Differences in Leukocyte Telomere Length between Coronary Heart Disease and Normal Population: A Multipopulation Meta-Analysis

Abstract

Coronary heart disease (CHD) is one of the most common causes of death in the world. Numerous studies have shown that as the degree of atherosclerotic disease increases, leukocyte telomere length gradually decreases. Short telomeres increase the risk of all-cause death and cardiovascular death. However, the reported results are not consistent, since the experimental design method, the measurement method, and the disease outcome are different. Therefore, we searched five major literature databases (Pubmed, Web of science, Embase, CNKI, and Wangfang) and finally included 18 eligible articles (including 5,150 patients with CHD and 9341 controls). We found that telomere length in patients with CHD was significantly shorter than that in controls, and the telomere length was inversely correlated with the severity of CHD. Subgroup analysis showed that telomere shortening was the most significant in Asian patients with CHD, in CHD patients with an average age <65 years, and in men with CHD. The mechanism of shortening the telomere length leading to the occurrence and development of CHD is worthy of further study.

Figure 1

Overall model linking the telomere length with inflammation and oxidative stress. Route 1: in CHD patients, inflammation and oxidative stress accelerate the formation of atheroma. In order to repair the endothelial injury caused by atheroma, hematopoietic stem cells (HSC) will accelerate the replication in order to maintain its own reserve, accompanied by the shortening of telomeres in the cells. At the same time, telomere shortening will feed back to HSC, resulting in a decrease in replication rate and a decrease in their reserve. Atheroma becomes difficult to repair and more unstable. Route 2: oxidative stress and inflammation can use oxygen free radical (such as O²⁻) to increase the rate of telomere shortening by directly acting on the GGG-specific sequence in the telomere.

Figure 2

Flow diagram of eligible studies selection in present meta-analysis.

Figure 3

Standard mean difference of telomere length between CHD and control group by recorded study level characteristics.

Figure 4

Forest plot (a) and funnel plot (b) of telomere length in CHD. SD: standard difference; SMD: standard mean difference.

Figure 5

Egger tests for the assessment of publication bias of telomere length in CHD. SND: Standard.