Keywords

Introduction

Hypertension affects one in three adults in the USA. There is usually a slow progression of elevated blood pressure (BP) beyond what is optimal (<115/75; Lewington 2002) to hypertensive (>140/90) over time. The ultimate determination of a patient as hypertensive by the observant health-care professional (or patient) may take time to recognize as the sustained measurements that meet the criteria for hypertension are documented. The concept of BP as progression through optimal levels to prehypertensive to hypertensive may be instructive and illustrative of the cardiovascular (CV) risk factors and their influence on the pediatric population through young adulthood ages18–25 years old and thereafter. What happens to the adult exposed to years of hypertension or prehypertension are likely a cumulative effect of the impact on the vasculature and the target organ exposure to this potentially unrestrained hemodynamic insult throughout one’s life and not just as someone has an increased risk for CV disease at ages greater than 50 or 60. When we do not engage in studying the goals of BP control in adolescents , we then are limited in our ability to modify what this disease may do to those who age beyond this.

However, we do know that prehypertension unabated leads to hypertension. The overall prevalence of prehypertension (systolic BP of 120 to 139 mm Hg and a diastolic BP of 80–89 mm Hg) in adults was 28% of the US population based on data from the National Health and Nutrition Examination Survey (NHANES) 2005–2006 (Ventura and Lavie 2011; Ostchega et al. 2008). There is a heightened risk of progression to hypertension depending on lower or higher degrees of prehypertension (Winegarden 2005). Among people with BP 130 to 139 mm Hg systolic and/or 85 to 89 mm Hg diastolic (stage 2 prehypertension), the risk of developing hypertension is threefold that of normotensives with BP <120/<80 mm Hg (Selassie et al. 2011). Indeed, the continuous relationship with risk throughout the normal range of usual BP, above 115/75 in those age > 40, is strongly and directly related to vascular and overall mortality (Lewington 2002). Data from the Framingham Heart Study suggest that individuals who are normotensives at 55 years of age have a 90% lifetime risk for developing hypertension (Chobanian et al. 2003; Vasan et al. 2002). This illustrates that the aging process leads to the inevitability of hypertension in the Western world. Because hypertension is a major risk factor for CV and cerebrovascular disease , two of the leading causes of death in adult Americans, responsible for 25% and 10% of all annual deaths respectfully, as well as an enormous cost to health care; improvements in education, accurate and accessible measurements, early detection, risk modification and pharmaceutical treatment, as well as health insurance coverage is essential to reducing the burdens of the most common health-care malady in the USA.

This chapter is devoted to the young adult ages 18–25. The study of BP in pediatric patients and their target organ injury has been described in preceding chapters. The singular question is at what age hypertension should be treated to prevent ensuing target organ injury and to what degree in this population? Is there futility or benefit of controlling hypertension to reduce the untoward injury of repeated stress to the vessels and organs at the end of the vasculature? These adults aged 18–25 are not represented significantly in many of the landmark BP trials (Table 1) which will be discussed later. Given the paucity of data on outcomes of hypertension in this age group, this chapter will not present specific information on treatment goals. However, it will attempt to address the compelling question of what point in time, or age, does the vasculature sustain injury and therefore necessitate treatment. Whether the elevated BP is permanent or transient in nature because of modification of lifestyle or pharmaceutical management, the evidence appears to be mounting that treatment is of benefit.

Table 1 Landmark hypertension trials
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Cardiovascular Death Trends and Age Groups

