Introduction
The annual meeting of the American Heart Association's (AHA's) Basic Cardiovascular
Science (BCVS) council met from July 30 to August 2 in San Antonio, Texas. This meeting
highlighted cutting‐edge basic and translational cardiovascular research from established
investigators and trainees across a variety of disciplines. The BCVS 2018 meeting
drew nearly 600 attendees and featured 105 oral presentations across 28 general and
special‐emphasis sessions and 328 abstracts. The meeting hosted researchers from across
the United States and around the globe, with 91 international researchers representing
14 countries. This confluence of the top minds in cardiovascular research provided
an outstanding environment to discuss emerging ideas and generate collaborations across
this community. Here, we highlight a small selection from the range of session topics
from BCVS 2018.
Welcome Address
Ivor Benjamin, MD, the incoming president of the AHA, officially commenced the meeting.
Dr Benjamin, who has been a long‐time member of the BCVS council, outlined the importance
of the BCVS to impact and improve cardiovascular health through basic, clinical, and
population science, and investment in trainees to expand the biomedical workforce.
Dr Benjamin reviewed the AHA's evolving funding objectives, laying out initiatives
the association is taking to fund the most promising research and make real changes
in the lives of people with heart disease. Dr Benjamin highlighted the importance
of the BCVS council to the AHA's overall mission, noting the inspirational work presented
at BCVS 2018 from “the individuals doing the best basic cardiovascular science.”
Keynote Lecture
Stefanie Dimmeler, PhD from Goethe University Frankfurt, Germany, delivered the keynote
address on cellular heterogeneity and plasticity in cardiovascular disease. Dr Dimmeler's
expansive list of publications, professional accolades, and editorial positions with
several key cardiovascular journals illustrate the impact of her research career.
She shared 2 major stories that her laboratory has developed. The first concerned
how endothelial cells contribute to the formation of new blood vessels following myocardial
ischemia. Her experiments used lineage‐tracing reporters to provide data that regeneration
of blood vessels occurs via clonal expansion of a small number of endothelial cells
that are able to migrate and expand into the postischemic myocardium. The second story
Dr Dimmeler shared focused on the heterogeneity of inflammatory cells in the hearts
of patients with heart failure. By collecting circulating blood monocytes, she identified
that patients with heart failure have a higher amount of transcriptional heterogeneity,
with a high occurrence of clonal hematopoiesis. These circulating monocytes alter
inflammatory signaling in the progression of heart failure. These findings may have
prognostic value in the assessment and treatment of patients with heart failure. Her
ongoing focus is to develop microRNAs for clinical use and apply recent advances in
single‐cell sequencing to patients with cardiovascular disease.
Changing the Landscape of Cardiac Fibrosis
One of the kickoff sessions highlighted the importance of cardiac fibrosis in normal
and pathological heart function. Modulation of cardiac fibrosis has been identified
as a key target in the treatment of heart failure with preserved ejection fraction
(HFpEF), and the talks in this session provided a wealth of data on many potential
strategies to reduce pathological fibrosis.
Jeff Molkentin, PhD from Cincinnati Children's Hospital shared data that establish
the origin and migration of the fibroblasts that contribute to the fibrotic response
following myocardial infarction. Dr Molkentin's study utilized the Postn‐ and Tcf21‐MerCreMer
and Actn2‐CreERT2 linage‐tracing reporters driving fluorescent reporters to identify
the origin of fibroblasts that proliferate into the site of cardiac ischemic injury.1
His data showed that myofibroblasts in the infarct border zone migrate into the ischemic
tissue within a week of infarct, stabilizing the scar at early time points. Once incorporated
into the scar, the myofibroblasts stopped proliferating and began depositing extracellular
matrix and disappear weeks later. A subset of endothelial cell‐derived fibroblasts
proliferated within the scar and persisted. These cells originated from an endothelial
lineage that migrate into the site of injury and loses α‐smooth muscle actin expression
after they integrate into the tissue. These cells, termed matrifibrocytes, may play
a role in maintaining the mature scar, as evidenced by their unique expression signature
including genes involved in bone, cartilage, and tendon production.2 These findings
provide specific cellular targets for regulating the development of fibrosis for attenuating
pathological fibrosis following ischemic injury.
