Cardiovascular Health, 2010 to 2020: A Systematic Review of a Decade of Research on Life's Simple 7

Abstract

Background

In 2010, the American Heart Association introduced Life's Simple 7, a construct to measure, monitor, and modify cardiovascular health (CVH) across the lifespan. We aimed to summarize the knowledge on outcomes, prevalence, determinants, and mechanisms of Life's Simple 7.

Methods

We systematically searched PubMed, Web of Science, and Scopus databases for publications in English examining Life's Simple 7 or 3 or more CVH metrics from January 1, 2010 to January 1, 2021. Risk of bias was assessed with the Mixed Methods Appraisal Tool for studies of outcomes, prevalence, and determinants.

Results

Of 4624 publications screened, 483 were included; most had low risk of bias. Studies of outcomes (n=259) showed that ideal/high CVH (score ≥12/14 or 6/7 ideal metrics) consistently associates with benefits in multiple bodily systems from brain to toe and from gestation to extreme old age. Low prevalence of ideal/high CVH (n=84) was reported worldwide. Longitudinal studies (n=144) showed CVH is higher at younger ages and declines with age. CVH disparities persist, with lower CVH among underrepresented individuals, in lower levels of urbanization, and greater exposure to adverse social determinants. Studies of mechanisms (n=23) showed the benefits of ideal/high CVH are partly due to lower inflammation and pathways yet to be defined.

Conclusions

Less is known about CVH among children and diverse populations, the benefits of modest improvements, and underlying mechanisms. Consistent evidence supports targeting social, psychological, and prenatal factors to improve individual and population CVH across the lifespan. Publication bias and overrepresentation of studies reporting significant associations cannot be excluded.

Nonstandard Abbreviations and Acronyms

AHA

American Heart Association

CVH

cardiovascular health

LS7

Life's Simple 7

RESEARCH PERSPECTIVE.

What Is New?

• This comprehensive systematic review shows that the construct of cardiovascular health, formally defined by the American Heart Association as Life's Simple 7, is a powerful predictor of cardiovascular disease risk, other chronic diseases, health care use and costs, and overall individual and population health from brain to toe, as well as longevity and holistic well‐being.

What Question Should Be Addressed Next?

• To unlock the full potential of the powerful cardiovascular health metric in the decades ahead, research must harness the greater granularity of the revised concept, Life's Essential 8 to: (1) better define and track cardiovascular health from early childhood ages, (2) assess the impact of modest and more attainable improvements on long‐term health outcomes, and (3) inform the development of sustainable strategies that promote maintenance and improvements of CVH with an equity lenses to help all individuals live longer, healthier lives.

In 2010, the American Heart Association (AHA) introduced a formal definition for the concept of cardiovascular health (CVH), creating a new paradigm that characterized and promoted a state of cardiovascular well‐being. ¹ This paradigm shift offered a proactive, long‐term strategy that expanded the scope of cardiology to include primary and primordial prevention. It also encouraged addressing health threats before they manifest and the promotion of CVH across the lifespan, which could be examined with the Life's Simple 7 (LS7) metric. To this end, the LS7 metric combined 3 health behaviors (diet, physical activity, and smoking status) and 4 health factors (body mass index, blood pressure, total cholesterol, and glucose) into a single CVH score, with separate criteria for adults and children. This novel definition encompassed the entire spectrum of values within the health behaviors and health factors, including levels below clinical thresholds for risk. The construct had relevance at all ages and phases of health and disease, and allowed for individuals, clinicians, and policymakers to consider the full spectrum of health promotion and disease prevention.

Now, >10 years after its inception, a plethora of studies have demonstrated the significance of the LS7 definition to quantify and track levels of CVH across the lifespan in individuals and, over time, in populations. Prior systematic reviews and meta‐analyses have evidenced the consistent dose–response relationship of CVH with cardiovascular disease (CVD), and both CVD and all‐cause mortality. ² , ³ , ⁴ The worldwide prevalence of CVH has also been previously summarized in a meta‐analysis. ⁵ This review updates prior work and advances the literature by summarizing all evidence associated with CVH including CVD and noncardiovascular outcomes, as well as other aspects of the LS7 metric (eg, determinants and mechanisms). This review provides a capstone for the first decade of research on CVH, defined by LS7, including a summary and an organized catalog of current understanding of the worldwide prevalence, outcomes, determinants, interventions, and mechanisms of CVH.

METHODS

A comprehensive systematic review was conducted by a research librarian using the PubMed, Web of Science, and Scopus databases from January 1, 2010 to January 1, 2021. The search algorithm (Data S1) included all English‐language articles that cited Lloyd‐Jones et al (2010) or Steinberger et al (2016), or a combination of CVH terms. The search was conducted in October 2019 and January 2021 to include articles published through 2020.

