and then it goes away when I stop walking, or get to the top and
relax, or walk up a hill is a typical situation, or sometimes when people just get emotionally upset. They can get angina. Now, medical therapy, particularly, well, I’ll take a step back. PCI is an abbreviation for percutaneous coronary intervention, basically, putting in a stent. When people develop symptoms, the typical thing that happens is they report them to their doctor, typically a primary care physician, who may then order a stress test. Stress test is gonna be abnormal, and the person gets referred
for cardiac catheterization. Pictures are taken of
the coronary arteries, and if there’s a significant narrowing, a stent is often inserted
to open up the artery, which results in relief of the angina. And this artery at this location, the way it’s represented,
is it’s not really inflamed where it’s healed, it’s more like a scar, and in this particular
area, as represented here, it’s less likely to cause a heart attack in that specific location. But that’s the area that
calls out because of symptoms and gets a lot of
attention and gets stented. This area, the fibrous cap, can be treated with medical therapy. High intensity statins
result in this liquid core becoming more solid, with the fibrous cap becoming thicker, and less
vulnerable to rupture. So those are the concepts
that are our understanding of what causes heart attacks
and what they look like. Here is a picture of
someone who didn’t make it. Again, it’s a cross-section. This is the fibrous cap that has ruptured. This is where the lipid core was. This is where the blood should be flowing, and that’s a big blood clot
that caused a heart attack. And that is responsible for the majority of heart attacks, the rupture of plaque. And here, I may or may
not be able to show you, looks like I’m not gonna
be able to show you. I was hoping to, I was gonna show you what a heart attack looked like, and what it looks like
when you put in a stent. So what should you do if
you have a heart attack? Acutely, you go to the
hospital as fast as you can, and you get a stent inserted
to reduce the damage to the heart muscle. But what do you do after a heart attack? So cardiac rehabilitation is a program that’s multiple risk factor intervention. Traditionally, it’s based on exercise, but it should be much
more than just exercise, it should include
counseling about nutrition, education about what is cholesterol, blood pressure, how to manage them, how to manage diabetes, and associated with an exercise program
and social support. And people who participate
in cardiac rehabilitation have about a 30% lower risk of dying compared with people who don’t. And it’s something that
the minority of patients, after a heart attack, participate in. And so that’s one key message. I would ask you, but I’m
not gonna interrupt my flow by doing so, there are, you
could separate risk factors into non-modifiable and modifiable, and the ones that you can’t change are things like your age, and your sex, and your history, and your family. And the things that you can change are behaviors, like smoking. You can treat high blood pressure and high cholesterol, or triglycerides, you can treat diabetes,
you eat more healthfully, you can be more physically active, and you can lose weight. The recommendations that are all based on clinical trials, and
these are in our guidelines, are to eat a Mediterranean-like diet, to take a shortcut. There’s a lot of controversy, what about saturated
fat, what about red meat, what about processed
meat, what about salt, and sugar, and cheese, and ice cream, and other dairy fats, and butter? There’s a lot of consensus
that a healthy diet looks like this, lots of
fruits and vegetables, whole grains, nuts, seeds, fish, if I left it out, nuts, and low-fat dairy. Weight control is
important in reducing risk. Being physically active,
and the recommendation is 30 minutes, at least five times a week, of moderate intensity exercise. The 30 minutes can be accumulated, it doesn’t have to be
one 30-minute session. Stop smoking, low-dose
aspirin, high-dose statin, a blood pressure goal of less than 130/80. Dr. Stafford was on the
guideline writing committee that came up with that number, and certain diabetes medications that reduce the risk of
having a heart attack, stroke, or dying. The cholesterol guidelines for
people with coronary disease, really shown on both sides of the slide, basically there’s a lot of stuff up here, but the goal is to get
the LDL less than 70. Start with high-intensity statin, and if that doesn’t work,
add a drug called ezetimibe, and if that doesn’t work, add a drug called a PCSK9 inhibitor, which is a relatively new class of drugs that’s injected every two weeks, and lowers the cholesterol
quite effectively. From one of the trials
that I spent about a decade of my life working on,
called the COURAGE trial, we did a long-term follow-up. These are all people with
coronary artery disease documented on a cardiac catheterization. They all had a narrowing, at least 70%, in at least one artery. And we compared stenting
versus good medical therapy, and found, after about 4 1/2 years, that there was no
