Original Article
Low Grade Inflammation and ECG Left Ventricular Hypertrophy in Urban African Males: The SABPA Study

https://doi.org/10.1016/j.hlc.2013.03.075Get rights and content

Background

Hypertension and vascular hyperresponsiveness have been associated with structural wall abnormalities in black Africans. Whether low grade inflammation would have an additive effect is uncertain. Therefore, a novel investigation aimed to assess whether inflammation and pressure overload would have an additive association with ECG left ventricular hypertrophy (LVH).

Methods

We included 75 African and 87 Caucasian males. Ambulatory blood pressure monitoring was done in the working week. A resting 12-lead ECG recording was used for the determination of LVH with the Cornell product formula. Fasting blood samples were obtained for high sensitivity C-reactive protein (hs-CRP) analyses after a controlled overnight stay. Men were stratified into low (≤3 mg/L) and high (>3 mg/L) hs-CRP groups.

Results

African men revealed higher ambulatory blood pressure levels compared to Caucasian men independent of hs-CRP levels after adjustment for age, physical activity, cotinine, log γ-GT and body surface area. In forward stepwise linear regression analyses, SBP was positively associated with ECG LVH in all Africans. Considering low grade inflammatory status (>3 mg/L hs-CRP), SBP [Adj R2 = 0.49 (β = 0.99, 0.45, 1.44), p  0.01] and pulse pressure [Adj R2 = 0.61 (β = 0.0.34, 0.88), p  0.01] respectively, predicted ECG LVH in African but not in Caucasian men.

Conclusions

Hyperdynamic blood pressure and inflammation acted in tandem as possible promoting factors to structural wall abnormalities in African men.

Introduction

In 2011, Schutte et al. [1] reported a significant association between ECG left ventricular hypertrophy and ambulatory blood pressure in hypertensive African men. This association was not found in hypertensive Caucasian men. One of the most compelling reasons for this finding could be differences observed in ambulatory blood pressure between ethnic groups [1], [2], [3], [4], [5]. There exists a growing belief that declining African cardiovascular health status is due to Westernisation or acculturation of black Africans during urbanisation [6], [7], [8], [9], [10]. Urbanisation is believed to elevate a person's blood pressure due to their adaptation to an urbanised lifestyle [7]. Additionally, increased inflammation levels have been reported in Africans [11]. Inflammation has also been positively correlated with left ventricular hypertrophy (LVH) in numerous studies, especially in Afro Americans [12], [13]. It has also been shown to be a powerful mediator to elevate blood pressure [14], [15] and in turn high blood pressure further stimulates pro-inflammatory responses [15]. The promotion of ECG-LVH caused by the additive effect of elevated blood pressure and inflammation has not been extensively studied and no findings exist for black Africans.

General concerns have been raised pertaining to ECG-LVH or Cornell product as measure of LVH. Measurement of ECG-LVH by means of the Cornell-product incorporates QRS-complex voltage as well as QRS-complex duration to identify the existence of ECG-LVH. This is done by using the sum of the R-wave and S-wave's amplitudes and multiplying it with the QRS duration [16]. It has been suggested that such voltage-duration products are the most accurate measurements of conventional ECH-LVH [17]. In 1998, Chapman et al. [18] reported greater ECG voltages in Africans, even when closely matched for LVH. This was attributed to ethnic differences in ECG voltages that were unrelated to differences in left ventricular mass index and overall added no difference in test accuracy. Currently accepted ECG voltage criteria for the detection of ECG-LVH remain equal or of greater value in black hypertensive's compared to whites [18].

There have been a large number of international studies assessing the separate effects of increased blood pressure and inflammation on LVH [12], [13], [14], [15], [16], [17], [18]. The aim of our sub-study was therefore to assess if low grade inflammation and pressure overload would have an additive association with ECG left ventricular hypertrophy in an ethnic male cohort from South Africa.

Section snippets

Participants

The SABPA (Sympathetic activity and Ambulatory Blood Pressure in Africans) study was performed in 2008 and 2009 and involved the participation of 101 African- and 101 Caucasian males. A power analysis was based on the largest standard deviation of ambulatory blood pressure indicating that a group consisting of 50 participants is enough to indicate significant differences in biological profiles [19]. The participants were urban teachers from the North-West Province, South Africa aged between 25

Results

From the 162 male participants of the SABPA study, a total of 19 participants’ (13 African and 6 Caucasian) had missing Cornell Product data. As seen in Table 1, the overall baseline characteristics of the participants largely show an unfavourable cardiovascular health profile for the African males. Africans showed a significantly higher ambulatory systolic (p < 0.01), diastolic blood pressure (p < 0.01), pulse pressure (p = 0.07), heart rate (p = 0.03), hs-CRP (p = 0.01) and higher Cornell product (p = 

Discussion

Our main aim was to assess the association between elevated ambulatory blood pressure, inflammation and a possible additive effect on ECG-LVH in a sub-Saharan African male cohort. The main finding in this study was the strong association between ECG LVH, SBP and pulse pressure in African men who also revealed elevated inflammation. Noteworthy is the fact that African men clearly showed elevated blood pressure levels when compared to Caucasian men regardless of inflammation. This finding has

Conflict of Interest

The authors declare no conflict of interest.

Acknowledgements

The Sympathetic activity and Ambulatory Blood Pressure in African study would not have been possible without the voluntary participation of the participants and consent from the Department of Education, North-West Province, South Africa. This work was partially supported by the National Research Foundation (UID 65607); the ROCHE Diagnostics, North-West University, North West Department of Education, South Africa; and the Metabolic Syndrome Institute, France.

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