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 Table of Contents  
REVIEW ARTICLE
Year : 2017  |  Volume : 9  |  Issue : 6  |  Page : 150-153

Prevention and management of cardiovascular disease risk factors during childhood


Department of Pediatric, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, Abu Dhabi, UAE

Date of Web Publication8-Nov-2017

Correspondence Address:
Elhadi H Aburawi
Department of Pediatric, College of Medicine and Health Sciences, United Arab Emirates University, P. O. Box 17666, Al Ain, Abu Dhabi
UAE
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmbs.ijmbs_40_17

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  Abstract 


Coronary artery disease (CAD) or alternatively called atherosclerosis is the leading cause of death worldwide. There are multiple cardiovascular disease risk factors (CVDRFs), which are the precursors for CAD. A chronic inflammation prompted by cholesterol-rich lipoproteins and other noxious CVDRF is central in the pathogenesis of CAD. Endothelial dysfunction is the first step in the development of CAD. There are many theories in the development of the atherosclerotic process such as the hygiene theory, genetic susceptibility, and the endothelial injury. For the modification and management of CVDRF, the disturbances in lipid and glucose metabolism, hypertension, obesity, and smoking are the most important targets. The main aim of both primordial and primary preventions is to prevent the first cardiovascular event rather than preventing the further myocardial infarction. The prevention should be considered and started early in childhood and not after the first cardiac event. The primary healthcare physicians, obstetricians, neonatologists, and pediatricians need to work together on prevention of CAD early in life and as early as in fetal life.

Keywords: Cardiovascular disease risk factor, coronary artery disease, endothelial cell dysfunction, infection, inflammation


How to cite this article:
Aburawi EH. Prevention and management of cardiovascular disease risk factors during childhood. Ibnosina J Med Biomed Sci 2017;9:150-3

How to cite this URL:
Aburawi EH. Prevention and management of cardiovascular disease risk factors during childhood. Ibnosina J Med Biomed Sci [serial online] 2017 [cited 2019 Dec 6];9:150-3. Available from: http://www.ijmbs.org/text.asp?2017/9/6/150/217869




  Cardiovascular Disease Risk Factors Top


There are multiple cardiovascular disease risk factors (CVDRFs) that have been reported as precursors for atherosclerosis or coronary artery disease (CAD), which then progresses gradually throughout life. These include a family history of premature CAD, hyperlipidemia, diabetes mellitus, obesity, cigarette smoking, sedentary lifestyle, and hypertension. Other noxious CVDRFs are recurrent attacks of infection and inflammation, hyperhomocysteinemia, and stress.[1] Atherosclerosis is considered as a chronic inflammatory disease with an autoimmune element. These independent risk factors hasten or adjust recurrent infections or chronic inflammatory vascular courses that finally present as atherosclerotic plaque.[2],[3],[4]

There are many theories behind the development of CAD such as the hygiene theory, genetic susceptibility, and the endothelial injury following infection and inflammation. The endothelial injury and consequently dysfunction could be the result of CVDRF. The endothelial dysfunction is considered the first step for the atherosclerosis development. However, probably the most putative theory is the endothelial injury and the body's endeavor to heal, leading to loss of the coronary artery vascular tone and formation of atherosclerotic plaque. Eventually, the fibrous cap is formed, which is composed of extracellular lipid core and layers of smooth muscle and connective tissue matrix. Plaque rupture leads to dissemination of thrombogenic core of lipid and necrotic material to the circulation. This in turn will lead to platelet adherence, aggregation, and progressive narrowing of the lumen of the coronary artery, which can quickly progress to atherosclerosis.

A chronic inflammation triggered by cholesterol-rich lipoproteins and other noxious factors is central in the pathogenesis of CAD.[2],[3],[4] The biochemical markers for CVDRF, for example, increased high sensitive or ultrasensitive C-reactive protein in the absence of acute infection or inflammation, are considered to indicate a high risk of and probably rapidly advancing CAD, where there is a real need for aggressive preventive actions.[5] Commonly, viral and also bacterial infections in children, especially when they occur together with abnormal lipid profile, become proatherosclerotic and are associated with intima-media thickness of the coronary arteries of children.[6],[7] Minor induction of inflammatory reaction by influenza vaccination in children has led to abnormal brachial arterial function and low-density lipoprotein (LDL) oxidation, which persisted for up to at least 2 weeks.[8]

