Circulation
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Circulation is available at www.ahajournals.org/journal/circ
February 14, 2023 Circulation. 2023;147:e76–e91. DOI: 10.1161/CIR.0000000000001124
Dr Wei is employed by the National Heart, Lung, and Blood Institute. The content of this article is solely the responsibility of the authors and does not necessarily repre-
sent the official views of the National Heart, Lung, and Blood Institute; National Institutes of Health; or US Department of Health and Human Services.
? 2023 American Heart Association, Inc.
AHA SCIENTIFIC STATEMENT
Optimizing Prepregnancy Cardiovascular
Health to Improve Outcomes in Pregnant and
Postpartum Individuals and Offspring: A Scientific
Statement From the American Heart Association
Sadiya S. Khan, MD, MSc, FAHA, Chair; LaPrincess C. Brewer, MD, MPH; Mary M. Canobbio, RN, MN, FAHA;
Marilyn J. Cipolla, PhD, FAHA; William A. Grobman, MD, MBA; Jennifer Lewey, MD, MPH; Erin D. Michos, MD, MHS;
Eliza C. Miller, MD, MS; Amanda M. Perak, MD, MS, FAHA; Gina S. Wei, MD, MPH, FAHA; Holly Gooding, MD, MSc, Vice Chair;
on behalf of the American Heart Association Council on Epidemiology and Prevention; Council on Clinical Cardiology; Council
on Cardiovascular and Stroke Nursing; Council on Arteriosclerosis, Thrombosis and Vascular Biology; Council on Hypertension;
Council on Lifestyle and Cardiometabolic Health; Council on Peripheral Vascular Disease; and Stroke Council
ABSTRACT: This scientific statement summarizes the available preclinical, epidemiological, and clinical trial evidence that
supports the contributions of prepregnancy (and interpregnancy) cardiovascular health to risk of adverse pregnancy
outcomes and cardiovascular disease in birthing individuals and offspring. Unfavorable cardiovascular health, as originally
defined by the American Heart Association in 2010 and revised in 2022, is prevalent in reproductive-aged individuals.
Significant disparities exist in ideal cardiovascular health by race and ethnicity, socioeconomic status, and geography.
Because the biological processes leading to adverse pregnancy outcomes begin before conception, interventions
focused only during pregnancy may have limited impact on both the pregnant individual and offspring. Therefore, focused
attention on the prepregnancy period as a critical life period for optimization of cardiovascular health is needed. This
scientific statement applies a life course and intergenerational framework to measure, modify, and monitor prepregnancy
cardiovascular health. All clinicians who interact with pregnancy-capable individuals can emphasize optimization of
cardiovascular health beginning early in childhood. Clinical trials are needed to investigate prepregnancy interventions to
comprehensively target cardiovascular health. Beyond individual-level interventions, community-level interventions must
include and engage key stakeholders (eg, community leaders, birthing individuals, families) and target a broad range of
antecedent psychosocial and social determinants. In addition, policy-level changes are needed to dismantle structural
racism and to improve equitable and high-quality health care delivery because many reproductive-aged individuals have
inadequate, fragmented health care before and after pregnancy and between pregnancies (interpregnancy). Leveraging
these opportunities to target cardiovascular health has the potential to improve health across the life course and for
subsequent generations.
Key Words: AHA Scientific Statements ? cardiovascular diseases ? pregnancy ? pregnancy complications ? primary prevention ? risk factors
T
here is a growing burden of cardiovascular-related
morbidity and mortality in pregnant and postpartum
individuals in the United States.
1
Cardiovascular
disease (CVD) is the leading cause of death during preg-
nancy and the postpartum period and represents 26.5%
of pregnancy-related deaths.
2
This topic was the focus
of the 2021 American Heart Association (AHA) policy
statement “Call to Action: Maternal Health and Saving
Mothers,” which outlined multilevel opportunities aimed
at improving health literacy, public awareness, cultural
competency, and bias reduction in optimizing maternal
cardiovascular health (CVH).
3
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Currently, nearly 1 in 5 births is complicated by an
adverse pregnancy outcome (APO), which includes
hypertensive disorders of pregnancy (HDP), preterm
birth, small-for-gestational-age (SGA) birth, and gesta-
tional diabetes.
4,5
Over the past decade, rates of APOs
have increased significantly, with a near doubling in
rates of HDP.
4,5
There are persistent disparities, with
non-Hispanic Black individuals significantly more likely
to experience APOs.
6
Available data demonstrate a
strong association between APOs and risk for subse-
quent CVD, which was detailed in the 2021 AHA sci-
entific statement “Adverse Pregnancy Outcomes and
Cardiovascular Disease Risk: Unique Opportunities for
Cardiovascular Disease Prevention in Women.”
7
Among
individuals who experience APOs, emerging data also
identify higher risk of long-term kidney disease, which
is itself an important risk factor for CVD.
8
Although the
pathophysiology of pregnancy-related complications is
complex and likely multifactorial, emerging data sug-
gest that these complications have, at least in part,
prepregnancy origins. Thus, the prepregnancy period
may be a critical window during which interventions
have a great potential for benefit in birthing individu-
als and their offspring. In addition, interventions in the
postpartum/interpregnancy period may offer a unique
opportunity to target the prepregnancy period before a
subsequent pregnancy.
In this AHA scientific statement, we critically review
the evidence for prepregnancy CVH as a key target to
improve the health of the birthing individual and offspring
over the life course (Figure). We highlight the impor-
tance of a life course and intergenerational framework
to assess and intervene on CVH. We offer consider-
ations for multilevel interventions (eg, individual, com-
munity, and societal) to equitably improve prepregnancy
CVH. We anchor this discussion on the AHA’s construct
of CVH. This was originally defined as Life’s Simple 7
in 2010, which integrates 7 health factors (diet, physi-
cal activity, nonsmoking, body mass index, blood pres-
sure, lipids, and glycemia) and has since been revised
to Life’s Essential 8, incorporating sleep health as the
eighth metric (Table 1).
9,10
CVH is oriented on promotion
Figure. The intergenerational life
cycle of cardiovascular health and its
foundational determinants.
Life’s Essential 8 image reprinted from
Lloyd-Jones et al.
9
Copyright ? 2022
American Heart Association.