Eligible original research studies had to examine the construct of CVH, or a similar composite that included ≥3 of the LS7 metrics (Table 1) with a health‐oriented approach. We focused on studies that measured CVH using AHA criteria to estimate an ordinal, semicontinuous, or categorical variable. Briefly, following the cutoff points outlined by the AHA (Table 1), a semicontinuous score ranging from 0 to 14 is calculated by assigning 2 points for each metric at ideal/high status, 1 point for intermediate/moderate status, and 0 points for poor/low status and adding the total points. An ordinal CVH variable is estimated by counting the number of ideal CVH metrics from 0 to 7. Last, a categorical variable is derived from the ordinal or semicontinuous CVH score by categorizing it into 3 strata: poor/low (semicontinuous score ≤4 or 0–2 ideal metrics), intermediate/moderate (score of 5–11 or 3–5 ideal metrics), and ideal/high (score ≥12 or 6–7 ideal metrics).

Table 1.

American Heart Association's Life's Simple 7 Scoring Criteria for Adult Cardiovascular Health

Cardiovascular health Life's Simple 7 factors		Scoring criteria
		Poor/low	Intermediate/moderate	Ideal/high
		Unfavorable		Optimal
Behavioral	Healthy diet (components*)	0–1	2–3	4–5
	Physical activity (min/wk)	None	1–149 min/wk moderate or 1–74 min/wk vigorous or 1–149 min/wk moderate and vigorous †	≥150 min/wk moderate or ≥75 min/wk vigorous or ≥150 min/wk moderate and vigorous †
	Smoking	Current	Former <1 year	Never or former >1 year
Clinical	Body mass index (kg/m2)	≥30	25.0–29.9	<25.0
	Blood pressure (mm Hg)	SBP ≥140 or DBP ≥90	SBP 120–139 or DBP 80–89 or treated to goal	<120/80 untreated
	Total cholesterol (mg/dL)	≥240	200–239 or treated to goal	<200 untreated
	Fasting plasma glucose (mg/dL)	≥126	100–125 or treated to goal	<100 untreated
Total cardiovascular health score categories‡		0 points	1 point	2 points
		0–4 points, 0–2 metrics	5–9 points, 3–5 metrics	10–14 points, 6–7 metrics

Adapted from Lloyd‐Jones et al. ¹ DBP indicates diastolic blood pressure; and SBP, systolic blood pressure.

^*Healthy diet components include any of the following: ≥4–5 cups/d of fruits and vegetables; ≥2, 3.5‐oz servings per wk of fish; fiber rich whole grains (≥1.1 g of fiber per 10 g of carbohydrate), ≥3, 1‐oz servings per day; ≤1500 mg/d of sodium and <36 fluid oz (≤450 kcal) per wk of sugar‐sweetened beverages. Dietary recommendations are scaled according to a 2000 kcal/d diet.

^† Minutes of vigorous activity are equal to 2 times the minutes of moderate activity when moderate and vigorous activities are combined.

^‡ Total cardiovascular health scores are estimated by assigning 2 points for each metric at ideal/high status, 1 point for intermediate/moderate status and 0 points for poor/low status, and adding the total points or by counting the number of metrics in the ideal category.

We excluded studies that examined disease‐oriented constructs, such as metabolic syndrome or the Framingham Risk Score. Studies focused on the awareness of the CVH definition without measuring CVH, conference abstracts, qualitative studies, systematic reviews without meta‐analyses, and non‐peer‐reviewed publications were excluded. The review protocol was not registered. Supplemental files detail the screening process (Data S2) per current Preferred Reporting Items for Systematic reviews and Meta‐Analyses guidelines. ⁶

Statistical Analysis

Two authors (L.A. and A.M.P.) independently reviewed the title and abstract of 4624 citations using Rayyan software to identify 605 articles that were potentially eligible. Three reviewers (L.A., C.C., J.W.G.) examined the full text of the 605 articles screened to determine eligibility. Disagreements about eligibility were resolved through consensus with the senior author (A.M.P.). Following these steps, 483 articles were selected and summarized using a standardized form adapted from the Participants/population, Exposure/interventions, Comparator, and Outcomes (PECO) framework. We defined associations with CVH based on significant statistical findings at the α<0.05 level. To evaluate the methodological quality of the studies that examined the prevalence, outcomes, and determinants of CVH, we conducted a critical appraisal using a modified version of the Mixed Methods Appraisal Tool. ⁷ We evaluated the methodological quality of studies that examined the prevalence and outcomes of CVH, including interventions that aimed to modify CVH, with the same instrument. This approach enabled us to quantitatively compare them, despite the differences in design (eg, cross‐sectional, longitudinal cohort, randomized, and nonrandomized trials). In the version implemented, we modified question 4.4 (Is the risk of nonresponse bias low?) to introduce ≤30% as objective criteria for low nonresponse bias. Results are reported based on the percentage of the 5 quality criteria that was met (range from 0% to 100%). Description of the results and broader literature on CVH was approached in a narrative fashion to succinctly summarize the essence of what this large body of literature has established. Institutional review board approval and informed consent were not required for this systematic review of published studies. Search algorithm and all review data analyzed are available within the article and its online supplementary files.

