Causal Relationship Observed Between Angina Pectoris and Gout Onset

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Results of a 2-sample Mendelian randomization (MR) study showed a clear causal relationship between angina pectoris and the onset of gout, according to research published in Pain Management and Research.¹

The incidence of both gout and angina pectoris continues to rise annually, with the global prevalence of gout currently ranging from .1% to 10.0%. Additionally, deaths due to cardiovascular disease have increased by 12.5% over the past decade and now accounts for approximately one-third of overall deaths globally.²

Investigators believe understanding the relationship between these conditions and evaluating the possibility of the development of both could help to more precisely prevent and control angina combined with gout.

“The relationship between angina pectoris and the incidence of gout lacks detailed evidence and warrants support from high-quality clinical research, and the relationship between angina pectoris and the incidence of gout needs to be elucidated as soon as possible,” wrote a group of investigators from Chengdu University of Traditional Chinese Medicine in Chengdu, China.

Single nucleotide polymorphisms (SNPs) linked with gout were collected from the UK Biobank-Neale Lab to be used as genetic instrumental variables. As gout is defined by elevated blood uric acid levels, the SNPs related to blood uric acid levels were collected from BioBank Japan and used as auxiliary gene instrumental variables. Similarly, SNPs linked to angina pectoris onset were collected from the FINN dataset as outcome variables.

The inverse variance weighting (IVW) of the random effects model was the primary result of the MR, along with the weighted median method (WME) and the MR-Egger regression method. A meta-analysis was performed on the IVW results of the European and Japanese biobanks.

In the UK biobank, the odds ratios (ORs) and 95% confidence intervals (CIs) of the IVW, WME, and MR-Egger were OR = 33.72; 95% CI: 2.07∼550.38; OR = 57.94; 95% CI: 2.75∼1219.82; and OR = 96.38; 95% CI: 0.6∼15556.93, respectively. Angina pectoris was significantly linked with the incidence of gout according to the values of IVW and WME (both .014, P <.05).

In the Japanese biobank, the ORs and 95% CIs of the IVW, WME, and MR-Egger were OR = 1.20; 95% CI: 1.07∼1.34; OR = 1.19; 95% CI: 1.02∼1.38; and OR = 1.30; 95% CI; 1.06∼1.60, respectively. Similarly, the values of the IVW, WME, and MR-Egger indicated a significant correlation between angina and blood uric acid levels (.001, .027, and .017, respectively; P <.05).

Scatter plots confirmed the causal association estimates of the MR-Egger, IVW, and weighted median methods were comparable, and the results of the MR were accurate. The meta-analysis of the IVW for the European and Japanese biobanks demonstrated gout with high blood uric acid levels significantly increases the risk of experiencing angina attacks (OR = 1.20; 95% CI: 1.07–1.34).

Investigators noted limitations including the heterogeneity in the results of the meta-analysis, which warrants further research using more datasets and larger sample sizes to confirm the findings and reduce heterogeneity. Additionally, all patients analyzed were of either European or East Asian ancestry, which may have reduced generalizability.

“Patients with gout often experience cardiovascular diseases in combination, and few guidelines have recommended drug treatment programs,” they wrote. “We expect that subsequent studies will focus on the group of patients with gout combined with angina pectoris and report on the risk factors for angina pectoris in patients with acute gout, as well as the anti-inflammatory and analgesic treatment programs for the 2 diseases, to reduce the acute attacks of angina pectoris in patients with gout and provide a basis for decision-making in terms of clinical drug treatment.”

References

1. ^{Xiong J, Sun Y, Huang H, et al. The Causal Relationship between Angina Pectoris and Gout Based on Two Sample Mendelian Randomization. Pain Res Manag. 2024;2024:4564596. Published 2024 Apr 9. doi:10.1155/2024/4564596}
2. ^{G. A. Roth, D. Abate, K. H. Abate et al. et al., “Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017,” The Lancet, vol. 392, no. 10159, pp. 1736–1788, 2018.}