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of wellness, with higher CVH scores (ie, scores reflecting
better health) associated with lower risk for a multitude
of downstream cardiovascular and noncardiovascular
outcomes in nonpregnant and pregnant individuals.
11
The
clinical relevance of the CVH construct as a key target
in birthing individuals was recently highlighted in a joint
presidential advisory from the AHA and the American
College of Obstetricians and Gynecologists that high-
lights the pivotal role of primary care clinicians, pediatri-
cians, obstetricians, and cardiologists in optimizing the
CVH of pregnancy-capable individuals.
12
For the purposes of this scientific statement, we
refer to individuals as females or males based on gen-
der assigned at birth and as women or men based on
presumed gender identity when these terms have been
used in prior literature. There remains a dearth of data on
CVH and its relationship with APOs and CVD in individu-
als with diverse gender identities.
Table 1. CVH Metrics and Scoring as Originally Defined in 2010 and Revised in 2022 for Nonpregnant Adults by the AHA
CVH construct definition: 2010
10
Ideal=2 points Intermediate=1 point Poor=0 points
Diet, Healthy Eating Index–2015 score 80–100 40–79 0–39
Physical activity, min/wk moderate to vigor-
ous leisure-time activity
≥150 >0 but <150 0
Smoking Never or quit >12 mo ago Former, quit ≤12 mo ago Current
Body mass index, kg/m
2
<25 25–29.9 ≥30
Blood pressure, mm Hg <120/<80 Systolic 120–139 or diastolic 80–89 and not on
blood pressure–lowering medications
Systolic ≥140 or dia-
stolic ≥90
Total cholesterol, mg/dL <200 without medication 200–239 or treated to <200 ≥240
Fasting glucose, mg/dL <100 without medication 100–125 and not on glucose-lowering medications ≥126
CVH construct definition: 2022
9
Ideal=100 points Suboptimal <100 points
Sleep health or average sleep per night, h 7–<9 70 points: 6–<7
20 points: 4–<5
0 points: <4
Diet, Healthy Eating Index–2015 score or
DASH (MEPA)
≥95th percentile
(MEPA score 15–16)
80 points: 75th–94th percentile (MEPA score 2–14)
25 points: 25th–49th percentile (MEPA score 4–7)
0 points: 1st–24th percentile (MEPA score 0–3)
Physical activity, min/wk moderate to vigor-
ous leisure-time activity
≥150 80 points: 90–119
20 points: 1–29
0 points: 0
Smoking Never smoker and no second-
hand exposure in home
75 points: former smoker, quit ≥5 y
20 points: former smoker, quit <1 y, or inhaled NDS
0 points: current smoker
Subtract 20 points for living with active indoor smoker in home (unless score
is 0)
Body mass index, kg/m
2
<25 70 points: 25.0–29.9
30 points: 30.0–34.9
0 points: ≥40.0
Blood pressure, mm Hg <120/<80 75 points: 120–129/<80
25 points: 140–159 or 90–99
0 points: ≥160 or ≥100
Subtract 20 points if treated level
Non-HDL cholesterol, mg/dL <130 60 points: 130–159
20 points: 190–219
0 points: ≥220
Subtract 20 points if treated level
Fasting glucose, mg/dL (HbA1c, %) <100
(<5.7%)
No history of diabetes
60 points: 100–125 (5.7%–6.4%)
20 points: diabetes (8.0%–8.9%)
0 points: diabetes (≥10.0%)
AHA indicates American Heart Association; CVH, cardiovascular health; DASH, Dietary Approaches to Stop Hypertension; HbA1c, hemoglobin A1c; HDL, high-
density lipoprotein; MEPA, Mediterranean Eating Pattern for Americans; and NDS, nicotine-delivery system.
Adapted from Lloyd-Jones et al.
9,10
Copyright ? 2010 American Heart Association, Inc. and Copyright ? 2022 American Heart Association, Inc.
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CURRENT STATUS OF CVH IN BIRTHING
INDIVIDUALS IN THE UNITED STATES
As of 2020, there were an estimated 64.5 million repro-
ductive-aged (age, 15–44 years) females in the United
States.
13
Approximately 3.5 to 4 million live births occur
in the United States annually, and by 40 to 44 years of
age, an estimated 86% of females in the United States
have given birth at least once.
14
Unfavorable CVH is prevalent in reproductive-aged
young adults, with few people (<1%) having ideal levels of
all CVH metrics.
11,15
According to data from the National
Health and Nutrition Examination Survey (2013–2016),
the prevalence of having ideal levels in ≥5 of 7 CVH met-
rics (using the 2010 CVH scoring system) was 45.0%
among adolescents 12 to 19 years of age, 31.6% among
young adults 20 to 39 years of age, and 10.6% among
adults 40 to 59 years of age.
16
Gender-specific data sug-
gest that CVH is slightly higher among females compared
with males of reproductive age (eg, for adults ≥20 years
of age, 21.5% of females versus 18.4% of males have ≥5
of 7 CVH metrics ideal). Similar findings were reported in
data from the National Health and Nutrition Examination
Survey (2013–2018) according to the revised 2022 CVH
scoring system, with a mean CVH score (of 100 possible
points) in women of 68.1 (SD, 0.48) compared with 63.6
(SD 0.44) in men. There are significant racial and ethnic
disparities in CVH, with non-Hispanic Black females hav-
ing lower mean CVH scores and worse values of most
CVH metrics, including worse sleep quality, than women
of other races and ethnicities.
17,18
Limited data are avail-
able for prepregnancy CVH in disaggregated Asian and
Hispanic subgroups and American Indian and Alaska
Native individuals. This is particularly critical given the
high rates of maternal morbidity and mortality observed
among American Indian and Alaska Native individuals.
19
Because race and ethnicity are social constructs, these
racial and ethnic differences have been attributed to dif-
ferences in upstream social factors such as education,
income, and access to health care.
11
When individual CVH
factors were examined among reproductive-aged females,
≈25% reported current smoking, ≈40% had obesity, 9.3%
had hypertension, 4.5% had diabetes, and up to 33% had
hyperlipidemia.
11,15,20–22
Lack of awareness and control of
CVD risk factors is an important problem in reproductive-
aged females; for example, of the 9.3% with hypertension
and 4.5% with diabetes, ≈17% and 30%, respectively,
were unaware of these diagnoses, and about half did not
achieve optimal blood pressure or glycemic control.
