Skip to main content
Download PDF

Obesity, hypertension, and tobacco use associated with left ventricular remodeling and hypertrophy in South African women: Birth to Twenty Plus Cohort

BMC Cardiovascular Disorders volume 22, Article number: 403 (2022) Cite this article

Abstract

Background

Left ventricular hypertrophy (LVH) is a marker of increased risk in developing future life-threatening cardiovascular disease (CVD), however, it is unclear how CVD risk factors, such as obesity, blood pressure (BP), and tobacco use, are associated with left ventricular (LV) remodeling and LVH in urban African populations. Therefore, we aimed to identify the prevalence of LVH as well as the health factors associated with LV remodeling and LVH, within black South African adult women and their pre-pubescent children.

Methods

Black female adults (n = 123; age: 29–68 years) and their children (n = 64; age: 4–10; 55% female) were recruited from the Birth to Twenty Plus Cohort in Soweto, South Africa. Tobacco and alcohol use, physical activity, presence of diabetes mellitus, heart disease, and medication were self-reported. Height, weight, and blood pressure were measured in triplicate to determine the prevalence of obesity and hypertension respectively. Echocardiography was used to assess LV mass at end-diastole, based on linear measurements, and indexed to body surface area to determine LVH.

Results

Hypertension and obesity prevalences were 35.8% and 59.3% for adults and 45.3% and 6.3% for children. Self-reported tobacco use in adults was 22.8%. LVH prevalence was 35.8% in adults (75% eccentric: 25% concentric), and 6.3% in children. Concentric remodeling was observed in 15.4% of adults, however, concentric remodeling was only found in one child. In adults, obesity [OR: 2.54 (1.07–6.02; p = 0.02)] and hypertension [3.39 (1.08–10.62; p = 0.04)] significantly increased the odds of LVH, specifically eccentric LVH, while concentric LVH was associated with self-reported tobacco use [OR: 4.58 (1.18–17.73; p = 0.03)]. Although no logistic regression was run within children, of the four children LVH, three had elevated blood pressure and the child with normal blood pressure was overweight.

Conclusions

The association between obesity, hypertension, tobacco use, and LVH in adults, and the 6% prevalence of LVH in children, calls for stronger public health efforts to control risk factors and monitor children who are at risk.

Peer Review reports

Background

Despite medical advances, cardiovascular disease (CVD) remains a global health concern affecting more than 37 million individuals [1]. CVDs are a leading cause of death globally [2,3,4]. CVD risk factors, such as hypertension, obesity, type II diabetes mellitus (T2DM), smoking, dyslipidaemia, a sedentary lifestyle, unhealthy diets, and excess alcohol intake [4, 5], are increasing in sub-Saharan Africa. South Africa is no exception, with a rising prevalence of known CVD risk factors, largely as a consequence of urbanisation and marked changes in health behaviour [6,7,8]. Thus, prevention of CVD is an important national public health goal.

Heart failure is the dominant form of CVD in South Africa, of which the main causes include hypertension, diabetes, coronary artery disease, dilated and or hypertrophic cardiomyopathy and valvular disease [9]. Unlike high-income countries, in South Africa heart failure typically affects younger working individuals and has an in-hospital mortality rate of approximately 8.4%, while 6 months post-hospital discharge, the fatality rate stands at approximately 26% [10]. As a result of the impact on young, economically active individuals, as well as the high fatality rate, heart failure in South Africa has a disproportional impact on an already fragile economy.

A key aspect of the pathological process of CVD, ultimately leading to heart failure and stroke [11, 12], is cardiac remodeling. The term is most applied to the left ventricle (LV) in which the chamber changes in size, shape, or structure [13]. Left ventricular hypertrophy (LVH), defined as an increase in muscle mass of the LV, is associated with a four-fold increase in heart failure [14,15,16,17,18,19,20]. As a result, regression of LVH is a goal of cardiovascular risk reduction [21,22,23,24]. Many of the risk factors contributing to the systemic and regional hemodynamic changes that drive the development of LVH [25] are modifiable, including obesity [26], tobacco and alcohol use [27], and elevated blood pressure and hypertension [26].

In South African adult women, there has been a sharp rise in prevalence of overweight/obesity (68%), hypertension (46%), regular alcohol use (17%) [28], and current tobacco smokers (7.6%) [29]. Given the increasing CVD rates and the restricted access to echocardiography in the public health sector [30], understanding the role of CVD risk factors in LVH development may have major implications for preventing LVH or interventions for regression of LVH. Furthermore, the growing burden of cardiovascular risk factors could lead to a growing burden of LVH [25,26,27] and potentially increase the risk of their offspring developing CVD risk factors and life-threatening CVD disease. Therefore, the study aimed to identify the prevalence of LVH as well as the CVD risk factors associated with LV remodeling and LVH, within black South African adult women and their pre-pubescent children. This could help inform public health efforts to reduce CVD risk in South Africa.

Methods

Study population

Data was collected during a cross-sectional study of vascular health in an existing birth cohort known as the Birth to Twenty Plus (BT20 +) Cohort, which started in 1990 in an urban historically disadvantaged setting, Soweto, Johannesburg, South Africa (described previously [31]), and now includes three generations. The cross-sectional study aimed to investigate the intergenerational transmission of cardiovascular health; the BT20 index female (known as 2nd generation or 2G; aged 28–29 years); their birth children or 3rd generation (3G, aged 4–10 years, female or male); and their biological mothers or 1st generation (1G, aged 43–68 years, female). For the present study, the first and second-generation participants were combined and classified as the “adult group”. Thus, 79 families, 237 participants (n = 158 adults and n = 79 children) were invited to attend for cardiovascular assessment where left ventricular remodeling and hypertrophy were assessed using echocardiography. All data were collected at the Developmental Pathways for Health Research Unit, at Chris Hani Baragwanath Academic Hospital in Soweto. Of the 237 participants recruited, n = 45 (19%) did not return to the study site and thus no echocardiography could be performed. Of the remaining 192 participants that returned to the study site, n = 5 (2.1%) was excluded due to the inability to obtain accurate linear measurements (due to excessive breast tissue), thus n = 187 (78.9%) were included in the analysis (Fig. 1). Trained researchers who spoke the participant's home language explained the study and all participants gave written informed consent (adults) or assent (children aged 7–10 years) before data collection. The Human Research Ethics Committee (Medical) of the University of the Witwatersrand approved the protocol (M190263).

