- [Announcer] Please welcome
the American Heart Association's
Chief Executive Officer,
Nancy Brown.
(majestic music)
- Welcome to the American
Heart Association's
Scientific Sessions 2016,
the world's premiere
conference for cutting edge
cardiovascular disease and stroke science.
We are honored that you have joined us,
and we hope you'll
embrace this opportunity
to engage with colleagues
and hear from thought leaders
in your field.
Before we begin, I'd like to
comment on the significance
of this meeting being held in New Orleans.
Last year, New Orleans
passed comprehensive
smoke-free legislation,
a great demonstration
of this city's commitment to the health
of its residents and to visitors like us.
We are proud to be supporting New Orleans
by hosting our meeting here.
(audience applauding)
I have the privilege today to announce
several partnerships that will improve
the lives of patients.
Last year, at this meeting,
we announced a partnership
between the American Heart Association
and the patient-centered
Outcomes Research Institute
to crowdsource compelling
ideas for comparative
effectiveness research
in precision medicine.
Since then, we have sought
insights from patients,
care givers, clinicians and researchers
to help us better understand
the needs of patients.
Today, I'm proud to
announce a new $5 million
AHA PCORI co-funded Grand Challenge Award
to build on these insights.
This partnership has been made possible
by the extraordinary
generosity of dear friends
and longtime supporters of the
American Heart Association,
David and Stevie Spina,
who have donated $2.5 million,
which PCORI has matched.
(audience applauding)
This gift adds to the
Spina's powerful legacy
of philanthropy.
We are so grateful to David and Stevie
for setting this pace.
As you know, one in three
Americans are living
with high blood pressure, which is why
the American Heart
Association has made this
a major focus of our work.
Last year, we announced
Target Blood Pressure
and a new relationship with the
American Medical Association
to improve clinical
care for blood pressure.
Today, it's my honor to announce
a new nationwide venture
between the American Heart Association
and the YMCA of the USA.
Leveraging the Y's
extraordinary community presence
and self management program with the AHA's
hypertension resources,
we intend to transform communities.
We are pleased to have
in the audience today
several national and
local leaders of the YMCA.
We thank them for this
tremendous partnership.
(audience applauding)
Last month, we announced
that the American College
of Cardiology and the
American Heart Association
have joined together to
create a single, comprehensive
set of cardiovascular accreditation
services for hospitals.
Starting in 2017, hospitals
will be able to take advantage
of this suite of AHA/ACC
co-branded accreditation services
focused on all aspects of cardiac care.
By leveraging our unique capabilities,
the AHA and ACC will accelerate
and expand our impact
on patients' lives across the country.
And as part of the AHA's
Institute for Precision
Cardiovascular Medicine, I'm
pleased to announce today
the launch of a new AHA Bayer
Innovation and Discovery
Grants Program focused on
research that addresses
unmet medical needs.
And finally, I'm excited
to announce the launch
of Target Cholesterol, made
possible by a $6 million
gift from Sanofi Regeneron.
I'm inspired by the difference that each
of these partnerships will
make on the lives of patients
across the country.
I'd like to also give special thanks today
for the outstanding work
and leadership of the
American Heart Association's Committee on
Scientific Sessions program.
The committee is led by
Chairman, Doctor Frank Sellke,
of Brown University Medical School and
the Rhode Island Hospital
and Vice Chairman
Doctor Eric Peterson,
from the Duke Clinical
Research Institute.
Please join me in a round of applause
for Doctors Sellke,
Peterson and the entire
Committee on Scientific Sessions Program.
(audience applauding)
And now, it's my honor to introduce
Doctor Steven Houser, President of
The American Heart Association.
Doctor Houser is Senior
Associate Dean of Research
and Chairperson of the
Department of Physiology
as well as Director of the
Cardiovascular Research Center
at Temple University School
of Medicine in Philadelphia.
During nearly 40 years
of volunteer service
to the American Heart Association,
he has made countless
enduring contributions
to our mission of building healthier lives
free of cardiovascular
diseases and stroke.
Please join me in welcoming
a wonderful volunteer
and dear friend, Doctor Steven Houser.
(majestic music)
- Thank you.
Good afternoon.
Welcome to Scientific Sessions 2016
in the finally smoke-free
city of New Orleans.
(audience applauding)
It's a pleasure to be back
in this exciting environment.
I truly hope your next few days are filled
with memorable and meaningful experiences.