22
Maternal data on some CVH factors (prepregnancy
body mass index, diabetes, hypertension, and smoking
status based on a combination of self-recall and health
records) are available from the National Center for Health
Statistics for all live births in the United States. Fewer than
half of birthing individuals have favorable prepregnancy
CVH (using an abbreviated CVH defined as absence of
obesity, hypertension, diabetes, and smoking).
23
Further-
more, prepregnancy CVH declined between 2011 and
2019 in all subgroups (race and ethnicity, geography,
and socioeconomic status); lower CVH persisted among
non-Hispanic Black females, pregnant individuals living
in the South and Midwest United States, and those with
Medicaid insurance during pregnancy.
23,24
With regard
to specific factors, <50% of birthing individuals in 2018
had a normal prepregnancy body mass index (18.5–24.9
kg/m
2
).
25,26
Levels of CVH metrics are highly correlated
between the prepregnancy period and pregnancy.
15,27
ASSOCIATIONS BETWEEN
PREPREGNANCY CVH AND APOs
Prepregnancy CVH and individual CVH metrics are
associated with risk of APOs in many observational stud-
ies.
11,25,28–37
According to National Center for Health Sta-
tistics data, there is a consistent and graded association
between worse prepregnancy CVH and APOs (preterm
birth, SGA birth, and fetal death).
28
Adjusted relative risks
for preterm birth with poor levels of prepregnancy CVH
metrics in 1, 2, 3, or 4 metrics (overweight or obesity,
diabetes, hypertension, and smoking) were 1.15 (95%
CI, 1.15–1.16), 1.62 (95% CI, 1.61–162), 2.85 (95% CI,
2.81–2.90), and 3.89 (95% CI, 3.68–4.10), respectively,
compared with individuals with no poor prepregnancy
CVH metrics.
28
Similar findings were observed in the
multinational HAPO study (Hyperglycemia and Adverse
Pregnancy Outcome), which found that lower CVH based
on clinical factors at 28 weeks’ gestation was associated
with higher risk of APOs (preeclampsia, SGA infant).
38
Among individual CVH metrics, prepregnancy dietary
patterns are associated with risks for APOs, with healthier
patterns associated with lower risk of gestational diabe-
tes, preterm birth, SGA infant, and HDP.
39
Better prepreg-
nancy fitness, assessed with a graded symptom-limited
maximal exercise treadmill test, is associated with lower
risk of gestational diabetes,
40
and greater leisure-time
physical activity at the beginning of pregnancy is associ-
ated with lower risk for APOs.
41
Obesity is also associated
with APOs and estimated to have a population attribut-
able fraction resulting from HDP of between 26.5% and
30.3% in 2018 in the United States.
25
In a meta-analysis,
the odds ratio was 1.31 (95% CI, 1.11–1.53) for each
1–kg/m
2
increase in body mass index from the start of
one pregnancy to the next associated with HDP.
42
Pre-
pregnancy blood pressure is associated with risk for
HDP, and treatment of mild chronic hypertension starting
in early pregnancy led to reduced risks for preterm birth,
SGA birth, and preeclampsia in the recent CHAP trial
(Chronic Hypertension and Pregnancy).
43,44
Prepregnancy
lipid levels (triglycerides, high-density lipoprotein choles-
terol) are associated with risk for gestational diabetes and
H DP.
45
Prepregnancy glycemic status across the spec-
trum is associated with risk for large-for-gestational-age
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birth, preterm birth, and HDP.
33,46
Poor sleep quality and
duration are associated with APOs, specifically gesta-
tional diabetes and HDP.
47, 4 8
These data, which demon-
strate a similar magnitude of associations between CVH
and APOs across individual CVH metrics, underscore the
relevance of a strategy that comprehensively targets total
CVH. Beyond the traditional CVH metrics, chronic kidney
disease is an important risk factor for APOs and long-
term CVD in birthing individuals.
49
ASSOCIATIONS BETWEEN
PREPREGNANCY CVH AND OFFSPRING
OUTCOMES
Epidemiological studies support the association between
prepregnancy CVH in the birthing person and offspring
health outcomes, broadly called the developmental origins
of health and disease.
50
As detailed previously, prepreg-
nancy CVH and individual CVH metrics are associated
with risk for APOs; in addition, these APOs are associated
with higher risks for premature CVD among exposed off-
spring.
14,51–56
As an example, preterm birth is associated
with 53% higher adjusted hazards for premature ischemic
heart disease by 43 years of age in the offspring.
52
Longer-term studies are emerging to provide direct
evidence for links between maternal prepregnancy CVH
metrics and offspring CVD risk factors and even CVD
events.
54,56–60
For example, prepregnancy type 2 dia-
betes was associated with an adjusted hazards ratio of
1.39 (95% CI, 1.23–1.57) for offspring premature CVD
by 40 years of age in a registry study.
56
No study has
reported maternal prepregnancy total CVH and offspring
cardiovascular outcomes. Although there are physiologi-
cal changes to CVH metrics in pregnancy (eg, increase in
body mass index, glucose, lipids), data demonstrate that
CVD risk factor levels measured before pregnancy were
highly correlated with risk factor levels during pregnancy.
27
This suggests that associations between unfavorable
CVH in pregnant individuals and in offspring may stem,
at least in part, from the prepregnancy period.
61
Of note,
studies of maternal body mass index indicate that pre-
pregnancy body mass index is more strongly associated
with both APOs and offspring cardiovascular risk factors
in adolescence compared with gestational weight gain.
34,35
However, whether the association between maternal CVH
and offspring CVH is an epiphenomenon or the two are
causally related requires further investigation.
POTENTIAL PATHOPHYSIOLOGICAL
MECHANISMS LINKING PREPREGNANCY
CVH AND APOs
Several factors shed light on the potential pathophysi-
ological link between prepregnancy CVH and APOs.
The periconceptional period before and after conception
covers critical events: oocyte meiotic maturation, sper-
matozoa differentiation, fertilization, transition to the em-
bryonic genome, resumption of mitotic cell cycles in the
newly formed zygote, initial morphogenesis, and implan-
tation. During this brief window, the genome is globally
reprogrammed through extensive epigenetic reorgani-
zation, which determines lineage-specific gene expres-
sion—including divergence of placental and embryonic
cell lineages—and establishment of metabolic controls
for energy supply and growth.