CVD risk factors

Tobacco use was assessed using the Global Adult Tobacco Survey [32], alcohol use with the WHO Alcohol Use Disorders (WHO-AUDIT) test [33], and physical activity using the Global Physical Activity Questionnaire (GPAQ) [34]. Self-reported medical history (diabetes mellitus [T2DM], hypertension, high cholesterol, or previous heart disease, and current medication use) was assessed by questionnaire. Thereafter, height and weight were measured in triplicate using standardised World Health Organization measurement protocols [35]. Brachial blood pressure (BP) was measured using automated devices (MIT5 for adults; HBP-1300 for children [36]; Omron Healthcare, Kyoto, Japan). Following the International Society of Hypertension (ISH) measurement guidelines [37], participants were seated and asked to rest for at least 5 min before measurement of BP in their right arm three times in a quiet room with the monitor facing away from the participant; there was a 2 min rest interval between the measurements. The first BP measurement was discarded and the second and third measurements were averaged for analysis.

Echocardiography

Transthoracic echocardiography examination was performed by a single echocardiographer, with the Mindray DC-70 Ultrasound system (Mindray, Shenzhen China). Measurements of chamber dimensions were taken from 2D mode and left ventricular (LV) mass and relative wall thickness (RWT) were calculated. Linear measurements were made according to the American Society of Echocardiography (ASE) Guidelines: Recommendations for Cardiac Chamber Quantification in Adults [38]. LV mass was assessed at end-diastole perpendicular to the long axis of the LV. LVM was calculated according to the Devereux formula: LVM (g) = 0.8 × 1.04 ((LVDd + IVSd + LVPWd)3 – LVDd3) + 0.6 where LVDd = left ventricular diastolic diameter; IVSd = intraventricular septal diameter, LVPWd = left ventricular posterior wall thickness in diastole [38]. The left ventricular mass index (LVMI) was calculated as a ratio of LVM indexed to body surface area [38]. The RWT was defined as 2 × LVPWd/LVDd, where LVPWd = left ventricular posterior wall thickness in diastole; LVDd = left ventricular diastolic diameter [38]. RWT was used to categorise LV mass and the pattern of remodeling. Left ventricular hypertrophy (LVH) was defined as LVMI > 95 g/m2 for adult women [38] and LVMI > 95th percentile (85.6 g/m2) for children [39], and eccentric LVH (LVH with RWT ≤ 0.42) and concentric LVH (LVH with RWT > 0.42) as well as concentric remodeling (normal LVMI with RWT > 0.42) [38].

Data management

In adults, body mass index (BMI; weight (kg)/height (m)2) was categorised according to the World Health Organisation (WHO) classification, as follows: < 18.5 kg/m2 as underweight; 18.5–24.9 kg/m2 as normal; 25–29.9 kg/m2 as overweight; and ≥ 30 kg/m2 as obese [40]. In children (> 5 years), age-adjusted z-scores for BMI were calculated using the WHO reference, and children were categorised as overweight if their BMI z-score was between 1–2, and obese if their BMI z-score was > 2 [40]. While in children aged four years, age-adjusted z-scores for BMI were categorised as overweight if their BMI z-score was between 2–3, and obese if their BMI z-score was > 3 [41]. In adults, hypertension was defined as a BP ≥ 140 mmHg systolic or ≥ 90 mmHg diastolic or currently taking antihypertensive medication; in those who were not on anti-hypertensive medication, elevated BP was defined as a BP 130–139 mmHg systolic or 85–89 mmHg diastolic, following the International Society of Hypertension (ISH) Global Hypertension Practice Guidelines [37]. For children, elevated BP was defined as BP ≥ 90th percentile to < 95th percentile for height and age, while hypertension was defined as BP ≥ 95th percentile for age and height following the American Academy of Paediatrics Clinical Practice 2017 guidelines [42].

Statistical analysis

SPSS statistics 25.0 (IBM, Chicago, IL, USA) was used for statistical analysis. Non-normality of data was confirmed using visual inspection of histograms and the Shapiro–Wilk test. Continuous variables are expressed as median, interquartile range unless stated. Dichotomous variables are expressed as percentages. Multivariable logistic regression, after checking for multicollinearity by confirming a variance inflation factor of less than five [43], was conducted to examine the relationship between LVH/LV remodeling and the following health factors: age, moderate-vigorous physical activity, sedentary behaviour, obesity, hypertension, previous diagnosis of T2DM, high cholesterol, ever tobacco use and alcohol use. Statistical significance for all analyses was set at p < 0.05. Due to the low prevalence of LVH in children, regression analysis was only performed in adults.

Results

Adult women characteristics

The median age for adults was 41 years (range 28 to 68 years, n = 123) (Table 1). Median BMI was 32.5 kg/m2 (IQR: 26.6–37.7 kg/m2) with 59.3% of adults classified as obese. Forty-four out of 123 adults (35.8%) were classified as hypertensive, of whom 75% were on treatment, primarily a diuretic. Of the 123 adults, 22.8% were current or past tobacco users (self-reported smoking and smokeless tobacco), and 55.3% regularly consumed alcohol. Three adults reported having previous heart disease. A small percentage of adults reported having high cholesterol and T2DM (12.2% and 2.4% respectively). While all participants with self-reported diabetes were on treatment, only 26.7% of adults with high cholesterol were. The median LVMI for adults was 84.75 (IQR: 71.36–102.33) g/m2. Sixty out of 123 adults (48.8%) had normal LV geometry, while 19 out of 123 (15.4%) had concentric remodeling. Forty-four out of 123 women (35.8%) had LVH, of whom 33 out of 123 (26.8%) had eccentric LVH and 11 out of 123 adults (8.9%) had concentric LVH (Table 1).