Amy Bradshaw, PhD from the Medical University of South Carolina highlighted her recent
work on the contribution of collagen fibrosis, a hallmark of diastolic dysfunction
in HFpEF. Deposition of collagen in fibrosis requires secreted protein acidic and
rich in cysteine proteins to process soluble collagen into insoluble, fibrotic collagen.
Dr Bradshaw shared data showing that increased macrophage secretion of these collagen‐converting
secreted protein acidic and rich in cysteine proteins was evident in a model of pressure‐overload
hypertrophy. Additionally, mice deficient for secreted protein acidic and rich in
cysteine proteins with wild‐type bone marrow transplantation showed mitigation of
fibrotic remodeling following pressure overload. These data add to our understanding
of the growing importance of noncardiac cell types in the fibrotic processes that
occur during pathological remodeling and provide novel targets for reducing diastolic
dysfunction in HFpEF.
Taben Hale, PhD from the University of Arizona provided data supporting the antifibrotic
effects of angiotensin‐converting enzyme inhibitor treatment. Angiotensin‐converting
enzyme inhibitors have had a role in the treatment of cardiovascular disease by lowering
blood pressure. Dr Hale showed that transient inhibition of the renin‐angiotensin
system reduces fibrosis and this reduction persists following the cessation of acute
treatment. Pretreatment with renin‐angiotensin system inhibitors appears to change
the fibroblast response to cardiac injury, resulting in milder fibrosis. These data
provide a potential direct mechanism of action of angiotensin‐converting enzyme inhibitors
in regulating fibroblast activity.
Timothy McKinsey, PhD from the University of Colorado presented his work on inhibition
of histone deacetylases to treat diastolic dysfunction in HFpEF. Dr McKinsey's study
used the histone deacetylase (HDAC) givinostat to treat fibrosis and improve myofilament
relaxation. HDAC inhibition has been shown to reduce fibrosis by limiting fibroblast
proliferation through epigenetic modulation of fibroblasts. However, in Dr McKinsey's
work, the direct effect of HDAC inhibition on myofilament relaxation was evaluated
using direct measurements of single myofibril relaxation. This work showed that HDAC
inhibition by givinostat reversed the slowed myofibril relaxation found in 2 small
animal models of diastolic heart failure. This provides a novel role for HDACs directly
altering posttranslational modifications on myofilament proteins. HDAC inhibitors
are already used clinically as a cancer therapy, and these data demonstrate a promising
potential alternative use of HDAC inhibitors to treat HFpEF.
Karla Maria Pires, PhD from the University of Utah presented the oral abstract for
this session describing her research on the transcription factor PR domain containing
16 (Prdm16). Dr Pires used germline knockout and conditional deletion mouse models
of Prdm16 for her studies. Homozygous loss of Prdm16 causes early lethality, whereas
heterozygous mice and inducible Prdm16 knockout cause robust hypertrophy that was
associated with increased transforming growth factor‐β and Smad signaling. These data
suggest that Prdm16 protection against hypertrophy and fibrosis occurs by suppressing
transforming growth factor‐β/Smad signaling and through regulation of mitochondrial
function.
Together, these presentations underscored the growing appreciation of the multifaceted
role of pathological fibrosis and the diverse approaches that are being pursued to
develop treatments for HFpEF and other fibrotic cardiovascular diseases.
Transcriptional Regulation and Epigenetics
This session started with a talk from D. Brian Foster, PhD of Johns Hopkins School
of Medicine who reported on the importance of retinoic acid signaling in hypertension
and heart failure. Retinoic acid is a vitamin A–derived transcriptional regulator
that has been shown to be reduced in patients with heart failure and dilated cardiomyopathy.