50
In animal experiments,
epigenetic modifications link the metabolic status of the
pregnant animal to gene expression programs in the
developing embryo and placenta.
62,63
As an example, in
mice with obesity, the follicular fluid and oocyte are lipid
enriched, resulting in endoplasmic reticulum stress, pro-
tein misfolding, and increased mitochondrial respiration
and reactive oxygen species generation, with dramatic
implications for energy metabolism in the oocyte and
subsequently the zygote.
64–66
Although animal and in vitro experiments provide
much of the mechanistic data linking prepregnancy
CVH metrics with maternal and offspring outcomes,
parallel clinical observations align with these proposed
periconceptional mechanisms. For example, in mice,
transfer of 1-cell zygotes from diabetic dams to control
recipients demonstrates that exposures around fertil-
ization are sufficient to permanently program the post-
natal phenotype. This experimental finding is mirrored
by the clinical observation that in humans with diabetes,
glycemic control must be achieved before pregnancy
to reduce the risk of congenital anomalies and adverse
neonatal outcomes.
67
The placenta, which develops soon after fertiliza-
tion and implantation occur, is a major focus of studies
underlying mechanisms of APOs. Placental malperfu-
sion is central to a cascade of vascular injury in many
APOs, is secondary to inappropriate vascular remodel-
ing of uterine spinal arteries, and begins long before
clinical manifestations of APOs are apparent.
68
This
abnormal placental development has been proposed to
be affected by the maternal environment such as pres-
ence of prepregnancy CVD risk factors, with potential
mechanisms related to angiogenesis and inflamma-
tion.
69–72
Thus, APOs may reflect the unmasking of
preexisting CVD risk in response to the physiological
stress of pregnancy. Indeed, markers of vascular dys-
function (eg, decreased arterial compliance, retinal
microvascular constriction, diastolic dysfunction) before
or in early pregnancy are associated with higher risk of
APOs.
73–75
Although not conclusive, these studies add
to the evidence base that unfavorable prepregnancy
CVH temporally precedes and contributes to APO risk.
Advancing our mechanistic understanding of the under-
lying pathophysiology can inform the design of poten-
tial interventions. Last, establishing whether CVH and
APOs are causally related is foundationally important to
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decrease the risk of APOs and future CVD by interven-
ing on CVH.
76
EVIDENCE FOR PREPREGNANCY AND
INTERPREGNANCY CVH INTERVENTIONS
There are currently no large, randomized trials with suffi-
cient power to test whether improving CVH before preg-
nancy will improve maternal and offspring outcomes (eg,
reduced frequency of APOs, severe maternal morbidity,
maternal mortality). Available data rely on studies that
have intervened on single risk factors such as weight
loss to reduce gestational diabetes risk rather than
comprehensive CVH promotion.
77
Randomized controlled
trials that have focused on prepregnancy behavioral in-
terventions have improved individual CVH metrics such
as diet, smoking cessation, or body mass index before
pregnancy.
78–84
In a cohort study of individuals with severe
obesity, bariatric surgery before pregnancy was associ-
ated with substantially lower risks of gestational diabetes
(odds ratio, 0.21 [95% CI, 0.12–0.36]) and HDP (odds
ratio, 0.38 [95% CI, 0.27–0.53]) but higher risks of SGA
birth (odds ratio, 2.18 [95% CI, 1.41–3.38]).
85
Data are even more limited for longer-term maternal
and offspring outcomes after prepregnancy interven-
tions. Among 2 studies with 6-year postpartum follow-up
after a randomized prepregnancy lifestyle intervention for
individuals with obesity and infertility before fertility care,
1 study found that mothers who successfully lost weight
with the intervention had better cardiometabolic health
6 years postpartum compared with control subjects, and
the other found that children of individuals who under-
went the lifestyle intervention had better left ventricular
structure and function.
86,87
However, data are limited by
small sample sizes, attrition bias, and conflicting findings
across studies for better CVH in offspring.
87, 8 8
Postpartum interventions, especially those that
result in weight loss, have been shown to improve
CVH, but the consequences of these interventions on
CVD outcomes in subsequent pregnancy are limited
but could inform similar prepregnancy interventions.
Among women with a history of preeclampsia, small
trials focused on behavior changes have demonstrated
improvement in physical activity postpartum.
89–91
Among women with a history of gestational diabe-
tes, lifestyle interventions conducted in the year after
delivery that targeted overweight/obesity resulted in
modest weight loss, increased physical activity, and
improved glycemic measures.
92
Health care delivery
strategies such as transitional clinics for postpartum
care after APOs, patient navigation, and integration of
maternal care at pediatric visits have been suggested
as potential opportunities to improve health but have
not yet been rigorously evaluated for their effects on
CVH outcomes.
93–95
A NEED FOR CLINICAL TRIALS
TARGETING PREPREGNANCY CVH
The American College of Obstetricians and Gynecolo-
gists strongly advocates the assessment and promotion
of preconception health behaviors and factors in indi-
viduals of reproductive age.
96
However, as just reviewed,
intervening on CVH before conception remains a critical
research gap. If a trial promoting CVH yielded positive
results in mitigating APOs and improving maternal and
offspring outcomes, it could be practice changing and
provide needed impetus for clinicians and reproductive-
aged individuals to be more cognizant about achieving
better CVH. At the population level, primordial prevention
with maintenance of ideal CVH is an overarching goal
throughout the life course. Specifically, in the context of
prepregnancy CVH, adolescence (before a first preg-
nancy) marks a critical transition in the life course when
health behaviors are becoming more firmly established
and distinct CVH trajectories are identifiable.
97
Key Considerations for Trial Design Focused on
Clinical Outcomes
Multiple elements need to be considered in the design
of a trial that tests whether interventions initiated before
pregnancy aimed at holistically promoting CVH will mod-
ify maternal and offspring outcomes. First, careful plan-
ning will be needed to recruit and retain a large, diverse
sample population. Particular attention will need to be
given to developing culturally cognizant strategies and to
oversample individuals from groups who are underrep-
resented in clinical trials and who bear a disproportion-
ate burden of unfavorable CVH, APOs, and CVD. These
groups include populations that are underrepresented
on the basis of racial and ethnic identity and sexual and
gender identity and individuals with adverse social de-
terminants of health. Within racial and ethnic groups,
disaggregation of larger categories such as Asian (eg,
Chinese, Filipina, Japanese, Korean, Vietnamese, Asian
Indian) and Hispanic (eg, Mexican, Puerto Rican, Central
and South American) is necessary given the heterogene-
ity across subgroups. Rigorous collection of self-reported
race and ethnicity, sexual and gender identity, and social
determinants of health, along with strategies to ensure
diversity and inclusion in recruitment, will be important to
understand generalizability of the treatment effect of an
intervention on APOs and offspring outcomes in differ-
ent populations.
