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 Table of Contents  
Year : 2019  |  Volume : 16  |  Issue : 1  |  Page : 25-31

Serum chemerin as a predictor of left ventricle hypertrophy in patients with coronary artery disease

1 Department of Cardiovascular Diseases, Faculty of Medicine, Cairo University, Cairo, Egypt
2 Department of Clinical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt

Date of Submission06-Aug-2018
Date of Decision24-Apr-2019
Date of Acceptance12-Jun-2019
Date of Web Publication22-Oct-2019

Correspondence Address:
Prof. Noha Hasssanin Hanboly
Department of Cardiovascular Diseases, Cairo University, Cairo
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njc.njc_20_18

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Background: Left ventricular hypertrophy (LVH) is an important predictor of cardiovascular risk and its detection contributes to risk stratification. Chemerin is a secreted protein with a complex but well-established role in immune function. It regulates adipocyte development and metabolic function as well as glucose metabolism in liver and skeletal muscle tissues.
Purpose of the Study: The aim of the current study was to investigate the correlation between the serum chemerin level and occurrence of LVH in patients with coronary artery disease (CAD).
Patients and Methods: The study included 100 patients with CAD. Patients were classified according to their body mass index (BMI) into two groups, 50 patients (Group A) with BMI (≥30 kg/m2) and 50 patients (Group B) with BMI ≤25 kg/m2. Transthoracic echocardiography was done for all patients after a thorough clinical assessment. Left ventricular study was done according to the guidelines endorsed by the American society of echocardiography.
Results: Serum chemerin level was positively correlated with BMI, waist circumference, and left ventricle mass index (P < 0.005 for all).
Conclusion: Serum chemerin levels were higher in obese patients with CAD. Levels were associated with LVH and increased high-sensitivity C-reactive protein as a marker of inflammation.

Keywords: Coronary artery disease, left ventricle hypertrophy, obesity, serum chemerin

How to cite this article:
Hanboly NH, Sharaf Y, Al-Anany M, Saeed E. Serum chemerin as a predictor of left ventricle hypertrophy in patients with coronary artery disease. Nig J Cardiol 2019;16:25-31

How to cite this URL:
Hanboly NH, Sharaf Y, Al-Anany M, Saeed E. Serum chemerin as a predictor of left ventricle hypertrophy in patients with coronary artery disease. Nig J Cardiol [serial online] 2019 [cited 2020 Sep 25];16:25-31. Available from: http://www.nigjcardiol.org/text.asp?2019/16/1/25/269649

  Introduction Top

Left ventricular hypertrophy (LVH) is defined by the increased left ventricular (LV) mass, myocardial cell hypertrophy, and an increase in collagen within the myocardium.[1]

It was found that LVH is present in the obese population. Obesity-related LVH is a powerful risk factor for systolic/diastolic dysfunction.[2]

An individual would be considered to be underweight if his/her body mass index (BMI) was in the range of 15–19.9, normal weight if the BMI was 20–24.9, overweight if the BMI was 25–29.9, and obese if it was 30–35 or greater.[3]

Other factors such as age, race, and gender can influence cardiac mass; this might occur through the cardiac load.[4] Hypertensive LVH is a risk factor for high insulin level and insulin resistance. Significant correlation between LV mass, insulin-like growth factor–I, and insulin was observed in a cohort study.[5]

The remodeling process in long-standing hypertension (HTN) consists of hypertrophy, fibrosis, and impaired microvascular circulation with arterial stiffness. It is accompanied by higher pulse pressure and systolic blood pressure (SBP), which are well-known risk factors for cardiovascular diseases.[6]

Systemic inflammation and endothelial damage were associated with LVH occurrence. These relationships offer insight into the pathophysiological mechanisms linking LVH to atherosclerosis and to increased cardiovascular morbidity and mortality.[7]

C-reactive protein (CRP) is a marker of systemic inflammation, predictor of poor cardiovascular prognosis, and its levels are generally elevated in patients with HTN.[8]

