Cardiovascular diseases (CVDs) are comprised of major clinical heart and circulatory conditions deserving of clinical attention, including but not limited to hypertension, stroke, myocardial infarction, congenital heart disease, rhythm disorders, atherosclerosis, coronary heart disease, congestive heart failure, valvular disease, venous disease, and peripheral arterial disease (Stewart, Manmathan, & Wilkinson, 2017), all of which have implications for economic costs, procedures, and quality of care. The conditions that fall under the umbrella of CVDs produce immense health and economic burdens in the United States and abroad. In 2011, a policy statement was released by the American Heart Association that claimed cardiovascular disease was the leading cause of death in the United States and was responsible for 17% of national health expenditures (Heidenreich et al., 2011). They noted as the general population ages and life expectancy increases, these costs were expected to increase substantially. Despite the fact that from 2001 to 2014 some improvements have been noted in the United States, such as heart failure (HF) admissions and in-hospital mortality rates significantly declining (Akintoye et al., 2017), since 2000, medical costs of CVDs have grown at an average annual rate of 6%. By .2030, 40.5% of the US population is projected to have some form of CVD (Heidenreich et al., 2011).
Along with increases in prevalence comes increases in socioeconomic burden (Carter, Schofield, & Shrestha, 2019). Based on current estimates, between 2010 and 2030, direct medical costs of CVD are projected to triple, from $273 billion to $818 billion, while indirect costs (due to lost productivity) are estimated to increase 61%, from $172 billion in 2010 to $276 billion in 2030 (Heidenreich et al., 2011). As of 2011, US medical expenditures were the highest in the world, increasing beyond 15% of Gross Domestic Product. Since that time, extensive research has demonstrated that we are on pace to meet or exceed these expectations, remaining stable for those aged 18 to 44, but increasing for everyone over the age of 45, as the average annual direct and indirect cost of CVD and stroke in the United States was an estimated $351.2 billion in 2014 to 2015 (Benjamin et al., 2019; Fryar et al., 2017). From 2013 to 2016, the prevalence of CVD in adults over the age of 20 was 48% overall, with increases noted with age. In 2015 alone, CVD was responsible for nearly 1 in 3 of all deaths worldwide (Roth et al., 2015). In the UK, 34% of deaths were accounted for by CVD, th ough approximately 40% of deaths in the European Union were due to CVD (Stewart et al., 2017). With over 121 million cases in 2016, about 18 million deaths were attributed to CVD globally, which marked a substantial increase of nearly 15% when compared to 10 years prior (Benjamin et al., 2019).
The purpose of this chapter will be to underline the well-known and lesser-known prevalence estimates and risks that contribute to CVD development based on the current state of research to date in order to paint an accurate picture of the world’s rising numbers and the challenges ahead. It is well known that risk factors such as family history, diabetes, obesity, smoking, alcohol use, substance use, and physical inactivity are responsible for a significant proportion of the overall cardiovascular risk; however, a number of other risk factors such as age, gender, race and ethnicity, mental illness, and socioeconomic status (SES) possess a bi-directional relationship with CVDs, such that they are both influenced by and contribute to one another. It should be noted that in talking about prevalence and risk factors, it can be difficult to disentangle information in order for it to be presented with clear, linear, or singular causal pathways. It is simply a fact that too much comorbidity (i.e., coexisting physical and/or mental health problems) and intersectionality (i.e., age, gender, race, ethnicity, socioeconomic status, etc.) exist that it becomes nearly impossible to discuss any disorder or risk factor in a vacuum, which is often a problem in and of itself, as this issue alone can complicate disease management (Chen, Thomas, Sadatsafavi, & FitzGerald, 2015). As such, in describing what is currently known about the risks and the figures, there will be a great deal of overlap; however, a concerted effort will be made to try and maintain some semblance of structure.