Table 1 Characteristics of the adults and children (n = 187)
Full size table

Children characteristics

The median age for children was 7 years (range 4 to 10 years, n = 64, 54.7% female) (Table 1). Children had a median BMI of 15.8 kg/m2 (IQR: 14.8–17.2 kg/m2) with 6.3% of children classified as obese. Nine out of sixty-four children (14.1%) had elevated BP, while twenty-nine out of sixty-four children (45.3%) were hypertensive. The median LVMI in children was 56.29 (IQR: 47.61–69.17) g/m2. Fifty-nine out of 64 (92.2%) of children had normal LV geometry, one child had concentric remodeling, while the remaining 4 children (6.3%) had eccentric LVH. No concentric LVH was observed within the children of the current study (Table 1).

Left ventricular (LV) remodeling and left ventricular hypertrophy (LVH) in adults

Table 2 compares characteristics of adults with and without LVH. Overall, women with LVH were significantly older (48 (min: 29, max 66) vs 29 (min: 28, max: 68) years, p = 0.04), were more often obese (73% vs 52%, p = 0.04), and more often had hypertension (52% vs 27%, p = 0.01) compared to those without LVH. When considering LVH regardless of pattern, after adjusting for age, moderate-vigorous physical activity, sedentary behaviour, obesity, hypertension, T2DM, high cholesterol, ever tobacco use, and regular alcohol use, hypertension (OR: 3.39 (1.08–10.62), p = 0.04), and obesity (OR: 2.54 (1.07–6.02) were significantly associated with LVH. Obesity was the only factor significantly associated with eccentric LVH (OR: 3.46 (1.28–9.37), p = 0.02), and ever tobacco use was the only factor significantly associated with concentric LVH (OR: 5.06 (1.24–20.69), p = 0.02), although the number of adults with this condition was small. No other significant associations were found with LV remodeling in the multivariable logistic regression models (Table 3).

Table 2 Sociodemographic characteristics of the women adults with and without left ventricular hypertrophy
Full size table
Table 3 Multivariable adjusted associations between health risk factors and left ventricular remodelling and left ventricular hypertrophy in adults
Full size table

Figure 2 depicts those adults with LVH and the number of CVD risk factors. The prevalence of LVH in adults significantly increased (p = 0.002) with the number of CVD risk factors reported.

Fig. 1
figure 1

Study flow diagram

Full size image
Fig. 2
figure 2

Percentage of South African adult women and children with left ventricular hypertrophy (LVH) according to the number of cardiovascular disease (CVD) risk factors. CVD risk factors for women included: obesity, hypertension, self-reported type II diabetes mellitus, self-reported high cholesterol, physical activity, tobacco use, and alcohol consumption. CVD risk factors for children included: obesity, hypertension, whether their mother and or grandmother use tobacco

Full size image

Left ventricular (LV) remodeling and left ventricular hypertrophy (LVH) in children

Over 90% of children (median age 7 years, range 4–10, 59.3% female) had normal LV geometry despite 14.1% (n = 9) having elevated BP, 45.3% (n = 29) being hypertensive and 17.2% (n = 11) being overweight and 6.3% (n = 4) being obese (Table 1). Of the four children with LVH (all eccentric LVH), three had elevated BP and were normal weight, while the fourth child had normal BP, but was overweight. Figure 2 illustrates that in the current study, three out of the four children with LVH had a known CVD risk factor.

Discussion

In the present study, we assessed the prevalence of LVH in black South African women and their children/grandchildren and health factors associated with LVH. We found a high prevalence of LVH in South African black adult women (28–68 years), with over a quarter having eccentric LVH. Obesity and hypertension, two modifiable health factors, were associated with eccentric LVH, while self-reported tobacco use was related to concentric LVH. Of the women with LVH, half had at least three CVD risk factors. Despite the small sample size, 6% of children aged 4–10 years had eccentric LVH, of which three had elevated blood pressure (BP). The current study highlights that multiple factors significantly drive the development of LVH in adult women. In addition, although only four children had LVH, the high prevalence of elevated BP in children is concerning and supports ongoing calls for prevention efforts, particularly for youth.

In African countries, CVD is increasing rapidly. LVH is a known marker of increased risk for developing future life-threatening CVD and there is evidence to suggest that LVH is higher in black populations of African descent [44]. Various studies conducted over the past decade in Sub-Saharan Africa have reported the prevalence of LVH among women (mean age range: 43–57 years) to vary from 19.9% to 44.5% [19, 45,46,47], which is consistent with the current study’s findings (35.8% of South African women; mean age: 41.3 years). Our estimates are, however, higher than previously reported South African data by Maseko et al. and Libhaber et al. (LVH prevalence of 19.9% and 21.7% respectively, despite similar ages (44 years)) [45, 46]. This increase in LVH prevalence may be, in part, due to increased risk cardiovascular risk factors from 2013. However, although the populations in both studies were similar to that of the current study (both black South African), the methodology was different. Both studies used LVM indexed to height2.7 [45, 46], whilst the current study used LVM indexed to body surface area. However, when indexing LVM to height2.7, the current study’s prevalence increased slightly from 35.8% (n = 44) to 38.2% (n = 47) (data not shown). To date, there remains controversy around the method to index LVM to accurately identify LVH within individuals in the Southern African region. Due to the high prevalence of stunting observed within the South African population [48, 49], LVM indexed to body surface area was identified as the most appropriate method so as not to under or overestimate LVH calculated by height2.7. This, in conjunction with the guidelines from The American Society of Echocardiography Recommendations for Cardiac Chamber Quantification in Adults [38], further supports the use of body surface area over height2.7.