RESULTS

We identified 483 articles that satisfied inclusion criteria and are cataloged in Tables S1 through S5. Most studies examined health outcomes associated with exposure to different levels of CVH (n=259). The remaining studies focused on the prevalence, trends, or distribution of CVH in samples around the world (n=84), study determinants or predictors of CVH (n=99), examined CVH in intervention studies (n=18), and investigated mechanisms through which CVH may influence health outcomes (n=23). Of the 483 studies cataloged, 11 studies were included as outcomes and mechanisms. Overall, most studies were considered of high quality with low risk of bias. Among studies of the prevalence, outcomes, and determinants or predictors, 84.5%, 86%, and 83% of the MMAT items were fulfilled, respectively. See Figure S1 for the distribution and criteria examined.

Prevalence and Distributions of CVH in Populations

Most of the 84 studies that presented the prevalence of 7 ideal CVH metrics showed it is extremely low, ranging from 0% to 4%, with higher prevalence in youth (12–17‐year‐old adolescents). ⁸ When using a less strict definition, such as having at least 5 metrics at ideal levels, the prevalence remained low, but ranged from <1% to 70%. Previous meta‐analysis showed rates of 5 ideal CVH metrics ranged from 13% to 20% among US adults. ⁴ We found a wider range with higher prevalence likely due to the inclusion of international samples, younger populations, and earlier generations. ⁹ , ¹⁰ The highest prevalence of high CVH was observed in a nationally representative sample from Nepal in 2013, where 71.5% of youth aged 15 to 29 years had 5 to 7 ideal CVH metrics. ¹¹ In contrast, the highest prevalence reported in the United States was 40%, found in 1988 among White adults aged 25 to 44 years with ≥5 ideal metrics. ⁹ By 2011, this prevalence had dramatically declined, with only 15.3% of young White adults meeting this threshold. ⁹ Meanwhile, in Denmark, the prevalence of ideal CVH metrics increased from 1978 to 2006 from 2% to 13% among women and from 1% to 5% among men.

Beyond the generational differences, we noticed that there are no universally accepted thresholds for categorizing LS7 scores into ideal/high, intermediate/moderate, and poor/low categories. As a result, the criteria for these classifications differed across studies. Furthermore, reporting is inconsistent: some studies focused solely on the prevalence of ideal/high or low/poor CVH, whereas others used a continuous scoring method and may not have reported prevalence data for each specific CVH category. Last, a handful of studies used the LS7 criteria to score each of the CVH metrics but did not combine all metrics into a single variable.

CVH Worldwide

The World Health Organization's 6 world regions criteria was used to catalog the countries in which CVH has been characterized (Data S1). The prevalence of ideal, intermediate, or poor CVH status was most often characterized among adults and in the United States and China. Only 2 studies examined the prevalence of ideal CVH of adults in Africa, ¹² , ¹³ and 1 in the Eastern Mediterranean Region (Iran ¹⁴ ). Cross‐country comparisons were limited, but 2 studies that compared the CVH levels of urban Ghanaian ¹² and rural Ecuadorian ¹⁵ adults with multiple European and US counterparts, respectively, revealed an advantage for African and Latin American adults.

Individual CVH Metrics

Of the 7 CVH metrics, the prevalence of ideal diet is consistently negligible (<1%) at all ages. Meanwhile, not smoking is the metric most frequently achieved by adults in the United States and North America, ¹⁶ Latin America, ¹⁷ Asia, ¹⁸ , ¹⁹ and Europe. ²⁰ In the United States, the annual statistics introduced by the AHA consistently show that the prevalence of ideal status for nonsmoking is highest in 12‐ to 18‐year‐old adolescents (~94%), nadir in young adults aged 19 to 44 years (75%), and increasing thereafter through older adulthood (87%). ²¹ The opposite pattern is documented for ideal physical activity, with the peak in young adulthood (42%) and the lowest levels for adolescents (25%) and older adults aged ≥65 years (28%). ²¹ Prevalence of ideal status is steadily lower with increasing age for body mass index (from 60.1% in adolescence to 24% in older adulthood), blood pressure (85%–16%), total cholesterol (78%–25%), and fasting glucose (86%–32%). ²¹

