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Published on: September 25, 2017
Soluble tumor necrosis factor receptor 1 level is associated with left ventricular hypertrophy: the northern
Yasuyoshi Takei1, Marco R Di Tullio, Shunichi Homma
1Division of Cardiology, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York, USA.
Insights
Soluble tumor necrosis factor receptor 1 (sTNFR1) is linked to increased left ventricular mass, suggesting inflammation contributes to left ventricular hypertrophy (LVH). Other markers like hsCRP and IL-6 were not independently associated with LVH.
Area of Science:
- Cardiology
- Inflammation Research
- Biomarkers
Background:
- Inflammatory markers are linked to cardiovascular events.
- Limited data exist on inflammatory markers and left ventricular hypertrophy (LVH).
- This study investigates inflammatory markers and LVH in a multiethnic cohort.
Purpose of the Study:
- To evaluate the independent association between inflammatory markers and LVH.
- To assess the role of specific inflammatory markers in LVH development.
Main Methods:
- Cross-sectional study of 660 participants without stroke.
- Echocardiography performed for LV mass calculation.
- Assessed soluble tumor necrosis factor receptor 1 (sTNFR1), interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hsCRP).
Main Results:
- Univariate analyses showed hsCRP, IL-6, and sTNFR1 associated with LV mass.
- sTNFR1 remained independently associated with LV mass after adjustments.
- hsCRP and IL-6 were not independently associated with LV mass in multivariate models.
Conclusions:
- sTNFR1 is independently associated with increased LV mass.
- Chronic subclinical inflammation, particularly the TNFR1 system, may contribute to LVH.
- hsCRP and IL-6 are not independently associated with LVH in this population.
Background:
Although inflammatory markers may be associated with risk of cardiovascular events, few data are available regarding these markers and their association with left ventricular hypertrophy (LVH). We sought to evaluate whether inflammatory markers were independently associated with LVH in a multiethnic population in northern Manhattan.
Methods:
A population-based cross-sectional study was conducted in 660 participants without stroke, who had undergone both transthoracic echocardiography and testing for soluble tumor necrosis factor receptor (sTNFR) 1, interleukin (IL)-6, and high-sensitivity C-reactive protein (hsCRP). LV mass was calculated according to an established formula. LVH was defined as LV mass >90th percentile of the participants.
Results:
The mean age was 67.4 +/- 8.8 years, 35.5% were men, 61.7% were Hispanic, 19.7% were black, and 18.6% were white. In univariate analyses, hsCRP, IL-6, and sTNFR1 were significantly associated with LV mass. Multiple linear regression analyses demonstrated that sTNFR1 (P = 0.0008) was associated with LV mass after adjusting for demographic and medical risk factors, but hsCRP and IL-6 were not. When all markers were included in the same model, sTNFR1 remained significant, but hsCRP and IL-6 did not. Compared with the lowest quartile of sTNFR1, those in the highest quartile were more likely to have LVH (odds ratio = 1.84, 95% confidence interval, 0.97-3.64, P = 0.06).
Conclusions:
sTNFR1, but not hsCRP nor IL-6, is independently associated with increased LV mass. Chronic subclinical inflammation including the TNFR1-associated system may contribute to LVH.
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