Dr Foster demonstrated that treatment with retinoic acid mitigates hypertrophy in
a phenylephrine‐induced murine hypertrophic cell model. Treatment with talarozole,
a CYP26 inhibitor that prevents retinoic acid degradation, increased retinoic acid
levels and reduced cardiomyocyte hypertrophy in cultured cardiomyocytes and pulmonary
edema in a guinea pig model of heart failure. These findings add to the growing appreciation
of retinoic acid and vitamin A in cardiac function and provide potential cardiac disease
targets for retinoic acid therapy.
Enzo Porello, PhD from the Murdoch Children's Research Institute in Australia presented
data examining how transcriptomes change in cell types that lose regenerative potential,
including cardiomyocytes. By comparing transcriptomes of developing, adult, and post‐injury
cardiomyocytes, Dr Porello revealed a failure of cardiomyocytes to reactivate developmental
gene networks after myocardial infarction. Interestingly, while developmental networks
were silenced in adult cardiomyocytes, the chromatin environment also changed, making
transcription factor binding sites inaccessible for genes in developmental networks.
This was not observed in other cells that remain proliferative as they mature. These
findings identify an epigenetic basis for the loss of cardiomyocyte regenerative potential
following the transition to the adult cell phenotype and provide a regulatory target
for ongoing efforts to reactivate cardiomyocyte proliferation.
Tom Vondriska, PhD from the University of California, Los Angeles, presented data
on chromatin organization in cardiomyocytes and how the chromatin landscape changes
following the development of heart failure. Dr Vondriska used a genetic mouse model
lacking the ubiquitous chromatin structural protein CTCF to alter normal chromatin
structure. Physically interacting regions of DNA, topologically associating domains,
were mapped using chromatin conformation capture to identify how different regions
of the genome normally interact and regulate each other. The interacting chromatin
domains were disrupted in a mouse model of pressure‐overload heart failure compared
with sham control mice and underlie the activation or inactivation of gene neighborhoods
by epigenetic chromatin restructuring. These data provide insight into the physical
interaction of the epigenome and how alterations in this architecture can regulate
different disease states.3
Samadrita Bhattacharyya, MS from the University of Texas Southwestern Medical Center
delivered this session's oral abstract on her work deciphering the enhancers that
specify cardiac conduction system cell types. Using a mouse model with a sinoatrial
node marker, nuclei from sinoatrial node cells were isolated from the surrounding
atrial tissue. The open regions of chromatin were then assessed using these isolated
nuclei. These data were combined with sinoatrial node RNA‐Seq data to identify novel
enhancer elements that drive cardiac conduction system gene expression programs. Identification
of these enhancers provides a better understanding of the biology of these cell types,
as well as establishing regions of noncoding DNA where mutations can occur that lead
to cardiac rhythm disorders.
This session illustrated the recent advances of understanding epigenomic control of
gene expression in the context of heart disease and displayed many exciting tools
that are being used to provide translational insights into human disease.
Resurgence of Cardiac Metabolism
This year's conference offered a number of presentations on mitochondrial biology
and cardiac metabolism in cardiovascular disease. Zoltan Arany, MD, PhD from the University
of Pennsylvania described recent work using a genome‐wide clustered regularly interspaced
short palindromic repeats (CRISPR) screen to identify accelerators and decelerators
of mitophagy. This screen revealed that knockout of the adenine nucleotide translocator
(ANT) impairs mitophagy. Subsequent work suggested that ANT's ability to promote mitophagy
is independent of its ATP/ADP exchanger activity, but instead may be related to the
closure of the TIM22 complex in response to mitochondrial stress and subsequent recruitment
of PINK/PARKIN to the mitochondria. This novel role of ANT as a gatekeeper for mitophagy
points to the potential for ANT mutations to contribute to dilated cardiomyopathy
by disrupting mitophagy, even in patients with intact ANT activity.