LVH is a compensatory response to cardiac insult through interactions between pressure and/or volume overload [50]. Increasing age, hypertension, and obesity are the three main cardiovascular risk factors that drive pressure and volume overload within the heart [50, 51]. The current study found that obesity and hypertension were associated with a two-fold and a three-fold respective risk of developing LVH (irrespective of type), and a three-fold risk of developing eccentric LVH. This is in line with results from the Framingham study that suggest a 7% increase for risk for developing LVH per one unit increase of body mass index (BMI) in women [52, 53]. Furthermore, there is a three-fold risk of developing CVD in individuals with BP ≥ 130/90 mmHg compared to individuals with BP < 120/80 mmHg [54]. In South Africa, approximately 68% of women (≥ 15 years) are overweight or obese [55] and hypertension is currently reported as one of the most common causes of CVD [19, 55]. Current understanding of hemodynamic alterations accompanying obesity and hypertension suggests that they drive an increase in LV filling and stroke volume, which specifically causes LV dilation and eccentric, rather than concentric, LVH [26, 56,57,58,59]. However, studies by Woodiwiss et al. [60] and Avelar et al. [58] found that adiposity was associated with concentric LVH, independently of BP. Our smaller sample size (n = 123, of which 11 had concentric LVH) may explain the lack of an association between obesity and concentric LVH in our study. In addition, due to the confounding effects of both hypertension and obesity, their interactions and duration within the same individual, left ventricular remodeling and hypertrophy may be different. Therefore, before definitive conclusions can be reached within this population, further studies investigating interactions of obesity and hypertension are required.

Along with obesity and hypertension, smoking prevalence in South Africa is currently on the rise [55]. There is sound evidence that smoking affects cardiac structure and function [61, 62], and results from other studies suggest significant increases in left ventricular mass index, and thus left ventricular hypertrophy, in individuals who smoke compared to those that don’t [61,62,63,64]. Similarly, although our sample of women that had concentric left ventricular hypertrophy was small, our data showed an association between smoking and concentric left ventricular hypertrophy.

The current study found a high prevalence of elevated blood pressure (59.4%) in children. Other recent studies from South Africa have also found high rates of elevated blood pressure in children [65, 66], and a stark increasing trend in paediatric hypertension was identified by a recent meta-analysis [67]. It should be noted that the present study was not designed to determine clinical prevalence, which would require confirmation of abnormal readings at multiple follow-ups and through auscultation, and we did not have data on the extent to which secondary or white-coat hypertension contributed to high blood pressure. Nevertheless, the worrying levels of paediatric elevated blood pressure require further exploration. Although only four children had LVH, of these, three had elevated blood pressure and the one child that was normotensive was overweight. Thus, following the same pattern observed in adults, rising CVD risk factors in children, namely elevated blood pressure and weight gain, are the driving factors behind CVD risk in children that also may persist into adulthood. This further support calls for earlier identification of children that are at risk and for interventions where necessary, especially within children.

A strength of this study is the indexing of LVM to body surface area, since indexing LVM to body height may result in an error in LVH classification due to the prevalence of stunting in this population [48, 49]. A limitation of the present study was the ages within the adult group. As this study recruited from within an existing birth cohort with all index children recruited at birth in 1990, these ‘children’ were all 29 years old adults at the time of the measurements, resulting in a clustering of adults around 29 years with their parents aged 45–65 years. Additionally, as we recruited participants that were from the same family (three generations), several cardiac measures may be heritable within families, which could account for the high prevalence of LVH noticed within the current study. Previous studies have shown that LV function and LVM may be heritable within European [68] and American [69] families, thus, future research is needed to identify a potential heritable component within South African families of three generations. Furthermore, we relied on self-reported data for medical history (previously diagnosed T2Dm, high cholesterol and heart disease) and CVD risk factors (tobacco and alcohol use, physical activity). We acknowledge that self-reported data may underestimate CVD risk factors and their potential association with LVH. Future studies should consider objective measures where available. Furthermore, given the potential association between self-reported tobacco use and LVH in adults, analysing biomarkers of tobacco exposure could be a useful next step in a bigger sample size. In addition, we did not have access to medical records around maternal pre-eclampsia and drug use during pregnancy, and therefore could not explore the impact of these factors on the prevalence of LVH, however, we will aim to include this in future studies. There is scant data on LVH prevalence within pre-pubescent children in Africa, thus this study has highlighted the need for additional studies to confirm the most appropriate cut-off points for identifying children with, or at risk of developing, LVH, so that appropriate intervention measures can occur to prevent the progression into severe heart disease and heart failure. As the low frequency of children with LVH prevented further statistical analysis, additional studies with larger sample sizes are needed to assess potential relationships between modifiable health behaviours and LVH.

Conclusions

In conclusion, the results have highlighted the need for specific call to action policies around obesity and hypertension in adult women and target intervention around weight management and elevated BP as well as hypertension in prepubescent children. Due to the high risk of developing LVH due to obesity and hypertension, specific interventions, before the development of obesity and hypertension (i.e. overweight and elevated BP individuals), are needed to prevent the development of LVH, and, in cases where LVH is evident, regress LVH. As obesity and hypertension have both additive and interactive effects on LVH development, both weight loss programs and BP-lowering medications (such as hydrochlorothiazide [70, 71]) are required to achieve appropriate LVH regression, particular in this population where obesity and hypertension are prevalent.