LVH is associated with increased cardiovascular morbidity and mortality, especially for hypertensive patients.[9] Echo criteria for LVH have been shown to have good sensitivity, specificity when compared with postmortem LV mass.[10] It was found that the prevalence of LVH in hypertensive cases varies from 20% to 70%.[11]

Adipose tissue and Chemerin

The traditional view of adipose tissue as a passive reservoir for energy storage is no longer valid. Adipose tissue is now known to express and secrete a variety of bioactive peptides, known as adipokines, which act at both the local (autocrine/paracrine) and systemic (endocrine) level.[12]

The discovery of leptin in 1994 heralded a new era in the discovery of a number of adipocytokines, such as adiponectin, leptin, resistin, visfatin, apelin, omentin, chemerin, nesfatin, and other cytokines, for example, interleukin-6 (IL-6), plasminogen activator inhibitor-1, monocyte chemoattractant protein-1, and tumor necrosis factor-alpha (TNF-α)[13] [Figure 1].
Figure 1: Timeline of adipokines discovery. IL-6 – Interleukin-6; PAI-1 – Plasminogenactivator inhibitor-1; RBP-4 –Retinol-binding protein-4; SAA – Serum amyloid A; TNF- α – Tumour necrosis factor alpha; ZAG – Zinc-α2-glycoprotein

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Chemerin is an adipokine known as a ligand for G protein-coupled chemokine-like receptor 1 (CMKLR1), also known as chemerin receptor 23, which was first identified in macrophages and dendritic cells.[14],[15]

Chemerin acts as a chemotactic factor for leukocyte populations expressing ChemR23, particularly immature plasmacytoid dendritic cells (pDCs) but also immature myeloid dendritic cells, macrophages and natural killer cell.[16]

Chemerin, also known as tazarotene-induced gene 2 or retinoic acid receptor responder protein 2, is a broadly expressed leukocyte attractant ligand for serpentine, G protein-associated receptor CMKLR1.[17]

CMKLR1, pDCs, macrophages, and natural killer cells are critical in bridging the innate and adaptive immune responses.[18]

In addition to its chemotactic effect, chemerin was found to regulate adipocyte differentiation angiogenesis, osteoblastogenesis, myogenesis, and glucose homeostasis [Figure 2].[19],[20]
Figure 2: Obesity, inflammation and chemerin. WAT – white adipose tissue

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The main source of chemerin is white adipose tissue, but a high concentration was also found in the liver, lower lungs, brown adipose tissue, heart, ovaries, kidneys, skeletal muscle, and pancreas.[21]

Aim of work

The aim of this study was to examine whether serum levels of chemerin are associated with metabolic parameters and the occurrence of LVH in patients with coronary artery disease (CAD).

  Patients and Methods Top

This was a prospective observational study that was conducted on 100 patients presented to the Department of Cardiology at Cairo University hospital with a picture of CAD.

Patients were divided into two groups, Group A included 50 obese patients (BMI ≥30 kg/m2) and Group B included 50 nonobese patients (BMI = 18–25 kg/m2).

Patients who refused to participate in the study or those with significant renal impairment (serum creatinine ≥2 mg/dl or creatinine clearance ≤60 ml/min) were excluded from the study. The study protocol was approved by the Local Ethics Committee. All patients were subjected to detailed medical history and clinical examination.

Diabetes mellitus was defined as fasting plasma glucose (FPG) ≥126 mg/dl and/or random plasma glucose ≥200 mg/dl and/or self-reported diabetes.[22]

Office BP was measured twice by a trained physician, with patients in the sitting position, using a calibrated mercury sphygmomanometer. HTN was defined according to the recently released American College of Cardiology/American Heart Association HTN guidelines.[23]

Dyslipidemia defined as total cholesterol >200 mg/dl, low-density lipoprotein cholesterol >100 mg/dl, high-density lipoprotein cholesterol <40 mg in males and <50 mg/dl in females or use of lipid-lowering medication. Hypertriglyceridemia was defined as triglycerides (TGs) >150 mg/dl.[24]

Anthropometric measurement

BMI was calculated according to the following formula: BMI = body weight (kg)/height (m2). Waist circumference (WC) was measured at the level of mid-distance between the bottom of the rib cage and the top of the iliac crest after expiration. Obesity was defined as BMI ≥30 kg/m2. Abnormal WC was defined as WC ≥94 cm for men and ≥80 cm for women.[3]

Laboratory work up

Complete blood count, FPG, high-sensitivity CRP (hs-CRP), serum creatinine, liver function tests, lipid profile, and serum chemerin level.

