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When cholesterol travels through the bloodstream, it does not do so alone; it is bound to particles called lipoproteins that circulate according to certain patterns of size and composition. These patterns are individual, variable and dependent on multiple factors. Cardiovascular risk (CVR) factors can affect the size, number and composition of the particles, determine a specific pattern and thus increase CVR.

To assess CVR properly it is necessary to know the number and size of cholesterol-carrying lipoprotein particles and not just their lipid content or cholesterol concentration, since two people with the same cholesterol concentration can have patterns with a different number and size of lipoprotein particles and therefore a different risk of cardiovascular disease (CVD).

A large number of LDL particles (LDL-P) with a predominance of the small LDL subclass over the large LDL subclass defines a pattern that dramatically increases the risk of CVD but goes undetected by traditional risk estimation scales. That's why a number of clinical guidelines now recommend measuring LDL-P size and number in addition to cholesterol content to set therapeutic targets and to assess a patient’s CVR or the efficacy of different prescribed treatments.
Since the validation of how to measure cholesterol was published in 1972, it has been and still is the standard measurement used as a therapeutic target and to control progression and determine CVR.

Currently, LDL cholesterol (LDL-C) is the primary and most important lipid factor routinely used to diagnose dyslipidaemia and determine an individual’s cardiovascular risk. Thirty-one per cent of the risk of CVD in people over the age of 30 is attributed to cholesterol, considered an independent individual factor (1). Hence its importance.

However, we know that a high percentage of individuals with CVD have and have always had normal LDL-C levels. In this regard, there are studies showing that up to 50% of subjects who suffer a cardiovascular accident have healthy LDL-C levels (LDL-C<100 mg/dl) (2). Standard lipid tests therefore fail to provide accurate predictive information about the risk of CVD.

It is important to study the distribution of cholesterol particles because it plays a very important role as an individual risk factor for CVD: up to 31% of CVD risk could be attributed to alterations in lipid profile (1). Advanced lipoprotein tests show the distribution patterns, number and size of cholesterol particles and use values to calculate individual CVR that are different to the risk traditionally determined by total cholesterol (TC) or LDL-C concentration.
Cholesterol is considered to be 'good' when it is transported by HDL particles (HDL-P), since they are responsible for carrying cholesterol back to the liver for it to be destroyed, and high levels of HDL cholesterol (HDL-C) have been related to a reduction in CVD (3). On the other hand, cholesterol is considered to be 'bad' when it is bound to LDL-P, and high levels, especially of small particles, have been related to the formation of atheroma plaques and the onset of cardiovascular events. <br><br>

It is actually the carrier that matters; there is little difference in the type of cholesterol.

An advanced lipoprotein test measures not only the concentration of cholesterol the particles carry but also the number and size of the different types of lipoprotein particles (VLDL, LDL and HDL) in the blood serum. Nine categories of lipoproteins can be established based on their size (large, medium and small for each type: VLDL, LDL and HDL). These lipoprotein particles carry cholesterol throughout the body and the number and size of particles varies from one person to another. Certain types, sizes and concentrations are more closely related to cardiovascular risk than the concentration of LDL-C (4).
Although it is always advisable to know your lipid profile, there are some groups of people for whom this test is of particular interest. American guidelines on endocrinology (American Association of Clinical Endocrinologists and American College of Endocrinology) and lipids (National Lipid Association) recommend having an advanced lipoprotein test (5,6):
  • Every 5 years in people over the age of 20 or younger under a doctor’s recommendation.
  • Every 1-2 years in people over the age of 55 who have not been tested previously, even if they have no other known CVR factors.
  • Every year in people over the age of 55 with known CVR factors.
It is especially appropriate to perform an advanced lipoprotein test in people who have two or more CVR factors, e.g. regular smoking, heavy drinking, obesity or overweight, sedentary lifestyle, stress, sleep disorders, polluted environments and, in particular, those who:
  • Have a family history of CVD in grandparents, parents or siblings detected before the age of 55
  • Padezcan una enfermedad dislipémica, como hiperlipidemia o hipercolesterolemia familiar, dislipemia aterogénica (DA) yaquellas en las que se detecten alteraciones en las concentraciones de c-LDL, c-HDL o Triglicéridos (TG)en sus perfiles lipídicos básicos, por ser potencialmente un indicador inicial de enfermedad dislipémica y por ende generar RCV.
  • Padezcan alguna enfermedad que requiera un seguimiento estrecho del perfil lipídico debido a la su alta relación con eventos cardiovasculares; p. ej. Diabetes mellitus (DM), hipertensión arterial (HTA), enfermedad tiroidea o insuficiencia renal crónica (IRC).
Advanced lipoprotein tests are performed by taking a routine blood sample, much as with most common haematological or biochemical tests. All you need to do is go to your nearest site and have a conventional blood test (1 ml is enough).

The blood serum/plasma sample is analysed by a technique based on two-dimensional nuclear magnetic resonance (2D MNR) using a non-destructive technique on the sample.

With this technique it is not only possible to obtain the usual lipid concentrations but also an accurate measurement of the number and size of lipoprotein particles. Once your sample has been analysed, you can discuss the results with your doctor, who will prescribe you the best treatment option, if necessary
Once you have identified it, tell your doctor where you would prefer to have the test
Dyslipidaemias are a set of metabolic alterations affecting lipids, such as hypercholesterolaemia, hypertriglyceridaemia, AD, mixed dyslipidaemia or discordant lipid patterns, which tend to favour the appearance of atherosclerosis, the process underlying most CVDs.