Second, selection of inclusion criteria may need to
focus on subsets of individuals who are capable of, open
to, or actively seeking to become pregnant. To adequately
power a study, it may be prudent to enrich the trial sample
with a population at higher risk. For example, a trial could
focus on only 1 metric such as overweight or obesity,
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given that this is the most prevalent risk factor for APOs
in pregnant individuals. However, risk factors often co-
occur in birthing and pregnant individuals, and associa-
tions of maternal CVH with APOs and offspring CVH
are not driven by any single CVH metric.
15,61
Therefore,
inclusion criteria should consider selection of individuals
based on unfavorable levels of multiple CVH metrics. A
trial could be designed that excludes those at highest
risk who already meet medical treatment thresholds for
hypertension, diabetes, or hyperlipidemia, thereby focus-
ing on the population with intermediate risk factor levels
(elevated blood pressure not characterized as hyper-
tension, prediabetes, borderline dyslipidemia) for whom
intervention guidelines are especially lacking.
Third, interventions tested should include multiple
components that include a focus on health behavior
changes (eg, diet, exercise) with or without pharma-
cotherapies based on options known to be safe dur-
ing pregnancy. For example, although statins have long
been avoided in pregnancy, there is growing consensus
that some agents (ie, hydrophilic statins such as pravas-
tatin) may be safe and may reduce the risk of APOs.
98,99
However, it is not known whether particular components
of CVH are most salient to focus on to improve preg-
nancy and long-term outcomes. To inform optimal trial
design, foundational work, including feasibility studies
to test recruitment approaches, retention strategies,
and acceptability of interventions, will be needed. One
hypothetical trial is outlined with the PICOTS (popula-
tion, intervention, comparison, outcome, timing, setting)
framework in Table 2 and is meant as a single example
of what could be considered.
Targeting Stress to Promote CVH
Psychological health, stress, and resilience are inextrica-
bly linked with CVH and are identified by the AHA as
foundational determinants in optimizing CVH.
9
This is
based on robust evidence of the association between
stress and health outcomes, which include APOs and
CVD.
100,101
Racism is a structural driver of disproportion-
ate burden of psychosocial stress, and historically ex-
cluded women have different life experiences such as
repeated episodes of discrimination that are associated
with unfavorable CVH and risk of APOs compared with
White women. Long-term exposures to stress cumula-
tively over the life course leads to weathering, increased
allostatic load (ie, cumulative biological stress), and im-
paired health.
102–104
One coping mechanism among Black
women, called the superwoman schema
105
because of
the need to display strength in the face of long-term ad-
versity, may also negatively affect maternal health out-
comes.
106,107
Culturally responsive stress reduction and
mindfulness-based interventions
108–111
that are sensitive
to systemic barriers may offer a means to buffer stress
and reduce maladaptive coping. Interventions targeting
Table 2. Design of a Potential Clinical Trial to Test Whether
Promoting CVH Before Pregnancy Improves Outcomes in
Pregnant and Postpartum Individuals and Offspring Using
the PICOTS Framework
Population Pregnancy-capable individuals open to or actively seek-
ing to become pregnant, with consideration for the
following:
Age: 25–44 y
CVH metrics: with overweight or obesity and intermedi-
ate levels for blood pressure, glucose, and cholesterol
who do not currently meet criteria for pharmacotherapy
Exclusions: history of infertility
Inclusive of transgender and gender-diverse individuals
Oversample individuals with adverse social determinants
of health (eg, household income at >200% of the federal
poverty level, receiving WIC support)
Oversample historically excluded racial and ethnic groups
(eg, Black, Hispanic, and Asian American/Native Hawai-
ian/Pacific Islander individuals)
Oversample individuals with prior APOs to further increase
study power
Intervention Moderate-intensity lifestyle intervention targeting multiple
CVH factors (diet, physical activity, sleep)
Adjunctive pharmacotherapy at cardiovascular risk factor
levels below current standard of care for pharmacological
intervention:
BP >120/80 mm Hg
Fasting blood glucose >100 mg/dL or HbA1c >5.7%
Non-HDL cholesterol >160 mg/dL or total cholesterol/
HDL ratio >5
Comparison Standard of care, including provision of relevant health
information on promoting CVH and referral to clinicians if
any abnormal CVH metrics
Outcome Coprimary outcomes
Maternal composite outcome consisting of the following:
Preeclampsia
Gestational hypertension
Gestational diabetes
Severe maternal morbidity (eg, acute myocardial in-
farction, cardiac arrest, heart failure)
Pregnancy-related mortality
Offspring composite outcome consisting of the following:
Fetal death
Preterm birth
SGA birth
Secondary outcomes
Individual components of the above composite out-
comes
Rigorous data collection and reporting of subgroup analy-
ses based on sociodemographic factors (eg, race and
ethnicity, gender identity)
Timing 5-y trial phase with 4 y of enrollment and an additional 1 y
of follow-up (average follow-up, 3 y; range, 1–5 y)
Setting Pragmatic trial that leverages health care systems such
as federally qualified health centers, Indian Health Service
clinics, HMOs, and large research networks
APO indicates adverse pregnancy outcome; BP, blood pressure; CVH, car-
diovascular health; HbA1c, hemoglobin A1c; HDL, high-density lipoprotein;
HMO, health maintenance organization; PICOTS, population, intervention, com-
parison, outcome, timing, setting; SGA, small for gestational age; and WIC,
Women, Infants, and Children supplemental nutrition program.
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stress in the prepregnancy period to improve maternal
health outcomes are a critical evidence gap and should
be considered in the context of multilevel policy changes
that simultaneously address structural and systemic bar-
riers to optimal health.
