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Tc to hdl ratio: Cholesterol ratio or non-HDL cholesterol: Which is most important?

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Cholesterol ratio or non-HDL cholesterol: Which is most important?

How important is cholesterol ratio and non-HDL cholesterol?

Answer From Francisco Lopez-Jimenez, M.D.

For predicting your risk of heart disease, many doctors now believe that determining your non-HDL cholesterol level may be more useful than calculating your cholesterol ratio. And either option appears to be a better risk predictor than your total cholesterol level or even your low-density lipoprotein (LDL, or “bad”) cholesterol level.

Non-HDL cholesterol, as its name implies, simply subtracts your high-density lipoprotein (HDL, or “good”) cholesterol number from your total cholesterol number. So it contains all the “bad” types of cholesterol.

An optimal level of non-HDL cholesterol is less than 130 milligrams per deciliter (mg/dL), or 3.37 millimoles per liter (mmol/L). Higher numbers mean a higher risk of heart disease.

To calculate your cholesterol ratio, divide your total cholesterol number by your HDL cholesterol number. So if your total cholesterol is 200 mg/dL (5.2 mmol/L) and your HDL is 50 mg/dL (1.3 mmol/L), your ratio would be 4-to-1. Higher ratios mean a higher risk of heart disease.

With

Francisco Lopez-Jimenez, M.D.

Jan. 29, 2020

Show references

  1. Ballantyne CM. Cholesterol: Concentration, ratio and particle number. In: Clinical Lipidology: A Companion to Braunwald’s Heart Disease. 2nd ed.
    Saunders Elsevier, 2015. https://www.clinicalkey.com. Accessed Jan. 7, 2020.
  2. Sandeep V. Screening for lipid disorders. https://www.uptodate.com/contents/search. Accessed Jan. 7, 2020.
  3. Non-high density lipoprotein cholesterol. Lab Tests Online. American Association for Clinical Chemistry. https://labtestsonline.org/tests/non-high-density-lipoprotein-cholesterol. Accessed Jan. 7, 2020.
  4. Heart and stroke encyclopedia: Cholesterol ratio. American Heart Association. http://www. heart.org/HEARTORG/Encyclopedia/Heart-and-Stroke-Encyclopedia_UCM_445084_ContentIndex.jsp?title=cholesterol%20ratio. Accessed Dec. 14, 2017.

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Finding the Ideal Cholesterol Ratio

Cholesterol is a fatty substance that naturally occurs in human blood. It is formed in the liver or comes from the foods you eat. Cholesterol performs important functions in your body. It aids in tissue and hormone formation. It protects your nerves. It helps with digestion. In fact, cholesterol helps form the structure of every cell in your body.

 

You’ve probably heard your doctor talk about good and bad cholesterol. It’s true we need cholesterol to maintain good health. But too much LDL — or “bad” — cholesterol and not enough HDL — or “good” — cholesterol may lead to heart disease and stroke. To help avoid these problems, you need to maintain the proper ratio between good and total cholesterol.

How do you know what that ratio is? Once you know your cholesterol numbers, you can work with your doctor to find the ideal cholesterol ratio for you. Then, by making simple lifestyle changes such as eating a heart-healthy diet, exercising regularly, and taking cholesterol medications such as statins, if necessary, you can work your way toward that ratio. By lowering your level of LDL cholesterol and increasing the level of HDL cholesterol, you can reduce your risk of cardiovascular disease.

How Do Good and Bad Cholesterol Affect the Body?

High-density lipoprotein, or HDL, is the good cholesterol. The benefit of HDL lies in the fact that it carries bad cholesterol back to the liver. In doing so, it cleanses cholesterol from the bloodstream.

Low-density lipoprotein, or LDL cholesterol, is the bad cholesterol. The higher the level of LDL cholesterol, the greater your risk of a heart attack. When the level of LDL cholesterol goes up, excess cholesterol can build up and stick to the walls of your arteries. This causes damage. The buildup is called plaque, and the formation of plaque can cause arteries to harden and narrow. This hardening is called atherosclerosis. It’s also known as hardening of the arteries. If a plaque becomes unstable, a blood clot can form, suddenly blocking an artery. This causes a heart attack or stroke.

What Is Total Cholesterol?

When your cholesterol is checked, you get a number for total cholesterol, one for the HDL level, and one for the LDL level. Your total cholesterol will be more than the sum of the HDL and LDL numbers.

Either a high HDL number or a high LDL number can make your total cholesterol number high. If it’s high because of a high HDL number, your health is not necessarily in danger. However, if it’s high because your LDL cholesterol level is high, it’s important to talk with your doctor about your health .

What Is Cholesterol Ratio and What Should Yours Be?

To find your cholesterol ratio, you divide your total cholesterol number by your HDL, or good, cholesterol number. For example, if your total cholesterol number is 200 and your good cholesterol is 50, your total cholesterol ratio is 4:1.

Cholesterol ratio may be used as a monitoring tool by some health care specialists. However, the AHA suggests that doctors use LDLcholesterol with patients rather than cholesterol ratio. That’s because the total cholesterol number is considered a better tool for guiding the doctor in planning the best patient care and helping patients understand their health risks. Discuss with your doctor what the best numbers to monitor for you are.

What Are Triglycerides?

Triglycerides are another form of fat in the blood. Just as with HDL and LDL cholesterol, your body makes triglycerides and also gets them from foods you eat. Foods that are high in trans fats and saturated fats can raise triglyceride levels. So can simple carbohydrates and food that are high in sugar. Also, when you eat more calories than you burn, your triglyceride levels may soar.

Are High Cholesterol Levels Dangerous?

A high cholesterol level can be a risk factor for heart attack and stroke. These devastating events happen when a cholesterol plaque ruptures. This causes blood to suddenly clot and block an artery in the heart or brain.

Blockages that prevent sufficient blood flow in the coronary arteries can lead to a form of chest pain called angina. Angina is a common symptom of coronary artery disease. Symptoms usually occur with exertion and go away with rest.

Are There Ways to Manage High Cholesterol Levels?

Yes, there are ways to manage high cholesterol levels, including the following:

  1. Increase HDL (“good”) cholesterol levels and decrease LDL (“bad”) cholesterol by getting regular aerobic exercise. Exercise also helps relax blood vessels and lowers blood pressure.
  2. Lower LDL cholesterol by eating foods low in saturated fat, cholesterol, and trans fat. You can replace these bad fat foods with foods high in monounsaturated and polyunsaturated fats. This includes eating fish with omega-3 fatty acids like salmon. In addition, eating soluble fibers — such as oats, pectin, and psyllium — will help reduce LDL cholesterol. So will cholesterol-lowering foods, such as margarines, enriched with plant sterols and stanols.
  3. Medications such as statins help lower LDL cholesterol levels. They also help lower triglycerides and slightly increase HDL cholesterol levels. Statins reduce the risk of heart disease in many people.

If your cholesterol is high, it will take time and effort to improve your cholesterol levels and cholesterol ratio. You should count on at least three months of lifestyle changes and possibly taking daily medication. The results, though — a healthier heart and lower risk of heart attack or stroke — are well worth the effort.

Cholesterol and Risk of Heart Attack

Q1. I often read that a person’s cholesterol should be under 200, yet have also read (on several occasions) that most people that have heart attacks have cholesterol in the 180 to 200 range. Can you help me to understand this? Thank you!

