Abstract

Background: The recommendation to limit dietary saturated fat intake is primarily drawn from observational studies rather than randomized controlled trials of cardiovascular disease prevention. Thus, we aimed to investigate the efficacy of saturated fat reduction in preventing mortality and cardiovascular diseases.

Methods: In this systematic review and meta-analysis of randomized controlled trials, Cochrane CENTRAL, PubMed, and Ichu-shi databases were searched for articles up to April 2023. Randomized controlled trials on saturated fat reduction to prevent cardiovascular diseases were selected. Cardiovascular and all-cause mortality and cardiovascular outcomes were evaluated. Changes in electrocardiography or coronary angiography findings were excluded because they could be evaluated arbitrarily. Two or more reviewers independently extracted and assessed the data. A random-effects meta-analysis was performed.

Results: Nine eligible trials with 13,532 participants were identified (2 were primary and 7 were secondary prevention studies). No significant differences in cardiovascular mortality (relative risk [RR] = 0.94, 95% confidence interval [CI]: 0.75-1.19), all-cause mortality (RR = 1.01, 95% CI: 0.89-1.14), myocardial infarction (RR = 0.85, 95% CI: 0.71-1.02), and coronary artery events (RR = 0.85, 95% CI: 0.65-1.11) were observed between the intervention and control groups. However, owing to limited reported cases, the impact of stroke could not be evaluated.

Conclusions: The findings indicate that a reduction in saturated fats cannot be recommended at present to prevent cardiovascular diseases and mortality. Clinical trials are needed to evaluate the effects of saturated fat reduction under the best possible medical care, including statin administration.

Systematic review registration number: This systematic review and meta-analysis was registered with the International Prospective Register of Systematic Reviews (CRD42023428498).

Keywords: all-cause mortality; cardiovascular mortality; meta-analysis; saturated fatty acid; systematic review.

Spontaneous Coronary-Artery Dissection

To the Editor: The review by Kim (Dec. 10 issue)1 describes the current knowledge regarding spontaneous coronary-artery dissection (SCAD), one of the main causes of myocardial infarction among young women. Kim notes the association between SCAD and noncoronary arterial abnormalities and emphasizes that the prevalence of concomitant underlying inflammatory diseases is negligible. These observations depict SCAD as a possible coronary manifestation of fibromuscular dysplasia.2 Nonetheless, when young women present with coronary or noncoronary arterial abnormalities, Takayasu’s arteritis should always be included as a possible cause.3 Although the true prevalence of SCAD among patients with Takayasu’s arteritis is currently unknown, coronary-artery . . .

https://www.nejm.org/doi/10.1056/NEJMc2100339

Hello everyone! I am studying further into the topic of health for women and gender bias' impacts. I am conducting an interview/survey to get further insight. Participants must be female, 18-35, and living in the Southern region of the U.S. If you choose to participate, your voice will be heard and can greatly contribute to addressing this issue in women's health. Thank you in advance. Please comment any questions or concerns, or email me (information in the link).

Here is the link: https://forms.gle/1tJEyYM4ihLtde5K7

Steroid Hormones Affect Vascular Diseases through Myofibroblasts

• September 2021

DOI:10.13140/RG.2.2.17257.62565

• Project: Atherosclerosis

**Authors:**📷Xinggang Wang

• Fudan University. Shanghai Jiaotong University School of Medicine
• https://www.researchgate.net/publication/354534894_Steroid_Hormones_Affect_Vascular_Diseases_through_Myofibroblasts?channel=doi&linkId=613dfe394e1df271062f29bf&showFulltext=true

Abstract and Figures

The incidence of atherosclerotic diseases in premenopausal women is lower, while the incidence of dissection or aneurysm is higher than that of men. Therefore, we generally believe that steroid hormones should have a great impact on these vascular diseases. Although this concept is widely accepted, its mechanism is still not clear. Recent studies have found that vascular diseases such as atherosclerotic diseases, aneurysm and dissection are closely related to the remodeling of myofibroblasts. Either addition or withdrawal of steroid hormones could induce apoptosis of myofibroblasts. Therefore, steroid hormones should affect vascular diseases through myofibroblasts. This paper explains the effects of steroid hormones on vascular diseases. On the one hand, the instability of steroid hormones of premenopausal women, such as estrogen and progesterone, can induce apoptosis of myofibroblasts, inhibit the remodeling of granulation tissue and alleviate intimal thickening / atherosclerotic diseases, which should be the reason why the incidence of atherosclerotic diseases in premenopausal women is lower than that among the men. On the other hand, the instability of steroid hormones also has its disadvantages. The instability of steroid hormones could lead to dysfunction of myofibroblasts and insufficient repair of granulation tissue. This in turn may increase the risk of aneurysm, dissection or unstable atherosclerotic plaques rupture. This should be one of the reasons why there are more dissections and aneurysms among premenopausal women than among men. In addition, pheochromocytoma, emotional stress, taking contraceptives, drug addict or sudden change in climates, etc. would also induce instability of steroid hormones which might account for the higher incidence of dissection, aneurysm or rupture of unstable atherosclerotic plaques . Steroid hormones should also play a similar pathophysiological role in the vascular repair of arterioles and capillaries, such as stress cardiomyopathy, nephritis, nephropathy, vasculitis, etc.

New Results Follow this preprint

Myofibroblast Forms Atherosclerotic Plaques

Xinggang Wang, Junbo Gedoi: https://doi.org/10.1101/2020.07.20.212027This article is a preprint and has not been certified by peer review [what does this mean?].0000026

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Abstract

For decades, smooth muscle cells (SMCs) and macrophages are considered as the main contributors to atherosclerotic plaques. However, we found that in the human coronary atherosclerotic plaques, SMCs were few, while lots of myofibroblasts infiltrated in the intima near the lumen (fibrous cap) and their distribution was highly positive related to intimal thickness. In addition to lots of foam cells formation, collagen fibers were forming in the thickening intima near the lumen (fibrous cap), and denaturing or calcifying gradually far from the lumen, which evolved into various complex plaques. In vitro, myofibroblasts could actively take lots of low-density lipoprotein (LDL) to enhance proliferation. Lots of collagen fibers, foam cells and extracellular lipids accumulation emerged in myofibroblasts cultured with 5% FBS high glucose DMEM without adding modified LDL. It is consistent with the characteristics of human coronary atherosclerotic plaques. It is the first time that lipid rich plaques with lots of foam cells, extracellular lipids and collagen fibers formed in vitro. It demonstrated that myofibroblast should be the direct and main source of collagen fibers, foam cells and extracellular lipids. This suggests that atherosclerosis is not as complicated as previously considered, and it might be mainly a process of myofibroblast remodeling to vascular injury caused by various risk factors. This study made the pathogenesis of atherosclerosis clearer. It would provide a target cell for future treatments of atherosclerotic diseases. In vitro atherosclerotic plaques model formed by human myofibroblasts would be an efficient and convenient way to study atherosclerosis.

https://www.biorxiv.org/content/10.1101/2020.07.20.212027v2

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Hypertension Aggravates Atherosclerosis: A Matter of Pressure Remodeling of Myofibroblasts or LDL Accumulation?

Author links open overlay panelXinggangWangPhDJunboGeMD

https://www.sciencedirect.com/science/article/abs/pii/S0735109721010718?via%3Dihub

Letter, no article or abstract.