Digital Technologies to Promote CVH
Given that adolescents and young adults are frequent
users of digital technologies (eg, smartphones, social
media, mobile applications [apps]), leveraging these tools
to deliver counseling could be an effective method to
promote prepregnancy CVH.
112
Digital health interven-
tions may offer increased accessibility to support indi-
viduals with low socioeconomic status, who often have
more barriers to health care access and in-person visits.
The integration of digital, face-to-face, and telephone
interactions with health care teams may increase en-
gagement with healthy behavior change interventions
for sustainability and long-term impact.
112
In 1 study,
a health information tool was used to screen for 102
health risks and to deliver tailored prepregnancy coun-
seling to empower high-risk Black individuals to improve
prepregnancy health across various domains, including
emotional and mental health, nutrition and activity, and
substance use.
83,84
The tool included a conversational
agent, Gabby, who provided culturally sensitive and em-
pathetic prepregnancy risk assessment and increased
the proportion of individuals engaged in behavior change
through person-centered decision making and goal set-
ting. Social marketing campaigns through media outlets
have shown promise in increasing awareness of the im-
portance of prepregnancy health and existing maternal
health outcomes disparities.
107,113
Further adaptation of
evidence-based mobile health lifestyle interventions pro-
moting ideal CVH
107,113
to focus on prepregnancy health
should also be studied.
COMMUNITY-ENGAGED DESIGN AND
IMPLEMENTATION OF PREPREGNANCY
CVH INTERVENTIONS
To achieve health equity among birthing individuals, at-
tentive design of community-based interventions is cru-
cial and will require community-centered engagement at
every stage of the research process. This is especially
imperative for populations with an increased frequency
of unfavorable CVH, including people of underrepresent-
ed races and ethnicities who have intersecting barriers
to optimal health attributable to social determinants of
health before, during, and after pregnancy.
107,114
Innovative strategies that are culturally cognizant and
recognize sociocultural and environmental contexts to
optimize CVH are needed. For example, Black women
are significantly more likely than White women to have
unfavorable CVH with multiple prepregnancy cardiovas-
cular risk factors (eg, obesity, diabetes), and risk is higher
among individuals within lower economic strata.
115,116
Hispanic women, in particular those from certain sub-
groups (eg, Puerto Rican women), may experience a
disproportionate burden of adverse social determinants
of health such as poor health care access and quality
and language barriers that contribute to disparate risk
of APOs and CVD.
117
In the limited data that are avail-
able from birthing individuals from Asian subgroups,
Asian Indian compared with White pregnant individuals
have a higher risk of gestational diabetes. Thus, consid-
eration of sociocultural context of individuals from vari-
ous backgrounds, including consideration of nativity and
acculturation along with experience of structural barriers
(eg, racism, built environment, health care access), is of
key importance in the design of interventions. Specifi-
cally, tailoring and adaption through user-centered and
participatory approaches can bolster the effectiveness
and relevance of interventions.
Effectiveness and relevance can also be optimized
through engagement with community steering com-
mittees or advisory boards with key stakeholders and
participants from the target population.
118–123
This will
also facilitate the design of interventions that maximize
strengths and resources present within communities to
promote an asset-based approach that empowers disen-
franchised communities. For example, the harnessing of
civic engagement and community advocacy as a means
to collectively address health disparities has resulted in
improved cardiovascular risk factors (eg, blood pressure,
physical activity) in Black women.
124,125
There is also evi-
dence to support integration of similar models fostering
volunteerism to promote favorable CVH among Hispanic
females.
126
Such interventions can incorporate peer lead-
ers (such as community health workers, or promotoras)
who serve as role models and provide social support to
promote CVH.
127–129
Meeting women in the community
by embedding place-based interventions within their
neighborhoods—at venues such as hair salons, churches,
public housing, college campuses, and workplaces—is
another potential strategy to promote CVH.
115,116,130
Fur-
ther investigation is needed to understand how incor-
porating interpersonal relationships and social support
through partners, friends, and community may also opti-
mize interventions.
ADDRESSING STRUCTURAL
DETERMINANTS OF CVH WITH POLICY-
LEVEL INTERVENTIONS
To substantially improve prepregnancy CVH and down-
stream maternal and offspring outcomes, the wider influ-
ence of multifaceted structural and social determinants
of health must be acknowledged and addressed. This
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requires a sincere appreciation that optimizing opportu-
nities for CVH is not solely an individual responsibility but
requires health system and society-level interventions.
There is well-established evidence that structural inequi-
ties such as disenfranchised neighborhoods and physi-
cal environments, the wealth gap, inadequate access to
quality health care, and food and housing insecurity are
barriers for optimal CVH.
131,132
Dismantling structural rac-
ism and discriminatory policies, the root causes of dispar-
ities in CVH and APOs, is therefore critical.
131,133
Building
CVH-promoting environments and contexts that support
optimal CVH for all birthing individuals requires will for
policy change.
134
Policy-level interventions are needed
to ensure social and reproductive justice and to enable
health over the life course, including during the continu-
um of prepregnancy and perinatal care.
135,136
Making ide-
al CVH the social norm in a community can be achieved
with the integration of equitable opportunities to maintain
healthier lifestyle practices such as increasing access to
healthier and affordable foods (local supermarkets, gro-
cery stores), greener and walkable neighborhoods, free
or subsidized fitness center memberships, and safe and
proximate parks and recreational facilities.
135
Enhancing
economic empowerment and investment in neighbor-
hoods through access to employment and education
opportunities can profoundly influence the CVH and
well-being of socioeconomically disenfranchised indi-
viduals
107,134,137
because these factors are directly linked
to access to high-quality health care. The Black Maternal
Health Caucus through the Black Maternal Health Mom-
nibus has introduced legislation to address the maternal
health crisis through community partnerships, diversity
in the perinatal health care workforce, digital tools, and
optimized health care coverage models that promote
continuity and access (eg, prepregnancy and interpreg-
nancy care) to improve quality of care and to mitigate dis-
parities.
107
Given data that lacking preconception health
insurance is associated with lower levels of pregnancy
care, later initiation of prenatal care, and lower levels of
postpartum care, ensuring uninterrupted access remains
a critical gap, with insurance transitions or “churn” being
common before and after childbirth.
138,139
Multilevel in-
terventions will be needed that are tailored to the unique
stages of the prepregnancy period. Potential examples
are outlined in Table 3.
