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The role of inflammation and the possibilities of inflammation reduction to prevent cardiovascular events.

ABSTRACT: Chronic systemic inflammation is a risk factor for cardiovascular (CV) disease (CVD). Whether this relationship extends to subclinical inflammation, quantified by values of circulating markers associated with inflammation in the high range of the normal interval, remains debatable. This narrative review evaluates evidence exploring this relationship. A review of pharmacological and non-pharmacological interventions, including diet and lifestyle strategies, supplements, nutraceuticals, and other natural substances aimed at reducing inflammation was also conducted, since few reviews have synthesized this literature. PubMed and EMBASE were used to search the literature and several well-studied triggers of inflammation [oxidized LDL, Lp(a), as well as C-reactive protein (CRP)/high-sensitivity CRP (hs-CRP)] were included to increase sensitivity and address the lack of existing reviews summarizing their influence in the context of inflammation. All resulting references were assessed. Overall, there is good data supporting associations between circulating hs-CRP and CV outcomes. However, the same was not seen in studies evaluating triggers of inflammation, such as oxidized LDL or Lp(a). There is also insufficient evidence showing treatments to target inflammation and lead to reductions in hs-CRP result in improvements in CV outcomes, particularly in those with normal baseline levels of hs-CRP. Regarding pharmacological interventions, statins, bempedoic acid, and apabetalone significantly reduce circulating hs-CRP, unlike PCSK-9 inhibitors. A variety of natural substances and vitamins were also evaluated and none reduced hs-CRP. Regarding non-pharmacological interventions, weight loss was strongly associated with reductions in circulating hs-CRP, whereas various dietary interventions and exercise regimens were not, unless accompanied by weight loss.

SUBMITTER: Maierean S

PROVIDER: S-EPMC9271640 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature

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The role of inflammation and the possibilities of inflammation reduction to prevent cardiovascular events.

Maierean Serban S Webb Richard R Banach Maciej M Mazidi Mohsen M

European heart journal open 20220614 4

Chronic systemic inflammation is a risk factor for cardiovascular (CV) disease (CVD). Whether this relationship extends to subclinical inflammation, quantified by values of circulating markers associated with inflammation in the high range of the normal interval, remains debatable. This narrative review evaluates evidence exploring this relationship. A review of pharmacological and non-pharmacological interventions, including diet and lifestyle strategies, supplements, nutraceuticals, and other ...[more]

PMID: 35919577

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Project description:ObjectivesTo examine the contemporary effect of smoking in a multiethnic sample, and to explore the respective contributions of inflammation and subclinical atherosclerosis to the cardiovascular consequences of smoking.Approach and resultsWe studied 6814 participants free of cardiovascular disease and coronary heart disease (CHD) from the Multiethnic Study of Atherosclerosis. Smoking status and cumulative exposure were determined by self-report and confirmed by urinary cotinine. Multivariable Cox regression was used to estimate the association between smoking parameters and all-cause cardiovascular disease, all-cause CHD, and hard CHD events. We further adjusted for high-sensitivity C-reactive protein and coronary artery calcium (CAC) in hierarchical Cox models. We identified 3218 never smokers, 2607 former smokers, and 971 current smokers. Median follow-up was 10.2 years. Compared with never smokers, adjusted hazard ratios in current smokers were 1.7 (95% confidence interval, 1.3-2.2) for all-cause cardiovascular disease, 1.6 (1.1-2.1) for all-cause CHD, and 1.7 (1.2-2.4) for hard CHD. Similarly, among current smokers, hazard ratios were higher in the 4th versus 1st quartile of pack-years (eg, all-cause CHD hazard ratio=2.7 [1.1-6.6]). Both CAC>100 and high-sensitivity C-reactive protein ≥3 mg/L identified higher relative risk among current smokers (eg, all-cause CHD hazard ratio of 3.0 [1.5-6.0, compared with CAC=0] and 2.6 [1.4-4.8, compared with high-sensitivity C-reactive protein <2 mg/L], respectively). However, CAC was a stronger mediator of events and adversely modified the effect of smoking on events (eg, P-interaction=0.02 for hard CHD). Compared with never smokers, former smokers (median cessation interval=22 years) had similar adjusted hazard for events.ConclusionsIn this multiethnic cohort, current smoking and cumulative exposure remain important modifiable determinants of cardiovascular disease. Both high-sensitivity C-reactive protein ≥3 mg/L and, particularly, CAC>100 identified high-risk smokers who may benefit from more intensive smoking-cessation efforts.

Project description:BACKGROUND AND OBJECTIVES:In the Systolic Blood Pressure Intervention Trial (SPRINT), intensive systolic BP treatment (target <120 mm Hg) was associated with fewer cardiovascular events and higher incidence of kidney function decline compared with standard treatment (target <140 mm Hg). We evaluated the association between mean arterial pressure reduction, kidney function decline, and cardiovascular events in patients without CKD. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:We categorized patients in the intensive treatment group of the SPRINT according to mean arterial pressure reduction throughout follow-up: <20, 20 to <40, and ≥40 mm Hg. We defined the primary outcome as kidney function decline (≥30% reduction in eGFR to <60 ml/min per 1.73 m2 on two consecutive determinations at 3-month intervals), and we defined the secondary outcome as cardiovascular events. In a propensity score analysis, patients in each mean arterial pressure reduction category from the intensive treatment group were matched with patients from the standard treatment group to calculate the number needed to treat regarding cardiovascular events and the number needed to harm regarding kidney function decline. RESULTS:In the intensive treatment group, 1138 (34%) patients attained mean arterial pressure reduction <20 mm Hg, 1857 (56%) attained 20 to <40 mm Hg, and 309 (9%) attained ≥40 mm Hg. Adjusted hazard ratios for kidney function decline were 2.10 (95% confidence interval, 1.22 to 3.59) for mean arterial pressure reduction between 20 and 40 mm Hg and 6.22 (95% confidence interval, 2.75 to 14.08) for mean arterial pressure reduction ≥40 mm Hg. In propensity score analysis, mean arterial pressure reduction <20 mm Hg presented a number needed to treat of 44 and a number needed to harm of 65, reduction between 20 and <40 mm Hg presented a number needed to treat of 42 and a number needed to harm of 35, and reduction ≥40 mm Hg presented a number needed to treat of 95 and a number needed to harm of 16. CONCLUSIONS:In the intensive treatment group of SPRINT, larger declines in mean arterial pressure were associated with higher incidence of kidney function decline. Intensive treatment seemed to be less favorable when a larger reduction in mean arterial pressure was needed to attain the BP target.

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The role of inflammation and the possibilities of inflammation reduction to prevent cardiovascular events.

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The role of inflammation and the possibilities of inflammation reduction to prevent cardiovascular events.

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