difference in the incidence of death or heart attack
between the groups. So stenting didn’t prevent heart attacks. There wasn’t any difference
in survival, either, although it was not really,
there weren’t enough patients to study whether or not
survival would be improved during the 4 1/2 years. But we did a long-term follow-up and found that there
was still no difference between the group that got
stents and the group that didn’t. However, there was a difference in those people who achieved
the risk factor goals that I just quickly went over. So this just shows, this
curve, this set of curves shows what the death rate
was among people who had, who achieved no goals,
and then one, two, three, four, five, and six, and
those goals that we studied were diet, smoking, physical activity, blood pressure, weight, LDL cholesterol. And for every risk factor goal attained, there was a 16% further reduction in the risk of dying over
the period of follow-up. Now, none of us gets out
of here alive, ultimately, but we wanna be as healthy as we can, and be free of symptoms
for as long as we can, and doing what are relatively
straightforward things, walking, if you can walk, taking medicine to control blood pressure, taking medicine to control cholesterol, eating a healthy diet, not smoking, those simple things can dramatically reduce the chances of dying
if you have heart disease. You know, I don’t wanna
take too much time. I have only 100 more slides
that I could show you. But I don’t know if I should stop there, or talk about some of
the newer medications. I’m looking at Dr. Stafford. – [Randall] Yeah, I think introducing the newer medications is important. – Okay, so I’ll talk a little bit more. First, an older medication,
and that’s beta-blockers. Many of you have heard of beta-blockers. One of the most popular
ones that’s prescribed is metoprolol, maybe
atenolol, maybe carvedilol, those are generic names,
Lopressor, Toprol, Tenormin, Coreg, those are examples
of beta-blockers. If someone’s had a heart attack, they should be on a beta-blocker
for at least a year. The guidelines say up to three years. If someone has a reduced squeeze,
called ejection fraction, the fraction of blood
ejected with each beat. If they have a weakened heart, they should be on a
beta-blocker indefinitely. And if someone has angina, and they prefer to be
treated with medication instead of having a
stent, or bypass surgery, beta-blockers reduce angina, and that’s another reason for their use. Now, some newer drugs I’m gonna talk about are on this slide, but
I’ll just go straight to, I have a couple slides on each drug. There was a big trial
presented a couple years ago, called REDUCE-IT, which was a trial in people with heart disease
who had high triglycerides, or diabetes, and had high triglycerides. And the intervention was giving a drug that is pure EPA, eicosapentaenoic acid, or the actual formulation
is called icosapent ethyl. The brand name of the drug is vascepa, you probably have heard, or may have seen
commercials, V-A-S-C-E-P-A. And so these are people with heart disease and high triglycerides,
defined as 135 or higher. And they were already on statins, and it was a placebo
control, so they either got the active drug,
icosapent ethyl, or a placebo, and there was a significant reduction in cardiovascular death,
heart attack, and stroke. And there was a significant difference in many of the other
endpoints that were measured. So this is fish oil, pure EPA, but it’s not over-the-counter, I don’t know if your over-the-counter would have the same benefit. And if you have high
triglycerides and heart disease, talk to your doctor
about getting on vascepa. That sounded like a commercial. (audience laughs) I mentioned PCSK9 inhibitors, drugs that are injected twice a month that lower cholesterol. Here is one of the two large trials. This one was called ODYSSEY. This drug, when given to people
who were already on statins, which can lower LDL cholesterol by 50%, when they take this drug, there’s an additional 55% reduction, shown in this red line,
compared with the placebo group. And there was a significant reduction in the primary endpoint, which included cardiovascular death,
heart attack, stroke, and something called unstable angina. Now, you can see the separation, it’s called statistically significant. None of these are huge reductions, but this is something that can be taken in combination with statins,
which also reduce the risk of dying and having a
heart attack and stroke. Here was the difference in mortality. So there’s a survival
benefit with that drug. Now, looking at something
completely different, doesn’t have to do with lipids, it has to do with blood-clotting. Some of you have heard of,
I believe the brand name for this drug, rivaroxaban, is Xarelto, I think that’s correct. Well, this is a blood
thinner, an anticoagulant, which was tested in low-dose in people with established
atherosclerosis, mostly heart disease. They got either the low-dose rivaroxaban, plus low-dose aspirin,
or intermediate dose of rivaroxaban, the
anticoagulant without aspirin, or low-dose aspirin. And the group that won
was low-dose rivaroxaban, the low-dose anticoagulant plus aspirin. These are people with
