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Review
. 2023 Aug 23;11(9):2353.
doi: 10.3390/biomedicines11092353.

Non-Conventional Risk Factors: "Fact" or "Fake" in Cardiovascular Disease Prevention?

Giovanni Cimmino  1   2 , Francesco Natale  3 , Roberta Alfieri  1   3 , Luigi Cante  1   3 , Simona Covino  1   3 , Rosa Franzese  1   3 , Mirella Limatola  1   3 , Luigi Marotta  1   3 , Riccardo Molinari  1   3 , Noemi Mollo  1   3 , Francesco S Loffredo  1   3 , Paolo Golino  1   3
Affiliations
Review

Non-Conventional Risk Factors: "Fact" or "Fake" in Cardiovascular Disease Prevention?

Giovanni Cimmino et al. Biomedicines. .

Abstract

Cardiovascular diseases (CVDs), such as arterial hypertension, myocardial infarction, stroke, heart failure, atrial fibrillation, etc., still represent the main cause of morbidity and mortality worldwide. They significantly modify the patients' quality of life with a tremendous economic impact. It is well established that cardiovascular risk factors increase the probability of fatal and non-fatal cardiac events. These risk factors are classified into modifiable (smoking, arterial hypertension, hypercholesterolemia, low HDL cholesterol, diabetes, excessive alcohol consumption, high-fat and high-calorie diet, reduced physical activity) and non-modifiable (sex, age, family history, of previous cardiovascular disease). Hence, CVD prevention is based on early identification and management of modifiable risk factors whose impact on the CV outcome is now performed by the use of CV risk assessment models, such as the Framingham Risk Score, Pooled Cohort Equations, or the SCORE2. However, in recent years, emerging, non-traditional factors (metabolic and non-metabolic) seem to significantly affect this assessment. In this article, we aim at defining these emerging factors and describe the potential mechanisms by which they might contribute to the development of CVD.

Keywords: cardiovascular diseases; cardiovascular prevention; conventional risk factors; emerging risk factors.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Possible role of homocysteine in CVD.
Figure 2
Figure 2
Major pathways UA related involved in pathogenesis of CVD.
Figure 3
Figure 3
Putative cardiovascular pathways Vitamin D-related: see text for details.
Figure 4
Figure 4
Summary of the main mechanisms by which gut microbiota, in condition of dysbiosis, influences the pathogenesis of atherosclerosis. * Precursors to TMAO: choline, L-carnitine and betaine. See text for details.
Figure 5
Figure 5
Lp(a) connection with CVD.
Figure 6
Figure 6
Schematic view of metabolic syndrome leading to CVD.
Figure 7
Figure 7
Pathophysiological pathways OSA related leading to CVD.
Figure 8
Figure 8
Molecular mechanisms linked air pollution to CVD.
Figure 9
Figure 9
Correlation between climate changes and CVD: possible basic mechanisms. Several variables affect the response to temperature changes.
Figure 10
Figure 10
Association between Sleep duration and CVD.
See this image and copyright information in PMC

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