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A Major Cause of Cardiovascular Disease is Dyslipidaemia
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Journal of Hypertension: Open Access

ISSN: 2167-1095

Open Access

Perspective - (2022) Volume 11, Issue 11

A Major Cause of Cardiovascular Disease is Dyslipidaemia

Vincent Auffret*
*Correspondence: Vincent Auffret, Department of Cardiology and Vascular Diseases, Pontchaillou University Hospital, University of Rennes, Rennes, France, Email:
Department of Cardiology and Vascular Diseases, Pontchaillou University Hospital, University of Rennes, Rennes, France

Received: 24-Oct-2022, Manuscript No. jhoa-23-86101; Editor assigned: 26-Oct-2022, Pre QC No. P-86101; Reviewed: 09-Nov-2022, QC No. Q-86101; Revised: 16-Nov-2022, Manuscript No. R-86101; Published: 24-Nov-2022 , DOI: 10.37421/2167-1095.2022.11.375
Citation: Auffret, Vincent. “A Major Cause of Cardiovascular Disease is Dyslipidaemia.” J hypertens 11 (2022): 375.
Copyright: © 2022 Auffret V. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Introduction

A condition known as dyslipidemia is characterized by an abnormally high blood level of lipids such as triglycerides, cholesterol, and fat phospholipids [1]. A factor that increases the likelihood of developing atherosclerotic cardiovascular disease (ASCVD) is dyslipidemia. Coronary artery disease, cerebrovascular disease, and peripheral artery disease are all examples of ASCVD. Dyslipidemia is a risk factor for ASCVD, but high levels do not necessitate lipid-lowering medications. In addition to dyslipidemia, other factors like concurrent conditions and lifestyle are taken into account in a cardiovascular risk assessment. In wealthy nations, the majority of dyslipidemias are caused by hyperlipidemia, or an increase in blood lipid levels. Most of the time, this is attributed to factors in one's diet and lifestyle. Dyslipidemia can result from prolonged insulin resistance. O-GlcNAc transferase (OGT) concentrations can also rise.

Description

There are two ways that doctors and basic scientists classify dyslipidemias. One method is the body's appearance (including the particular type of lipid that is elevated). The alternative is a result of the disease's underlying cause (genetic or secondary to another condition) [2]. The majority of illnesses are brought on by a combination of genetics and lifestyle choices, making this classification challenging. However, there are a few distinct genetic conditions that are typically simple to identify.

Triglycerides (TG), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C) (LDL-C) are the three primary blood values used to diagnose dyslipidemia. High triglyceride levels (fasting >1.7 mmol/L) are a sign of dyslipidemia. The bloodstream's triglyceride transporters are VLDLs (very low density lipoproteins). Because non-fasting TG results can be misleading, it is essential to keep in mind that when measuring triglyceride levels, you will need to fast for eight to twelve hours to obtain an accurate result. TG levels greater than 10 mmol/L should be treated due to the increased risk of acute pancreatitis posed by severe hypertriglyceridemia. HDL-C, a blood test that looks for dyslipidemia, is another one. HDL cholesterol is mostly protein with a few lipids. It has a beneficial effect on the body because it works by getting to the tissues and removing excess cholesterol and fat [3,4]. HDL-C is referred to as "good cholesterol" because of its beneficial effects on preventing plaque formation. Among HDL-other C's functions are protection against thrombosis, endothelial function maintenance, and maintaining low blood viscosity. A low HDL cholesterol level indicates dyslipidemia and is a risk factor for problems due to its beneficial effects. LDL cholesterol is yet another diagnostic test that is frequently looked into. Cholesterol, TG, phospholipids, and apolipoproteins make up low density lipoproteins. Plaque forms when LDL-C molecules bind to the endothelium of blood arteries. Once plaques have formed, LDL-C in the bloodstream may cling to them, resulting in additional accumulation. LDL-C molecules can be oxidized, which can lead to plaque formation. Oxidation can result in elevated cholesterol levels and the production of inflammatory cytokines, both of which damage blood vessels [5]. High levels of LDL-C indicate dyslipidemia and raise the risk of cardiovascular disease due to its negative effects.

Additionally, dyslipidemias can be categorized according to whether the underlying cause is primary, secondary, or a combination of the two. The genetic defects known as primary dyslipidemias result in elevated lipid levels without any other obvious risk factors. People who have primary dyslipidemias are more likely to develop issues related to dyslipidemia, such as atherosclerotic cardiovascular disease, when they are younger. Essential dyslipidemias are hereditary imperfections that cause expanded lipid levels with next to no other clear gamble factors. People who have primary dyslipidemias are more likely to develop issues related to dyslipidemia, such as atherosclerotic cardiovascular disease, when they are younger. Homozygous or heterozygous hypercholesterolemia, familial hypertriglyceridemia, mixed hyperlipidemia, and HDL-C metabolism anomalies are among the most prevalent genetic disorders linked to primary dyslipidemias. Typically, mutations in the LDLR, PCSK9, or APOB genes are the cause of familial hypercholesterolemia, which results in elevated LDL cholesterol. In patients with concurrent hyperlipidemia, the liver produces an excessive amount of apoB-100. Numerous LDL and VLDL molecules are formed as a result of this. Numerous LDL and VLDL molecules are formed as a result of this. Patients with primary dyslipidemias frequently exhibit acute pancreatitis or xanthomas on the skin, eyelids, or cornea [1]. In contrast to primary dyslipidemias, secondary dyslipidemias are caused by environmental or lifestyle factors that can be changed. Uncontrolled diabetes, cholestatic liver disease, chronic renal disease, hypothyroidism, and polycystic ovarian syndrome all increase dyslipidemia risk.

Conclusion

When it comes to dyslipidemia screening, there is no universal agreement. Males between the ages of 25 and 30 and females between the ages of 30 and 35 should be screened at a younger age if they have a high risk of cardiovascular disease. It is unknown whether screening people under the age of 40 who have no symptoms are beneficial. Males and females who are not at risk of cardiovascular disease should be screened at the ages of 35 and 45, respectively, according to Up to Date. You should get screened regardless of your age if you have any of the risk factors listed below. The Framingham Risk Score (FRS) can be used to assess cardiovascular risk and should be updated on a regular basis.

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