stable coronary disease given an anticoagulant, a low dose, and they had fewer deaths,
heart attacks, and strokes. For people with diabetes,
there are two classes of drugs that in the last few years have been shown to prevent heart attacks,
strokes, and death in people with heart disease. These are results from a
placebo-controlled trial called EMPA-REG, and the blue lines, so this is time, I should
have explained this, in the x-axis is time,
and these are events, in the y-axis, percent of
participants that had events. And for each of these different outcomes, this is death, heart attack and stroke, this is cardiovascular death, people who got the drug lived longer, had fewer heart attacks, fewer strokes. And then there is a class of drugs, well, I didn’t say what
this class was called. This has a really difficult
name to pronounce, this one is called Empagliflozin. It’s an SGLT2 inhibitor. But if you have diabetes
and heart disease, ask your doctor if you are a candidate for this kind of drug. And then there’s another class of drugs for patients with diabetes
and heart disease, they’re called GLP-1 receptor agonists. And, oh yeah, a simple name, liraglutide is the name of the drug
tested in this trial. But again, small but
significant reductions in cardiovascular
endpoints with that drug. And this is the last
drug that I’ll mention and then I’ll stop. So we talked a little
about blood pressure. Blood pressure lowering reduces
heart attacks, and strokes, and prolongs life in
people with hypertension and heart disease. Same with LDL cholesterol lowering. Now, diabetes drugs that aren’t so much about treating the diabetes, they’re about reducing
the risk of heart attack in people with diabetes. We talked about an
anticoagulant, a blood thinner, that reduces the risk, and you
can sort of understand that from what I showed you
when the blood clot forms, you’re preventing blood clots from forming with the anticoagulant. Now, this is something
completely different, it doesn’t affect blood clotting, doesn’t affect blood pressure, doesn’t affect cholesterol or blood sugar. This is a test of a very
familiar drug called colchicine, which is used for the treatment of gout, and a much less common condition called familial Mediterranean fever. It is an antiinflammatory drug, and this is a recent study, called the Colchicine
Cardiovascular Outcome Trial, or COLCOT, and compared with placebo, colchicine reduced the risk
of cardiovascular events. I think that this was
also cardiovascular death, heart attack, and stroke was the endpoint. These are not huge differences, but it’s a couple percent,
and you put it all together with lifestyle and the right medicines, you can do quite a lot to
prevent having a heart attack, and I’ll stop there. Thank you. (audience applauds)
– Thank you so much, David. I hope it’s okay if I continue
to have you up here, and. – What about the mic? – While you have the mic, I
will pay special attention to yakking a lot, if I can. But what I, I thought
we would transition now, a little bit, I’m a primary care doctor. I see these people who come in to see me, and, all, I would say 90% of the time, coronary artery disease is
just one among many conditions that they have. And so part of my goal is
really to help the patient think about what to prioritize. So I was very, it’s
very encouraging to see the data from the COURAGE
trial, which suggests that kinda the more things you have under control, the better. But the sort of question
I get from patients, and the one I wanna ask you, what do you prioritize? What health behaviors do you really put at the top of your list, and which ones maybe do you put lower down the risk. All of ’em are important. I think that’s, you know,
one indication here, and it almost seemed like, to
really get the huge benefit, you had to really be
working on everything. But I have patients who ask me, “Well, what one thing can I do “to really help my risk?” – Well, we don’t see a
lot of patients who smoke here in this community, but
that would be number one. And when we looked at, I’m
sorry I don’t have the slide, but when we looked at which of those goals had the greatest benefit,
physical activity was, I think it was, came after smoking, and then blood pressure came third, having a systolic blood
pressure less than 130. And lower down came diet. Now, almost everybody in that trial, over 95% were already on a statin. And so we didn’t compare
no statin versus statin. If there was, if there
were two medications that I would say are
really critical to take, it would be low-dose aspirin
and high-dose statin. – Great, thank you. So another question that my
patients come to me with. You know, some of the more
learned of my patients have heard of the trial
with the icosapent, with the part of what’s in fish oil, and their question is, “Well, you guys “keep going back and forth on this. “A couple decades ago, fish oil was in, “then it was maybe we weren’t
sure of the proof of that, “and then it really fell out of favor, “but now it seems to be coming back. “But these capsules are really expensive, “can’t I just, like, eat more fish, “or just use an over-the-counter fish oil “in place of this really expensive drug?” – Really good question. A very learned patient