Serum Chemerin level

A volume of 5 ml blood sample was drawn from patients. The samples were separated and stored at −20°C. An enzyme-linked immunosorbent assay kit was used to assay human chemerin in the sample according to the manufacturer's instructions (SinoGeneclon Co., Ltd., Product No: SG-10352).

Echocardiographic assessment

The echocardiographic machines used were General Electric VIVID 7 (GE Health Medical, Horten, Norway) and Philips IE 33 (USA). Patients were examined in the left lateral decubitus position.

Using two-dimensional and M-mode echocardiography LV end-diastolic and end-systolic dimensions, LV posterior wall thickness in diastole, dimensions of the ascending aorta, and end-systolic dimension of the left atrium were studied according to the American society of echocardiography.[25]

LV ejection fraction percentage was measured with the biplane Simpson's method and was used as a parameter of LV systolic function. Regional wall motion abnormalities were assessed in different views. LV mass index (LVMI) was measured through the linear method with the Devereux formula:

LV mass was calculated using Devereux formula = 0.8 (1.04([LVID+PWT+IVST]3 – [LVID]3)) + 0.6 g where LVID is the left ventricle internal dimension, PWT is the posterior wall thickness, IVST is the interventricular septal thickness, 1.04 is the specific gravity of the myocardium, and 0.8 is the correction factor.[26]

The diagnosis of LVH was defined by LV mass indexed to body surface area equal to or higher 125 g/m2 in men and 110 g/m2 in women.[27]

Statistical analysis

After data were collected, they were analyzed using the Statistical Package for the Social Sciences version 19 (SPSS Inc., Chicago, IL, USA). Unless denoted otherwise, categorical data are described as count and percentages and continuous data are described as means ± standard deviation or median. Logarithmic transformation was used for chemerin due to the high degree of skewing.

A Student's t-test (for data that was normally distributed) or a Mann–Whitney test (for data that was not normally distributed) and Pearson's Chi-squared test (for data that were categorical variables) were used to compare the obese and nonobese samples.

Correlations between serum chemerin levels and continuous variables were determined using Pearson's correlation (for normally distributed data) or Spearman's correlation (for nonnormally distributed data). Two-tailed P < 0.05 was considered statistically significant.

  Results Top

This observational cross-sectional study was carried out in the Department of Cardiovascular at Cairo University hospital. The study included 100 patients with CAD who underwent coronary angiography for clinically indicated reasons. Patients were classified according to BMI into two groups (Group A) with BMI (≥30 kg/m2) and (Group B) having BMI ≤25 kg/m2.

Male gender predominated in our sample, and 70% of participants were older than 50 years.

50 patients were diabetics and 55 patients were hypertensives. According to the mode of presentation, 40 patients presented with the acute coronary syndrome and 60 patients were diagnosed with stable CAD [Table 1].
Table 1: The demographic, clinical characteristics and mode of presentation of the study patients

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It was found that obese patients had significantly higher levels of FPG, glycated hemoglobin (HbA1c), and chemerin levels than nonobese patients [Table 2]. Positive correlation was found between BMI and several study variables [Table 3].
Table 2: Laboratory data of obese versus nonobese patients classified according to body mass index

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Table 3: Body mass index correlated to different study parameters

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The more participants had a higher BMI, the higher their WC (r = 0.842, P < 0.001), SBP (r = 0.188, P = 0.061), serum TGs level (r = 0.369, P < 0.001), FPG (r = 0.246, P = 0.014), HbA1c (r = 0.331, P = 0.001), and serum chemerin level (r = 0.323, P = 0.001) [Figure 3].
Figure 3: Serum Chemerin level according to body mass index