Larry, California

It is confusing, but I’ll try to clarify. The problem is that what’s considered “normal” or average cholesterol in our society is not biologically normal for our arteries. So when I hear people say heart attacks occur when cholesterol is normal (e.g., 180 to 200 mg/dL), I cringe.

Total cholesterol is made up of good and bad cholesterol. You can have a total cholesterol level of less than 200 mg/dL but that may be because your good (HDL) cholesterol is low, which may put you at risk of heart disease. That’s why I like to look at all the numbers, the good (HDL) cholesterol, the bad (LDL) cholesterol, and the “ugly” (triglycerides) in addition to the total cholesterol. The goal for total cholesterol is less than 200 mg/dL, the goal for bad (LDL) cholesterol is less than 100 mg/dL, the goal for good (HDL) cholesterol is 40 mg/dL or higher in men and 50 mg/dL or higher in women, and the goal for triglycerides is less than 150 mg/dL.

The higher your cholesterol levels (total and LDL), the greater the likelihood of heart disease. The Multiple Risk Factor Intervention Trial (a national heart-disease prevention study conducted from 1973 to 1982) showed that the likelihood of heart attack in people with cholesterol levels in the highest 20 percent was three times that of people whose levels were in the lowest 20 percent. Another well-known survey, the Framingham study, also illustrated the link between high cholesterol levels and heart disease.

In both studies, however, a significant number of heart attacks still occurred in people with low or “normal” cholesterol values. In the Framingham study, four of five people fell into a large middle range of cholesterol levels, whether or not they developed heart disease. Those with extremely low total cholesterol (less than 50 mg/dL) had low (though not zero) risk for heart attack; those with extremely high cholesterol (over 300 mg/dL) had a threefold higher risk for heart attack. But the great majority of people fell in between these extremes, and the greatest number of heart attacks developed in people with cholesterol levels in this middle range. Why? Because people with low or middle-range cholesterol values vastly outnumber those with high cholesterol levels. As a result, there are at least as many heart attack victims with low and intermediate cholesterol levels as there are those with high cholesterol.

The bottom line: The higher the cholesterol, the higher the statistical risk of heart attack, yet a surprising number of heart attacks still occur in people who have “normal” cholesterol levels because “normal” in our society is too high. I hope that helps.

Q2. I just got cholesterol test results and the TC/HDL ratio is 3.5. What is the risk factor and what does the number mean?

– Kathi, Oregon

I’m glad you asked this question since deciphering your results can be confusing. The total cholesterol to HDL cholesterol ratio is a number that is helpful in predicting atherosclerosis, the process of fatty buildup in the walls of the arteries. The number is obtained by dividing total cholesterol by HDL (good) cholesterol. For example, if a person has a total cholesterol of 200 mg/dL and an HDL cholesterol level of 50 mg/dL, the ratio would be 4.0. A high ratio indicates a higher risk of heart attack while a low ratio indicates a lower risk. High total cholesterol (an indicator that your body has a lot of the lipoproteins that contribute to atherosclerosis) and low HDL cholesterol increases the ratio, so that scenario is undesirable. Conversely, low total cholesterol and high HDL cholesterol lowers the ratio and is good news.

The goal is to keep the ratio below 5.0; the optimum ratio is 3.5. But even though this ratio can be a powerful predictor of heart disease risk, it is not used as a sole indicator for therapy. So while this ratio will help you understand your risk, keep in mind that your physician will be making treatment choices based upon your other lipoprotein numbers, specifically your LDL and HDL levels.

Q3. I’m already taking a statin — shouldn’t this protect me from a heart attack?

— Chris, Indiana

Possibly, but most of the time, the answer is no! Statins are not a magic bullet. They reduce the number of cardiovascular events, including heart attacks, by about 30 percent over five years. This means that 70 percent of individuals who were destined for a cardiac event without the statin will still have one, which is why we need to get more aggressive and consider other therapies, like taking niacin to increase high-density lipoprotein(HDL) — the good cholesterol. Other medications, such as metformin (Glucophage) and insulin sensitizers (the thiazolidinediones, or TZDs), are typically used to treat insulin resistance in patients with type 2 diabetes, but some have been found to have beneficial effects on blood fats as well. The TZD troglitazone, for example, can have a lipid-lowering effect and increases HDL levels. Another TZD, pioglitazone, can also decrease triglycerides.

Bottom line: Don’t assume that a statin is going to do all the work. You still need to adopt a healthy lifestyle with a proper diet and regular exercise (and no smoking, of course!) to give yourself the greatest protection against heart disease.

Learn more in the Everyday Health Heart Health Center.

Physiological significance and clinical usefulness in cardiovascular prevention

Vasc Health Risk Manag. 2009; 5: 757–765.

Published online 2009 Sep 18.

,1,2,3,4,5,6,7,8,9,10,11 and 12

Jesús Millán

1 Hospital Universitario Gregorio Marañón, Madrid, Spain

Xavier Pintó

2 Hospital Universitario Bellvitge, L’Hospitalet de Llobregat, Barcelona, Spain

Anna Muñoz

3 Solvay Pharma, Barcelona, Spain

Manuel Zúñiga

4 Hospital Marqués de Valdecilla, Santander, Spain

Joan Rubiés-Prat

5 Hospital Vall d’Hebrón, Barcelona, Spain

Luis Felipe Pallardo

6 Hospital Universitario La Paz, Madrid, Spain

Luis Masana

7 Hospital Sant Joan, Reus, Tarragona, Spain

Alipio Mangas

8 Hospital Universitario Puerta del Mar, Cádiz, Spain

Antonio Hernández-Mijares

9 Hospital Universitario Dr Peset, Valencia, Spain

Pedro González-Santos

10 Hospital Clínico Universitario Virgen de la Victoria, Málaga, Spain

Juan F Ascaso

11 Hospital Clínico Universitario, Valencia, Spain

Juan Pedro-Botet

12 Hospital del Mar, Barcelona, Spain

1 Hospital Universitario Gregorio Marañón, Madrid, Spain

2 Hospital Universitario Bellvitge, L’Hospitalet de Llobregat, Barcelona, Spain

3 Solvay Pharma, Barcelona, Spain

4 Hospital Marqués de Valdecilla, Santander, Spain

5 Hospital Vall d’Hebrón, Barcelona, Spain

6 Hospital Universitario La Paz, Madrid, Spain

7 Hospital Sant Joan, Reus, Tarragona, Spain

8 Hospital Universitario Puerta del Mar, Cádiz, Spain

9 Hospital Universitario Dr Peset, Valencia, Spain

10 Hospital Clínico Universitario Virgen de la Victoria, Málaga, Spain

11 Hospital Clínico Universitario, Valencia, Spain

12 Hospital del Mar, Barcelona, Spain

Correspondence: Anna Muñoz, Solvay Pharma, Av. Diagonal, 507, 08029, Barcelona, Spain, Tel +34 93 495 4500, Fax +34 93 430 3727, Email
[email protected] © 2009 Millán et al, publisher and licensee Dove Medical Press Ltd.

This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

This article has been cited by other articles in PMC.