Lifespan
CVDs affect people across the lifespan, with each developmental period experiencing its own set of unique problems. From childbirth to elder years, CVD prevalence, risk, and symptom expression can change dramatically. Much of this can be accounted for by genetics, hormonal shifts, environment, lifestyle choices, or merely normal age-related deterioration, and each has their own set of consequences for the nature and course of how diseases progress (e.g., Webster, Shu-Ching Yan, & Marsden, 2013). Regardless of the epigenetic determinants of cardiovascular health, having a sense of what problems appear in target populations is necessary in assisting the process of identification, assessment, treatment, and growth.
Infancy
It is estimated that more than 2.4 million children and adults are living with a congenital heart disease (CHD) in the United States, with new cases occurring in as many as 1% of total live births annually (Dray & Marelli, 2015; Gilboa et al., 2016). CHDs are present at birth and involve the heart or major associated blood vessels, which can include a number of chronic conditions, with very different phenotypes, prevalence, risk factors, and outcomes. CHD is a significant contributor to birth-defect—related morbidity, mortality, and health care costs in early life and later in adolescence and adulthood (Jenkins et al., 2019). Obese women are thought to be at high risk of giving birth to a child with a CHD (Zhu, Chen, Feng, Yu, & Mo, 2018), which is among the most common birth defects in newborns worldwide, accounting for nearly one-third of all congenital abnormalities, with estimates varying between studies from 1.9 to 9.3 per 1,000 live births globally (Van Der Linde et al., 2011) and 1 per every 110 (Jenkins et al., 2019) in the US, marking a significant increase over the past 80 years (10% every 5 years between 1970 and 2017; Liu, Tian, Liu, Nigatu, & Wang, 2019). Despite this exponential growth, it is postulated that over 90% of this increase is probably due to increased detection of milder lesions through the availability of better technology, which is especially emblematic of developed countries with higher incomes and better access to health care (Liu et al., 2019).
These defects not only produce large numbers of adults with congenital diseases (Hoffman, Kaplan, & Liberthson, 2004), but are believed to also contribute to onset of developmental delays by school age, necessitating additional educational resources and potential mental health support for these children (Majnemer et al., 2009). These children are also linked to having greater risk of attentional, behavioral, conduct-related, impulse control, and autism spectrum-related issues in childhood and mood, anxiety, and substance use disorders in later adulthood, with as many as 1 in 3 adults being diagnosed with a mental illness (Khanna et al., 2019). Several genetic disorders present at birth are also associated with both CHDs and mental illness, such as schizophrenia (Bassett & Chow, 1999; Schneider et al., 2014). The risk of developing a mental illness increases as the number of corrective procedures increase beyond two, up to 4.5-fold (Khanna et al., 2019).
Other birth defects such as down syndrome have also been implicated in the development of cardiovascular illness; however, advances in early detection and surgical techniques have prolonged the lives of those with trisomy 21 and similar conditions (Versacci, Di Carlo, Digilio, & Marino, 2018). Considerably higher or lower birth weight has been associated with diabetes, coronary heart disease, and hypertension later in life (Huang et al., 2007) . Interestingly, the long-term risk of these problems can apply to the health outcomes of both the child and the mother (see Plows, Stanley. Baker, Reynolds, & Vickers, 2018 for a review). One consequence of obesity during pregnancy in a meta-analysis of 33 studies spanning from 1980 to 2017 has been increased risk of fetal congenital heart defects, as well as the onset gestational diabetes. This problem in particular affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic; some consequences include increased risk of maternal cardiovascular disease, type 2 diabetes, and macrosomia and birth complications in the infant (Plows et al., 2018).
A relationship has been established between birth weight and later metabolic syndrome in a well-nourished Western population of fullterm newborns, with higher and lower birth weights (significantly higher or lower than 7.7 lbs) suggesting the highest risk (Andersson & Vasan, 2018). Among mothers who smoke during pregnancy, these effects have been magnified (Huang et al., 2007). In general, smokers comprise over 15% of the global population with tobacco use remaining a leading cause of preventable death in the United States and globally, accounting for an estimated 7.1 million deaths worldwide in 2016, especially among those of lower SES or with mental illness (World Health Organization, 2017). Meta analytic reports suggest that the current prevalence among pregnant women is somewhere between 3.6% and 7.0% (McNeill, Brose, Calder, Bauld, & Robson, 2020). Though these figures mark a decrease in recent years of the prevalence of pregnant smokers, there has been a steady rise in those who vape instead; however, a 2018 report by the National Academy of Sciences, Engineering and Medicine (NASEM) concluded that there was no available evidence concerning whether or not vaping affects pregnancy outcomes and whether there is sufficient evidence as to whether or not maternal vaping affects fetal development (Fairchild, Holyfield, &Byington, 2018). Despite the dearth of available data, the issue deserves careful monitoring as preliminary studies have shown that nicotine use of any kind during pregnancy alters metabolic markers in mice and their offspring (Li et al., 2020).This was supposed to appear earlier along with the information on birth weight.