Cardiovascular disease in 2010 accounted for approximately 30% of all deaths in the USA, about 800,000 (Murphy et al. 2013). Deaths from CV and cerebrovascular disease can be avoided through improving lifestyle behaviors, treating modifiable risk factors, and addressing social determinants of health . From 2001 to 2010, the mortality data from the National Vital Statistics System were analyzed amid the improvements in risk factors and changes in cardiac treatments (CDC 2013; Ford and Capewell 2011). From 2001–2010, the avoidable death rate from heart disease, stroke, and hypertensive disease decreased 29% overall. The average annual percentage change (AAPC) shows that rates decreased sharply for 65–74-year-olds (AAPC = −5.1%), declined more gradually for 55–64-year-olds (AAPC = −3.3%), even more gradually for 35–54-year-olds (AAPC = −0.8%), and did not change at all in 0–34-year-olds. The death rate in 2010 for 0–34-year-olds was 1.9 per 100,000 population versus 401.5 per 100,000 in those aged 65–74 – compared to 640 per 100,000 in 2001 for the same age group (CDC 2013). This illustrates the benefits of improvements in risk factors and changes in CV treatments (Towfighi et al. 2011). However, as noted, there was no change in mortality for those between the ages of 0–34 years. Reasons for slower declines in death rates among younger populations may be attributable to greater benefits in modifying risks for older people, or in better health insurance coverage for those older than 65, or unavoidable losses in youth that could never be modified by any population-wide intervention.

Health Insurance and Blood Pressure Control

In adults aged 18–64 years, the percentage of those without health insurance increased from 17% in 2001 to 22% in 2010 but remained at <2% among adults aged >65 years because of Medicare coverage in this population (CDC 2013; US Census Bureau 2012). The increase in percentage of those without insurance among the younger age groups might have limited their access to preventive screenings and early treatment of high BP and other health-care interventions to reduce CV risk factors. Compared with persons aged ≥60 years, during 2009–2010, adults aged 18–39 years with high BP experienced lower rates of treatment (43.5% versus 83.6%) and control (28.6% versus 47.0%) (Table 2) and saw no improvements in those rates from 2001 to 2010 (Centers for Disease Control and Prevention 2013; US Census Bureau 2012). From 1997–2006, stroke hospitalization rates decreased among those 55–64 years old; stayed the same for those aged 45–54, and actually increased in those aged 35–44 years old (Towfighi et al. 2011). Those aged 18–25 were not analyzed. CDC data for young adults with hypertension ages 20–24 from 2011–2014 (Table 3) was 6.9% of males and 4.3% of females, and uncontrolled high BP was seen in 74.1% of the males and 55.5% of the females. These numbers for the same years 2011–2014 in those 65–74 years old demonstrated hypertension in 63.4% of the male and 64.3% of the female population with uncontrolled BP in 38.2% of males and 44.5% of females (National Center for Health Statistics 2016).

Table 2 Blood pressure treatment and control by age group , 2009–2010
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Table 3 Hypertension prevalence and control by age group and gender, 2011–2014
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The point is clear that BP increases as we age, and management improves similarly, and uncontrolled hypertension in young adults is far greater than in the elderly. In 2014 for those under 18 years old, 6.5% had no health insurance coverage (Table 4) compared to 18.1% uninsured in those aged 18–24 years old, 22.7% for those aged 25–34, 17.7% in those aged 35–44, and 11.8% for those aged 45–65 (National Center for Health Statistics 2016). The control of BP parallels insurance coverage. The Affordable Care Act (ACA) and its expanded coverage of young adults who can stay on their parents’ plans until they turn 26 likely influences not only coverage but also potentially treatment and control. An estimated 20 million uninsured people have gained health coverage, and a large number of these (an estimated around 2.3 million) are young adults ages 19–25 who gained health insurance between the enactment of the ACA in 2010 and the initial open enrollment period in October 2013 (Fig. 1) (Furman and Fielder 2015; Uberoi et al. 2016). Whether this will impact CV complications as these young people age will only be understood over time.

Table 4 Uninsured populations by age, 2014
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Fig. 1
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Adult uninsured rates, 1997–2014 (Source: Furman and Fielder 2015)

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Cardiovascular Risk Assessment