Abstract

Low-density lipoprotein (LDL) cholesterol concentration has been the prime index of cardiovascular disease risk and the main target for therapy. However, several lipoprotein ratios or “atherogenic indices” have been defined in an attempt to optimize the predictive capacity of the lipid profile. In this review, we summarize their pathophysiological aspects, and highlight the rationale for using these lipoprotein ratios as cardiovascular risk factors in clinical practice, specifying their cut-off risk levels and a target for lipid-lowering therapy. Total/high-density lipoprotein (HDL) cholesterol and LDL/HDL cholesterol ratios are risk indicators with greater predictive value than isolated parameters used independently, particularly LDL. Future recommendations regarding the diagnosis and treatment of dyslipidemia, including instruments for calculating cardiovascular risk or action guidelines, should include the lipoprotein ratios with greater predictive power which, in view of the evidence-based results, are none other than those which include HDL cholesterol.

Keywords: apolipoproteins, cholesterol ratios, predictive power, cardiovascular disorders

Introduction

Estimation of cardiovascular risk has become the cornerstone of cardiovascular prevention. Although atherogenesis is a multifactorial process, abnormalities in lipoprotein metabolism are one of the key factors, representing around 50% of the population-attributable risk of developing cardiovascular disease.1 Despite of the considerable progress made in cardiovascular disease management in recent decades, there is almost unanimous agreement among epidemiologists and clinicians that coronary risk assessment based exclusively on low-density lipoprotein (LDL) cholesterol is not optimal,2 particularly in individuals at intermediate risk. 3 Efforts have been made in seeking emergent or new cardiovascular risk factors to improve cardiovascular disease prediction.1 However, it must be emphasized that in an attempt to optimize the predictive capacity of the lipid profile, several lipoprotein ratios or “atherogenic indices” have been defined. These ratios can provide information on risk factors difficult to quantify by routine analyses and could be a better mirror of the metabolic and clinical interactions between lipid fractions. Since lipoprotein ratios are under-used in cardiovascular prevention, but can add to risk assessment, in this review, we briefly summarize their physiological and pathophysiological aspects. Furthermore, we highlight the rationale for using these lipoprotein ratios as cardiovascular risk factors in clinical practice, specifying their cut-off risk levels and a target for lipid-lowering therapy ().

Table 1

Risk categories and target levels for total cholesterol/HDL-C, LDL-C/HDL-C and apoB/apoA-I ratios, in primary and secondary prevention, stratified by gender6,7,14

Ratio Primary prevention Secondary prevention*


Risk level


Target


Risk level


Target


Men Women Men Women Men Women Men Women
TC/HDL-C >5. 0 >4.5 <4.5 <4.0 >4.0 >3.5 <3.5 <3.0
LDL-C/HDL-C >3.5 >3.0 <3.0 <2.5 >3.0 >2.5 <2.5 <2.0
ApoB/ApoA-I >1.0 >0. 9 <0.9 <0.8 >0.8 >0.7 <0.7 <0.6

Total cholesterol/HDL cholesterol and LDL/HDL cholesterol ratios

The total/high-density lipoprotein (HDL) cholesterol ratio, known as the atherogenic or Castelli index and the LDL/HDL cholesterol ratio are two important components and indicators of vascular risk, the predictive value of which is greater than the isolated parameters. In this respect, an increase in total cholesterol concentration, and specifically LDL cholesterol, is an atherogenic lipid marker, whereas reduced HDL cholesterol concentration is correlated with numerous risk factors, including the components of the metabolic syndrome, and probably involves independent risk. 4 When total cholesterol, HDL cholesterol, and total/HDL cholesterol ratio are compared between an apparently healthy population and myocardial infarction survivors, the total/HDL cholesterol ratio is found to present less superposition of populations.5 This illustrates the high discriminatory power for coronary heart disease presented by the total/HDL cholesterol ratio, as well as its great predictive capacity. The value of this parameter when the lipid profile is within desirable range should be emphasized. For example, total cholesterol of 231 mg/dL (5.89 mmol/L) and HDL cholesterol of 42 mg/dL (1.09 mmol/L) gives a total/HDL cholesterol ratio of 5.5, which indicates moderate atherogenic risk.6 On the other hand, with the same level of total cholesterol, if HDL cholesterol were 60 mg/dL (1.55 mmol/L), the ratio would be 3.8. As total cholesterol/HDL ratio is considered a more sensitive and specific index of cardiovascular risk than total cholesterol, the Canadian working group has chosen this lipid ratio as a secondary goal of theraphy. 7

The LDL/HDL cholesterol ratio appears to be as useful as the total/HDL cholesterol ratio. Their similarity can be explained by the fact that approximately two thirds of plasma cholesterol are found in LDL and, consequently, total and LDL cholesterol are closely related. Like the total/HDL cholesterol ratio, LDL/HDL cholesterol may have more predictive power if triglyceridemia is taken into account.8 Although, the increase in these ratios predicted a greater cardiovascular risk in a wide range of cholesterol or triglyceride concentrations, the risk is significantly higher when hypertriglyceridemia is present, as shown by the Helsinki Heart Study.9

However, it is clear than when there is no reliable calculation of LDL cholesterol, as when triglyceridemia exceeds 300mg/dL (3.36 mmol/L), it is preferable to use the total/HDL cholesterol ratio; furthermore, the very-low-density lipoprotein (VLDL) fraction shows cholesterol enrichment in individuals with high triglyceride concentrations, and thus the LDL/HDL cholesterol ratio may underestimate the magnitude of the lipoprotein abnormality in these patients.

Individuals with a high total/HDL cholesterol or LDL/HDL cholesterol ratio have greater cardiovascular risk owing to the imbalance between the cholesterol carried by atherogenic and protective lipoproteins. This may be due to an increase in the atherogenic component contained in the numerator, a decrease in the anti-atherosclerotic trait of the denominator, or both.10

Some studies have calculated inverse ratios, ie, HDL/total cholesterol and HDL/LDL cholesterol. Although their predictive value is identical but in the opposite order, few authors suggest they more clearly express the proportion of HDL cholesterol (protective) compared with the rest.8

ApoB/ApoA-I ratio

Apolipoprotein (apo) B represents most of the protein content in LDL and is also present in intermediate-density lipoproteins (IDL) and VLDL. ApoA-I is the principal apolipoprotein in HDL. Both apolipoproteins, therefore, separately provide information for detecting high-risk individuals. ApoA-I is also believed to be a more reliable parameter for measuring HDL than cholesterol content since it is not subject to variation. Therefore, the apoB/apoA-I ratio is also highly valuable for detecting atherogenic risk, and there is currently sufficient evidence to demonstrate that it is better for estimating vascular risk than the total/HDL cholesterol ratio.1114 The apoB/apoA-I ratio was stronger than the total cholesterol/HDL holesterol and LDL/HDL cholesterol ratios in predicting risk.11 Furthermore, Walldius and colleagues have reported that addition of lipids, lipoproteins or any cholesterol ratio to apoB/apoA-I in risk models did not further improve the strong predictive value of apoB/apoA-I.13

This ratio reflects the balance between two completely opposite processes (): transport of cholesterol to peripheral tissues, with its subsequent arterial internalization, and reverse transport to the liver.15 shows that the greater the apoB/apoA-I ratio, the larger will be the amount of cholesterol from atherogenic lipoproteins circulating through the plasma compartment and likely to induce endothelial dysfunction and trigger the atherogenic process. On the other hand, a lower apoB/apoA-I ratio will lead to less vascular aggression by plasma cholesterol and increased and more effective reverse transport of cholesterol, as well as other beneficial effects, thereby reducing the risk of cardiovascular disease.