Next, Dan Kelly, MD of the University of Pennsylvania shared data examining the importance
of the shift in mitochondrial fuel use to favor ketone oxidation over fatty acid metabolism
in the failing heart. Dr Kelly showed that mice with cardiac‐specific deletion of
3‐hydroxybutyrate dehydrogenase 1, preventing the use of ketones as fuel for the heart,
exhibit exaggerated left ventricular remodeling in response to transverse aortic constriction.
Pathological cardiac remodeling was attenuated when these animals were fed a ketogenic
diet, supporting the hypothesis that the shift to ketone oxidation in heart failure
is an adaptive response. Dr Kelly backed up this conclusion with exciting results
from a canine model of heart failure demonstrating that infusion of 3‐hydroxybutyrate
is sufficient to protect against tachypacing‐induced cardiac dysfunction and remodeling.
Together, these findings suggest that targeting fuel metabolism may be a therapeutic
strategy for heart failure.
Brad Hill, PhD from the University of Louisville continued the theme of myocardial
substrate use by discussing the idea of “autopoiesis,” how a system maintains or reproduces
itself. Dr Hill examined how glucose metabolism affects anabolic processes and regulation
of cardiac homeostasis in the contexts of hypertrophy, dilation, and failure. He noted
that glycolysis is higher in the exercise‐adapted heart, and described evidence for
exercise‐induced periodicity in cardiac metabolism. Dr Hill then shared data from
a recent study showing that fixing the heart's glycolytic capacity at a constant level
and impairing its metabolic flexibility is sufficient to drive physiologic or pathologic
hypertrophy.4 He demonstrated that failing hearts have diminished use of carbon substrates
in ancillary biosynthetic pathways and proposed that inhibition of such anabolic pathways
may drive pathologic cardiac remodeling and heart failure.
The cardiac metabolism session wrapped up with an oral abstract presentation by postdoctoral
researcher Jessica Pfleger, PhD from Temple University about her investigations of
the direct role of G protein–coupled receptor kinase 2 (GRK2) in metabolic dysfunction
of the failing heart. Dr Pfleger showed that transgenic hearts with increased GRK2
expression have compromised fatty acid uptake coupled with a diminished bioenergetic
reserve, which was associated with increased phosphorylation, ubiquitination, and
degradation of the fatty acid transporter CD36. Experimentally decreasing GRK2 expression
restores CD36 levels in the failing heart. Dr Pfleger's findings support a model in
which increased GRK2 expression in the failing heart diminishes CD36 expression and
so impairs myocardial fatty acid uptake, leading to impaired cardiomyocyte ATP production
and survival.
Together, the studies presented in this session provided ample evidence for the investigation
of cardiac metabolism as a promising avenue for the development of novel interventions
for cardiac hypertrophy and heart failure.
Functional Genomics and Pathogenicity Assessment
The advent of next‐generation sequencing has provided a wealth of data about cardiovascular
disease but has also presented many challenges in interpreting genetic variation in
the context of an individual's disease. The Functional Genomics and Pathogenicity
Assessment session focused on several facets of this problem. Quinn Wells, MD, PharmD
from Vanderbilt University Medical Center explained that the rate of identification
of new mutations associated with heart disease has increased well beyond the rate
at which the pathogenicity of these mutations can be verified. Dr Wells demonstrated
the power of mining large data sets of genetic information to assess the potential
role of novel variants to contribute to cardiovascular disease.
Beth McNally, MD, PhD from Northwestern University shared 2 stories evaluating the
genetic causes of different types of heart disease. Dr McNally presented data demonstrating
that myotonic dystrophy type 1 and type 2 are caused by different genetic mechanisms.