Trends in CVH

Ten studies examined trends of CVH over time in the United States, 2 in China, ²² , ²³ 3 in Western Europe, ²⁰ , ²⁴ , ²⁵ and 1 in Korea. ¹⁹ The analysis of CVH trends included data from as early as 1987 ²⁶ for US children aged 9 to 19 years and from 1988 ⁹ for adults. Most US‐based studies evidenced small CVH declines, albeit significant, even during the 2008 to 2009 economic recession. ²⁷ This led the authors to suggest CVH scores appeared stagnant, particularly from 1999 to 2010. ⁸ , ²⁸ Few studies evidence improvements in specific US subsamples, but these were often negligible, such as changes in ideal CVH from 0.3% to 0.6%. ²⁹

Analyses of trends outside the United States showed CVH worsen among more recent generations of Chinese adults ²² and children (aged 6–18 years), ²³ remained unchanged among Korean adults, and in contrast, improved among later born adults in Berlin, ²⁰ France, ²⁵ and Denmark. ²⁴

Differences in CVH Between Subgroups in the United States

Studies that evaluated sex differences found women and girls had higher CVH than adult men and boys, but not all sex comparisons were statistically different. Nonsignificant differences were most often shown in studies using nonrepresentative ³⁰ or small samples, ³¹ which may explain the results. Important variations also exist within samples of women; pregnant women ³² and sexual minority women ³³ had worse CVH than their nonpregnant and heterosexual counterparts. However, evidence of these differences is limited to single studies conducted exclusively in the United States.

The prevalence of high CVH also varied by race and ethnicity. The AHA 2022 statistical report showed that the prevalence of having ≥5 ideal metrics among adolescents aged 12 to 19 years and adults aged ≥20 years was highest among non‐Hispanic Asian individuals (63% and 26%), followed by non‐Hispanic White individuals (49% and 19%), Hispanic individuals (41% and 12%), and non‐Hispanic Black individuals (35% and 12%). ²¹ The prevalence of ideal CVH also varied by region, but fewer studies documented geographic differences. Higher rates were reported among the Northeast, Pacific, and Mountain regions of the United States compared with the South, Central, and South Atlantic regions, ³⁴ , ³⁵ and among urban adults ³⁶ compared with their rural counterparts.

Outcomes Associated With High Levels of CVH

Figure 1 and Table 2 introduce the health outcomes associated with CVH (see Data S2 for a detailed list of outcomes associated with more optimal levels of CVH).

Figure 1. Benefits to human health associated with optimal cardiovascular health: optimal health from brain to toe.

Table 2.

Alphabetical List of Outcomes Associated With More Optimal CVH

Higher CVH is associated with lower risk of:

Cancer 41 , 49 , 102 , 103 , 104 , 105

CVD clinical outcomes 37 , 41 , 42 , 43 , 44 , 48 , 57 , 59 , 93 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 , 120 , 121 , 122 , 123 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153

CVD mortality 41 , 57 , 121 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 , 164 , 165

CVD subclinical outcomes: cIMT, 38 , 39 , 40 , 166 , 167 , 168 , 169 , 170 , 171 , 172 , 173 , 174 , 175 , 176 ventricular mass, 177 , 178 , 179 , 180 coronary artery calcification,  17 , 39 , 169 , 173 , 174 , 181 , 182 , 183 , 184 , 185 atherosclerosis, 186 , 187 , 188 , 189 , 190 , 191 ambulatory arterial stiffness, 192 , 193 , 194 , 195 , 196 carotid plaques, 38 , 182 , 197 pulse wave velocity, 198 , 199 , 200 other outcomes 38 , 46 , 65 , 170 , 201 , 202 , 203 , 204 , 205 , 206 , 207 , 208 , 209 , 210 , 211 , 212 Null associations with: cIMT 46 , 202 , 204

CVH/CVD risk profile, suboptimal 64 , 208 , 213 , 214 , 215

Cerebral volumes, 216 , 217 , 218 , 219 , 220 , 221 , 222 , 223 , 224 , 225 , 226 , 227 cognition declines, 220 , 228 , 229 , 230 including MMSE scores, 217 , 231 , 232 , 233 and dementia (Alzheimer)  21 , 47 , 234 , 235 , 236 , 237 , 238 , 239 Null associations with: cognitive function (MMSE) 240 , 241

Diabetes 59 , 242 , 243 , 244 , 245 , 246 , 247 , 248 , 249 , 250

Eye health problems 251 , 252 , 253

Health care costs (high) 51 , 52 , 53 , 254 , 255

Hearing loss 256

Health‐related quality of life, poor 55 , 257 , 258 , 259 , 260

Hypertension  59 , 175 , 248 , 261 , 262 , 263 , 264 , 265 , 266 , 267 , 268 /ideal blood pressure 269 , 270

Chronic kidney disease  59 , 271 , 272 and end‐stage renal disease 273 , 274

Lipids: hypercholesterolemia (LDL‐C ≥186 mg/dL) 175 , 275 /lower atherogenic index of plasma 276