Children & Adolescence
Many of the risk factors for heart disease have recently been shown to develop during childhood, such as the buildup of arterial plaques, left ventricular hypertrophy, and hypertension (Gartlehner et al., 2020). In a meta-analytic review of 63 studies comprised of 49,220 children, many revealed systolic and diastolic blood pressure, left ventricular mass as well as blood lipids, total cholesterol and triglycerides, fasting insulin, and insulin resistance were higher in overweight and in obese children than in children of normal weight (Friedemann et al., 2012). Obesity (body mass index >30) among children and adolescents is at an all-time high. In fact, since 1985, obesity prevalence has been 8.7 times greater in children and 38.1 times greater for adolescents, and they are still not meeting ideal levels for physical activity (60 minutes per day; Daniels, Pratt, & 1 layman. 2011), sufficient fruit and vegetable intake, body mass index (BMI), and blood glucose (Benjamin, 2019). As it stands, obesity in childhood and adolescence has become a major public health problem to say the least.
In 2010 alone, just under 43 million children younger than five years were overweight (Friedemann et al., 2012). Cumulatively over the last 30 years, the prevalence of obesity in children and adolescents has more than tripled to their current levels (18.5% of children ages 2 to 19 in the US; Fryar, Carroll, & Ogden, 2018) leading to an increase in cardiovascular risk factors including type 2 diabetes, hypertension (at doubled or tripled the rates of normal weight children; Friedemann et al., 2012), dyslipidemia, hyperlipidemia, increased fasting insulin concentration, inflammation, metabolic syndrome, sleep apnea, left ventricular hypertrophy, arterial stiffness, coronary heart disease, and atherosclerotic cardiovascular disease (as early as age 9, with increased risk among those with obesity; Friedemann et al., 2012), along with up to a 4 times greater likelihood of obesity persisting into adulthood (Fobian, Elliott, & Louie, 2018). One systematic review found that childhood obesity is significantly and positively associated with adult systolic blood pressure, diastolic blood pressure, and triglycerides and significantly and negatively associated with adult high-density lipoproteins (HDL) that actually help lower risk of heart attack and stroke (Umer et al., 2017).
The increasing prevalence of obesity and higher rates of type 2 diabetes in children and adolescents are of serious concern, with the prevalence of diabetes mellitus estimated to be 4.1 per 1,000 among 12- to 19-yearolds (with up to a 10-fold increase in some areas; Fobian, Elliot, & Louie, 2018). Some research has demonstrated that 70—75% of children in the 90th percentile of lipid levels and who are between the ages of 5 and 18 years of age will likely have elevated lipid levels persist into adulthood, necessitating a greater need for screening and tracking, especially among those who are obese (Daniels et al., 2011). Obesity has also been linked to another correlate of CVD, body dissatisfaction, via lower self-esteem and depression (Cruz-Sáez, Pascual, Wlodarczyk, & Echeburúa, 2020); however, in terms of primary pathways to CVD, one of the strongest predictors of hypertension in young adults is obesity in childhood and adolescence (Andersson & Vasan, 2018), as reflected in biomarkers such as interlukin-6 and C-reactive protein (Fobian et al., 2018). Most notably, a population-based study estimated that 70% of obese children and adolescents between the ages of 5 to 17 have at least one risk factor for CVD (Freedman, Mei, Srinivasan, Berenson, & Dietz, 2007). Ther...