In childhood, the endothelial function gets worse after respiratory tract viral infections.[9] Furthermore, the endothelial dysfunction existed for up to 5 years after the onset of Kawasaki disease.[10] In general, exposure to CVDRF in childhood may induce preatherocslerotic changes as demonstrated by increased carotid intima-media thickness (IMT) two decades later, which also increases with the number of risk factors involved.[11] Furthermore, endothelial dysfunction in adulthood at mean ages of 27 and 33 years was associated with early childhood (<5 years of life) infection-related hospitalization.[12]


  Coronary Artery Disease Top


CAD is a chronic process, due to the decrease of antegrade coronary blood flow into the myocardium, which leads to ischemia. The myocardial ischemia results in an imbalance between myocardial oxygen supply and demand with accumulation of the metabolic products. This is caused by a combination of a narrowing of the lumen and abnormal vascular tone of the epicardial coronary arteries due to the endothelial dysfunction and atherosclerotic plaque. This could be symptomatic or asymptomatic, which may occur with or without exertion, depending on the severity and speed of its development. When the myocardial ischemia is severe and long enough together with the accumulation of metabolic products, myocardial infarction (MI) or ischemic heart disease develops. CAD is the most common type of heart disease, and it is the leading cause of death in the USA in men and women of all major ethnic group. It was alone estimated to cost over $100.00 billion/year (in the US for example) in the last few years.[13]

Early histological features of CAD are fatty streaks and intimal thickening, which were found in postmortem coronary arteries of the newborn babies and children.[6],[14] Intimal mesenchymal reaction to injury was reported by Haust and his colleagues.[15] The first step after the endothelial injury is the development of fatty streaks, which contain atherogenic lipoproteins and macrophage foam cells at the intima media, between the endothelium and internal elastic lamina.


  Management and Prevention of Cardiovascular Disease Risk Factors Top


The management and preventive measures of CVDRF should be started in fetal life and continued throughout childhood and all the way through adulthood. The roots of CAD go back to the intrauterine life, where the risk factors especially the genetic factors and maternal diet and smoking start to have their effects on the fetal coronary arteries with fatty streaks formation and endothelial dysfunction. The prevention of CVDRF development (primordial prevention) and the prevention of future CAD by active management of identified risk factors (primary prevention) are the main target to tackle the CVD and specially the CAD.[16],[17] It is too late to start managing these risk factors when the patients already have symptoms and signs or even after the treatment of MI. The prevention program of CAD may be the best to be done in collaboration with the obstetricians, neonatologists, pediatricians, and primary healthcare physicians. The recommendation from the expert panel documented three impending areas for attention: maternal obesity, maternal cessation of smoking, and choice of neonatal feeding method.[16],[17]

Dyslipidemia with or without obesity

Dyslipidemia means composite of high levels of “bad” or LDL cholesterol and low levels of “good” or high-density lipoprotein (HDL) cholesterol. It can be acquired genetically, for example, homozygous hypercholesterolemia and obesity, but also secondary to specific conditions such as obesity, diabetes mellitus, chronic renal disease, a history of Kawasaki disease with current coronary involvement, chronic inflammatory disease, nephrotic syndrome, postorthotopic heart transplant, and hypothyroidism. Familial hypercholesterolemia is defined as raised LDL cholesterol in the child in concurrence with the positive family history of high LDL cholesterol and/or CAD.[16],[17] Those with a positive family history of premature MI and sudden cardiac death in relatives <55 years for males and 65 years for females have a high CVDRF for CAD. The most common form of dyslipidemia in children is the combined one, which is seen commonly in obesity. Lipid assessment in overweight and obese children and especially in those with morbid obesity detects an important percentage of those with substantial lipid abnormalities.[16],[17]