Liver dysfunction: elevated liver enzymes (ALT/γ‐GT), 277 , 278 nonalcoholic fatty liver disease, 279 , 280 , 281 , 282 , 283 , 284 , 285 hepatic steatosis 286

Longevity, low or unhealthy 52 , 54

Mental health: alexithymia, 287 anxiety, and stress, 288 depressive symptoms, 50 , 288 , 289 , 290 , 291 , 292 mood disorder, 293 work engagement 294

Metabolic syndrome 80 , 175 , 295 , 296 , 297

Mortality: all‐cause mortality 2 , 3 , 41 , 92 , 161 , 298 , 299 , 300 , 301 , 302 , 303 , 304 , 305 , 306

Other diseases: obesity, 307 erectile dysfunction, 308 chronic obstructive pulmonary disease 49 , 309 pneumonia, 49 lower exhaled carbon monoxide, 310 reduced risk of venous thromboembolism, 49 , 311 , 312 , 313 multisystem suboptimal health status 314

Physical fitness, lower cardiorespiratory fitness, 315 and muscular fitness 316

Physical functioning: functional disability 317 , 318 ; frailty, 319 , 320 , 321 mobility problems, 322 poor physical function, 323 at least 2 disability d off work, 324 physical performance (Short Physical Performance Battery) scores 325 ; worse gross motor function 219 and grip strength levels 326

Pregnancy/reproductive outcomes: preeclampsia, unplanned primary cesarean delivery, newborn birthweight >90th percentile, newborn sum of skinfolds >90th percentile, and newborn insulin sensitivity <10th percentile 327 ; preterm birth and small for gestational age in women with lupus, 328 and CVD among women with premature ovarian insufficiency 329

Self‐reported poorer health 55 , 257 ,  258 ,  330

Sleep disturbances: sleep‐disordered breathing and excessive daytime sleepiness 66

Null associations with: sleep duration, insomnia symptoms 66

ALT/y‐GT, alanine aminotransferase (ALT) and y‐glutamyl transpeptidase (ALT/y‐GT) ratio; cIMT, carotid intima‐media thickness; CVD indicates cardiovascular disease; CVH, cardiovascular health; LDL‐C, low‐density lipoprotein cholesterol; and MMSE, Mini‐Mental State Examination.

Detailed list of specific associations is available in the Supplemental Table.

Associations of CVH Status With CVD and Mortality

Better CVH is consistently associated with multiple indicators of subclinical CVD, such as peripheral artery disease, ³⁷ coronary artery calcification, and carotid plaques. ³⁸ , ³⁹ , ⁴⁰ Numerous investigations evidenced an a inverse, log‐linear, dose–response relationship between ideal/higher CVH and lower risks for total CVD, ⁴¹ , ⁴² stroke, ⁴³ myocardial infarction, ⁴⁴ CVD mortality, and all‐cause mortality. ⁴¹ , ⁴⁴

However, these associations were not always consistent. One study found no association between CVH and the prevalence of stroke or ischemic heart disease. ⁴⁵ Another study found discrepancies in the association with carotid intima‐media thickness, particularly among women. ⁴⁶ These discrepancies suggest the need for further research to explore potential sex‐specific modifiers.

Other Health Outcomes

Beyond CVD, several studies showed that ideal/high CVH (versus poor/low) is associated with lower risk for incidence or prevalence of numerous chronic diseases, including dementia (86% lower risk), ⁴⁷ , ⁴⁸ cancer (20%), ⁴¹ , ⁴⁹ chronic kidney disease (62%), ⁴⁹ and depression (10% lower risk per each additional ideal CVH metric). ⁵⁰ This comprehensive array of health benefits translates into lower medical expenditures and health care use, ⁵¹ , ⁵² , ⁵³ greater longevity, ⁵⁴ compression of morbidity, ⁵² and higher quality of life. ⁵⁵

Life Course and Intergenerational CVH Outcomes

Only 4 studies examined intergenerational CVH transmission. Of these, Perak et al showed that early in the life course, ideal/high (versus poor/low) maternal gestational CVH is associated with nearly an 8‐times lower risk for offsprings’ low CVH by adolescence. ⁵⁶ Better CVH in younger ages is associated with lower risk for subclinical CVD in adulthood ⁴⁰ and subsequent premature CVD events and CVD mortality. ⁵⁷ On the opposite end of the age spectrum, better CVH is associated with better quality of life, ⁵⁵ even among centenarians aged ≥85 years. ⁵⁴ , ⁵⁸