who asks that question, because what’s happened
in the United States is there have been a series of trials using fish oil that showed no benefit, and every time one of those was published, sales of fish oil went up. (audience laughs)
You know, go figure, I mean, it’s really kinda kooky. But there have been a couple of trials, one in people that didn’t have
established heart disease, and then this most recent one in people with established heart disease, using this specific preparation. (phone beeping) That might be me. Icosapent ethyl, and
they both were positive, they both showed a benefit. And so unfortunately, it’s expensive, and if you have a drug
plan, it may not cover it, or it may cover it a little. But, the general rule is, if you want to practice
evidence-based medicine is you use the evidence
from clinical trials, and it’s anyone’s guess if
over-the-counter fish oil is as good as, you would
derive a benefit from, as compared with the icosapent ethyl. So I can’t in good conscience say that it’s just as good to take
over-the-counter fish oil. There was just a trial that
was stopped, using DHA, Docosahexaenoic acid,
because there was no benefit. So you have to use the
evidence from clinical trials, and, unfortunately, I would say that you might be wasting your money if you take over-the-counter. – But if I read kinda
between the lines there, you know, thinking about myself, or, let’s say, my father who
has coronary artery disease, I might look for a
over-the-counter fish oil with lots of EPA in it, would that be the wrong thing to do? – It’s a guess, you’re flipping a coin. I guess I would look at all of, look at the big picture, what
are his greatest risk factors, how much benefit in
the best case scenario, if you applied the results
from that clinical trial, and, you know, I look at that as treating high triglycerides, people
with high triglycerides, although we actually don’t
know if it would work in people with low triglycerides,
’cause that wasn’t tested. So I would look at his
specific risk factors and see which interventions might yield the greatest benefit for him. – So you talked a little
bit about cardiac rehab. And, actually, one of my other roles that Nora mentioned was
on this national committee looking at falling measures. How would we measure quality
of clinical practice? And cardiac rehab has come up as something we ought to be
paying more attention to. And some of the data that
the group was presented with are really astounding,
which basically suggests that if we look at the whole country, cardiac rehab is essentially unused. Very few people are
referred to cardiac rehab, and even among the people who I referred, very few people make it
to even six sessions, which is well below
what we would recommend. And this was quite startling to me, ’cause I think living
in this geographic area, we know of multiple different
cardiac rehab locations, and we send patients there all the time. But clearly, something is different in other parts of the country. What can patients do to try to kind of make sure they’re
getting the best care, and getting referred to cardiac rehab? – Well, first of all, I would say that I’m not sure that we’re much better than the rest of the world. The referral rates are not close to 100%, and the showing up rates
are, for the first visit, are not close to 100%, for
those people who are referred, and then completion, it’s probably more like 30% completion rate. Maybe if they go to the first visit it might be closer to 50%. So we’re not fantastic,
but if you don’t know that you should go to cardiac rehab if you are a candidate, and
your doctor doesn’t refer you, you lose out. And really, what cardiac rehab is, is it’s multiple risk factor intervention. It addresses all of those risk factors, smoking, cholesterol,
blood pressure, diabetes, weight, physical activity, and nutrition. So that’s why the reduction
in mortality is so big. You know, people talk about how effective cardiac rehab is, and it’s just the sum of all of those individual interventions. – So, just one last question. You know, one issue that I run into a lot with my primary care patients, is not only do they have
the coronary artery disease, they have all these other things. And, you know, quite
often those were competing with one another for
the patient’s attention. There’s a kind of limited
capacity each of us has to deal with kind of
complexity in our lives. And one of the things
that I often emphasize is that some of those other conditions, like diabetes, or high blood pressure, or high cholesterol, things
like being overweight, all of those also tie back to some of these health behaviors. And so I view the health behavior route as something that not only addresses the cardiovascular disease, but can also deal with some of these other conditions that the patient may have simultaneously. And again, in my patient population, it’s incredibly rare to have somebody who just has the coronary artery disease, and, you know, often it
goes along with diabetes, and high blood pressure,
even heart failure in many cases. So one question for you is, how to help those patients