The indication for pharmacologic treatment of dyslipidemia is elevated LDL cholesterol level of >250 mg/dL, triglyceride level of >500 mg/dL, and HDL cholesterol levels <40 mg/dL. The objective of LDL-lowering therapy (e.g., statin) in childhood and adolescence is to decrease the LDL cholesterol level to the <95th percentile (130 mg/dL). Statins have been shown to decrease LDL cholesterol in children and adolescents with markedly high LDL cholesterol. The other indications for treatment of dyslipidemia in children are in those with hypertension (blood pressure >99th percentile), current cigarette smokers and obesity (body mass index >95th percentile), plus dyslipidemia.[16],[17] Furthermore, those who are at high risk for accelerated atherosclerosis such as those with chronic kidney disease, Type 1 or Type 2 diabetes mellitus, and Kawasaki disease with coronary aneurysms and those with a positive family history of MI and sudden cardiac death should be considered for initiation of medication therapy. The most important modifiable CVDRFs for the development of atherosclerosis are disturbances in lipid and glucose metabolism, hypertension, obesity, and smoking. The United States Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents recommends healthy food, adequate physical exercise, and nonsmoking. Measurement of lipid profile of all children has raised critique. The recommendation states that a pathological measurement must be checked with a repeated test.[16],[17]

Inflammation and infection

Validation of reliable and reproducible indices ideally measured using noninvasive techniques for vascular risk assessment remains an important task in cardiovascular research in the young. Inflammation is central in the pathogenesis of atherosclerosis.[2],[3] Even in asymptomatic individuals, a decrease in coronary microvascular function is accompanied by a systemic inflammatory response, independent of CVDRF.[18]

Uses of anti-inflammatory agents in selected groups of high-risk individuals such as those with chronic inflammatory disease and diabetes should be encouraged. The interleukin-1 receptor antagonist (Anakinra) was found to be effective and promotes myocardial deformation recovery in patients with rheumatoid arthritis.[19]

Furthermore, given the evidence that the most common etiology of infections is viral in origin, antibiotics use are of less value in those high CVDRF groups. The use of antibiotics for the secondary prevention of CAD is not proven.[20]

Lifestyle and dietary intervention

The international data put forward that only 5%–50% of children and adolescents are meeting the current exercise guidelines.[21],[22],[23],[24],[25] The main causes of obesity in children and adolescents are decreased physical activity and reduced nutrition. According to the exercise guidelines, the energy intake in obese children is often greater than in healthy weight children.[26],[27] Lifestyle is important to be modified and to be started early in childhood both at schools and at home. Physical exertion does decrease overweight and improve endothelial function due to an increased blood flow and shear rate during the exercise.[16],[17] In the strip study, the dietary intervention started in infancy, which was continued to early adulthood,[28] led to lowered LDL cholesterol and improved high blood pressure, plus insulin sensitivity, and diminished clustering of CVDRF. The dietary intervention was in the form of replacing saturated fat with unsaturated fat and the increases use of vegetables, fruits, and whole grain products and a low intake of salt. In another study, 2-year weight loss diets induced a significant regression of measurable carotid vessel wall volume.[29] The effect was similar in low-fat, Mediterranean, or low-carbohydrate strategies and appears to be mediated mainly by the weight loss–induced decline in blood pressure.[29] Individuals with a history of coarctation of aorta (CoA) demonstrate excess morbidity and premature mortality associated with hypertension and CAD.[30] Intrinsic vascular abnormalities might contribute to the risk for premature CAD, independent of hypertension. Elevated blood pressure should be treated medically.[30]

According to the Expert Panel, the recommendation for routine blood pressure measurements should be started after 3 years of the age.[16],[17]

Given the multifactorial etiology of the arterial endothelial dysfunction, and its implications in both atherosclerosis and the regulation of coronary flow, strategies aimed at decreasing the burden of CVDRF in childhood should be considered. Factors to be paid attention to are family history of heart events in the relatives, overweight, serum lipid concentrations, blood glucose levels, and blood pressure.


  Recommendation Top


The recommendation is to encourage and pursue screening programs for more treatable CVDRF including hypertension, diabetes mellitus, and hyperlipidemia especially familial hypercholesterolemia, which should be implemented as early as 3 years of age. Preventive sequence of measures are immediate termination of smoking and having free smoking and pollution environment, and lifestyle modifications including healthy diet and organized physical activity in schools and at home. Multidisciplinary approach teams and specialized clinics need to be started for treating CVDRF, for example, obesity, hypertension, and diabetes mellitus. Early diagnosis and modification and treatment of the CVDRF over long term may eradicate or at least delay CAD. These measures should be implemented in each country at its own national level according to the resource availability.