Availability of data and materials

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

Abbreviations

ASE:

American Society of Echocardiography

BMI:

Body mass index

BT20 + :

Birth to Twenty Plus Cohort

BP:

Blood pressure

CI:

Confidence interval

CVD:

Cardiovascular disease

GPAQ:

Global physical activity questionnaire

IQR:

Interquartile range

ISH:

International Society of Hypertension

IVSd:

Intraventricular septal diameter

LVDd:

Left ventricular diastolic diameter

LVPWd:

Left ventricular posterior wall thickness in diastole

LV:

Left ventricular

LVH:

Left ventricular hypertrophy

LVM:

Left ventricular mass

LVMI:

Left ventricular mass index

MVPA:

Moderate-vigorous physical activity

OR:

Odds ratio

RWT:

Relative wall thickness

T2DM:

Type II diabetes mellitus

WHO:

World health organisation

WHO-AUDIT:

WHO Alcohol Use Disorders

1G:

First generation

2G:

Second generation

3G:

Third generation

References

  1. Ziaeian B, Fonarow GC. Epidemiology and aetiology of heart failure. Nat Rev Cardiol. 2016;13:368–78.

    Article  PubMed  PubMed Central  Google Scholar 

  2. Bradshaw D, Groenewald P, Laubscher R, Nannan N, Nojilana B, Norman R, et al. Initial burden of disease estimates for South Africa, 2000 : original article. Samj. 2003.

  3. Bhatia RS, Tu JV, Lee DS, Austin PC, Fang J, Haouzi A, et al. Outcome of heart failure with preserved ejection fraction in a population-based study. N Engl J Med. 2006. https://doi.org/10.1056/NEJMoa051530.

    Article  PubMed  Google Scholar 

  4. Mozaffarian D, Benjamin EJ, Go AS, Arnett DK, Blaha MJ, Cushman M, et al. Heart disease and stroke statistics-2015 update : a report from the American Heart Association. Circulation. 2015. https://doi.org/10.1161/CIR.0000000000000152.

    Article  PubMed  PubMed Central  Google Scholar 

  5. Lee DS, Gona P, Vasan RS, Larson MG, Benjamin EJ, Wang TJ, et al. Relation of disease pathogenesis and risk factors to heart failure with preserved or reduced ejection fraction: Insights from the framingham heart study of the national heart, lung, and blood institute. Circulation. 2009. https://doi.org/10.1161/CIRCULATIONAHA.108.815944.

    Article  PubMed  PubMed Central  Google Scholar 

  6. Steyn K, Damasceno A. Lifestyle and related risk factors for chronic diseases. 2006.

  7. Rayner B. Hypertension: Detection and management in South Africa. Nephron - Clinical Practice. 2010.

  8. Maredza M, Bertram MY, Tollman SM. Disease burden of stroke in rural South Africa: An estimate of incidence, mortality and disability adjusted life years. BMC Neurol. 2015. https://doi.org/10.1186/s12883-015-0311-7.

    Article  PubMed  PubMed Central  Google Scholar 

  9. Hitzeroth J, Mpe M, Klug E, Ranjith N, Sliwa K, Steingo L, et al. 2020 Heart Failure Society of South Africa perspective on the 2016 European Society of Cardiology Chronic Heart Failure Guidelines. S Afr Med J. 2020;110:13057.

    CAS  PubMed  Google Scholar 

  10. Szymanski PZ, Badri M, Mayosi BM. Clinical characteristics and causes of heart failure, adherence to treatment guidelines, and mortality of patients with acute heart failure: experience at Groote Schuur Hospital, Cape Town, South Africa. South Afr Med J. 2018;108:94–8.

    Article  CAS  Google Scholar 

  11. Bots ML, Nikitin Y, Salonen JT, Elwood PC, Malyutina S, FreiredeConcalves A, et al. Left ventricular hypertrophy and risk of fatal and non-fatal stroke. EUROSTROKE: a collaborative study among research centres in Europe. J Epidemiol Commun Health. 2002;56(1):8.

    Article  Google Scholar 

  12. Ranganai E, Matizirofa L. An analysis of recent stroke cases in South Africa: trend, seasonality and predictors. S Afr Med J. 2020;110:92–9.

    Article  CAS  PubMed  Google Scholar 

  13. Alpert MA, Karthikeyan K, Abdullah O, Ghadban R. Obesity and cardiac remodeling in adults: mechanisms and clinical implications. Prog Cardiovasc Dis. 2018;61:114–23.

    Article  PubMed  Google Scholar 

  14. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the framingham heart study. N Engl J Med. 1990;322:1561–6.

    Article  CAS  PubMed  Google Scholar 

  15. Levy D, Anderson KM, Savage DD, Kannel WB, Christiansen JC, Castelli WP. Echocardiographically detected left ventricular hypertrophy: prevalence and risk factors. The Framingham heart study. Ann Internal Med. 1988;108:7–13.

    Article  CAS  Google Scholar 

  16. Wright GA, Ang DS, Stonebridge PA, Belch JJ, Struthers AD. Left ventricular hypertrophy is present in one-half of newly-diagnosed peripheral arterial disease patients. J Hypertens. 2007;25:463–9.

    Article  CAS  PubMed  Google Scholar 

  17. Katholi RE, Couri DM. Left ventricular hypertrophy: Major risk factor in patients with hypertension: Update and practical clinical applications. Int J Hypertens. 2011;2011:1–10.

    Article  Google Scholar 

  18. Schirmer H, Lunde P, Rasmussen K. Prevalence of left ventricular hypertrophy in a general population. Tromso Study Eur Heart J. 1999;20:429–38.

    Article  CAS  PubMed  Google Scholar 

  19. Baldo MP, Gonçalves MA, Capingana DP, Magalhães P, da Silva ABT, Mill JG. Prevalence and clinical correlates of left ventricular hypertrophy in black Africans. High Blood Press Cardiovasc Prev. 2018;25:283–9.

    Article  PubMed  Google Scholar 

  20. Brady TM. The role of obesity in the development of left ventricular hypertrophy among children and adolescents. Curr Hypertens Rep. 2016;18:1–7.