kind of see the full benefits of those health behavior changes? Clearly, it’s easier when
people are holding your hand, as happens in cardiac
rehab, but how do patients take on those kind of
health behavior changes, especially when they’re
seeing their cardiologist for 30 minutes, or seeing
their primary care physician for just 15 minutes. How do we, how do we help people? – That’s a really tough question, thank you very much. (audience laughs) Well, from a physician’s standpoint, first of all, I totally
agree with what you said about health behaviors, and, yes, the typical accompaniments of the diagnosis of heart disease is high blood pressure,
high cholesterol, diabetes, overweight, and not so much smoking, as I said earlier, in this community. To start with, it’s making a connection. For me, it’s making a connection with the individual patient. It’s just making a human connection, and that’s kind of hard to teach in medical school. But that’s one of the prerequisites if we’re gonna make any progress. It’s finding out from the patient what’s important to them,
what is important to you? Because, you know, habits
are really hard to change, and you have to really be motivated. What motivates you to make a change? Is it to see a child
graduate, get married, watch a grandchild grow up, attend some important family event? What is it that motivates you? So that’s something to leverage. To say, if you wanna achieve this, this is what you need to do. And then, for me, it’s having a team. A dietitian, maybe a nurse
who’s particularly good at following up to see if
laboratory tests are done, if medications are being
picked up at the pharmacy, are they being refilled. It takes a team. Maybe engaging the spouse
or other family member to help support changes. I see, you’d be amazed, that some couples are not perfect. (audience laughs) And there can be undermining
of trying to reach goals, people working at cross-purposes. It’s not easy, but it
starts with education, building a connection with the patient. It’s the one of the reasons why I think cardiac rehab is so successful is because of the social support. There are other people there, physically, going through the same thing, having the same diagnosis that
you can share tricks with, support each other, learn from each other. It’s all of that, I don’t know the answer. – So I’m gonna open it up for questions in just a moment, but I did wanna go back to your risk factor slide. Couple things there
that sometimes I’ve seen on such slides, but I didn’t on yours, perhaps because they’re
a little bit borderline in terms of their causal relationship. But what about stress reduction and sleep? Are those risk factors for
having another heart attack? – Another great question. One of the, one of the difficulties with those potential
risk factors, let’s say, is that there have not been
randomized controlled trials to prove that, for
example, stress reduction reduces the risk of heart attacks. Now, there’s good
evidence that acute stress triggers heart attacks. There’s plenty of evidence. You can take natural disasters and see the heart attack rate spike when there’s a huge earthquake. We see people who are going
through stressful situations have heart attacks. As far as sleep, I actually
don’t know the evidence so well to indicate that poor
sleep causes heart disease, but I’m sure there aren’t
any clinical trials showing that improving sleep hygiene, or sleeping more reduces the risk. So there is a difference
between risk factors and things that have been
proven to cause heart attacks. For example, low HDL, you’ve heard of high density lipoprotein cholesterol? A lot of people, I would bet
some people in this room, still believe that low
HDL causes heart attacks, but the evidence actually
doesn’t support that. Raising HDL doesn’t reduce
the risk of heart attacks. Now, in 10 years from now, somebody else will be standing up here, telling you that raising HDL does indeed, if it’s the right type of HDL, reduce the risk of heart disease. But with our current
understanding, it doesn’t. So I’m sort of a purist on the one hand, and I just wanna use the evidence. The highest forms of evidence is a randomized controlled trial, where you take a group of
people with a certain exposure, let’s say it’s high blood pressure, and you treat one group, and
you don’t treat the other, or you treat one more intensively than you treat the other,
and you see what happens. And it’s that kind of random assignment where people don’t get to
choose which group they’re in, that is the highest form of truth in trying to understand causation. – So I hope the time you’d
ask really hard questions for Dr. Maron, here. Why don’t we start over here? – [Man] I have a question. You mentioned one of the drugs, which is a beta-blocker, and also there’s another
class called ACE inhibitor. My question is, what is the
difference between the two, and what each one does,
if a person only has artery disease and has stents? – Okay, the question is,
what’s the difference between a beta-blocker
and an ACE inhibitor. And, boy, I’d love
that, since Dr. Stafford was on the guideline writing
committee for hypertension, would you like to answer
that, or not do it? – Sure.