No matter whether this is your first time
at Scientific Sessions,
or if you've come so often
that you've stopped counting,
I thank you for joining us
from across the U.S. and
around the world to explore
the latest developments
in cardiovascular science.
I am honored to stand
before you as the President
of the American Heart Association and
the American Stroke Association.
It's my privilege today to
share my personal journey
as a cardiovascular scientist
and as an AHA volunteer,
and to delve into the key themes
of my presidential tenure,
scientific discovery,
developing the next generation
of cardiovascular
scientists, and of course,
the prevention of cardiovascular
diseases and stroke.
My personal journey as a
cardiovascular scientist began,
oddly enough, on the basketball court.
I love basketball.
After four years of
shooting almost every ball
that was passed my way
at a Division III school,
it turned out that no
NBA team was interested
in an undersized power forward.
So I moved to a graduate
program in medical physiology
at Temple University School of Medicine
in my hometown of Philadephia.
Two years into my training,
I was involved in the study
of the neuromuscular
junction in the lobster,
which is a model of the synapses in
the human central nervous system.
It was a great project.
My duties included
weekly trips to the docks
to pick out fresh lobsters.
I ate really well as a graduate student.
But then the real world intervened.
My dad became very sick.
So let me tell you a
little bit about my dad.
Robert Harold Houser was
a great husband to my mom
and a great father to me and my sister.
Baseball and fishing
were our shared passions.
If he wasn't helping me get
better at hitting curve balls
or stopping grounders, then
we were probably catching bass
in Maine or sitting on the
sofa watching a Phillies game
or an Eagles game.
Like many men of his
generation, my father served
in World War II.
He didn't talk much about the war with me.
All I really know was that he
was a radio man in the Navy
and he saw action in the Pacific.
And he came home with a three
pack a day smoking habit
that he never kicked.
Bob Houser was a hard working
member of the middle class.
His primary goals in life were to love
his high school sweetheart,
my mom, and to provide
for his children so that we could have
greater opportunities than
he had, like all of you do
for your families.
My dad was also soft-spoken.
He was not a complainer,
not even when his body
sent him warning signals
that something was wrong.
My dad was 43 when he
suffered what he dismissed
as a chest cold.
He never sought treatment.
He missed just one day of work.
About seven years later,
my dad was diagnosed
with congestive heart failure,
and that's when things
got really bad really quickly.
I was in the lab at Temple
studying my lobsters
when my mom called and said,
"You've got to come home."
Those were the early days
of cardiac catheterizations,
and my dad had one.
And it showed that the episode
he considered a chest cold
actually had a been a large
myocardial infarction.
And now he had a ventricular aneurysm and
congestive heart failure.
His surgeon discussed
repairing the aneurysm
but didn't think my dad
would survive the surgery.
His care team tried
their best to treat him,
but he lived only a year longer.
Heart disease took my dad
at just 51 years of age,
and I'm 65 this year.
And his death changed my career.
During his decline I began
my education in cardiology.
I remember sitting in
my dad's hospital room
watching his PVC's and
then running to the library
to read what I could find
on ventricular arrhythmias.
Those were the days of libraries.
Every change in his
condition sent me in search
of more reading materials.
I especially devoured papers
from Gene Braunwald's group,
and I became hooked.
I love the field, and
of course, I now felt
a deep personal connection.
I went to my adviser and
I switched my thesis topic
to a study of failing cardiac muscle.
And I decided to devote my life's work
to helping develop the
knowledge needed to best treat
patients with heart failure, secondary
to myocardial infarction.
Let me frame it this way.
The American Heart
Association uses the tagline,
Life is Why.
It's a great tagline.
Well, starting in 1977,
defeating my dad's disease
became my why.
My initial work sought
to find ways to make
a failing heart stronger and to prevent
lethal cardiac arrhythmias.
I would go on to spend more than 25 years
working on those two topics.
It was an amazing period of
new scientific discovery.
A host of new tools such as
single cell electrophysiology
and calcium imaging came onto the scene.
And a collection of
cardiovascular scientists
throughout the world began
to unravel the mysteries
of normal cardiac myocyte physiology.
Studies in my field defined
the fundamental bases
of normal cardiac function
and the cellular and molecular
underpinnings of human heart failure.
These discoveries led to the development
of better therapies to
treat patients who suffer
from cardiovascular diseases,
including heart failure.
One early hypothesis of
heart failure research
was that if we could
increase the contractility
of weak myocytes in the failing heart,
we would improve its poor pump function.