UNANSWERED QUESTIONS AND FUTURE
DIRECTIONS
A growing body of evidence supports associations be-
tween CVH and APO and between APO and CVD and
builds on the well-established pathways known to ex-
ist between CVH and CVD across the life course and
intergenerationally. However, important knowledge gaps
(a selection of which are presented in Table 4) remain
in the epidemiology and pathophysiology of CVH and
effective interventional strategies to promote CVH. A
central question that remains is whether the associa-
tions among CVH, APOs, and CVD are epiphenomena or
causally related; this question has direct consequences
for the design of prevention and treatment strategies to
improve CVH to decrease the frequency of APOs and
the risk of CVD. Specifically, it is not known whether
Table 3. Tailored Interventions to Promote CVH at Various Prepregnancy Life Stages and Across Ecological Levels
Prepregnancy life stages
People with no current intention
to become pregnant (includes
adolescents)
People with intention to become pregnant
(prepregnancy)
People with intention to become pregnant again
(interpregnancy)
Individual Lifestyle coaching
Stress reduction
Sleep interventions
Weight loss pharmacotherapy/
bariatric surgery
Text-based interventions
In addition to those for people with no current
intention to become pregnant:
Lifestyle-based weight loss interventions
Pharmacotherapy safe during pregnancy to
achieve optimal risk factor control
Lifestyle-based interventions for people with a history of
APOs
Pharmacotherapy among individuals after a history of APOs
(eg, metformin or GLP-1RA after gestational diabetes)
Cognitive behavioral therapy and pharmacologic therapy for
postpartum depression
Community Civic engagement Peer-led support groups Peer-led parenting groups
Home visitation programs focused on stress, postpartum
depression
Population Social marketing campaigns to raise awareness about CVH promotion
Built environment changes (eg, access to healthy foods, green spaces)
Policy Dismantled structural racism
Fair housing practices
Access to education, equitable employment opportunities, and paid family leave
Diversity in health care workforce
Continuous health insurance coverage to ensure high-quality prepregnancy counseling and to minimize interruptions in access
APO indicates adverse pregnancy outcome; CVH, cardiovascular health; GLP-1RA, glucagon-like peptide-1 receptor agonist; SNAP, Supplemental Nutrition As-
sistance Program; and WIC, Women, Infants, and Children supplemental nutrition program.
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APOs are a marker or mediator of the CVH-CVD re-
lationship. Indeed, there are likely multiple direct and
indirect pathways by which CVH may influence mater-
nal and offspring CVH. This supports an emphasis on
primordial prevention to preserve or improve CVH be-
ginning in childhood; however, it is not known whether
specific metrics in the CVH construct are most salient
to focus on at different life stages (eg, before preg-
nancy to reduce risk of APOs). Similarly, it is not known
whether strategies that reduce the frequency of APOs,
by virtue of that reduction, also improve long-term health
outcomes for the birthing individual and offspring. Ob-
servational evidence for several shared pathways at the
CVH-APO-CVD intersection supports that the protec-
tion conferred by higher CVH for both APO and CVD
risk reduction may be more than the sum of its parts.
9,38,61
However, individual-level promotion of prepregnancy
CVH will be limited among individuals with unintended
pregnancies, which account for nearly half of all preg-
nancies; unintended pregnancies are disproportionately
higher among low-income individuals and people of un-
derrepresented races and ethnicities, who are also at
greater risk of poor CVH and CVD.
140
This emphasizes
that population health and policy-level interventions are
key, including strategies to equitably reduce unintended
pregnancies (eg, access to desired long-acting revers-
ible contraceptives, implementation of the One Key
Question) and targeting CVH beginning early in the life
course before the reproductive years.
141
CONCLUSIONS
Substantial opportunity exists to improve health across
the life course and generations by targeting prepreg-
nancy CVH in the birthing individual. Numerous epide-
miological studies demonstrate that CVH is a risk factor
for both APOs and CVD in the birthing individual and
offspring. Animal models and in vitro experiments sug-
gest a strong link among prepregnancy CVH, APOs,
and CVD. Poor prepregnancy CVH is highly prevalent in
reproductive-aged individuals and disproportionately so
among individuals with higher burden of adverse social
factors. Identification of individuals with unfavorable CVH
before pregnancy, as early in the life course as childhood
and adolescence, is a necessary first step to increase
awareness of risk. Clinical trial data are needed to dem-
onstrate whether CVH interventions beginning before
pregnancy will modify maternal and offspring outcomes,
including APOs and CVD. Unfavorable CVH has been
associated with a broad range of antecedent individual-
level and structural determinants. Therefore, effective
interventions should consider multilevel approaches at
the individual, community, and society levels. Persistent
racial, ethnic, and socioeconomic disparities illustrate the
critical importance of future investigations ensuring that
proposed interventions are created, implemented, and
evaluated with an equity focus. The prepregnancy period
offers a unique window of opportunity to address the
growing public health burden of APOs and to interrupt
the intergenerational transmission of poor CVH.
ARTICLE INFORMATION
The American Heart Association makes every effort to avoid any actual or po-
tential conflicts of interest that may arise as a result of an outside relationship or
a personal, professional, or business interest of a member of the writing panel.
Table 4. Key Knowledge Gaps in Mechanistic Pathways,
Effective Interventions, and Implementation of Strategies to
Equitably Promote Prepregnancy CVH
Pathophysiology What are the pathophysiological mechanisms and path-
ways linking prepregnancy CVH, APOs, and CVD?
Could proteomic markers assessed before pregnancy
identify individuals at highest risk of APOs for whom
increased surveillance or intensive risk factor modifica-
tion may reduce risk of APOs?
Are there mechanistic targets that can inform novel
therapeutic development to improve prepregnancy
CVH and pregnancy outcomes?
Interventional re-
search
Which metrics of the CVH construct are most salient
to target in a multicomponent intervention in the pre-
pregnancy period to improve maternal and offspring
outcomes?
Should thresholds for treatment of cardiovascular risk
factors be different in pregnancy-capable individuals
with hypertension (eg, goal BP level <130/80 mm Hg
vs <140/90 mm Hg before pregnancy)?
How should interventions be designed to incorporate
and address social determinants of health, psychologi-
cal health, and stress to improve prepregnancy CVH?