Reliable approaches to scoring 10-year and lifetime CV disease (CVD) risk for those >50 years old according to the presence or absence of specific risk factors have been developed. These risk factors were smoking history, body mass index (BMI), BP, cholesterol levels, and presence or absence of diabetes. Framingham Heart Study participants had risk factor assessments and were free of CVD (myocardial infarction, coronary insufficiency, angina, stroke, claudication) at 50 years of age. Those with optimal risks at age 50 had lifetime risks of atherosclerotic CVD to 95 years of age of 5.2% for men and 8.2% for women. This compared to participants with more adverse levels of single risk factors, who had lifetime risks of CVD events that were higher: 52.7% for men and 39.2% for women in the entire cohort studied (3564 men and 4362 women). The risk reduction in CVD events was 90% for men and 79% for women if participants did not have any risk factors at age 50 (Lloyd-Jones et al. 2006). Increasing BP and total cholesterol were associated with increased lifetime risk for CVD and shorter median survival, and the presence of diabetes at 50 years of age conferred the highest lifetime risk for CVD of any single risk factor. Median survival was substantially lower among diabetics compared with nondiabetics (Lloyd-Jones et al. 2006). Similarly, overweight status and obesity were associated with modest increases in lifetime risk and reductions in survival compared with normal weight status.

With respect to the continuum of disease, a 50-year-old patient does not flip a switch that has a sudden impact on one’s CVD risk and adverse outcomes. The influence of the perturbed milieu of metabolic and mechanical abnormalities is a steady continuum during one’s life that leads to detrimental effects on target organs, including the heart, brain, and kidneys. Clearly, behavioral habits and preventive efforts need to begin decades before the age of 50, since even the presence of a single major risk factor at that age is associated with substantially increased lifetime risk for CVD and markedly shorter survival (Lloyd-Jones et al. 2006). Patients who are 50 years of age or younger may have a very high lifetime CVD risk, which may be amenable to risk factor reduction but may be considered to be at low risk because they have a low 10-year CV risk (due to the weighting of age in 10-year risk equations) (Berger et al. 2010). Since the estimates for 10-year risk prevalence nationally for most men <50 years and most women <70 is <10%, it becomes difficult to capture the risk in those <30 years. This is illustrated in studies using the Framingham Risk Score (FRS) that classified all men <30 years as “low risk” by Adult Treatment Panel III definitions, despite a substantial risk factor burden (Berry et al. 2007; Ford et al. 2004). Therefore, the use of long-term (>30-year) risk assessment tools is necessary. Similarly necessary are recommendations for the institution of treatment prior to actual occurrence of clinical events. These shorter-term strategies have no effect on lowering short-term risk in younger patients and suboptimal effects on longer-term risk, since treatment introduced at some older age does not eliminate decades of exposure to high-risk factors. On the other hand, overweighting lifetime risk without studied outcomes beginning at an early age may potentially commit large numbers of individuals to lifelong drug therapy with unknown consequences (Cavanaugh-Hussey et al. 2008).

The 2013 American College of Cardiology/American Heart Association (ACC/AHA) guideline on the assessment of CV risk calculates the 10-year risk of heart disease or stroke and predicts risk in those with ages between 20 and 70. Extensive epidemiological, pathological, and basic science data indicate that the development of atherosclerosis , the precursor to atherosclerotic CV disease (ASCVD), occurs over decades and is related to long-term and cumulative exposure to causal, modifiable risk factors. In assessing for evidence of risk factors in young adults, individuals with extreme values for BP, particularly from secondary hypertension or familial hyperlipidemia, may be identified, and as a population data on risk prevalence and consequences may be studied for future benefit of lifestyle modification and or pharmaceutical treatment (Goff et al. 2014). The 2013 ACC/AHA guideline 6.2.2 recommendation 2 for long-term assessment of 30-year or lifetime ASCVD risk based on traditional risk factors may be considered in adults 20–59 years of age who are free from ASCVD and who are not at high short-term risk. The evidence here is weak, with very limited populations evaluated and only consensus opinion of experts, case studies, or standard of care. With respect to benefit of treatment versus risk for treatment, the usefulness/efficacy of lipid management is less well established (Goff et al. 2014). Also, evidence was not found regarding the utility of lifetime risk assessment for guiding pharmacologic therapy decisions, and the work group judged that long-term and lifetime risk information may be used more appropriately at that time to motivate therapeutic lifestyle change in younger individuals, and the choice of age 20 as the starting point for long-term risk assessment was used as a starting point for long-term risk assessment. Figure 2 illustrates their approach to these populations (Goff et al. 2014).