Atherogenic and anti-atherogenic lipoproteins. This diagram shows that there is one single apolipoprotein B (apoB) molecule in each large, buoyant or small, dense particle of very-low-density (VLDL), intermediate-density (IDL), and low-density lipoproteins (LDL). Therefore, apoB represents the total number of potentially atherogenic particles. Apolipoprotein A-I (apo A-I) is the principal protein component in high-density lipoproteins (HDL) and is responsible for starting reverse cholesterol transport. The balance between apoB and apoA-I is indicative of cardiovascular risk: the greater the ratio, the greater the risk.

Abbreviations: TG, triglycerides; C, cholesterol; + +, increased risk; − −, reduced risk.

Impact of the apoB/apoA-I ratio on atherogenic balance.

Abbreviation: Apo, apolipoproteins.

Logarithmic transformation of the triglyceride/HDL cholesterol molar concentration ratio

The association between triglycerides and HDL cholesterol reflected by this ratio depicts the balance between atherogenic and protective lipoproteins. Known as the atherogenic plasma index, it shows a positive correlation with the HDL esterification rate (FERHDL) and an inverse correlation with LDL size.16 Therefore, the phenotype of LDL and HDL particles is clearly synchronized with the FERHDL. Hypoalphalipoproteinemia and hypertriglyceridemia both induce an increase in the percentage of small HDL and small, dense LDL particles. Ultimately, the simultaneous use of triglycerides and HDL cholesterol in this ratio reflects the complex interactions of lipoprotein metabolism overall and can be useful for predicting plasma atherogenicity. 17 An atherogenic plasma index [log (triglycerides/HDL cholesterol)] over 0.5 has been proposed as the cut-off point indicating atherogenic risk.16

LDL cholesterol/apoB ratio

Although apoB is not an apolipoprotein exclusive to LDL, since it is present in other atherogenic lipoprotein fractions such as IDL and VLDL, the LDL cholesterol/apoB concentration ratio provides approximate information on LDL particle size. In this respect, it has been suggested that a ratio of less than 1.3 would indicate the predominance of LDL particles with lower cholesterol content, consistent with small, dense LDL particles.18 However, a study comparing LDL particle size determination by gradient-gel electrophoresis with the LDL cholesterol/apoB ratio in healthy and hyperlipidemic subjects failed to find a good correlation and did not recommend the use of this ratio as a surrogate LDL size marker.19

Non-HDL cholesterol/HDL cholesterol ratio

Non-HDL cholesterol, which is total cholesterol minus HDL cholesterol, is a measure of the cholesterol in LDL, IDL and VLDL particles. Non-HDL cholesterol has therefore been recommended as a secondary therapeutic target in individuals with high triglyceride concentration, and it has been suggested that it could be a surrogate marker of serum apoB concentration in clinical practice. However, non-HDL cholesterol is not always strongly associated with apoB, particularly in the presence of hypertriglyceridemia.20 The non-HDL cholesterol/HDL ratio is a lineal combination of total/HDL cholesterol. Although few studies have evaluated this lipoprotein ratio for predicting cardiovascular disease, and as it is a lineal combination of the results can be assumed to be similar to those of the total/HDL cholesterol or LDL/HDL cholesterol ratios.21

Predictive power of lipoprotein ratios for cardiovascular risk

The evidence derived from large observational studies, including the Framingham Study,22 the LRCP23 and the PROCAM,24,25 suggests that the total/HDL cholesterol ratio is a more powerful coronary risk predictor than independently-used total cholesterol, LDL cholesterol and HDL cholesterol. The predictive value for the development of coronary events of the baseline total/HDL cholesterol and LDL/HDL cholesterol ratios in the placebo groups of WOSCOPS,26 AFCAPS/TexCAPS,27 and 4S28 studies was higher than that of other lipid parameters in multivariate analyses. Indeed, the total/HDL cholesterol ratio was included in the Framingham equation to improve risk prediction.29 The LRC-CPPT study5 analysed the ability of the total/HDL cholesterol ratio to predict coronary risk and compared it to other lipid metabolism variables in three large population-based cohorts: the men in the placebo group of the LRCP-CPPT study; a group of individuals of both sexes subject to follow-up in the Framingham Study; and a group of men and women without coronary disease included in the LRCP Mortality Follow-up Study. The groups of men and women from the Framingham Study and the men from the LRCP-CPPT control group were divided into deciles, using a primary lipid end-point, and the deciles were subsequently divided into terciles using a secondary lipid end-point. When total cholesterol and LDL cholesterol were used as primary end-points, the total/HDL cholesterol and LDL/HDL cholesterol ratios identified significantly high- and low-risk groups within the deciles. For example, when the LRCP-CPPT men were divided into deciles according to LDL cholesterol, the absolute difference in risk within each decile between individuals in the upper and lower terciles of the total/HDL cholesterol ratio was 13% (95% confidence intervals [CI]: 8.2%–17.7%). The results were similar when the LDL/HDL cholesterol ratio was used. When the LDL/HDL cholesterol and total/HDL cholesterol ratios were used as primary end-points, neither total nor LDL cholesterol identified high- or low-risk groups within the deciles. These results of the stratified analysis were confirmed in the logistic regression analysis and suggest that the total/HDL cholesterol ratio adds risk prediction power to total and LDL cholesterol values. However, no other lipid parameter adds predictive power to the total/HDL cholesterol ratio. On the other hand, no conclusive data were obtained in relation to the superiority of the total/HDL cholesterol ratio over the LDL/HDL ratio, or vice versa. Only in women was the total/HDL cholesterol ratio found to have greater predictive power, which could be explained by the fact that this ratio, and not LDL/HDL cholesterol, includes triglyceride-rich lipoproteins in the numerator (VLDL and IDL), and triglycerides are a more powerful coronary risk predictor in women than in men.30 When there is no reliable calculation of LDL cholesterol, as occurs in individuals with serum triglycerides above 300 mg/dL (3.36 mmol/L), since in this scenario the Friedewald formula for estimating LDL cholesterol is not valid, the total/HDL cholesterol ratio will have to be used. The total/HDL cholesterol ratio was the best risk predictor in a subanalysis of the cohort of 14,916 men in the Physicians Health Study31 and, after adjusting for other factors, each unit increase in the ratio was found to be associated with a 53% increase in the risk of myocardial infarction. Similarly, in the cohort of 28,263 postmenopausal women undergoing a three-year follow-up in the Women’s Health Study,32 among lipid variables, various inflammation markers and homocysteine, the only independent predictors of risk for a cardiovascular event were C-reactive protein and the total cholesterol/HDL cholesterol ratio. Other studies33,34 have shown the total cholesterol/HDL cholesterol ratio to be the lipid parameter with the greatest predictive power with regard to the presence, severity and extension of coronary atherosclerosis in women.