Maintenance and Improvements in CVH

Overall, studies have shown that CVH declines with age, and fewer individuals are able to maintain or improve their CVH as they get older. Those who experience improvements reduced their CVD risks by >20%. A study among participants of the Framingham Offspring Study showed that each 5‐year period of ideal/high or intermediate/moderate (versus poor/low) CVH translated to 33% lower risk for hypertension; about 25% lower risks for diabetes, chronic kidney disease, or CVD; and 14% lower risk for all‐cause mortality. ⁵⁹ Among Korean adults, improvements of 1 CVH metric to the ideal category during young adulthood were associated with a 21% lower risk for CVD events. ⁶⁰ Improvements from low CVH reduced the lifetime risk for CVD from 45% to 38% for Chinese middle‐aged adults who improved to moderate CVH and to 24.4% for adults who improved to ideal CVH. ⁶¹ Among US adults, improvements from poor CVH to moderate or ideal levels were associated with 33% lower risk for CVD and 20% lower risk for all‐cause mortality. ⁶²

Role of Individual Metrics

Each additional ideal CVH metric contributes to lower lifetime risk of CVD events ⁴² and overall mortality. ⁶² Even among individuals with high genetic risk for coronary heart disease, maintenance of at least 3 CVH behaviors at ideal levels is associated with substantially lower risk of coronary events and longer CVD‐free survival. ⁴⁸ , ⁶³

Predictors or Determinants of CVH

Table S3 provides a list of factors associated with ideal/high CVH.

Health‐Related Behaviors

Individuals who maintain healthier LS7 behaviors from a young age are more likely to retain all LS7 metrics at ideal levels into middle age. ⁴⁰ , ⁶⁴ , ⁶⁵ Beyond the CVH behaviors included in the LS7 definition, sleep duration and quality are associated with ideal/high CVH. ⁶⁶ , ⁶⁷ Additionally, the circadian rhythm of health behaviors, such as shorter eating intervals and morning chronotype, are associated with ideal/high CVH, but research remains limited. ⁶⁸ , ⁶⁹

Behavioral Interventions

All interventions targeting CVH improvements (n=18) used a longitudinal framework to examine both immediate and long‐term effects (list available in Table S4). Most interventions successfully improved total CVH among adults by promoting lifestyle changes through mobile health, ⁷⁰ , ⁷¹ health partners, ⁷² community groups, ⁷³ , ⁷⁴ , ⁷⁵ and faith‐based organizations. ⁷⁰ , ⁷¹ Follow‐up examinations ranged from 8 weeks ⁷³ (immediately after the implementation ended) to 6 years. The study with the longest follow‐up was also the only study that focused on youth, reporting better CVH in adolescents (aged 9–13 years) who followed a dietary and lifestyle counseling intervention introduced during preschool ages. ⁶⁵

Psychological Health

Although psychological health appears to be critical for adopting and maintaining ideal CVH, only 8 studies focused on mental health. These studies showed that lower levels of perceived stress ⁷⁶ and depressive symptoms, ⁵⁰ as well as higher levels of positive emotions over time, ⁷⁷ , ⁷⁸ are associated with better CVH. ⁵⁰ , ⁷⁶ , ⁷⁷ , ⁷⁸

Social Determinants of Health

Most studies included social determinants of health as covariates in their analyses, but only 41 specifically focused on these determinants. Results from these show that better CVH levels are consistently observed for adults and children with more favorable conditions across each of the 5 Healthy People 2020 social determinants of health domains, ⁷⁹ including higher (1) economic stability, ⁸⁰ (2) health care access, ⁸¹ (3) education access and quality, ²⁴ (4) neighborhood status ⁸² and resources (such as living in neighborhoods with physical activity resources ⁸³ and more full‐service restaurants ⁸³ ), and (5) better social and community contexts, including higher median household income ⁸³ , ⁸⁴ and racial and ethnic heterogeneity. ⁸⁵ , ⁸⁶

Family‐Related Factors

Parental CVH is associated with offspring CVH in childhood and adulthood. ⁸⁰ These associations may be modulated by genetic predisposition, ⁸⁷ shared family environment and lifestyle, ⁸⁸ and the intrauterine environment. ⁵⁶

Mechanisms Associated With CVH

The mechanisms through which CVH influences the structure and response of multiple organ systems, and consequently resilience to many chronic diseases simultaneously, are complex and incompletely understood (Table S5). The known pathways suggest cyclical feedback resulting from a dose–response relationship in which loss of ideal CVH leads to higher levels of inflammation, ⁸⁹ , ⁹⁰ and subsequent additional CVH loss. Among young adults, the loss of CVH contributes to DNA methylation across multiple tissues and blood subtypes that simultaneously contribute to the pathogenesis of CVD. ⁹¹ Two studies examining cumulative multisystem alterations found that even a combination of intermediate circulating biomarkers across multiple systems (ie, concentrations of C‐reactive protein, D‐dimer, fibrinogen, homocysteine, and other markers) accounted for, at most, 24% of the relationship between CVH and incident CVD or death risk. ⁹² , ⁹³ These findings underscore that the biological mechanisms by which CVH metrics influence the occurrence of CVD and other health outcomes remains incompletely characterized.