Fig. 2
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Implementation of ACC/AHA risk assessment work group recommendations. ACC: American College of Cardiology; AHA: American Heart Association; ASCVD: atherosclerotic cardiovascular disease (Source: Goff et al. 2014)

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Blood Pressure Goal

The US Preventive Screening Task Force (USPSTF) recommends annual screening of BP for adults aged 40 years or older for those who are at increased risk for high BP, those with prehypertension 130–139/85–89 mm Hg, overweight or obese, and African Americans. Adults aged 18–39 years with normal BP (<130/85) who do not have other risk factors should be rescreened every 3 to 5 years (Siu AL; US Preventive Services Task Force 2015). (Note: their use of the term normal BP is not the same as optimal [<115/75 mm Hg] referenced elsewhere in this chapter.) The USPSTF recommends screening for high BP in adults aged 18 years or older and gives it an A recommendation. (There is high certainty that the net benefit is substantial.) This means the available evidence usually includes consistent results from well-designed, well-conducted studies in representative primary care populations. These studies assess the effects of the preventive service on health outcomes. The conclusion is therefore unlikely to be strongly affected by the results of future studies.) Furthermore, obtaining measurements outside of the clinical setting for diagnostic confirmation before starting treatment is also recommended.

Once the diagnosis of hypertension has been made in a young adult aged 18–25, management, particularly in someone who has coronary and other atherosclerotic disease, would be similar to recommendations for other adults based on the 2011 AHA/ACC guidelines, because no distinction for age is made. In light of the SPRINT study , evidence for those aged >50 with SBP 130–180 mm Hg untreated or treated with antihypertensive medications and at increased risks of CV events was that an SBP of 120 mm Hg resulted in lower rates of fatal and nonfatal major CV events and death from any cause (The SPRINT Research Group 2015). However, the age group from 18–25 was not studied. Does this mean there should be another goal if those 18–25 years of age have coronary and other atherosclerotic disease? What is the goal for these young adults who could be possibly at increased risk for CV events? The recommendations from members of the Joint National Committee panel stated that there is insufficient evidence from good or fair quality randomized controlled trials (RCTs) to support in hypertensive persons younger than 60 years a specific systolic goal, or in those younger than 30 years a specific diastolic goal, so based upon expert opinion, the panel recommended a goal BP of less than 140/90 mm Hg for these groups (James et al. 2014). More specifically, for ages 18–29 years, the systolic BP goal is <140 mm Hg and diastolic BP goal is <90 mm Hg, and this is completely based on expert opinion due to the lack of clinical trial evidence in this age group. With the release of SPRINT, future consensus bodies may change recommendations for those age ≥50 at increased CV risk, but for those ages 18–25, the goal systolic BP is the same as for those 25–49. Given the difficulty of informing and controlling this population, this is likely a good starting point for control. Nonetheless, both systolic and diastolic BP goals should be studied and extended to those less than the age of 50. There were several studies in Table 1 that included participants that were ages 18–25. To our knowledge the data were not analyzed separately for this age group, and there were too few patients within this age range, particularly in the MDRD and AASK trials, to yield useful information in managing them.

Atherosclerosis in Young Adults

The ability to assess atherosclerotic disease in the young adult population is irrecoverably linked to series of autopsy studies, including some conducted on combat fatalities, and others from population-based studies. The coronary arteries of 200 soldiers with the average age of 22 years who were killed in the Korean War demonstrated some evidence of coronary arteriosclerotic disease in 77.3% (Enos et al. 1953). Two decades later during the Vietnam War, postmortem coronary angiography and dissection of the hearts from 105 US soldiers (mean age of 22 years, range 18–37 years) demonstrated that 45% had some evidence of atherosclerosis, although none had angiographic evidence of severe coronary narrowing (Strong and McGill 1962).