The total/HDL cholesterol ratio has also been shown to be a good predictor of carotid intima-media thickness; it has greater power than the isolated variables and similar power to that of the apoB/apoA-I ratio and non-HDL cholesterol.35 More controversial is the role of the ratio between the principal protein fractions of LDL and HDL, apoB and A-I, which is the apoB/apoA-I ratio, as contradictory results regarding its use for predicting cardiovascular risk and its relative value compared with the LDL/HDL cholesterol and total/HDL cholesterol ratios have been obtained in the different observational studies. 36,37 In the Interheart study, which included around 30,000 subjects from 52 countries, the apoB/apoA-I ratio was the variable which predicted a larger proportion of risk of myocardial infarction. Indeed, nearly 50% of the population-attributable risk corresponded to that ratio.1 However, the Interheart study did not include any other lipid measurement, such as HDL or LDL cholesterol, and thus did not compare the relative usefulness of this ratio. In a recent study conducted in 3,322 Framingham inhabitants of both sexes with a 15-year follow-up, the apoB/apoA-I ratio was not superior to the total/HDL cholesterol ratio.38 In the EPIC-Norfolk study conducted in apparently healthy men and women, the apoB/apoA-I ratio was associated with the risk of future coronary events independently of the traditional lipid variables, including the total/HDL cholesterol ratio and the Framingham equation. However, the apoB/apoA-I ratio was not a better discriminatory factor between cases and controls than the total/HDL cholesterol ratio, and added little predictive power to the Framingham equation. 39 Recently, the Cardiovascular Risk in Young Finns Study40 has demonstrated that the apoB/apoA-I ratio measured in adolescence was higher than LDL/HDL cholesterol ratio in predicting increased carotid intima-media thickness in adulthood.

Considering these observations and given that apolipoprotein measurement methods are not as widely used as lipoprotein methods and the absence of consensus on reference values and therapeutic objectives, it would appear that the use of apoB/apoA-I ratio is limited for the time being.

Although the total/HDL cholesterol and LDL/HDL cholesterol ratios predict greater cardiovascular risk with a wide range of cholesterol or triglyceride concentrations, the risk is considerably higher in the presence of hypertriglyceridemia. In the Helsinki study,41 the LDL/HDL cholesterol ratio was a powerful predictor of cardiovascular risk, mainly in subjects with elevated triglycerides. The greatest risk was observed in subjects with an LDL/HDL ratio >5 and triglycerides >200 mg/dL (2. 24 mmol/L), who represented around 10% of the population studied; it was precisely this group which most benefited from treatment with gemfibrozil, with a remarkable 71% reduction in the incidence of coronary events, more than double that of the overall active-treatment group. In the cohort of 4,559 adult men in the PROCAM observational study,24,25 it was found that subjects with an LDL/HDL cholesterol ratio >5 presented more than six times the rate of coronary events of those with an LDL/HDL ratio <5; however, when the LDL/HDL cholesterol ratio was >5 and associated with triglycerides ≥200 mg/dL (2.24mmol/L), the risk was double that of subjects with triglycerides <200 mg/dL (2.24 mmol/L). In the Physicians Health Study,31 this synergic effect was also found between the increase in the atherogenic/protective cholesterol ratio and hypertriglyceridemia.

Predicting the magnitude of the preventive effect

The total/HDL cholesterol and LDL/HDL cholesterol ratios are also good predictors of the degree of clinical benefit to be derived from lipid-lowering intervention. 10 In the LRC-CPPT with cholestyramine, the drops in the total/HDL cholesterol ratio in the active treatment group were associated with clinical benefit. In the Helsinki study, multivariate analysis of the relationship between the lipid changes induced by gemfibrozil and the incidence of cardiovascular events in the treated group showed better predictive value for changes in HDL cholesterol and the total/HDL cholesterol ratio. In the placebo group of the AFCAPS/TexCAPS study,27 baseline LDL cholesterol had no predictive value for the incidence of coronary events, whereas predictive value was found in HDL cholesterol and the total/HDL cholesterol and LDL/HDL cholesterol ratios, both with greater significance than HDL cholesterol by adjusted logistic regression; in the active treatment group, only changes in apoB and the apoB/apoA-I ratio, which is largely equivalent to the LDL/HDL cholesterol ratio, predicted risk reduction. The total/HDL cholesterol ratio also had more predictive value than other lipid parameters in the control group of the 4S study;28 treatment-induced changes in this ratio were the best risk predictors in the group receiving simvastatin, with an estimated 17. 6% risk difference for every one-unit reduction in the ratio.

In two angiographic studies in which cholestyramine was used as a hypolipidemiant agent,42,43 changes in the total/HDL cholesterol or LDL/HDL cholesterol ratios were the only independent predictors of the benefit observed in coronary stenosis. The predictive capacity of the ratios in this study is also supported by data indicating that an increase in HDL cholesterol is associated with an independent effect on regression,44 and that combined treatment with lipid-lowering agents which reduce LDL cholesterol or increase HDL cholesterol more than monotherapy would be associated with a net regression, in comparison with monotherapy, which would only slow down progression. In a meta-analysis of coronary atherosclerosis follow-up studies with intravascular ultrasound scans in patients treated with statins, the apoB/apoA-I and HDL/LDL cholesterol ratios were powerful predictors of changes in atheroma burden. 45 This analysis clearly shows that an increase in HDL cholesterol and apoA-I is fundamental, as is a reduction in LDL cholesterol and apoB, for halting progression of coronary atherosclerosis.

At least in secondary prevention, the predictive power of the ratios in relation to the benefit of intervention can be extended to countries with a lower prevalence of coronary disease such as Spain. In a cohort of 882 coronary patients included in the Hospital de Bellvitge Secondary Prevention Programme who were followed up for a mean of 34 months, those who reached the established therapeutic target, an LDL/HDL cholesterol ratio <3.7, or reduced ratio by ≥15%, reduced their risk of hospitalization for cardiovascular disease and death to less than half, compared with those who did not reach the target. Of the different lipid and nonlipid risk factors, reaching the LDL/HDL ratio objective had the greatest power to predict a favorable outcome in the multiple regression analysis adjusted for possible confounding factors. 46

What do lipoprotein ratios provide that other conventional risk variables do not?

Classic cardiovascular risk factors such as age, sex, smoking, diabetes, hypertension, high LDL and low HDL cholesterol levels have been widely analyzed and established as independent cardiovascular risk factors. Many other predictors, such as triglycerides, apoB, lipoprotein(a), homocysteine, C-reactive protein and others have also been studied. Furthermore, the total/HDL cholesterol and LDL/HDL cholesterol ratios are of great interest as major predictors of cardiovascular disease.

Guidelines for lipid management are based on LDL cholesterol concentrations, although other parameters including the total/HDL cholesterol index are better cardiovascular risk predictors than LDL cholesterol and have not been included.47 The beneficial use of these indices as important cardiovascular risk predictors is based on multiple epidemiological studies which have shown that these ratios (total/HDL cholesterol and LDL/HDL cholesterol) have a greater correlation with cardiovascular disease and are therefore better predictors of cardiovascular disease than simple lipid parameters. 5,31,48

A study in 32,826 menopausal women49 with an eight-year follow-up, after adjusting for age, smoking, C-reactive protein levels, homocysteine, body mass index, family history, diabetes, hypertension, physical activity, and alcohol consumption, found a relative risk of cardiovascular disease (95% CI) of 0.6 (0.5–0.8) for HDL cholesterol; 1.3 (1.0–1.5) for triglyceride levels; 1.4 (1.1–1.7) for LDL cholesterol; 1.7 (1.4–2.1) for apoB concentration; 1.6 (1.3–1.9) for non-HDL cholesterol; 1.5 (1.3–1.9) for the LDL/HDL cholesterol index; and 1.6 (1.3–1.9) for the total/HDL cholesterol index. The total/HDL cholesterol index is therefore a good predictor of cardiovascular risk irrespective of other factors.

