Dual elevated remnant cholesterol and C-reactive protein in myocardial infarction, atherosclerotic cardiovascular disease, and mortality

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Background and aims: Elevated remnant cholesterol and low-grade inflammation each cause atherosclerotic cardiovascular disease (ASCVD); however, it is unknown whether joint elevation of both factors confers the highest risk. We tested the hypothesis that dual elevated remnant cholesterol and low-grade inflammation marked by elevated C-reactive protein is associated with the highest risk of myocardial infarction, ASCVD, and all-cause mortality. Methods: The Copenhagen General Population Study randomly recruited white Danish individuals aged 20–100 years in 2003–2015 and followed them for a median 9.5 years. ASCVD was cardiovascular mortality, myocardial infarction, stroke, and coronary revascularization. Results: In 103,221 individuals, we observed 2,454 (2.4%) myocardial infarctions, 5,437 (5.3%) ASCVD events, and 10,521 (10.2%) deaths. The hazard ratios increased with each of stepwise higher remnant cholesterol and stepwise higher C-reactive protein. In individuals with the highest tertile of both remnant cholesterol and C-reactive protein compared to individuals with the lowest tertile of both, the multivariable adjusted hazard ratios were 2.2 (95%CI:1.9–2.7) for myocardial infarction, 1.9 (1.7–2.2) for ASCVD, and 1.4 (1.3–1.5) for all-cause mortality. Corresponding values for only the highest tertile of remnant cholesterol were 1.6 (1.5–1.8), 1.4 (1.3–1.5), and 1.1 (1.0–1.1), and those for only the highest tertile of C-reactive protein were 1.7 (1.5–1.8), 1.6 (1.5–1.7), and 1.3 (1.3–1.4), respectively. There was no statistical evidence for interaction between elevated remnant cholesterol and elevated C-reactive protein on risk of myocardial infarction (p = 0.10), ASCVD (p = 0.40), or all-cause mortality (p = 0.74). Conclusions: Dual elevated remnant cholesterol and C-reactive protein confers the highest risk of myocardial infarction, ASCVD, and all-cause mortality, that is, compared to either of these two factors individually.

Original languageEnglish
Article number117141
JournalAtherosclerosis
Volume379
ISSN0021-9150
DOIs
Publication statusPublished - 2023

Bibliographical note

Funding Information:
The work reported here received no direct funding. This work was partly supported by the Capital Region of Denmark to BGN (the Global Excellence Programme) , to AL (Research Fund, grant number: A7160 ), and to TD (Research Fund, grant number: A7165 and A7272 ); the Department of Clinical Biochemistry , Copenhagen University Hospital, Herlev and Gentofte, Denmark ; and Japan Society for the Promotion of Science to TD (JSPS Overseas Research Fellowship) .

Publisher Copyright:
© 2023 The Authors

    Research areas

  • Cardiovascular disease, Death, Inflammation, Triglycerides-rich lipoproteins, Very low-density lipoproteins

ID: 371472408