    Article  CAS  Google Scholar 

  21. Devereux RB, Wachtell K, Gerdts E, Boman K, Nieminen MS, Papademetriou V, et al. Prognostic significance of left ventricular mass change during treatment of hypertension. J Am Med Assoc. 2004;292:2350–6.

    Article  CAS  Google Scholar 

  22. Pierdomenico S, … DL-A journal of, 2008 undefined. Regression of echocardiographic left ventricular hypertrophy after 2 years of therapy reduces cardiovascular risk in patients with essential hypertension. academic.oup.com. 2008. https://doi.org/10.1038/ajh.2008.2.

  23. Fagard RH, Celis H, Thijs L, Wouters S. Regression of left ventricular mass by antihypertensive treatment: a meta-analysis of randomized comparative studies. Hypertension. 2009;54:1084–91.

    Article  CAS  PubMed  Google Scholar 

  24. Lønnebakken MT, Izzo R, Mancusi C, Gerdts E, Losi MA, Canciello G, et al. Left ventricular hypertrophy regression during antihypertensive treatment in an outpatient clinic (the Campania salute network). J Am Heart Assoc. 2017;6:e004152.

    Article  PubMed  PubMed Central  Google Scholar 

  25. Messerli FH, Ketelhut R. Left ventricular hypertrophy: an independent risk factor - PubMed. J Cardiovasc Pharmacol. 1991;17 Suppl 4:S59–66; discussion S66–7. https://pubmed.ncbi.nlm.nih.gov/1726010/. Accessed 26 Feb 2021.

  26. Woodiwiss AJ, Norton GR. Obesity and left ventricular hypertrophy: the hypertension connection. Curr Hypertens Reports. 2015;17:539.

  27. Park SK, Moon K, Ryoo JH, Oh CM, Choi JM, Kang JG, et al. The association between alcohol consumption and left ventricular diastolic function and geometry change in general Korean population. Eur Heart J Cardiovasc Imaging. 2018;19:271–8.

    Article  PubMed  Google Scholar 

  28. National Department of Health (NDoH), Statistics South Africa (Stats SA), South African Medical Research Council (SAMRC) and I, Survey H. South Africa Demographic and Health Survey 2016: Key Indicators. 2017.

  29. Reddy P, Zuma K, Shisana O, Jonas K, Sewpaul R. Prevalence of tobacco use among adults in South Africa: Results from the first South African national health and Nutrition Examination Survey. S Afr Med J. 2015;105:648–55.

    Article  PubMed  Google Scholar 

  30. Bedeker WF, Lachman AS, Borkum M, Hellenberg D, Cupido CS. Impact of transthoracic echocardiography at district hospital level. S Afr Med J. 2015;105:817–22.

    Article  CAS  PubMed  Google Scholar 

  31. Richter L, Norris S, Pettifor J, Yach D, Cameron N. Europe PMC Funders Group Cohort Profile : Mandela ’ s children : The 1990 birth to twenty study in South Africa. Int J Epidemiol. 2007;36:504–11.

    Article  PubMed  Google Scholar 

  32. Palipudi KM, Morton J, Hsia J, Andes L, Asma S, Talley B, Caixeta RD, Fouad H, Khoury RN, Ramanandraibe N, Rarick J, Sinha DN, Pujari S, Tursan d'Espaignet E; [On behalf of the GATS Collaborative Group]. Methodology of the Global Adult Tobacco Survey - 2008-2010. Glob Health Promot. 2016;23(2 Suppl):3–23. https://doi.org/10.1177/1757975913499800.

  33. Saunders JB, Aasland OG, Babor TF, de la Fuente JR, Grant M. Development of the alcohol use disorders identification test (AUDIT): WHO collaborative project on early detection of persons with harmful alcohol consumption-II. Addiction. 1993;88:791–804.

    Article  CAS  PubMed  Google Scholar 

  34. Cleland CL, Hunter RF, Kee F, Cupples ME, Sallis JF, Tully MA. Validity of the Global Physical Activity Questionnaire (GPAQ) in assessing levels and change in moderate-vigorous physical activity and sedentary behaviour. BMC Public Health. 2014;14:1–11.

    Article  Google Scholar 

  35. de Onis M, Garza C, Victora CG, Onyango AW, Frongillo EA, Martines J. The WHO multicentre growth reference study: planning, study design, and methodology. Food Nutr Bull. 2004;25(1 SUPPL. 1):15–26.

    Article  Google Scholar 

  36. Meng L, Zhao D, Pan Y, Ding W, Wei Q, Li H, et al. Validation of Omron HBP-1300 professional blood pressure monitor based on auscultation in children and adults. BMC Cardiovasc Disord. 2016;16:1–5.

    Article  CAS  Google Scholar 

  37. Unger T, Borghi C, Charchar F, Khan NA, Poulter NR, Prabhakaran D, et al. International society of hypertension global hypertension practice guidelines. Hypertension. 2020;2020:1334–57.

    Article  CAS  Google Scholar 

  38. Orsinelli DA, Armour A, De Cara J, Fey B, Frommelt P, Lopez-Mattei J, et al. The American society of echocardiography recommendations for cardiac chamber quantification in adults. J Am Soc Echocardiogr. 2015;28:1–39.

    Article  Google Scholar 

  39. Simpson JM, Savis A, Rawlins D, Qureshi S, Sinha MD. Incidence of left ventricular hypertrophy in children with kidney disease: Impact of method of indexation of left ventricular mass. Eur J Echocardiogr. 2010;11:271–7.

    Article  PubMed  Google Scholar 

  40. WHO/Europe | Nutrition - Body mass index - BMI. https://www.euro.who.int/en/health-topics/disease-prevention/nutrition/a-healthy-lifestyle/body-mass-index-bmi. Accessed 1 Jul 2020.

  41. WHO. Body mass index-for-age (BMI-for-age). https://www.who.int/toolkits/child-growth-standards/standards/body-mass-index-for-age-bmi-for-age. Accessed 17 Mar 2021.