  Conclusion Top


CAD is a disease that starts early in childhood and its roots go back to the intrauterine life. The CVDRF especially the genetic ones and maternal diet start to have their effects at the intrauterine life with the formation of fatty streaks and intimal thickening in the coronary arteries. It is too late to start managing and preventing these risk factors when the patients already have symptoms and signs or been diagnosed and treated for MI. The primordial and primary preventions should be the main aim to prevent the first cardiovascular event rather than preventing the recurrent and future MIs. The obstetricians, neonatologists, and primary healthcare physicians need to work together on the prevention of CAD early in life during antenatal care visits, neonatal period, and as early as 3 years of age.

Disclosures

Single author article.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

Ethical approval

Not applicable.



 
  References Top

1.
Dahlström S, Viikari J, Akerblom HK, Solakivi-Jaakkola T, Uhari M, Dahl M, et al. Atherosclerosis precursors in Finnish children and adolescents. II. Height, weight, body mass index, and skinfolds, and their correlation to metabolic variables. Acta Paediatr Scand Suppl 1985;318:65-78.  Back to cited text no. 1
    
2.
Singh RB, Mengi SA, Xu YJ, Arneja AS, Dhalla NS. Pathogenesis of atherosclerosis: A multifactorial process. Exp Clin Cardiol 2002;7:40-53.  Back to cited text no. 2
[PUBMED]    
3.
Farmer JA, Torre-Amione G. Atherosclerosis and inflammation. Curr Atheroscler Rep 2002;4:92-8.  Back to cited text no. 3
[PUBMED]    
4.
Adelmann GA. Cardiology Essentials in Clinical Practice. Springer Dordrecht Heidelberg London, New York, British Liberary Cataloguing in Publishing Data Library of Congress Control Number: 2010932881: Springer-Verlag London Limited; 2011. p. XVI, 365.  Back to cited text no. 4
    
5.
Aburawi EH, Liuba P, Berg A, Pesonen E. A transthoracic Doppler echocardiography study of C-reactive protein and coronary microcirculation in children after open heart surgery. Cardiol Young 2007;17:472-7.  Back to cited text no. 5
[PUBMED]    
6.
Pesonen E, Paakkari I, Rapola J. Infection-associated intimal thickening in the coronary arteries of children. Atherosclerosis 1999;142:425-9.  Back to cited text no. 6
[PUBMED]    
7.
Liuba P, Persson J, Luoma J, Ylä-Herttuala S, Pesonen E. Acute infections in children are accompanied by oxidative modification of LDL and decrease of HDL cholesterol, and are followed by thickening of carotid intima-media. Eur Heart J 2003;24:515-21.  Back to cited text no. 7
    
8.
Liuba P, Aburawi EH, Pesonen E, Andersson S, Truedsson L, Ylä-Herttuala S, et al. Residual adverse changes in arterial endothelial function and LDL oxidation after a mild systemic inflammation induced by influenza vaccination. Ann Med 2007;39:392-9.  Back to cited text no. 8
    
9.
Aburawi E, Liuba P, Pesonen E, Ylä-Herttuala S, Sjöblad S. Acute respiratory viral infections aggravate arterial endothelial dysfunction in children with type 1 diabetes. Diabetes Care 2004;27:2733-5.  Back to cited text no. 9
    
10.
Ishikawa T, Iwashima S. Endothelial dysfunction in children within 5 years after onset of Kawasaki disease. J Pediatr 2013;163:1117-21.  Back to cited text no. 10
[PUBMED]    
11.
Raitakari OT, Juonala M, Kähönen M, Taittonen L, Laitinen T, Mäki-Torkko N, et al. Cardiovascular risk factors in childhood and carotid artery intima-media thickness in adulthood: The Cardiovascular Risk in Young Finns Study. JAMA 2003;290:2277-83.  Back to cited text no. 11
    
12.
Burgner DP, Sabin MA, Magnussen CG, Cheung M, Sun C, Kähönen M, et al. Early childhood hospitalisation with infection and subclinical atherosclerosis in adulthood: The Cardiovascular Risk in Young Finns Study. Atherosclerosis 2015;239:496-502.  Back to cited text no. 12
    
13.
Kochanek KD, Murphy SL, Xu J, Tejada-Vera B. Division of Vital Statistics. Deaths: Final Data for 2014. Vol. 65. National Vital Statistics Reports; 2016. Available from: https://www.cdc.gov/nchs/data/nvsr/nvsr65/nvsr65_04.pdf. [Last accessed on 2017 Aug 16].  Back to cited text no. 13
    