How should we identify individuals at highest absolute
risk (eg, low CVH, biomarkers) to prioritize for testing
interventions?
Do interventions targeting the interpregnancy period
improve outcomes of the subsequent pregnancy and
offspring?
Do interventions targeting prepregnancy CVH reduce
the risk of long-term kidney disease?
Dissemination and
implementation
research
Is the proposed intervention adaptable for resource-
limited populations?
Is the proposed intervention culturally tailored to maxi-
mize benefit in diverse communities?
Can technology-based approaches (eg, virtual remind-
ers, mHealth) optimize delivery of interventions to
improve prepregnancy CVH?
Health equity con-
siderations
Can healthcare system–based models that provide
patient navigation and peer support to address barriers
that exist help to optimize prepregnancy CVH?
What are optimal strategies to ensure equitable recruit-
ment of individuals who do not have routine health care
access, particularly in the prepregnancy period?
What strategies are most effective in engaging key
stakeholders from communities from the beginning of
intervention development to process improvement in
the implementation phases?
Are interventions generalizable to different populations,
including across race and ethnicity, socioeconomic
status, and gender identity?
APO indicates adverse pregnancy outcome; BP, blood pressure; CVD, car-
diovascular disease; CVH, cardiovascular health; and mHealth, mobile health.
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Specifically, all members of the writing group are required to complete and sub-
mit a Disclosure Questionnaire showing all such relationships that might be per-
ceived as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science
Advisory and Coordinating Committee on October 15, 2022, and the American
Heart Association Executive Committee on December 12, 2022. A copy of the
document is available at https://professional.heart.org/statements by using
either “Search for Guidelines & Statements” or the “Browse by Topic” area. To
purchase additional reprints, call 215-356-2721 or email Meredith.Edelman@
wolterskluwer.com.
The American Heart Association requests that this document be cited as
follows: Khan SS, Brewer LC, Canobbio MM, Cipolla MJ, Grobman WA, Lewey J,
Michos ED, Miller EC, Perak AM, Wei GS, Gooding H; on behalf of the American
Heart Association Council on Epidemiology and Prevention; Council on Clinical
Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Arterio-
sclerosis, Thrombosis and Vascular Biology; Council on Hypertension; Council on
Lifestyle and Cardiometabolic Health; Council on Peripheral Vascular Disease;
and Stroke Council. Optimizing prepregnancy cardiovascular health to improve
outcomes in pregnant and postpartum individuals and offspring: a scientific state-
ment from the American Heart Association. Circulation. 2023;147:e76–e91. doi:
10.1161/CIR.0000000000001124
The expert peer review of AHA-commissioned documents (eg, scientific
statements, clinical practice guidelines, systematic reviews) is conducted by the
AHA Office of Science Operations. For more on AHA statements and guidelines
development, visit https://professional.heart.org/statements. Select the “Guide-
lines & Statements” drop-down menu, then click “Publication Development.”
Permissions: Multiple copies, modification, alteration, enhancement, and dis-
tribution of this document are not permitted without the express permission of the
American Heart Association. Instructions for obtaining permission are located at
https://www.heart.org/permissions. A link to the “Copyright Permissions Request
Form” appears in the second paragraph (https://www.heart.org/en/about-us/
statements-and-policies/copyright-request-form).
Disclosures
Writing Group Disclosures
Writing group
member Employment Research grant
Other
research
support
Speakers’
bureau/
honoraria
Expert
witness
Ownership
interest
Consultant/advisory
board Other
Sadiya S. Khan Northwestern Univer-
sity, Feinberg School
of Medicine
None None None None None None None
Holly Gooding Emory University
School of Medicine
NHLBI (R03 to create car-
diovascular prevention tool
for young women)?
None None None None None None
LaPrincess C.
Brewer
Mayo Clinic College
of Medicine
None None None None None None None
Mary M.
Canobbio
UCLA School of
Nursing
None None None None None None None
Marilyn J.
Cipolla
University of Vermont None None None None None None None
William A.
Grobman
The Ohio State
University
None None None None None None None
Jennifer Lewey University of Penn-
sylvania, Perelman
School of Medicine
None None None None None None None
Erin D. Michos Johns Hopkins
University School of
Medicine
None None None None None Amarin; Amgen;
AstraZeneca; Bayer;
Boehringer Ingelheim;
Esperion; Novartis;
Novo Nordisk; Pfizer
None
Eliza C. Miller Columbia University NIH NINDS
(K23NS107645)?; NIH NIA
(R21AG069111)?; NIH
NINDS (R01NS122815)?;
Gerstner Family Founda-
tion (Gerstner Scholars
Program)?
None None None None None None
Amanda M.
Perak
Lurie Children’s Hos-
pital and Northwest-
ern University
None None None None None None None
Gina S. Wei NHLBI None None None None None None None
This table represents the relationships of writing group members that may be perceived as actual or reasonably perceived conflicts of interest as reported on the
Disclosure Questionnaire, which all members of the writing group are required to complete and submit. A relationship is considered to be “significant” if (a) the person
receives $5000 or more during any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of
the entity, or owns $5000 or more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding
definition.
Modest.
?Significant.
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Reviewer Disclosures
Reviewer Employment
Research
grant
Other research
support
Speakers’
bureau/
honoraria
Expert
witness
Ownership
interest
Consultant/
advisory
board Other
Rachel M. Bond Chandler Regional Medical Center,
Dignity Health
None None None None None None None
Joshua D. Bundy Tulane University School of Public
Health and Tropical Medicine
None None None None None None None
Randi Foraker Washington University in St. Louis,
School of Medicine
None None None None None None None
Garima Sharma Johns Hopkins University School of
Medicine
None None None None None None None
Jennifer Stuart Brigham and Women’s Hospital and
Harvard Medical School
None None None None None None None
This table represents the relationships of reviewers that may be perceived as actual or reasonably perceived conflicts of interest as reported on the Disclosure
Questionnaire, which all reviewers are required to complete and submit. A relationship is considered to be “significant” if (a) the person receives $5000 or more during
any 12-month period, or 5% or more of the person’s gross income; or (b) the person owns 5% or more of the voting stock or share of the entity, or owns $5000 or
more of the fair market value of the entity. A relationship is considered to be “modest” if it is less than “significant” under the preceding definition.
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