– Okay. – So angiotensin converting
enzyme inhibitors or ACE inhibitors and beta-blockers, they’re both classes of drugs
that are very typically used to treat high blood pressure. So both reduce blood pressure, but in slightly different ways. And, in fact, both seem to have a benefit in the presence of some
types of heart disease, particularly the situation where the heart is not pumping strenuously enough, often called heart failure. Now, both of those drugs are probably have multiple benefits. Some is purely from the
reduction of blood pressure. In some sense, the less blood pressure the heart has to push against, the heart’s work load is reduced. However, there’s probably other benefits of both of those drugs,
and there’s a lot been said for kind of the hormonal
effects that happen as the heart starts to work harder, or the heart doesn’t
have enough oxygen supply to do it. Beta-blockers are the ones that have the greatest known benefit in the person who simply has coronary artery disease, that is this whole kind of range of things where the arteries supplying
blood to the heart muscle are either blocked slowly
or blocked suddenly. So the beta-blockers really come up on top in terms of that situation. Both probably have some benefit beyond their blood pressure controlling, and we see that in things
like kidney disease, where ACE inhibitors
clearly have a benefit of reducing the progression,
reducing the rate of which people lose
their kidney function. So it’s a very complicated area. Both of these blood pressure medicines have benefits, the type
of benefit they have may be more than just
reducing blood pressure. – [Man] The reason I asked the question, we moved from Texas here eight years ago and I have a doctor at Stanford, ’cause I just got done in
Houston, Texas Medical Center, so I contacted him, so I’m a patient of a cardiologist at Stanford. And so he saw my medicine,
which doctor in Houston had prescribed, beta-blocker, metoprolol. And first visit he says,
“Oh, that’s very good, “but I think giving you five milligram “of ACE inhibitor is no-brainer.” He used those words,
and I was very curious that he says no-brainer,
that means so obvious. What was it my doctor needs to list? – Well, I don’t know the whole story, that’s a little hard to speculate. But again, both are very good medications. Both of these medications
have been around forever, you know, back into the
1950s for beta-blockers, into the mid ’60s for ACE inhibitors. David talked about a number
of the brand new medicines. We’re still kind of figuring out how to get the most benefit out of them. But in terms of blood
pressure, we pretty much know how to treat blood pressure and do so pretty successfully with drugs that have been around a
while, and for that reason tend to be low cost. – Okay, and I would add that
not knowing the specifics, but if you had a reduced
ejection fraction, it would be a no-brainer
to add an ACE inhibitor. If you have diabetes and
some protein in your urine, it would be a no-brainer
to add an ACE inhibitor. So certain of these medicines have very specific, what
are called indications, or reasons to prescribe them. I don’t know what it is
in your specific case, but there may be something
where it’s obvious that you would benefit from the addition of an ACE.
– I do have insulin resistance. – Okay, yeah, could be, yeah.
– So that’s that. – [Randall] How about in the middle here? – [Man] A stupid, obvious question. But since you’re evidence-based, exercise, what kind of factor is there, I mean something we can do without actually taking medication? – Is the question what are
the benefits of exercise? – [Man] Yeah, I mean, do you
have, like, numbers on that, or anything that shows
what the exercise can do to help keep that? – Well, I don’t have anything on a slide, but I can recite to you some
of the benefits of exercise, and there’s a lot of literature on what exercise does. It lowers blood pressure, it
improves insulin sensitivity, so it reduces the risk
of developing diabetes, it helps to manage diabetes, it lowers triglycerides, it reduces the stickiness of platelets, it enlarges coronary arteries. People who exercise a lot
actually get larger diameter. – [Man] That’s it, that’s
what I’m looking for, yeah. – Okay.
(audience laughs) – [Man] Well, you should’ve been in front of the computer
for three, four hours a day, I should be out there running, right? – Yes.