A community-wide evaluation of atherosclerosis was conducted in New Orleans in 1962 as part of the Bogalusa Heart Study , reviewing 548 necropsies. Data on CV risk factors were collected cross-sectionally beginning in 1973 on 14,000 people from birth until the age of 38, with periodic repeat assessments. Autopsies were performed after the death of a young person (most deaths were due to accidents or homicide) to evaluate for pathological atherosclerotic findings in coronary arteries and aorta (Berenson et al. 1998). Coronary arteriosclerosis was found in those as young as 10–19 years old, with increasing prevalence paralleling age; these lesions were noted at least 20 years of age earlier than in the combat victim autopsy study mentioned previously (Strong and McGill 1962). Crucially, the investigators were able to link pathologic findings to antemortem CV risk factors. Specific antemortem risk factors such as elevations in BMI, systolic BP, serum triglycerides, LDL cholesterol concentration, and cigarette smoking were significantly related to the extent of atherosclerotic lesions in young people and are in agreement with the findings in other studies. With respect to these studies on populations in the twentieth century, presumably with the incidence of obesity, diabetes, and hypertension more prevalent in the twenty-first century, we would expect more pathologic lesions. This illustrates the occurrence of vascular disease that occurs in young healthy adults and the need to consider risk factor reduction management in this population despite the lack of studies to reduce CV disease outcomes. The chapter in this text on Epidemiology of Cardiovascular Disease in Children reviews this concept as it pertains to the pediatric population as well as those risk factors in childhood that predict atherosclerosis in adulthood.

The landmark Pathobiological Determinants of Atherosclerosis in Youth Study (PDAY) (McGill et al. 2008) is important to mention as well. This study examined autopsies looking at coronary arteries and aortas, estimating the percentage of intimal surface involved by fatty streaks and atherosclerotic lesions in persons 15 through 34 years of age who died of external causes (accidents, homicides, and suicides). Labs for total and lipoprotein cholesterol, glycohemoglobin, and thiocyanate levels to indicate smoking were drawn to assess exposure to these risks factors. Wall thickness of small renal arteries was measured to estimate mean arterial BP (increased renal artery thickness indicated hypertension), and BMIs were determined postmortem for obesity assessment. There was a relationship among 15–34 years of age between CV risk factors and quantifiable vascular injury. PDAY results have confirmed previous observations that atherosclerosis begins in childhood and progresses into young adulthood and beyond. By the third decade, many young adults already have significant coronary atherosclerosis, which includes not only calcified plaques seen by radiography but also carotid intima-media thickness seen on noninvasive methods. Intervention in the fourth decade and after may be too late for optimal CVD prevention (McGill et al. 2008). The theoretical and plausible likelihood of vascular injury in youth persisting to adulthood unless modified by risk reduction begs the question, when will researchers study the effects of intervention during youth to reduce the composite CV injury studied in adults of age greater than 50 as in such studies as the SPRINT BP trial?

Fitness in Young Adulthood and Cardiovascular Disease

Health fitness in the form of cardiopulmonary fitness is an established lifestyle attribute that modifies CV disease. A population-based longitudinal cohort study of 18–30-year-olds was studied in the Coronary Artery Risk Development in Young Adults (CARDIA) study (Carnethon et al. 2003). Participants who completed the treadmill examination protocol at baseline were followed up over 15 years. The main outcome measure was incident type 2 diabetes, hypertension, and the metabolic syndrome. During the 15-year study, the rates of incident diabetes, hypertension, and metabolic syndrome were assessed. Those participants with fitness <20th percentile were 3–6-fold more likely to develop diabetes, hypertension, and the metabolic syndrome than participants with fitness > 60th percentile. Improved fitness over 7 years was associated with a reduced risk of developing diabetes and the metabolic syndrome (Carnethon et al. 2003). Poor fitness in young adults followed longitudinally is associated with the development of CVD risk factors with low fitness increasing hypertension by 21% and diabetes 28%. Fitness in young adults has CV benefits, and the lack thereof has consequences that extend for decades.