In a retrospective study with a 20-year follow-up of 1,439 men and 2,812 women with cardiovascular disease,50 cardiovascular risk increased in relation to total/HDL cholesterol levels, regardless of total or LDL cholesterol. In men, the relative risk for quintile 5 over 1 of LDL cholesterol was 1.85, whereas the upper over the lower quintile of the total/HDL cholesterol ratio was 2.9. This cardiovascular risk difference between LDL cholesterol and total/HDL cholesterol was not found in women. The authors therefore conclude that men with elevated LDL cholesterol do not have to be treated aggressively if their total/HDL cholesterol index is low, and vice versa, with mild elevations of LDL cholesterol requiring more aggressive treatment if the total/HDL cholesterol ratio is high. This reveals that the total/HDL cholesterol ratio is an excellent cardiovascular risk predictor and a good parameter for deciding on the intensity and need for therapeutic intervention in each different situation.

Other authors51 studying subjects with peripheral arterial disease demonstrated the importance of the total/HDL cholesterol index in predicting atherosclerosis in this setting. Studying a cohort of 2,265 subjects with a five-year follow-up, they found disease progression to be significantly related to smoking, the total/HDL cholesterol index and plasma levels of lipoprotein(a) and C-reactive protein.

In an analysis of the Framingham Heart Study and the Coronary Primary Prevention Trial data,52 LDL cholesterol and the total/HDL cholesterol and LDL/HDL cholesterol ratios were found to be good cardiovascular disease predictors. However, when vascular changes and cardiovascular risk after intervention were studied, both ratios were better cardiovascular risk reduction predictors than total cholesterol or LDL cholesterol. These ratios should therefore be used when assessing vascular risk and in the reduction of such risk after therapeutic intervention.

There is reason to believe that these lipoprotein ratios, mainly total/HDL cholesterol, based on two values directly measured in a clinical laboratory and which indicate the relationship or proportion between the atherogenic and antiatherogenic lipid fraction, have predictive power for cardiovascular disease and cardiovascular risk reduction after intervention superior to that of classic lipid parameters and should be used in regular clinical practice.

With regard to identifying the “best” lipoprotein ratio, there is an interesting contrast between the use of cut-off points46 and quantiles.50 Thus it must be taken into account that while cut-off points can provide clinical relevant information, with regard to comparing ratios it would seem more logical to use quantiles within the cohort/population.

Conclusions and recommendations

LDL cholesterol concentration has been the prime index of cardiovascular disease risk and the main target for therapy. However, data now suggest that total/HDL cholesterol and LDL/HDL cholesterol ratios are risk indicators with greater predictive value than isolated parameters used independently, particularly the former. These two indices can be regarded as similar; since two thirds of plasma cholesterol are found in LDL, total and LDL cholesterol are closely correlated. The predictive capacity of these ratios is supported by data suggesting that an increase in HDL cholesterol is more prevalently associated with plaque regression, while a decrease in LDL cholesterol would slow down progression. Both predict greater cardiovascular risk for a wide range of cholesterol concentrations. However, when there is no reliable determination of LDL cholesterol, as in cases of hypertriglyceridemia, it is preferable to use the total/HDL cholesterol ratio. This may be particularly interesting in patients with features of the metabolic syndrome.

ApoB constitutes most of the protein content of LDL, as does apoA-I for HDL, even as parameters subject to less variation. Therefore, the apoB/apoAI ratio is also of great value for detecting atherogenic risk and often better than the total/HDL and LDL/HDL cholesterol ratios.

We suggest that future recommendations regarding the diagnosis and treatment of dyslipidemia, including instruments for calculating cardiovascular risk or action guidelines, should include the lipoprotein ratios with greater predictive power which, in view of the results, are none other than those which include HDL cholesterol. Meanwhile, we propose that lipoprotein ratios should be routinely determined to assess the atherogeneity lipids disorders, mainly those characterized by an elevation in plasma triglycerides.

Footnotes

Disclosures

The authors report no conflicts of interest in this work.

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  • Making sense of cholesterol tests

    The pros and cons of total cholesterol, HDL, LDL, and triglyceride testing

    Time to get your cholesterol checked. Okay, but which test should you get? It’s not so simple anymore. Here is a rundown of some of the choices and their pros and cons:

    Total cholesterol. This is the simplest and least expensive test. The test doesn’t require any sophisticated lab work, either. The simple, do-it-yourself home cholesterol tests measure total cholesterol.

    But total cholesterol includes both “good” high-density lipoprotein (HDL) cholesterol, and the “bad” varieties, chiefly low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL). So, if your total cholesterol is in the desirable category, it’s possible that you may have unhealthy levels of HDL (too low) and LDL and VLDL (too high). Think of total cholesterol as a first glimpse, a peek. Doctors are not supposed to make any treatment decisions based on this number alone.

    Cholesterol levels can be lowered by stress (physical or psychological) or infection. An injury, cancer, stroke, or heart attack may have the same effect. So, if your cholesterol levels are unusually high or low, your doctor will probably want to repeat the test some weeks later. Abnormal readings may also lead to tests for other medical problems.

    HDL cholesterol. HDL wins its laurels as the “good” cholesterol because it sponges up cholesterol from blood vessel walls and ferries it to the liver for disposal. In contrast, LDL deposits the harmful fat in vessel walls.

    An HDL level of 60 or above is associated with a lower risk of heart disease, and below 40 is associated with a higher risk.

    Cholesterol: The good and the bad of it

    HDL High-density lipoprotein
    • Makes up 20%–30% of total cholesterol
    • The “good” cholesterol
    • Moves cholesterol from arteries to the liver.
    LDL Low-density lipoprotein
    • Makes up 60%–70% of total cholesterol
    • Main form of “bad” cholesterol
    • Causes build-up of plaque inside arteries.
    VLDL Very-low-density lipoprotein
    • Makes up 10%–15% of total cholesterol
    • With LDL, the main form of “bad” cholesterol
    • A precursor of LDL.

    LDL cholesterol. The LDL measurement is usually considered the most important for assessing risk and deciding on treatment. The definition of a healthy level keeps on getting lower. For people at low risk of heart disease, an LDL of less than 100 is desirable, However, people at higher risk of heart disease, an LDL of less than 70 or perhaps even lower is considered “optimal.” Some experts say that an LDL of less than 70 would be a healthy LDL goal for all of us.

    Your LDL is computed by plugging the measurements for total cholesterol, HDL, and triglycerides into a: LDL = Total cholesterol – HDL – (Triglycerides ÷ 5). LDL can also be measured directly in a non-fasting blood sample.

    You have to fast for about 10 hours before the test because triglyceride levels can shoot up 20%–30% after a meal, which would throw off the equation. Alcohol also causes a triglyceride surge, so you shouldn’t drink alcohol for 24 hours before a fasting cholesterol test.

    The numbers to know

    Test

    Generally desirable level

    Total cholesterol

    under 200 mg/dL

    LDL (bad) cholesterol

    under 100 mg/dL

    HDL (good) cholesterol

    over 60 mg/dL

    Triglycerides

    under 150 mg/dL

    C-reactive protein (CRP) is a protein in the blood that increases with inflammation. Because atherosclerosis is fundamentally an inflammatory process, many experts believe that CRP testing could lead to early detection and therefore save lives. The American Heart Association says CRP tests are most helpful for people at intermediate risk for heart disease, but not those at the low and high ends of the risk spectrum.