DISCUSSION

The first decade of CVH research from 2010 to 2020 documented key features of CVH that identify its key determinants, examine potential mechanisms, and underline its unique usefulness (Figure 2). Optimal CVH is a powerful predictor of low long‐term CVD risk and future physical and psychological well‐being. We summarized a large array of multisystem and multilevel benefits associated with ideal/high CVH, spanning from brain to toe (see Figure 1 and Table 2). At the brain level, maintaining or achieving ideal/high levels of CVH is associated with more optimal cognitive health. ⁴⁷ , ⁴⁸ At the toe level, better CVH is associated with lower risk of peripheral artery disease‐lower limb amputations. ³⁷ Mainly, at the heart of CVH's benefits, individuals with optimal CVH experience low rates of CVD over long‐term follow‐ups ⁵⁷ and live longer, healthier lives. ⁵² , ⁵⁴ Social‐level benefits include the intergenerational transmission of optimal CVH profiles ⁵⁶ and economic savings from lower health care use and costs. ⁵¹ , ⁵² , ⁵³ In sum, optimal CVH is consistently associated with reduced risk for CVD and major noncommunicable diseases. Studies of CVH mechanisms suggest the influence of ideal/high CVH on long‐term health outcomes appear to be causal and exceeds the predictive power of any single CVH metric, perhaps reflecting other unmeasured aspects of healthy lifestyles or pathways not yet identified.

Figure 2. Summary of the determinants, mechanisms, and outcomes associated with ideal/high and poor/low levels of cardiovascular health.

CVH indicates cardiovascular health.

Unfortunately, worldwide, the prevalence of optimal CVH remains exceedingly low, particularly from middle age onward. Loss of CVH is greater among adults and children in disadvantaged social positions. Efforts to achieve the AHA 2028 Impact Goal, to advance CVH for everyone, everywhere, will require strategies to address inequities, particularly during childhood. Although improvements in CVH at any stage in life are highly beneficial, ⁶⁰ , ⁶² they are remedial, and far less feasible than preventing declines in CVH.

Primordial prevention of CVH loss and continual promotion of optimal CVH from the beginning of life offer the best opportunities for healthy longevity and quality of life in all populations. CVH studies in youth showed that early loss of high CVH, even without clinically elevated risk levels, conveys long‐lasting adverse consequences for cardiovascular ⁶⁵ and overall physical, ⁵⁷ cognitive, ⁴⁷ , ⁴⁸ and mental health. ⁵⁰ , ⁷⁶ In contrast, maintenance of ideal/high CVH and CVH improvements benefit individuals across the lifespan and may have intergenerational effects. Maternal gestational CVH is strongly associated with offspring CVH in adolescence, emphasizing the need to support CVH during gestation, and even earlier, via the mother's preconception CVH. ⁵⁶

Intervention studies improved CVH with promising community‐engagement strategies. The FAITH! intervention in Black churches ⁷⁰ , ⁷¹ and the Strong Hearts, Healthy Communities study in rural, underserved areas ⁷⁴ resulted in improved CVH knowledge and metrics in disadvantaged groups. Similarly, although it did not satisfy our criteria for inclusion in this review, it is worth noting the SI! Program for both preschoolers and its recent iteration on secondary schools. Findings from this multicomponent program showed promising long‐term improvements in physical activity, healthy diet knowledge, attitudes, and habits among preschool‐aged children, ⁹⁴ but no significant improvements when the program was administered to adolescents in secondary schools. ⁹⁵ These findings highlight the importance of promoting CVH from young ages, before substantial CVH losses have taken place. Even individuals at high genetic risk for CVD (as indicated by a poor polygenic risk score) benefit in terms of CVD risks by maintaining or pursuing better CVH. Findings suggest that early interventions to maintain and improve CVH could mitigate genetic risks, ⁴⁸ , ⁶³ and potentially also benefit their offspring.

Future Research

The relevance of the CVH construct and the decade of research summarized in this review led the AHA to refine its definition in 2022 to enhance the usefulness and applicability of CVH in the decades to come. ⁹⁶ The publication of the AHA's Life's Essential 8 (LE8), ⁹⁶ is spurring new research further examining the implications of this construct in various settings. Evidence is already accumulating showing that LE8 may be an even more powerful tool than LS7 for CVD prevention. The expectation of improvement is due to: (1) greater granularity in quantifying each metric and the overall score, which enables a better characterization of CVH status of children, ⁹⁷ adults, ⁹⁸ and populations; (2) the addition of sleep duration as the eighth metric, and (3) the characterization of nicotine exposure inclusive of secondhand smoke and vaping. LE8 will particularly benefit 2 understudied areas: (1) childhood CVH, which is better defined in LE8 and (2) implications of more modest (and perhaps more readily attainable) improvements in CVH, better discriminated by LE8's more granular CVH scoring system. Notably, LS7 and LE8 scores are highly correlated (r=0.88, P<0.0001), ⁹⁹ such that research on LS7 is expected to remain highly applicable. Thus, the conclusions reached about key benefits and determinants of CVH in populations that were well‐studied during this initial decade of research are unlikely to differ when LE8 is substituted for LS7.