  42. Flynn JT, Falkner BE. New clinical practice guideline for the management of high blood pressure in children and adolescents. Hypertension. 2017;70:683–6.

    Article  CAS  PubMed  Google Scholar 

  43. Kim JH. Multicollinearity and misleading statistical results. Korean J Anesthesiol. 2019;72:558–69.

    Article  PubMed  PubMed Central  Google Scholar 

  44. Kamath S, Markham D, Drazner MH. Increased prevalence of concentric left ventricular hypertrophy in African-Americans: Will an epidemic of heart failure follow? Heart Fail Rev. 2006;11:271–7.

    Article  PubMed  Google Scholar 

  45. Maseko MJ, Woodiwiss AJ, Libhaber CD, Brooksbank R, Majane OHI, Norton GR. Relations between white coat effects and left ventricular mass index or arterial stiffness: role of nocturnal blood pressure dipping. Am J Hypertens. 2013;26:1287–94.

    Article  PubMed  Google Scholar 

  46. Libhaber CD, Norton GR, Maseko MJ, Majane OHI, Millen AME, Maunganidze F, et al. Relationship between inappropriate left ventricular hypertrophy and ejection fraction independent of absolute or indexed mass in a community sample of black African ancestry. J Hypertens. 2013;31:169–76.

    Article  CAS  PubMed  Google Scholar 

  47. Isaac Kofi O, Emmanuel AA. Determinants of left ventricular hypertrophy in hypertensive patients seen in a teaching hospital in Ghana. J Hypertens Open Access. 2017;06:1–7.

    Article  Google Scholar 

  48. Willey BA, Cameron N, Norris SA, Pettifor JM, Griffiths PL. Socio-economic predictors of stunting in preschool children—a population-based study from Johannesburg and Soweto. S Afr Med J. 2009. https://doi.org/10.7196/SAMJ.2652.

    Article  PubMed  Google Scholar 

  49. Nyati LH, Pettifor JM, Norris SA. The prevalence of malnutrition and growth percentiles for urban South African children. BMC Public Health. 2019;19:1–13.

    Article  Google Scholar 

  50. Drazner MH. The progression of hypertensive heart disease. Circulation. 2011;123:327–34.

    Article  PubMed  Google Scholar 

  51. Aronow WS. Hypertension and left ventricular hypertrophy. Ann Transl Med. 2016;5(15):310. https://doi.org/10.21037/atm.2017.06.14.

    Article  Google Scholar 

  52. Horwich TB, Fonarow GC. Glucose, obesity, metabolic syndrome, and diabetes. Relevance to incidence of heart failure. J Am College Cardiol. 2010;55:283–93.

    Article  CAS  Google Scholar 

  53. Hamzeh N, Ghadimi F, Farzaneh R, Hosseini SK. Obesity, heart failure, and obesity paradox. J Tehran Univ Heart Center. 2017;12:1–5.

    Google Scholar 

  54. Vasan RS, Larson MG, Leip EP, Evans JC, O’Donnell CJ, Kannel WB, et al. Impact of high-normal blood pressure on the risk of cardiovascular disease. N Engl J Med. 2001;345:1291–7.

    Article  CAS  PubMed  Google Scholar 

  55. National Department of Health (NDoH), Statistics South Africa (Stats SA), South African Medical Research Council (SAMRC) and I. South Africa Demographic andd Health Survey 2016. 2019.

  56. Alpert MA, Lavie CJ, Agrawal H, Aggarwal KB, Kumar SA. Obesity and heart failure: Epidemiology, pathophysiology, clinical manifestations, and management. Transl Res. 2014;164:345–56.

    Article  CAS  PubMed  Google Scholar 

  57. Nauta JF, Hummel YM, Tromp J, Ouwerkerk W, van der Meer P, Jin X, et al. Concentric vs. eccentric remodelling in heart failure with reduced ejection fraction: clinical characteristics, pathophysiology and response to treatment. Eur J Heart Failure. 2020;22(7):1147–55.

  58. Avelar E, Cloward TV, Walker JM, Farney RJ, Strong M, Pendleton RC, et al. Left ventricular hypertrophy in severe obesity: interactions among blood pressure, nocturnal hypoxemia, and body mass. Hypertension. 2007;49:34–9.

    Article  CAS  PubMed  Google Scholar 

  59. Aurigemma GP, De Simone G, Fitzgibbons TP. Cardiac remodeling in obesity. Circ Cardiovasc Imaging. 2013;6:142–52.

    Article  PubMed  Google Scholar 

  60. Woodiwiss AJ, Libhaber CD, Majane OHI, Libhaber E, Maseko M, Norton GR. Obesity promotes left ventricular concentric rather than eccentric geometric remodeling and hypertrophy independent of blood pressure. Am J Hypertens. 2008;21:1144–51.

    Article  PubMed  Google Scholar 

  61. Fidelix MP, Tanni SE, Roscani MG, Mesquita CB, Schelini KNdM, Polegato BF, et al. Vitamin D role in smoking women and cardiac remodeling. Nutrire. 2016;41:1–7.

    Article  CAS  Google Scholar 

  62. Bullen C. Impact of tobacco smoking and smoking cessation on cardiovascular risk and disease. Expert Rev Cardiovasc Ther. 2008;6:883–95.

    Article  CAS  PubMed  Google Scholar 

  63. Leigh JA, Kaplan RC, Swett K, Balfour P, Kansal MM, Talavera GA, et al. Smoking intensity and duration is associated with cardiac structure and function: The ECHOcardiographic Study of Hispanics/Latinos. Open Heart. 2017;4:1–12.

    Article  Google Scholar 

  64. Kaplan A, Abidi E, Ghali R, Booz GW, Kobeissy F, Zouein FA. Functional, cellular, and molecular remodeling of the heart under influence of oxidative cigarette tobacco smoke. Oxid Med Cell Longev. 2017;2017.