Both diseases have been thought to be caused by dysregulation of mRNA splicing. However,
using human induced pluripotent stem cell–derived myotubes from patients with myotonic
dystrophy, Dr McNally demonstrated that myotonic dystrophy type 1 showed evidence
of aberrant splicing events, whereas myotonic dystrophy type 2 myotubes did not. She
also presented whole genome sequencing data from a large cohort of patients with dilated
and hypertrophic cardiomyopathy with cardiovascular phenotype information. This data
set showed that patients with dilated cardiomyopathy had a greater amount of variation
in genes encoding cardiac proteins, revealing a multigenic signature for dilated cardiomyopathy
compared with a monogenic signature for hypertrophic cardiomyopathy. Additionally,
the severity of disease correlated with an increased mutation burden in cardiac genes
in dilated cardiomyopathy, whereas this was not the case for hypertrophic cardiomyopathy.
Kiran Musunuru MD, PhD from the University of Pennsylvania highlighted the problem
of dismissing variants of uncertain significance in genetic testing because of our
limited understanding of the effect of these variants. Dr Musunuru shared his work
developing platforms to rapidly screen variants of unknown significance, the elucidation
of which will improve the diagnostic power of genetic sequencing for patients with
cardiovascular disease. Using dual integrase cassette exchange gene editing, he demonstrated
that he was able to efficiently model several troponin missense mutations in isogenic
cell lines. Adapting these concepts to develop simple higher‐throughput assays to
evaluate other common sources of variants of uncertain significance (eg, titin missense
variants) will allow greater utility for genetic testing in evaluating cardiovascular
disease risk.
Finally, Mingfu Wu, PhD from Albany Medical College presented the session's oral abstract
on the regulation of cardiac morphogenesis. Dr Wu presented data dissecting the role
of Numb family proteins in cardiac trabeculation. He demonstrated that Numb family
proteins regulate N‐cadherin levels by regulating N‐cadherin's endosomal recycling
from the plasma membrane during development, and loss of this activity resulted in
aberrant ventricular trabeculation. These findings shed light onto the developmental
regulation of this process and have implications for better understanding ventricular
noncompaction cardiomyopathy.
Architecture of Contraction
This session featured 4 talks focusing on diseases of the cardiac sarcomere. Jil Tardiff,
MD, PhD from the University of Arizona described her efforts to develop an integrated
platform to test sarcomeric mutations and sort them into hypertrophic or dilated cardiomyopathy
categories based on their effects on sarcomere structure and dynamics. Dr Tardiff
highlighted a recently developed atomistic model of the thin filament5 and her use
of this model in classifying mutations as dilated/hypertrophic by incorporating their
effects on tertiary and quaternary thin filament structure and function. She concluded
by emphasizing that sarcomeric mutations do not completely “break” the sarcomere,
but instead shift function slightly; thus, all that is needed for viable therapies
is to push the key affected parameter (eg, thin filament flexibility) back toward
normal in order to get a phenotypic improvement that may benefit a patient.
The University of Cincinnati's Sakthivel Sadayappan, PhD spoke next about his investigations
aimed at understanding the incomplete penetrance and variable cardiomyopathy phenotype
in individuals with a 25‐base pair deletion in cardiac myosin binding protein‐C (MYBPC3)
that is common among populations of South Asian ancestry. Dr Sadayappan and his team
identified a novel missense mutation (D389V) in the portion of myosin binding protein
C that binds the β‐myosin heavy chain S2 region.6 This D389V variant occurs on the
same MYPBC3 allele as the 25‐base pair deletion, and the combination of the 2 mutations
causes cardiomyocyte hypertrophy, an increased incidence of arrhythmia, and a significant
increase in cardiac contractility. Dr Sadayappan concluded that co‐segregation of
the 25‐base pair MYBPC3 deletion with additional variants such as D389V likely accounts
for the phenotypic variability in people harboring this deletion. These findings underscore
the potential impact of modifier genes on the clinical outcomes of patients with mutations
in genes of the cardiac sarcomere.