    You should get a fasting cholesterol test at least once every five years for everyone beginning at age 20. A fasting cholesterol test gives you the important numbers: total, LDL, and HDL cholesterol, as well as triglyceride levels.

    For more information, read “11 foods that lower cholesterol.”

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    should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.

    The Ideal Ratio of Total Cholesterol to HDL

    Your doctor can order blood tests that reveal your ratio of total cholesterol to HDL.

    Image Credit: Nomad/E+/GettyImages

    High cholesterol is one of the biggest risk factors for heart attack, stroke and cardiovascular disease, according to the Cleveland Clinic. Your cholesterol ratio, which compares your total cholesterol to your HDL, or “good,” cholesterol, can help better assess your risk.

    While a healthy total cholesterol is less than 200 milligrams per deciliter (mg/dL), the ideal ratio of total cholesterol to HDL is a bit more complicated. Here’s what you need to know.

    Read more: What Is a Dangerous Cholesterol Level?

    Good Cholesterol vs. Bad Cholesterol

    In order to understand cholesterol ratios, it’s good to know a bit more about the different types of cholesterol.

    Cholesterol is a waxy, fat-like substance that is crucial for the body to function properly, according to the Harvard T. H. Chan School of Public Health. You may think that all cholesterol is “bad.” But the truth is that only some kinds of cholesterol are a health concern, and then only in high quantities.

    Low-density lipoproteins (LDL) are the so-called “bad” kind of cholesterol, according to the American Heart Association (AHA). If there is too much LDL in the bloodstream, it can combine with other substances like calcium and form deposits on the artery walls. These deposits — called plaque — narrow and stiffen the arteries, a condition called atherosclerosis. Atherosclerosis significantly increases the risk of heart attack, stroke and cardiovascular disease.

    High-density lipoproteins (HDL) are the “good” kind of cholesterol, per the AHA. HDL moves through the bloodstream and picks up excess LDL particles before returning them to the liver for disposal. In this way, HDL helps prevent plaque buildup and heart disease.

    Read more: The Truth About How Your Diet Affects Cholesterol

    Is My Cholesterol Ratio Healthy?

    There are several types of cholesterol tests, sometimes called a lipid panel. One test measures a person’s total cholesterol level. A healthy total cholesterol is less than 200 mg/dL, according to the U.S. National Library of Medicine. But if a person has high HDL cholesterol (the good kind), it can cause elevated cholesterol overall. This is why measuring different types of cholesterol is so important.

    A ratio is simply a comparison between two numbers. A cholesterol ratio compares a person’s HDL cholesterol to the total cholesterol in the body, according to the Mayo Clinic.

    How to Calculate Cholesterol Ratio

    This number is found by dividing the total amount of cholesterol by the HDL number. For example, if a person has an overall cholesterol level of 225 mg/dL and an HDL of 80 mg/dL, his or her cholesterol ratio is 2.8-to-1, also written as 2.8:1 or simplified to cholesterol ratio 2.8.

    A healthy cholesterol level is no more than 5:1, according to the University of Rochester Medical Center. But the lower the ratio, the better. A ratio of 3.5:1 or lower is considered very good.

    However, Robert Eckel, MD, professor of medicine, emeritus, at the University of Colorado, Anschutz Medical Campus, former president of the American Heart Association and president of the American Diabetes Association, doesn’t think cholesterol ratios are the most accurate way to determine a person’s risk for cardiovascular disease.

    “Ratios are misleading. The result is related to HDL, but a person’s LDL level remains important,” Dr. Eckel says. Essentially, if a person has both high HDL and LDL, the ratio between the two can still be normal, even if their LDL cholesterol is in an unhealthy range. Instead, Dr. Eckel prefers measuring non-HDL cholesterol.

    Per the Mayo Clinic, many doctors now use non-HDL tests to assess a person’s risk. A non-HDL measurement is exactly what it sounds like — a measurement of all the cholesterol in the body, minus the HDL. A healthy, non-HDL cholesterol level is less than 130 mg/dL.

    Warning

    High cholesterol doesn’t usually cause symptoms, according to the American Academy of Family Physicians. Be sure to have your cholesterol level checked regularly, per your doctor’s instructions.

    High Cholesterol Risk Factors

    High cholesterol is often caused by poor lifestyle habits, according to the AHA. An unhealthy diet (particularly one high in saturated fats), along with a lack of exercise and being overweight can lead to high cholesterol. Smoking cigarettes is also a major risk factor for raising LDL cholesterol.

    But there is good news. Because many high cholesterol risk factors are lifestyle related, lifestyle changes can reduce your risk, per the AHA. Healthy diet choices, exercising regularly, reaching and maintaining a healthy weight and quitting smoking are some of the best things you can do to lower your cholesterol — and improve your overall health.

    Learn how to fill your plate with healthy, nutrient-dense foods by logging your meals on the MyPlate app. Download now to fine-tune your diet today!

    There are also non-lifestyle-related high cholesterol risk factors, per the AHA. These include genetics (inherited traits), older age and sex — men are more at risk for high cholesterol than women.

    If you’re concerned about your cholesterol, talk to your doctor about lifestyle changes or medications that might help get your numbers into a healthy range.

    Read more: Good vs. Bad Cholesterol: How to Raise HDL and Lower LDL Naturally

    90,000 Oxidative stress in lung cancer patients is associated with altered serum lipid markers

    Lung cancer has been the most common cancer in the world for several decades. This is a very serious disease that can often be fatal.

    Changes in the redox balance are widely observed in lung cancer (LC) and are a consequence of the disease in combination with smoking. Previously, the authors demonstrated that metabolic disorders such as the state of trace elements and changes in carbohydrate metabolism are associated with the redox state.

    The aim of this study was to assess the relationship between serum lipid metabolism and redox balance in patients with LC.

    Serum lipid metabolism parameters, i.e. total cholesterol (TC), HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), triglycerides (TG), TC: HDL-C ratio, HDL-C free, apolipoprotein A1 (Apo-A1), apolipoprotein B (Apo-B) and Apo-B: Apo-A1 ratio as well as systemic redox status, i.e. total antioxidant status (TAS), total oxidative status (TOS) , oxidative stress index (OSI), vitamin E (VE), vitamin C (VC), malonyldialdehyde (MDA), conjugated dienes (CD), and 4-hydroxynonenal (4-HNE) were determined in 92 LC patients and 82 control subjects (CS).

    Women with LC have significantly lower T-C and LDL-C, and higher TG, while HDL-C, Apo-A1 and Apo-B decreased significantly in patients with LC regardless of gender, compared to CS. Men with LC had changes in systemic overall redox balance, such as lower TAS and higher OSI, than men with CS. Women with LC had a lower VC, but in patients with LC, the VE was decreased regardless of gender. Higher lipid peroxidation was observed in patients with LC, expressed through higher 4-HNE and CD.Systemic redox abnormalities were associated with serum lipid changes: TOS and OSI were positively correlated with the T-C: HDL-C ratio and Apo-B: Apo-A1 ratio and negatively with HDL-C. The lipid peroxidation parameters CD and MDA were significantly associated with variables reflecting lipid abnormalities. The observed correlations were enhanced by overall overweight / obesity, abdominal obesity, hypertriglyceridemia, and lack of addiction to smoking.