  65. Boerstra BA, Soepnel LM, Nicolaou V, Kolkenbeck-Ruh A, Kagura J, Ware LJ, et al. The impact of maternal hyperglycaemia first detected in pregnancy on offspring blood pressure in Soweto, South Africa. J Hypertens. 2022;40:969–77.

    Article  CAS  PubMed  Google Scholar 

  66. Matjuda EN, Sewani-Rusike CR, Anye SNC, Engwa GA, Nkeh-Chungag BN. Relationship between high blood pressure and microalbuminuria in children aged 6–9 years in a South African population. Children. 2020;7:131.

    Article  PubMed Central  Google Scholar 

  67. Song P, Zhang Y, Yu J, Zha M, Zhu Y, Rahimi K, et al. Global prevalence of hypertension in children: a systematic review and meta-analysis. JAMA Pediatr. 2019;173:1154–63.

    Article  PubMed  PubMed Central  Google Scholar 

  68. Jin Y, Kuznetsova T, Bochud M, Richart T, Thijs L, Cusi D, et al. Heritability of left ventricular structure and function in Caucasian families. Eur J Echocardiogr. 2011;12:326–32.

    PubMed  PubMed Central  Google Scholar 

  69. Post WS, Larson MG, Myers RH, Galderisi M, Levy D. Heritability of left ventricular mass. Hypertension. 1997;30:1025–8.

    Article  CAS  PubMed  Google Scholar 

  70. Roush GC, Abdelfattah R, Song S, Ernst ME, Sica DA, Kostis JB. Hydrochlorothiazide vs chlorthalidone, indapamide, and potassium-sparing/hydrochlorothiazide diuretics for reducing left ventricular hypertrophy: a systematic review and meta-analysis. J Clin Hypertens. 2018;20:1507–15.

    Article  CAS  Google Scholar 

  71. Pierdomenico SD, Cuccurullo F. Risk reduction after regression of echocardiographic left ventricular hypertrophy in hypertension: a meta-analysis. Am J Hypertens. 2010;23:876–81.

    Article  PubMed  Google Scholar 

Download references

Acknowledgements

Funding support from the South African Medical Research Council, Wellcome Trust, and DSI-NRF Centre of Excellence in Human Development at the University of the Witwatersrand, Johannesburg, South Africa for the Birth to Twenty Plus Cohort.

Funding

This study was supported by a Wellcome Trust Seed Award to Lisa J. Ware (214082/Z/18/Z). This Award funded the study by providing travel reimbursement and refreshments for all the participants that were enrolled into the study, and by providing salaries for the research team that carried out all the data collection for the duration of the study.

Author information

Authors and Affiliations

  1. SAMRC/Wits Developmental Pathways for Health Research Unit, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, 2000, South Africa

    Andrea Kolkenbeck-Ruh, Larske M. Soepnel, Simone H. Crouch, Sanushka Naidoo, Shane A. Norris, Justine Davies & Lisa J. Ware

  2. Cardiovascular Pathophysiology and Genomics Research Unit, Faculty of Health Sciences, School of Physiology, University of the Witwatersrand, Johannesburg, South Africa

    Andrea Kolkenbeck-Ruh

  3. Julius Global Health, Julius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht, Utrecht University, Huispost number: STR 6.131, P.O. Box 85500, 3508 GA, Utrecht, The Netherlands

    Larske M. Soepnel

  4. Hypertension in Africa Research Team (HART), North-West University, Potchefstroom, South Africa

    Wayne Smith

  5. South African Medical Research Council: Unit for Hypertension and Cardiovascular Disease, North-West University, Potchefstroom, South Africa

    Wayne Smith

  6. School of Health and Human Development, University of Southampton, Southampton, UK

    Shane A. Norris

  7. Institute of Applied Health Research, University of Birmingham, Birmingham, UK

    Justine Davies

  8. DSI-NRF Centre of Excellence in Human Development, University of the Witwatersrand, Johannesburg, 2000, South Africa

    Lisa J. Ware

Authors
  1. Andrea Kolkenbeck-Ruh
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Larske M. Soepnel
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Simone H. Crouch
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Sanushka Naidoo
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Wayne Smith
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Shane A. Norris
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Justine Davies
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Lisa J. Ware
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

AKR and LJW, conceptualised and designed the study. AKR was responsible for data management, data analysis and wrote the original draft. AKR, LMS, SHC, SN, WS, SAN, JD, LJW, contributed to interpretation of data and critical review of manuscript. LW was the Principal Investigator of the project. All authors gave final approval of the version to be submitted.

Corresponding author

Correspondence to Larske M. Soepnel.

Ethics declarations

Ethical approval and consent to participate

Written informed consent was provided by all women and their children / grandchildren prior to their inclusion in the study. Trained researchers who spoke the participant’s home language explained the study and all participants provided written informed consent prior to taking part. For children, the mother of the child provided written consent that her child may take part in the study, with children older than 7 years additionally providing written assent to take part. The study was conducted according to the principles of the Declaration of Helsinki [67] and the Human Research Ethics Committee (Medical) of the University of the Witwatersrand approved the protocol with ethical clearance number M190263.

Consent for publication

Not applicable

Competing interests

The authors declare that they have no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Kolkenbeck-Ruh, A., Soepnel, L.M., Crouch, S.H. et al. Obesity, hypertension, and tobacco use associated with left ventricular remodeling and hypertrophy in South African women: Birth to Twenty Plus Cohort. BMC Cardiovasc Disord 22, 403 (2022). https://doi.org/10.1186/s12872-022-02837-w

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12872-022-02837-w

Keywords

  • Left ventricular hypertrophy
  • Ventricular remodeling
  • Sub-Saharan Africa
  • South Africa
  • Child health
  • Women's health

BMC Cardiovascular Disorders

ISSN: 1471-2261

Contact us