14.
Rapola J, Pesonen E. Coronary artery changes in newborn babies. A histological and electron microscopical study. Acta Pathol Microbiol Scand A 1977;85:286-96.  Back to cited text no. 14
[PUBMED]    
15.
Haust MD. Reaction patterns of intimal mesenchyme to injury, and repair in atherosclerosis. Adv Exp Med Biol 1974;43:35-57.  Back to cited text no. 15
[PUBMED]    
16.
Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents; National Heart, Lung, and Blood Institute. Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: Summary report. Pediatrics 2011;128 Suppl 5:S213-56.  Back to cited text no. 16
[PUBMED]    
17.
LaBresh KA, Lazorick S, Ariza AJ, Furberg RD, Whetstone L, Hobbs C, et al. Implementation of the NHLBI integrated guidelines for cardiovascular health and risk reduction in children and adolescents: Rationale and study design for young hearts, strong starts, a cluster-randomized trial targeting body mass index, blood pressure, and tobacco. Contemp Clin Trials 2014;37:98-105.  Back to cited text no. 17
[PUBMED]    
18.
Vaccarino V, Khan D, Votaw J, Faber T, Veledar E, Jones DP, et al. Inflammation is related to coronary flow reserve detected by positron emission tomography in asymptomatic male twins. J Am Coll Cardiol 2011;57:1271-9.  Back to cited text no. 18
[PUBMED]    
19.
Ikonomidis I, Tzortzis S, Lekakis J, Paraskevaidis I, Andreadou I, Nikolaou M, et al. Lowering interleukin-1 activity with anakinra improves myocardial deformation in rheumatoid arthritis. Heart 2009;95:1502-7.  Back to cited text no. 19
[PUBMED]    
20.
Grayston JT. Secondary prevention antibiotic treatment trials for coronary artery disease. Circulation 2000;102:1742-3.  Back to cited text no. 20
[PUBMED]    
21.
Schranz N, Olds T, Cliff D, Davern M, Engelen L, Giles-Corti B, et al. Results from Australia's 2014 report card on physical activity for children and youth. J Phys Act Health 2014;11 Suppl 1:S21-5.  Back to cited text no. 21
[PUBMED]    
22.
Gray CE, Barnes JD, Cowie Bonne J, Cameron C, Chaput JP, Faulkner G, et al. Results from Canada's 2014 report card on physical activity for children and youth. J Phys Act Health 2014;11 Suppl 1:S26-32.  Back to cited text no. 22
[PUBMED]    
23.
Standage M, Wilkie HJ, Jago R, Foster C, Goad MA, Cumming SP. Results from England's 2014 report card on physical activity for children and youth. J Phys Act Health 2014;11 Suppl 1:S45-50.  Back to cited text no. 23
[PUBMED]    
24.
Liukkonen J, Jaakkola T, Kokko S, Gråstén A, Yli-Piipari S, Koski P, et al. Results from Finland's 2014 report card on physical activity for children and youth. J Phys Act Health 2014;11 Suppl 1:S51-7.  Back to cited text no. 24
    
25.
Dentro KN, Beals K, Crouter SE, Eisenmann JC, McKenzie TL, Pate RR, et al. Results from the United states' 2014 report card on physical activity for children and youth. J Phys Act Health 2014;11 Suppl 1:S105-12.  Back to cited text no. 25
[PUBMED]    
26.
Hills AP, Andersen LB, Byrne NM. Physical activity and obesity in children. Br J Sports Med 2011;45:866-70.  Back to cited text no. 26
[PUBMED]    
27.
Skinner AC, Steiner MJ, Perrin EM. Self-reported energy intake by age in overweight and healthy-weight children in NHANES, 2001-2008. Pediatrics 2012;130:e936-42.  Back to cited text no. 27
[PUBMED]    
28.
Available from: http://www.stripstudy.utu.fi. [Last accessed on 2017 Aug 16].  Back to cited text no. 28
    
29.
Shai I, Spence JD, Schwarzfuchs D, Henkin Y, Parraga G, Rudich A, et al. Dietary intervention to reverse carotid atherosclerosis. Circulation 2010;121:1200-8.  Back to cited text no. 29
[PUBMED]    
30.
Bondy CA. Aortic coarctation and coronary artery disease: The XY factor. Circulation 2012;126:5-7.  Back to cited text no. 30
[PUBMED]    




 

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