– Right. – [Man] Okay. – Okay. – [Man] That’s my New Year’s goal. – [Randall] How about back here? – [Man] Could you say a few words about the research that’s
being conducted at Stanford, and as part of that,
I’ve been participating in a Stanford heart study
for quite a long time. Every day I enter my activities,
it tracks my numbers, and so on, but I haven’t got any feedback, I’ve been doing this for about two years, so I’m wondering what’s going on. – I don’t know which study that is, so I’m gonna refer you to whoever the principle investigator is. I’ll tell you a little bit about the trial that I was overseeing, that we finished not too long ago, called
the ischemia trial. It was a study of people with stable coronary artery disease, in other words, people with obstructive coronary arteries who were in a stable phase, they weren’t having a heart
attack when we met them. They all had an abnormal stress test. They had been referred for
stress testing of any type for, usually because
of symptoms of angina. And we randomly assigned them to a group that would go to the cath lab and get pictures of their arteries taken, and then go on to have either
a stent or bypass surgery, whichever is most appropriate, and optimal medical
treatment as described. That was the invasive strategy. Or they were randomly assigned
to the conservative strategy where they didn’t go to the cath lab, but they got the same
high-quality medical therapy. And we watched what happened to them over a period of years. And the bottom line is that
there was no difference between groups in terms
of the primary endpoint, which was a combination
of cardiovascular death, heart attack, hospitalization
for unstable angina, or heart failure, or cardiac arrest. And this followed the COURAGE trial which showed, in people who
were sent to the cath lab and had at least one narrowed artery, that there was no difference between stent or no stent, as long as they
both got good medical therapy. So that, I’m expecting to hear
from the “Journal” tomorrow with comments from reviewers. That study hasn’t been published yet, but we presented it last November, and it was covered broadly
in the “New York Times”, “Washington Post”, et cetera. So that’s a high profile
study that we did at Stanford. There was the Apple Watch study, that I think we called it the, not we, they called it the Stanford,
the Apple Heart Watch? Anyway.
– That’s the one that I’m in. – Oh.
– That’s the one. – Okay, well, you need
to talk to Marco Perez, and I’ll give you his
cell phone number after. (audience laughs) And that was looking for
evidence of atrial fibrillation using this heart watch,
or the Apple Watch, that is monitoring heart rate, and had an algorithm that thought it was, that could detect speeded up heart rates that increased the likelihood that atrial fibrillation was present. That was a very, that
was a momentous study, because it showed that you could enroll tens of thousands of
patients really quickly. It took us several years
to randomly assign 5,000 in the ischemia trial. – [Randall] Unfortunately,
we’re running out of time, so we’re gonna have two more questions, how about right here? – [Man] You mentioned high-dose statins. What is, give me a
number, for like Lipitor, and also, what about the
people who have side effects, muscle aches, what can they do? And is there something besides aspirin that can help the muscle aches? – Great question, I expected it. And, because in my clinic,
I see a lot of patients who want to be treated,
but don’t give me a statin. – [Randall] If I see those people, I immediately refer them to Dave. – Thank you.
(audience laughs) Well, that explains it, yeah. Just a comment about
muscle aches and statins. When people have been
studied in the context of a clinical trial, and
they’re getting a drug, and they don’t know if
it’s a statin or placebo, there’s no difference in the complaints about muscle symptoms. However, when they find out
that they’re taking a statin, the rate goes up. There is a large internet society that propagates worries
about side effects. Having said that, maybe 5%
of people who take statins get muscle aches. And whether or not they’re
caused by statins, I don’t know. But let’s just dismiss that question mark, and let’s say you’ve
got statin intolerance, you cannot take a statin. Well, when I see patients such as this, who really need to be on a
statin to reduce their risk, they have heart disease,
or they’ve had a stroke, and carotid artery narrowing. We try a lower dose, we try,
if that hasn’t been tried. We try a different statin. We try taking a low dose
of Crestor every other day. There are things that we can try. But let’s say you can’t
take a statin at all. Then, ezetimibe, Zetia, is a drug that lowers LDL, not
quite so much as a statin. If you can’t get your LDL below 70, and you have heart disease, and you can’t get down
there with just ezetimibe, then you should go on a PCSK9 inhibitor, and that’s the best solution. Another drug is probably
coming out this year. It’s, I don’t know what
it’s gonna be called, but the generic name is bempedoic acid, and it’s about as effective as ezetimibe, maybe a 15, 20% reduction in LDL, as opposed to a statin which
will lower your LDL by 50%. And give you some numbers, okay, Lipitor is
atorvastatin, and high dose is considered 40 to 80 milligrams. Crestor, which is rosuvastatin, high dose is considered 20 to 40 milligrams. – [Randall] One more
question here, in red. – [Man] I’ve actually got
two, and one’s real short. First short question is, I understand that something like only 6% of people who have a heart attack survive it, is that in fact true? – No.