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Echocardiography study

No significant difference was found between obese and nonobese participants [Table 4]. However, it was found that patients with LVH and abnormal LVMI were associated with high serum chemerin [Table 5].
Table 4: Echocardiography parameters according to body mass index

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Table 5: Serum chemerin and left ventricle hypertrophy

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Patients with LVH were older with high serum chemerin along with a trend of significance to be hypertensive than their comparators without LVH. Using binary logistic regression it was obvious that serum chemerin had significant independent value as a predictor of LVH [Figure 4].
Figure 4: Bivariate correlation of serum Chemerin with left ventricle mass index

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The study revealed that the more participants had higher BMI and WC, the higher their serum chemerin level. This positive correlation was noticed also with inflammatory status represented by elevated levels of hs-CRP [Figure 5].
Figure 5: Bivariate correlation of Chemerin with high sensitivity C-reactive protein

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  Discussion Top

The current prospective observational study was conducted on 100 participants divided into two groups, (Group A) 50 obese patients (BMI ≥ 30 kg/m2) with CAD and (Group B) 50 nonobese patients (BMI = 18–25 kg/m2) with CAD.

Patients had angiographically documented CAD. After taking informed consent, all candidate participants were subjected to full history taking, clinical examination, electrocardiogram (ECG) and to laboratory investigations, including serum chemerin level.

The relation between LVH and unfavorable cardiovascular prognosis may involve systemic inflammation and endothelial dysfunction/damage. However, the pathophysiologic mechanisms underlying the evolution from LVH to cardiovascular event development are still unclear, but they may involve accelerated atherosclerosis because of systemic inflammation and endothelial dysfunction.[28]

The circulating chemerin level strongly correlates with the level of inflammatory markers such as TNF-α, IL-6, hs-CRP, resistin, and leptin in humans and animals.[29]

The current study found that obese patients (group A) has a higher serum chemerin level than nonobese patients (Group B), (P = 0.019). This finding is concordant with other study that found a positive correlation of BMI with serum chemerin level in patients with CAD and metabolic syndrome.[30]

We found that serum chemerin levels were higher in females (P = 0.012) in contrast to previous studies that found similar levels in females and males.[31] This finding can be attributed to the higher prevalence of obesity among our female patients (only 7.7% are nonobese) with subsequent higher serum Chemerin level and also the fact that our study was not sex matched.

Among our participants, obese patients had significant lower prevalence of smoking (P = 0.002). Also, there was a significant higher serum Chemerin level in nonsmokers more than in smokers (P = 0.038) and this finding can be justified by the controversial fact that smoking is associated with lower body weights and with a lower prevalence of obesity. This is concordant with other studies that showed a nonsignificant trend toward a lower prevalence of smoking among obese subjects.[32]

Adipokines, especially leptin and adiponectin, have been linked to LVH in several studies.[33] Chemerin did not receive similar studies to determine its association with LVH. The current study revealed that Chemerin levels showed significant positive correlations with obesity parameters, LVMI, FPG, hs-CRP, and with the trend of significance with SBP.

Concordant with previous studies[34] Chemerin was elevated probably due to obesity and chronic inflammations that was reflected by a significant positive correlation with BMI and hs-CRP as well as with the severity of CAD evaluated by coronary angiography.[35],[36] hs-CRP had a significant positive correlation with serum Chemerin (r = 0.365, P = 0.001).

In our study, LVH was detected by echocardiography in 28% of our study patients and in 25% by ECG. No statically significant difference between obese and nonobese groups regarding the presence of LVH. However; serum chemerin level was statically significant higher in patients with LVH comparing with their comparators without LVH. After binary logistic regression analysis we found that serum chemerin level is a significant predictor of LVH (odds ratio = 0.98, 95% confidence interval = 0.006–0.994, P = 0.006).

  Conclusion Top

The study concluded that serum chemerin level was higher in obese patients with significant correlation to several cardiometabolic risk factors. Moreover; it had a significant correlation with hs-CRP as a marker of systemic inflammation. Serum chemerin had significant independent value as a predictor of LVH in patients with CAD.


The authors are grateful to all medical and paramedical staffs at echocardiography laboratory cardiovascular department Cairo University hospitals for their cooperation.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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