We learned what made failing myocytes weak
and we developed novel
inotropic therapeutics
to enhance their contractility.
Many of these drugs
improved cardiac function
and made patients feel better
and are still useful to
bridge patients through
transient periods of
acute cardiac dysfunction.
Unfortunately, some of these
drugs also had a propensity
to cause lethal cardiac arrhythmias.
Clinical trials showed
that chronic treatment
with many of these drugs
put patients at higher risk
of sudden death.
About this time, a brave
group of investigators
made the surprising discovery
that beta adrenergic
receptor antagonists, drugs
thought to be contraindicated
in heart failure, because
they have the potential
to make weak hearts even weaker.
Well, we found these drugs
could actually improve
cardiac structure and
function and would prolong
patients' lives.
So what had our collective
experimental results taught us?
After a heart attack,
the surviving myocytes
have to work harder than normal.
And this persistent, excessive workload
induces a change in their
phenotype, making them prone
to electrical abnormalities
that can cause sudden death.
Importantly, we also learned
that persistent disease stress
causes a slow rate of
cardiac muscle cell death,
and that this progression
of death contributes
to heart failure progression.
When I teach my students
about this scenario,
I use the analogy of people pushing a sled
up a snowy hill.
If you take away some of the pushers,
those who remain obviously
must push even harder.
And over time, they get tired,
and some might even die.
About ten years ago, I had one of my many
scientific epiphanies.
Clinical data showed that the
therapies that worked best
to prolong the lives of
heart failure patients
were those that limited,
rather than increased,
excessive myocyte workload.
Based on these data, I
concluded that progressive
weakening of myocytes
in the failing heart was
the effect of, rather than
the cause of, heart failure.
And that increasing the
contractility of these myocytes
does not address the actual
cause of the problem.
The answer was right in front of me.
There just were not
enough myocytes in a heart
with a myocardial infarction to perform
normal pump function.
Making overworked
myocytes work even harder
was not addressing the primary problem.
So using our analogy, forcing
tired workers to push harder,
was not likely to be a long term solution
to get that sled up the hill.
The problem was that we had lost pushers.
So the solution was simple.
We needed to add new pushers, restoring
the original conditions.
The data we had all collected
prompted me to reevaluate
the focus of my laboratory.
I was proud of the tremendous
advances that had been made
in my field.
When we started, we knew
little of the fundamental
biology of cardiac electrical
and mechanical function.
But now we understood them.
New drug therapies were
available, novel devices
to further improve cardiac performance
and treat lethal arrhythmias
had become commonplace.
However, I now believed that
increasing the contractility
of weakened myocytes in
heart failure patients
was not going to fix the actual problem.
So I changed the focus of my laboratory
and joined a host of new colleagues
who began to test the
hypothesis that a real cure
for myocardial infarction
requires regenerative therapies
that actually add new
myocytes and vasculature
to the failing heart.
When I started this new
journey, I was an old dog.
But I decided to change the
focus of my laboratory anyway.
Many of my colleagues questioned
the wisdom of my decision.
But I decided to go for it.
My goal had always been
to learn things that
could benefit patients.
And I felt that this was
my best path forward.
So once again, I turned to my dad's case
and I began to chart a new
course in trying to save others
from his fate.
When my dad has his
heart attack, a big part
of his heart died and was
replaced by scar tissue.
He simply didn't have
enough muscle mass left
to provide normal function.
So true repair of the heart
after myocardial infarction
would require replacing
the lost vasculature
and muscle mass.
Thus my current science studies
how a heart repairs itself
after an MI, and we are searching for new
therapeutic strategies to
replace lost heart tissue.
I am certain that if this field develops
the new knowledge required
to understand new myocyte
and vascular formation in the adult heart,
we can translate this knowledge into safe
and effective therapeutics.
The Holy Grail in this
relatively new field
is finding a safe way to regenerate
myocytes and vasculature that
are lost to ischemic insults.
As usual, I thought it would be easy.
We just find a therapeutic
that's cardiogenic,
treat the damaged heart,
and we're good to go.
However, as individuals
in this field have all
come to learn, inducing
cardiac regeneration
in the adult heart is not easy.
So my friends, the honeymoon
phase for this field
is over, and now it's time for
us to do the heavy lifting.
This is an important and
challenging clinical issue,
but I strongly believe that
given the scientific intellect
that's addressing this
problem, new therapies
that produce new cardiac
tissue can be developed
if we follow the data.
