Author + information
- Stephen R. Daniels, MD, PhD⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Stephen R. Daniels, University of Colorado School of Medicine and Children's Hospital Colorado, 13123 East 16th Avenue, B065, Aurora, Colorado 80045
Hypertension has long been recognized as an important risk factor for adverse cardiovascular disease outcomes, including cerebrovascular disease and myocardial infarction (1). Obesity has been recognized as an important determinant of elevated blood pressure (2). However, the vascular changes that are associated with obesity and hypertension and whether these are different across the age span have not been as well understood.
The arterial system has multiple functions, including the transportation of blood to vital tissues and organs and the conversion of highly pulsatile flow emanating from the heart to more continuous flow at the periphery. There are complex interrelationships between cardiac output and systemic vascular resistance. The mean arterial pressure represents the integrated mean of the pulsatile arterial waveform and represents the interaction between cardiac output and systemic vascular resistance. There are also important age-related changes in the arterial system (3,4). In children, the pulsatile flow is largely dampened by the central arteries, including the aorta and its main branches. In children, the aorta contains a predominance of elastin compared with collagen. However, with increasing age, the arterial system may change its composition with the addition of more collagen and may become stiffer. In Western populations, it has been demonstrated that blood pressure increases with age (5). This has been thought to be due to increasing vascular stiffness (6).
Research has led to a better understanding of age-related changes in the cardiovascular system and the relative roles of obesity, blood pressure elevation, and other factors in those changes. In adolescents, systolic hypertension associated with increased cardiac output is most common. In early to middle adulthood, systolic and diastolic blood pressure may both increase. This is a result of increasing vascular stiffness, systemic vascular resistance, and increased pulse wave velocity (3). After age 50, diastolic blood pressure tends to decrease, and pulse pressure widens as a result of even stiffer central arteries. This then results in the isolated systolic hypertension seen in the elderly (4).
The prevalence of obesity has increased dramatically in children and adolescents over the past 3 decades (7). In adults, the strong relationship between obesity and hypertension is quite clear (2). Similar relationships have also been demonstrated in young subjects (8). Although the mechanisms of obesity-associated hypertension are not understood completely, increased circulating volume and increased cardiac output have been shown to be important in obesity-related hypertension (8,9). In the early stages of hypertension associated with obesity, peripheral vascular resistance may be normal or only slightly elevated. A variety of factors, including insulin resistance, sympathetic nervous system activity, inflammation, the renin-angiotensin-aldosterone system, and structural changes in the kidney and cardiovascular system may all play interrelated roles in hypertension associated with obesity (9,10).
Elevated blood pressure itself may play an important role in vascular changes over time. Fracturing and disarray of elastin may occur in response to elevated arterial pressure and result in greater deposition of collagen and calcium, and a stiffer arterial system. Cytokines, inflammation, and oxidative metabolites associated with obesity may result in endothelial dysfunction and contribute to this arterial pathophysiology. These changes result in a vicious cycle in which obesity and elevated blood pressure, along with other factors, result in changes in the vascular system that in turn promote arterial stiffening and further elevation of blood pressure.
These changes in the vascular system may also result in adverse outcomes related to the heart. In young patients, obesity and hypertension are associated with eccentric left ventricular hypertrophy due to increased circulating volume (11). Over time, the changes in the arterial system, including increased systemic vascular resistance, result in the development of concentric left ventricular hypertrophy. Concentric hypertrophy is associated with a substantial increase in risk for subsequent adverse cardiovascular endpoints in adults (12).
These complex physiologic and pathophysiologic relationships make the determination of vascular health more difficult, especially in children and adolescents. In this issue of the Journal, Charakida et al. (13) report on the results from the ALSPAC (Avon Longitudinal Study of Parents and Children). They evaluated children age 10 to 11 years who had been followed since birth and found that overweight and obese children had higher heart rates and systolic blood pressures compared with children of normal weight. They also found that obese children had greater brachial artery diameter, as well as greater resting and hyperemic blood flow and lower arterial stiffness, compared with children of normal weight. These vascular findings may at first seem reassuring or even favorable. However, the combination of increased cardiac output, a higher heart rate, and higher blood pressure may be more ominous for future findings in the cardiovascular system in these children. The vascular system appears to be adapting to the early obesity-related hemodynamic changes. However, in the context of the anticipated large number of aortic and vascular expansions and stretching expected over a lifetime, the known relationships of these hemodynamic factors to vascular structural and functional changes, and the concomitant changes in insulin resistance, inflammation, and other vasoactive factors associated with obesity, these results suggest that these young subjects are on a path toward increasing vascular stiffness, increasing blood pressure, and concentric left ventricular hypertrophy as they grow into adulthood.
The findings of Charakida et al. (13) serve to emphasize the imperative to reduce the risk for cardiovascular disease early in life. This can best be accomplished by the prevention of obesity and hypertension. However, for those children and adolescents with obesity and elevated blood pressure, interventions are needed to improve the percentile of body mass index and blood pressure to avoid the longer-term risk for cerebrovascular disease and myocardial infarction.
Dr. Daniels has reported that the has no relationships relevant to the contents of this paper to disclose.
↵⁎ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
- American College of Cardiology Foundation
- Franklin S.S.,
- Gustin W. IV.,
- Wong N.D.,
- et al.
- Guo F.,
- He D.,
- Zhang W.,
- Walton R.G.
- Daniels S.R.,
- Loggie J.M.,
- Khoury P.,
- Kimball T.R.
- Bluemke D.A.,
- Kronmal R.A.,
- Lima J.A.,
- et al.
- Charakida M.,
- Jones A.,
- Falaschetti E.,
- et al.