One case warranting special consideration is AD, which is characterised by slightly low HDL-C levels, moderately high TG levels, normal (or slightly high) LDL-C levels and clearly increased LDL-P levels due to the presence of smaller LDL-P which are capable of crossing the arterial walls more easily.

AD is associated with a high risk of CVD and is the main cause of residual CV risk, defined as an excess of cardiovascular complications that occur in patients whose LDL-C concentration is well controlled. It is characteristically associated with type 2 diabetes (DM 2), obesity, metabolic syndrome, familial combined hyperlipidaemia and some types of kidney disease, all of which are closely linked to peripheral insulin resistance.

The high atherogenicity of AD, with a prevalence of 18 to 23% in the Spanish population, means that early detection and early action are very important for controlling the situation to prevent any potential CVD (7, 8).
Examples of CVD include:
  • Heart Attack
  • Coronary Heart Disease
  • Heart Failure
  • Dilated and hypertrophic cardiomyopathy
  • Arrhythmia and sudden cardiac death
  • Cerebrovascular disease (CeVD): Permanent or transient cerebrovascular accident (CVA) (ictus, cerebral infarction, apoplexy) and certain neurological deficits.
  • Peripheral vascular disease (PVD): inflammation, embolism, thrombosis, stenosis or aneurysms of the peripheral arterial vessels and aorta.
The development of a CVD is not a sudden phenomenon; rather, it develops as a long, slow, continuous process and the worst part is that there are generally no symptoms until the disease reaches an advanced stage.
According to the World Health Organization (WHO), it has been estimated that 17.5 million people died of CVD in 2012, representing 31% of deaths registered worldwide. Of these, approximately 7.4 million were due to coronary heart disease and 6.7 to CVA. Between now and 2030 almost 22.2 million people will die from some form of CVD, primarily heart disease and stroke. It is expected that these diseases will remain the leading cause of death in years to come.(9)

According to the Spanish National Institute of Statistics (INE), CVD accounts for approximately 29% of all-cause deaths. What is more, almost 50% of heart attacks are recorded in people under the age of 70, the most productive period of life (2). If we add to this the ageing population and changes in lifestyle that will take place in the coming decades, CVD will have an even greater impact on demography, health, social aspects and work.

According to the WHO, there are also a number of determining factors that underlie chronic diseases, i.e. “the causes of the causes”, which are a reflection of the major forces that govern social, economic and cultural changes: globalisation, urbanisation and the ageing population. Other determinants of CVD are poverty, stress and hereditary factors.


  1. Toth PP, Grabner M, Punekar RS, Quimbo RA, Cziraky MJ, Jacobson TA. Cardiovascular risk in patients achieving low-density lipoprotein cholesterol and particle targets. Atherosclerosis. 2014; 235: 585-591.
  2. Jellinger PS, Handelsman Y, Rosenblit PD, Bloomgarden ZT, Fonseca VA, Garber AJ, et al. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of dyslipidemia and prevention of atherosclerosis. Endocrpract. 2017; 23(4):479-497.
  3. Bays HE, Jones PH, Orringer CE, Brown WV, Jacobson TA. National Lipid Association Annual Summary of Clinical Lipidology 2016. J Clin Lipidol. 2016; 10(1 Suppl):S1-43.
  4. World Health Organization. Informe sobre salud en el mundo 2002: Reducir los riesgos y promover la vida sana.
  5. Sachdeva A, Cannon CP, Deedwania PC, Labresh KA, Smith SC Jr, Dai D, Hernandez A, et al. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. Am Heart J. 2009; 157(1):111-117.
  6. Kontush A. HDL particle number and size as predictor of cardiovascular disease. Front Pharmacol. 2015; 6:218.
  7. Pedro-Botet J, Flores-Le Roux JA, Mostaza JM, Pintó X, de la Cruz JJ, Banegas JR. Dislipemia aterogénica y control en las unidades de lípidos. Rev Clin Esp. 2014;214(9): 491-498.
  8. Guía Clínica para la detección, diagnóstico y tratamiento de la dislipemia aterogénica en Atención Primaria. 2013.
  9. World Health Organization. Global Status Report on Noncomunicable Diseases 2014.


  • VLDL: Very-low-density lipoprotein
  • LDL: Low-density lipoprotein
  • HDL: High-density lipoprotein
  • LDL-C: LDL cholesterol
  • CVD: Cardiovascular disease
  • AD: Atherogenic dyslipidaemia
  • HDL-C: HDL cholesterol
  • DM: Diabetes Mellitus
  • HBP: High blood pressure
  • CKD: Chronic kidney disease
  • 2D MNR: Two-dimensional nuclear magnetic resonance
  • CVR: Cardiovascular risk
  • TC: Total cholesterol
  • LDL-P: LDL particles
  • HDL-P: HDL particles
  • TG: Triglycerides
  • DM 2: Type 2 DM
  • CeVD: Cerebrovascular disease
  • CVA: Cerebrovascular accident
  • PVD: Peripheral vascular disease
  • WHO: World Health Organization
  • INE: Spanish National Institute of Statistics