– No, it’s just the opposite. It’s actually well above 90% of people who’ve had a heart attack survive. So you, what you, I think
what you were saying is that 94% of people do
not survive a heart attack. – [Man] That was the statistic I read. – No, absolutely not, no. – [Man] The other question is, every single person on my
mother’s side of the family, and there are plenty
of ’em, a large family, have all died of heart
disease, every single one. So I’ve taken a statin for 35, 40 years. My numbers have always been
100 and at least 128 or below. – For your total cholesterol or LDL? – [Man] The one that they told
me was (speaking faintly). – The LDL? – [Man] And it’s been, at times, as low as under 100. And I’m good on all the risk factors, and all of a sudden I found
that I have heart disease. We’re doing everything right, and it seemed like it
came on very quickly, within a period of about three months. And I don’t wanna brag,
but I went out dancing and was challenged by about
a 30, 35-year-old woman to a dance contest, and she
left immediately thereafter and never came back. (audience laughs) I think I’m doing something right. How does that, how does it, you know, how does it all come together? – A couple of comments. Now, this was supposed to be for people with heart disease, but
I see a lot of people who are at risk or have. (phone beeps)
Sorry, have a strong family history of heart disease, and one of the tests
that I get quite a bit is called a coronary artery calcium scan, where we can easily diagnose the presence of calcified plaque in
people who have no symptoms, and those, it’s a wonderful test to help make the decision about treatment of risk factors, how aggressive to be. That said, how could you, who
has done everything right, get heart disease? First of all, life’s not fair. Second of all, you know,
your LDL cholesterol, it sounds like, if you
were on a high dose statin, might’ve been in the 200s,
LDL cholesterol in the 200s without the statin, which suggests that you may have something called familial hypercholesterolemia, FH, which is a genetic disorder, it’s one of the most
common genetic disorders. And that may be why there’s
so much heart disease on your mother’s side of the family. If you have that fate,
you have a 50% chance of transmitting it to your child. You may have that, I don’t know. And so, and, an LDL in
the 100 to 115 range is the average LDL of somebody
who gets heart disease. It’s not particularly low,
it’s probably much lower than it would be if you
weren’t on the medicine. And then there’s another test that doctors generally don’t get, that if anyone develops heart disease and you’re scratching your head why, everything is good, lipoprotein little a, is a factor that causes
heart disease and stroke, and narrowing of the aortic valve that is not commonly tested, but it helps explain a fair
amount of heart disease. – [Man] So remedy then is that commonly a significant factor? – It’s a significant factor. People who are dealt
a bad hand genetically can improve their prognosis
by having a healthy lifestyle, just like people who are dealt a good hand and have a terrible lifestyle
can make bad things happen. So it sounds to me like you’ve
done a lot of good things and you’ve staved off heart disease, compared with your predecessors. – [Man] I happen to know
that my bone calcium is low, so I actually take calcium,
and if I remember right, my blood calcium is low. – Separate deal. – [Man] Pardon? – It’s a separate thing,
your bone density. – Thank you.
– Okay. – We wanted to thank all
of you for coming tonight. I think we had a really great conversation and hopefully you’ve
taken away quite a bit of new knowledge from this. I certainly wanna thank my colleague, David Maron, for joining me up here and providing a lot of expertise on a whole range of things. And this is one of those
topics that I’m sure, you know, given six hours,
David could easily fill it. So I really appreciate summarizing it down to what we can all
handle for one evening. I do wanna tell you that this
series is going to continue. The next one will be in April. Looking at this issue of heart failure, which we talked about a little bit today, and then we’ll have a subsequent session thinking about how to
use medical technology. And the question about
the Apple Watch Study brings us right to that point and kind of tells us some
of these technologies are out there, and maybe we
ought to be taking advantage of them a little bit more,
not only around things like detecting atrial fibrillation, but maybe also helping
us with behavior change. So I hope you’ll join us in the future. Thank you so much. (audience applauds)

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