I am humbled to be part of this
exciting new research area.
No matter my area of research
focus, I have both a passion
for scientific discovery
and a passion for training
the next generation of
cardiovascular scientists
who could develop better
therapies for patients
with sick hearts.
I believe the change of
focus in my laboratory
exemplifies this.
This is why I urge all
my colleagues, including
young investigators and
early career professionals
here today to have the
passion, confidence and courage
to follow their data rather
than any preconceived ideas
of how people think things might work.
For our science to have
an impact on patient care,
we will sll need to perform well designed,
basic translational and clinical research
that produces reliable,
readily validated data sets.
These results should
provide the foundation
for new therapies that
can improve and extend
patients' lives.
I must point out that the
American Heart Association's
support for my research fellows and for me
has been essential to
any success I have had
in my laboratory.
I love to tell the story
of my first AHA grant,
because of how pivotal
it was for my career.
When I started my
laboratory, I was determined
to study fundamental
aspects of cardiac myocyte
remodeling in human heart failure.
My first NIH grant on this
topic was turned down,
not once, not twice,
but back in my day, three straight times.
In fact, my score got progressively worse
with each resubmission.
Sometimes I'm not a good listener.
At that time, there was a
feeling that Ph.D. scientists
should not be studying
mechanisms of disease,
and my colleagues told me this.
How times have changed.
I was undeterred.
I took my ideas to what
was then the Philadelphia
chapter of the AHA, and
sought the equivalent of the
current scientist development grant.
My grant was awarded on
the first submission.
I received the grand sum of
$7,500 over two or three years.
I don't remember.
Emboldened by my success
and with a little more data,
I was ready to try again with the NIH.
I figured out how to
better present my ideas
and I've been an NIH funded
investigator ever since.
I've received NIH funding
in excess of $25 million.
Now that's a great return
on an AHA investment.
(audience applauding)
Thank you.
From the moment my AHA grant was awarded,
I proudly became an AHA volunteer.
I did my homework and
realized the AHA was the
professional organization
whose mission was aligned
with my career and personal goals.
During my 35 years as a volunteer,
I have reviewed countless AHA grants,
served my affiliate in numerous roles
and served as Chair of the
Basic Cardiovascular Sciences
Council and as the AHA
Research Committee Chair.
And now I'm so fortunate and honored
to serve as AHA President.
I also take great pride in
the fact that while I'm the
80th President, I am the
first Ph.D. basic scientist
to hold this position.
(audience applauding)
Thank you.
As my AHA involvement has ramped up,
so has my understanding of
this organization's scope,
which is really vast.
I discovered perspectives beyond science.
I learned that I could
also impact public health
through advocacy, consumer
awareness and fundraising.
The AHA has long been a top
funder of cardiovascular
and stroke research, investing
more than $4 billion to date.
Only the federal government spends more.
And of course, that NIH
funding is critical.
Our advocacy team is
always squarely focused
on increasing NIH funding.
Of course, they also
continue to rack up victories
in a number of other areas.
We all must ensure that
lawmakers on both sides
of the political aisle are
aware of the importance
of scientific discovery to save lives
and to improve our economy.
(audience applauding)
Thank you.
When I'm fortunate
enough to have face time
with an elected official,
I always keep my message
very simple.
I tell them we should
invest in health research
because a healthy America
is a productive, proud
and strong America.
I enjoy stretching
beyond science in my role
as AHA President.
I take special interest
in being a champion
for the next generation of
cardiovascular scientists
and thought leaders.
This summer we held our
first AHA Research Academy.
It was really great.
About 275 newcomers and
experienced investigators
discussed topics ranging from the future
of clinical trials in the
era of precision medicine
to the essential role of
patients acting as co-pilots
to their doctors.
In my view, today is an
incredibly exciting time
for early career investigators beginning
in academic medical research.
The scientific toolbox that
they have has expanded so much.
When I started, there were
no genomics, proteomics,
metabolomics.
There was no real precision medicine
as we think of it today.
But now we have the
ability to unravel so many
of nature's mysteries.
That's why we created the AHA's Institute
for Precision Cardiovascular Medicine.
This new knowledge will teach us things
about the fundamentals of
health and the bases of disease.
I am confident that this
will help us develop
better ways to treat patients
or groups of patients
with cardiovascular
diseases, including stroke.
But there are significant
challenges in front of us.