Beata Wolska, PhD of the University of Illinois at Chicago discussed the molecular
basis of inherited cardiomyopathies and the relationship between myofilament calcium
sensitivity and the type of cardiomyopathy. She noted that mutations leading to hypertrophic
cardiomyopathy are generally associated with increased myofilament calcium sensitivity,
while mutations giving rise to dilated cardiomyopathy are characterized by decreased
myofilament calcium sensitivity. Therefore, Dr Wolska tested whether overcoming increased
myofilament calcium sensitivity and associated diastolic dysfunction could prevent
the development of hypertrophic cardiomyopathy. Studies in mice with mutant tropomyosin
and exaggerated myofilament calcium sensitivity showed that the introduction of a
psuedophosphorylated troponin I to lower myofilament calcium sensitivity back toward
normal can prevent pathological hypertrophy. Dr Wolska ended by sharing a recent proof‐of‐concept
experiment showing that a green tea extract corrects calcium hypersensitivity in myofilaments
in vitro with a hypertrophic cardiomyopathy–linked cardiac troponin I mutation (K206I).
Finally, David Barefield, PhD from Northwestern University delivered the session's
oral abstract. Dr Barefield presented his work on a novel myofilament protein, myosin‐binding
protein H–like (MyBP‐HL). The data showed that MyBP‐HL is highly expressed in the
atria in humans and mice, as well as in a subset of the ventricular conduction system.7
Loss of MyBP‐HL in a mouse model causes dilated cardiomyopathy and atrial and ventricular
arrhythmias. Dr Barefield showed evidence of atrioventricular block in these mice
and localization of MyBP‐HL to the atrioventricular node. Molecularly, MyBP‐HL was
shown to be localized in the myofilament A band, and that MyBP‐HL and cardiac myosin‐binding
protein C have a reciprocal relationship, where reduction of 1 protein causes an increase
in the other, which may alter myofilament function.
Together, these 4 talks illustrate that the development of therapies for cardiomyopathy
aimed at normalizing the behavior of mutant sarcomeres is a practical and realistic
goal.
Outstanding Early Career Investigator Award Finalists and Awards Ceremony
Three exceptional young scientists competed for this year's Outstanding Early Career
Investigator Award. Lisandra de Castro Brás, PhD from East Carolina University opened
the competition with an account of her discovery that a novel collagen cleavage product,
p1158/59, accumulates in the heart following myocardial infarction. Administration
of p1158/59 to mice with experimental myocardial infarction reduces fibrosis, attenuates
left ventricular dysfunction, and promotes scar formation and maturation, likely by
stimulating fibroblast migration and alteration of collagen deposition. Dr de Castro
Brás's work provided intriguing proof‐of‐concept evidence that this endogenous peptide
can modulate adverse left ventricular remodeling to help preserve cardiac function
after a heart attack.
Next to the podium was Cristi Galindo, PhD from Vanderbilt University. Dr Galindo
shared her investigations into the phenotypic variability observed in the hearts of
patients with Duchenne muscular dystrophy and presented evidence that higher circulating
levels of brain‐derived neurotrophic factor correlate with better heart function in
these individuals. Pharmacologic stimulation of the brain‐derived neurotrophic factor
receptor, TrkB, improves cardiac output in a mouse model of Duchenne muscular dystrophy,
while pharmacologic inhibition of this receptor exacerbates cardiac dysfunction. Dr
Galindo concluded that brain‐derived neurotrophic factor is cardioprotective for dystrophic
hearts and may be an attractive therapeutic target for cardiomyopathy in Duchenne
muscular dystrophy.
Manuel Rosa‐Garrido, PhD from the University of California, Los Angeles, presented
elegant work using chromatin capture experiments to explore how gene regulation can
be coordinated by the spatial arrangement of chromatin into special microenvironments
within the nucleus. He explained that heart failure alters the normal 3‐dimensional
arrangement of chromatin and that sets of genes whose expression increases or decreases
in heart failure tend to be organized together into distinct nuclear “neighborhoods.”