Key areas of research gaps and recommendations for future research on CVH that need deliberate, focused attention are summarized in Table 3. The research gaps documented are exacerbated among low‐ and middle‐income countries. The AHA, ¹⁰⁰ the National Heart, Lung, and Blood Institute, ¹⁰¹ and others published several scientific statements with practical strategies to promote equity in CVH. It is imperative that future studies intentionally apply these strategies to increase representation of underrepresented groups and aim to promote CVH equity. Future efforts should also focus on advancing CVH equity by addressing current challenges that contribute to cardiovascular disparities. Specific issues, such as the effects of environmental factors like endocrine‐disrupting chemicals, forest fires, and pollution, need to be considered, because they may worsen current CVH disparities.

Table 3.

Research Gaps and Recommendations for Future Research on Cardiovascular Health

Areas of knowledge gaps	Needs and recommendations for future research
Underrepresented populations	Increasing representation of diverse populations in research designs and cohorts:
	Children
	Pregnant and lactating women
	Racial and ethnic subgroups (eg, disaggregated Asian, Hispanic and Latino, Indigenous, and multiracial populations)
	Migrant and refugee populations
	Sexual minorities
	Populations with intersecting identities/cumulative disadvantages
	Low‐ and middle‐income countries
Environmental exposures	Influence of the natural environment (eg, air pollution, extreme weather, forest fires)
	Endocrine disrupting chemicals and other pollutants
	Interplay of various environmental components (ie, exposome framework)
Life course and mechanism	Identification of important CVH inflections or periods of change and vulnerability
	Investigation of CVH patterns and assessment throughout the life course, especially at younger ages, including in utero
	Improved understanding of the influence of SDOH and how it influences CVH levels across the life course
	Further elucidation of biological pathways mediating the influence of CVH across the life course with optimal health outcomes, from gestation
Implementation	Intervention strategies to equitably improve CVH for individuals and for diverse populations (eg, clinical guidelines, policies, individual lifestyle interventions, community interventions and engagement, pharmacotherapy)
	Development and deployment of digital health applications and online tools for CVH assessment, as well as digital and remote online tools that yield sustainable improvements in CVH in populations of all ages and diverse backgrounds
	Intervention strategies that promote modest CVH improvements
	Better understanding of long‐term outcomes and barriers to sustainability of intervention strategies in clinical and community settings
	Using CVH scoring to predict health outcomes and identify populations at risk before clinical thresholds are reached
	Standardization of routine CVH and SDOH assessment in clinical settings

CVH indicates cardiovascular health; and SDOH, social determinants of health.

The purpose of this systematic and narrative review was to systematically catalog and succinctly summarize the large body of literature investigating LS7 from 2010 to 2020. In alignment with this purpose, methodologic choices were made that limit applicability for other uses. First, we chose to focus on the first decade of LS7 research, which includes the studies that preceded and informed the new LE8 definition. Second, this review was not preregistered because we did have a complete list of outcomes specified before data extraction, which could introduce publication bias and overrepresentation of studies reporting significant associations. Third, consistent with the planned scope and diversity of studies included, we did not include a uniform assessment of evidence quality, and quality assessment was restricted to studies evaluating health outcomes, prevalence of CVH, and its predictors. Last, publication biases and overrepresentation of studies that reported significant associations cannot be excluded.

CONCLUSIONS

Higher levels of CVH powerfully predict low risk for CVD and other chronic diseases and indicate holistic benefits to individuals and populations. It is possible, and urgent, to promote improvements in CVH and prevent loss of CVH at all ages, starting early in childhood. This systematic summary and catalog of a decade of studies on the prevalence, predictors, interventions, outcomes, and mechanisms of CVH/LS7 aimed to contribute to the acceleration of significant and innovative work with AHA's new LE8. We call for the development and implementation of strategies that mitigate and eliminate CVH disparities and promote optimal CVH for all people.

Sources of Funding

Dr Aguayo was supported by the American Heart Association (AHA 17SFRN33660752) and the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health (5R01DK115937‐02) and is currently supported by the American Heart Association (CDA: 938767), and the National Institute of Environmental Health Sciences of the National Institutes of Health (NIEHS K12ESO33593). Dr Marma‐Perak is supported by the National Heart, Lung, and Blood Institute (NHLBI K23 HL145101). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the American Heart Association.

Disclosures

None.

Supporting information

Data S1–S4

Tables S1–S5

Figure S1