    Thus, parameters associated with lipid changes are associated with oxidative stress in patients with LC.The largest contribution from lipid parameters was deduced for the ratio of T-C: HDL-C, HDL-C and Apo-B: Apo-A1, and the largest contribution from redox status was deduced for OSI and VE. Overweight, obesity, hypertriglyceridemia, and lack of attachment to smoking add to this relationship.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6459492/pdf/pone.0215246.pdf
    Katarzyna Zabłocka-Słowińska, Sylwia Płaczkowska, Katarzyna Skorska, Porika Preschał, Konrad Ięrad Kosacka, Halina Grajeta.Oxidative stress in lung cancer patients is associated with altered serum markers of lipid metabolism. PLoS ONE 14 (4). April 11, 2019.

    Article page: Clinical laboratory diagnostics

    Sniderman A.D., Jungner I., Holme I., Aastveit A., Walldius G. Errors that result from using the TC / HDL C ratio rather than the apoB / apoA-I ratio to identify the lipoproteinrelated risk of vascular disease. J. Intern. Med. 2006; 259: 455-61.

    Walldius G., Jungner I., Aasteveit A., Holme I., Furberg C.D., Sniderman A.D. The apoB / apoA-I ratio is better than cholesterol ratios to estimate the balance between plasma proatherogenic and antiatherogenic lipoproteins and to predict coronary risk. Clin. Chem. Lab. Med. 2004; 42: 1355-63.

    Johansson L., Schmidt C. Increased apoB / apoA-I ratio is predictive of peripheral arterial disease in initially healthy 58-year-old men during 8.9 years of follow-up. Angiology. 2009; 60: 539-45.

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    Genest J.Jr., McNamara J.R., Ordovas J.M., Jenner J.L., Silberman S.R., Anderson K.M. et al. Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. J. Am. Coll. Cardiol. 1992; 19: 792-802.

    Superko H.R.Beyond LDL cholesterol reduction. Circulation. 1996; 94: 2351-4.

    van Lennep J.E., Westerveld H.T., van Lennep H.W., Zwinderman A.H., Erkelens D.W., van der Wall E.E. Apolipoprotein concentrations during treatment and recurrent coronary artery disease events. Arterioscler Thromb. Vasc. Biol. 2000; 20: 2408-13.

    Srinivasan S.R., Berenson G.S. Serum apolipoproteins A-I and B as markers of coronary artery disease risk in early life: the Bogalusa Heart Study. Clin. Chem. 1995; 41: 159-64.

    Sniderman A.D., Kiss R.S. The strengths and limitations of the apoB / apoA-I ratio to predict the risk of vascular disease: a Hegelian analysis. Curr. Atheroscler. Rep. 2007; 9: 261-5.

    Sniderman A.D., Pedersen T., Kjekshus J. Putting low-density lipoproteins at center stage in atherogenesis. Am. J. Cardiol. 1997; 79: 64-7.

    Elovson J., Chatterton J.E., Bell G.T., Schumaker V.N., Reuben M.A., Puppione D.L. et al. Plasma very low density lipoproteins contain a single molecule of apolipoprotein B.J. Lipid Res. 1988; 29: 1461-73.

    Walldius G., Jungner I. Apolipoprotein B and apolipoprotein A-I: risk indicators of coronary heart disease and targets for lipid-modifying therapy. J. Intern. Med. 2004; 255: 188-205.

    Walldius G., Jungner I. Rationale for using apolipoprotein B and apolipoprotein A-I as indicators of cardiac risk and as targets for lipid-lowering therapy. Eur. Heart J. 2005; 26: 210-2.

    Thompson A., Danesh J. Associations between apolipoprotein B, apolipoprotein AI, the apolipoprotein B / AI ratio and coronary heart disease: a literature-based meta-analysis of prospective studies.J. Intern. Med. 2006; 259: 481-92.

    Carnevale Schianca G. P., Pedrazzoli R., Onolfo S., Colli E., Cornetti E., Bergamasco L. et al. ApoB / apoA-I ratio is better than LDL-C in detecting cardiovascular risk. Nutr. Metab. Cardiovasc. Dis. 2011; 21: 406-11.

    Biochemical reagents – Mindray

    Alanine aminotransferase (ALT), Aspartate aminotransferase (AST),
    γ-glutamyl transferase (GGT), Alkaline Phosphatase (ALP)
    Albumin (ALB), Total protein (TP),
    Prealbumin (PA), Total Bile Acid (TBA)
    Cholinesterase (CHE), Direct bilirubin – DSA method (DBI-D),
    Total bilirubin – DSA method (TBI-D), Direct bilirubin – VOX method (DBI-V),
    Total bilirubin – VOX method (TBI-V), α-L-fucosidase (AFU),
    5′-nucleotidase (5′-NT)

    Cum sunt influenţate de consumul de alcool riscurile cardiovasculare în sindromul metabolic?

    Consumul moderat de alcool este asociat ce reducerea
    riscurilor dezvoltării patologiei coronariene; consumul
    exagerat însă creşte mortalitatea provocată de ictusul hemoragic.Am examinat relaţia dintre consumul de alcool şi riscurile
    de dezvoltare a evenimentelor coronariene în următorii10
    ani la pacienţi cu sindrom metabolic.
    La 142 de pacienţi cu sindrom metabolic au fost evaluaţi
    factorii de risc pentru patologia coronariană. Am evaluat
    indexul masei corporale (IMC), nivelului colesterolului
    total (CT), lipoproteidelor de densitate înaltă (HDL) şi de
    densitate joasă (LDL), raportului CT / HDL şi nivelul glicemiei.
    Profi lul riscului cardiovascular a fost măsurat în
    funcţie de consumul de alcool: 50 ml / zi (nivelul înalt).Riscurile de dezvoltare a evenimentelor coronariene în următorii10
    ani au fost calculate în acord cu ecuaţia Framingham.
    Scorul riscului a fost predefi nit ca intermediar (≤
    20%) şi mare (> 20%).
    Creşterea consumului de alcool a fost asociată cu diferenţe
    semnifi cative statistic privind IMC – 31.89 ± 5.36
    vs 29.45 ± 6.18 ٭ vs 32.25 ± 5.65 ٭, p

    Moderate alcohol consumption is associated with
    reduction in coronary heart disease (CHD) risk, heavy
    drinking increases mortality, due to hemorrhagic stroke.We examined the relationship between reported alcohol
    consumption and 10-years risk of cardiovascular events in
    patient with metabolic syndrome.
    142 patients with metabolic syndrome underwent
    screening for CVD risk factors. We evaluated body
    mass index (BMI), total cholesterol (TC), high density
    lipoproteine ​​(HDL) and low density lipoproteine ​​(LDL),
    TC / HDL rate and glucose. The cardiovascular risk profi le
    we measured in groups of reported alcohol intake: 50 ml / day (heavy drinking). The
    10-years risk of cardiovascular events was calculated
    according to Framingham equation.The risk score were
    categorized using predefi ned cutoffs as intermediate (≤
    20%) and high (> 20%).
    Increasing consumption was associated with
    statistically signifi cant difference in BMI (- 31.89 ± 5.36 vs
    29.45 ± 6.18 ٭ vs 32.25 ± 5.65 ٭, p

    Moderate alcohol consumption is associated with reduced
    reducing the risk of developing coronary heart disease
    (Ischemic heart disease), at the same time, excessive use of alcohol
    la leads to an increase in mortality due to hemorrhoids
    ragic stroke.

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