Furthermore, genes found in these active or inactive neighborhoods were characterized
by distinct epigenetic marks. Dr Rosa‐Garrido proposed that this spatial organization
of the genome could be a mechanism allowing for coordinated changes in gene expression,
while rearrangement of such chromatin microenvironments may be a common feature of
heart failure.3
At the BCVS council dinner, the winner of the Outstanding Early Career Investigator
Award was announced, with Manuel Rosa‐Garrido from the University of California, Los
Angeles, claiming the top honor. All 3 finalists were selected based on their top‐scoring
abstract submissions. Other award winners were recognized at the event, including
8 recipients of the Cardiovascular Outreach Award, which promotes promising minority
or underrepresented early career investigators to attend the BCVS meeting. Additionally,
the BCVS sponsors travel awards for early‐stage investigators to promote the inclusion
of trainees. This year, the BCVS granted an astounding 41 New Investigator Travel
Awards.
Early Career Events
The BCVS has made a clear commitment to providing resources for new investigators
in training or at the beginning stages of their independent careers. This year's early
career programming kicked off with Dr Sakthivel Sadayappan's perspective on how to
overcome common career hurdles. Dr Sadayappan urged audience members to consider making
the best choice available to them, rather than a choice that is merely “comfortable”
when weighing different career options, and to actively seek out scientific discussions
with peers, mentors, and colleagues. He noted the importance of trainees finding a
mentor who will promote them, and emphasized the need for scientists to learn how
to promote themselves as well. The session concluded with Dr Sadayappan's reminder
that success requires passion and resourcefulness, which he defined as “the ability
to find quick and clever ways to achieve ones’ scientific and professional goals.”
A special early career session was held, entitled Navigating Your Career: Finding
Success and Happiness With a PhD. This session consisted of a series of presentations
from an established faculty, a postdoctoral fellow, and a current doctoral graduate
student. Mark Sussman, PhD from San Diego State University delivered a spirited analysis
of how scientists can cultivate an “omnivert” personality type to address the varied
aspects of a life in research, from quiet bench science to enthusiastically presenting
data to large crowds and being comfortable networking with your peers. Catherine Makarewich,
PhD, who has performed her postdoctoral training in Eric Olson's laboratory at UT
Southwestern Medical Center, presented some of the wisdom she has gathered during
her career. Adrian Arrieta, a graduate student at San Diego State University in Christopher
Glembotski's laboratory, contributed his perspective as an early stage trainee. A
panel discussion with these 3 researchers followed, covering topics from the audience
including mentorship, networking, and the importance of defining a career path and
goals as a developing researcher.
The Early Career Committee organized a sold‐out networking lunch and mentorship roundtable
forum with many of the scientific leaders within the BCVS. Dr Merry Lindsey, PhD from
the University of Mississippi Medical Center delivered a presentation on mentorship,
highlighting the challenges faced by trainees by using a host of her own current and
previous trainees as examples. This provided rich insight into the challenges of providing
mentorship to a wide range of trainees. The networking roundtable gave young investigators
the chance to sit down with many outstanding BCVS investigators. These conversations
provided excellent networking opportunities and a chance for these investigators to
pass on bits of career development wisdom for many trainees.
Conclusions
The 2018 BCVS meeting was an inspiring display of innovative research by the leaders
in basic cardiovascular science. The multitude of topics covered and the effort dedicated
to promoting collaboration and career development was a testament to the importance
of the BCVS council in fulfilling the AHA's mission. The new BCVS council chair, Joe
Wu from Stanford University, the Program Committee, and the Early Career Committee
of the BCVS deserve special thanks, as their efforts were evident in the high quality
of this meeting.
Disclosures
None.