How will we sift through
these huge new data sets
to find those few nuggets of information
that will guide us to
more effective therapies.
This will require new types
of scientific expertise.
And as I mentioned, the
AHA is keenly focused
on continuing its leadership role,
not only in training the next generation
of cardiovascular scientists,
but also by focusing
their explorations on
unmet clinical needs.
At the request of our donors and patients,
we have developed strategically focused
research networks that
address important unresolved
clinical issues.
We've launched networks
studying prevention,
hypertension, disparities, stroke,
and women and heart disease.
In May, we announced our Heart
Failure Research Network.
And next year, we will launch networks
dedicated to obesity and then to children.
A critical priority for
the AHA is working toward
enhanced prevention of
cardiovascular diseases.
And again, I start with my dad's case.
My dad smoked.
He ate a diet that was
not what we would call
heart healthy, and I along with him.
He likely had high cholesterol and
high blood pressure.
Of course, that was
typical for his generation.
I often wonder whether my dad could have
avoided heart disease had
he lived in today's era,
where we're empowered to reduce our risks.
For instance, what if he'd been exposed
to life's Simple Seven and had controlled
his blood pressure and his cholesterol?
What if I'd been able to
help him quit smoking?
I'm sure we all agree
that the best way to treat
ischemic heart disease is to keep people
from having it in the first place.
While our prevention
efforts, and of course,
our work in treating acute
cardiovascular events
have had a profound
impact, we cannot relax.
We must remain vigilent.
Because if this recent data holds,
then serious problems are on the horizon.
Adding to this concern is
the rise of Type II diabetes
among teens.
If these trends are not reversed,
we can expect to see a
rise in vascular disease
once these young people become adults.
And then we will give
back so many of the gains
we've made in recent years.
We also know that specific
prevention strategies
may work for some
individuals and populations,
but not for others.
So we need to do more
research to understand,
to help us understand
which strategies work best
in which circumstance.
The evidence we already
have and the new information
we can gain will help us
build a culture of health,
where the healthy choice
is the default choice.
This concept has no boundaries.
Just as the AHA likes to say Life is Why,
we also believe that science is how
and community is where.
This can happen is we
work together to continue
building on this culture of health.
For instance, my fellow basic scientists,
your discoveries can
provide key information
that is used in offices,
hospitals and classrooms
to improve health.
My personal prescription
for cardiovascular health
includes a brisk walk
each day and a few less
Philly cheese steaks.
Or while I'm here, a few less beignets.
I urge everyone to take
control of their own health
and to work collectively
to improve the culture
of health in the U.S.
and around the world.
This culture of health must be inclusive.
It must also be dedicated
to equal, respectful
treatment for people of all races, genders
and religions.
As I wrap up, I want to thank a few people
who have blessed my
professional and personal life.
I have been so fortunate
to spend my entire career
at the Lewis Katz School of
Medicine at Temple University.
This school has generously supported me
and given me the freedom
to pursue my passion.
And for this I am truly grateful.
I am also grateful for
the hundred plus students
and fellows who have
trained in my laboratory
and who have heard me
expand upon my philosophies
about science and life.
God bless them.
I am particularly
thankful for the hard work
of two longtime lab members,
Doctor Hajime Kubo and Remus Berretta.
I am also sincerely
thankful for my colleagues
in BCVS, who have generously
shared their ideas
and their collective spirit
with me for so many years.
I also would not be
standing here today without
my family and friends.
Two of my dearest friends,
Greg and Denise Day
are in the audience,
and I want to thank them
for their love and support
over the past decades.
Most of all, I need to thank my wife,
Doctor Beth Bailey, who puts up with me,
for her unconditional love and support.
She is my rock and she is my best friend.
I am also thankful for our daughters,
Ellie and Emily, great
young women who I am
extremely proud of.
I'm also grateful for my dad,
both as a parent and as my alpha patient.
As you've heard today,
he still fuels my passion
to help people who suffer
from ischemic heart disease.
I am as passionate
about this mission today
as I was sitting at his
bedside 40 years ago.
I'd like to leave you
with one final thought.
Today we have unprecedented opportunities
to improve people's health.
I urge you to find new
ways to help someone
live their life free of
cardiovascular diseases and stroke.
Something brought you
to Scientific Sessions.
Whatever that motivation
is, let this meeting
continue to stoke it and to inspire you.
So thank you again for
listening to my story,
and please enjoy this meeting.
It's a great meeting.
(audience applauding)