Young Adult Lifestyle Attributes that Lend Themeselves to Hypertension and Cardiovascular Disease

Data from the CDC 2011–2014 sheds light on several risk factors for CV disease and hypertension that could be modified by 18–25-year-olds to influence future outcomes. Males and females from 20 to 34 years old have a prevalence of obesity from 28.5% and 33.4%, respectively (National Center for Health Statistics 2016; Table 58). Among 12–19-year-olds obesity in both sexes was 20.5% of the population (National Center for Health Statistics 2016; Table 59). One can surmise that there is a steady rise in young adulthood and onward. In the ensuing decade from ages 35–44, they have a prevalence of obesity of 39%, and this changes little for males but goes up to 44.4% in females 55–65 years of age.

With respect to participation in both leisure-time aerobic and muscle-strengthening activities that meet the federal 2008 Physical Activity Guidelines for Americans among adults aged 18 and over, a recent analysis revealed for 18–24-year-olds, 31% met both these guidelines in 2014, but this figure declined to 25% for ages 25–44 years and continued to decrease for each decade thereafter (National Center for Health Statistics 2016; Table 57). Obesity and a sedentary lifestyle go hand-in-hand and tend to worsen as we age.

To reinforce the health-care coverage issue, which likely plays a role in awareness of health and management, in 2013–2014 for ages 19–25, there were 28.5% of young adults who did not have a usual source of health care (distinct from no health insurance coverage), and compared to those ages 6–17 years old who did not have usual sources of health care, they were about 4.4% (National Center for Health Statistics 2016; Tables 61 and 62). This is compared to those 25–44 years old where 22.8% did not have a usual source of health care, and from 45–54 years, it is 12.8%, and from 55–64, it is 8.6% (National Center for Health Statistics 2016; Table 61).

Smoking as a risk factor for CV events is a public health issue, and of note in 2013–2014, CDC data indicates that cigarette smoking in 18–24-year-olds was 18.5% for males and 14.8% for females and increased in 25–34-year-olds to 23.7% and 17.5% in males and females, respectively. This relationship between lower health insurance coverage (Table 4) for 25–34-year-olds may be telling. However, those over 25 years old had a usual source of health care greater than the 19–25-year-olds. Perhaps health-care personnel needs to be more vigilant in noting and modifying CV risk factors, or those in that age group need to be better informed of the risks of smoking. Smoking cessation in later decades decreases for each decade thereafter.

It appears when looking at obesity, physical activity, smoking, and hypertension, the tipping point to the development of good or bad habits or increased or decreased risk factors for CV disease occurs in adults in the 18–25-year age group. After this, physical activity typically diminishes, obesity skyrockets, smoking prevalence increases, and the prevalence of hypertension in the population increases, with control rates <50% of the population until we are 45–54 years old. To add further insult, health insurance and usual sources of health care is not as utilized or available for the young adult at this time in their life. Clearly the young adult does not have financial coverage or incentives to have CV risk assessed, screened, or managed. The psychology of this is likely related to the invincibility of youth as well as the distractions of moving into lifelong employment, careers, and their own relationships and families outside their childhood formative years. It would seem that for those 18–25 years old, a transition into adulthood with significant medical guidance would be warranted to avoid irreparable harm from a stroke, heart attack, or incessant atherosclerosis destined for a significant part of our population.

Summary

Recognizing lifetime risk at an early age should provoke policy makers and an informed electorate to better promote public interest in prevention, screening, studying and treatment of CVD especially in younger adults who have more years at risk to protect from CV harm when risk modification has more potential benefit. This information could potentially guide the allocation of resources to improve public health and preventive services for the leading cause of death in the USA. Discrepancies in health insurance coverage, uncontrolled high BP, lack of studies directed at this population, and lifestyle factors expose future 50-year-olds to CV risk and injury over time. The 2016 scientific statement from the American Heart Association, “Cardiovascular Health Promotion in Children: Challenges and Opportunities for 2020 and Beyond,” delivers this summation. The principles in their summary reflect the AHA’s new dynamic and proactive goal to promote CV health throughout the life course. “The primary focus is on adult CV health and disease prevention, but critical to achievement of this goal is maintenance of ideal CV health from birth through childhood to young adulthood and beyond” (Steinberger et al. 2016).

Cross-References