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Measurement of blood lipids and lipoproteins

Measurement of blood lipids and lipoproteins
Literature review current through: Jan 2024.
This topic last updated: Oct 14, 2022.

INTRODUCTION — Lipids, such as cholesterol and triglyceride, are insoluble in plasma. They are made soluble by attachment to circulating lipoproteins that transport lipids to various tissues for energy utilization, lipid deposition, steroid hormone production, and bile acid formation. The lipoprotein consists of esterified and unesterified cholesterol, triglycerides, and phospholipids, and protein.

There are five major lipoproteins in blood: chylomicrons, very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Each of these classes of lipoproteins carries cholesterol and triglyceride to a varying degree, with LDL carrying the majority of cholesterol and VLDL carrying the majority of triglyceride.

In general, patient care issues related to screening, diagnosis, and treatment are based on the results of the measurement of serum lipids, which is generally accomplished by obtaining a lipid profile. On occasion, measurement of serum lipoproteins is necessary for one or more of these purposes. This topic will discuss the issues relevant to the measurement of serum lipids and lipoproteins. Other issues related to lipids and lipoproteins, such as their role in atherosclerosis, are discussed separately. (See "Lipoprotein classification, metabolism, and role in atherosclerosis".)

INDICATIONS

Overview — The lipid profile typically includes total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides. The most common indications for ordering a complete lipid profile include:

Screening for a familial lipid disorder

Establishing the risk of cardiovascular disease in an individual without prior disease

The first lipid test in any patient being tested for a lipid disorder

Total and HDL cholesterol — For patients who have had documentation (first test) of a full lipid profile and the triglyceride level was not elevated, subsequent measurement of a total cholesterol and HDL cholesterol is sufficient. These measurements can be used to calculate non-HDL cholesterol (total cholesterol – HDL cholesterol). (See "HDL cholesterol: Clinical aspects of abnormal values".)

However, it is important to recognize that LDL cholesterol remains the primary lipid measure for cardiovascular disease risk assessment and guide to therapy. (See "Low-density lipoprotein cholesterol-lowering therapy in the primary prevention of cardiovascular disease".)

LDL cholesterol — Measuring LDL cholesterol periodically can be helpful in determining whether a patient has met an LDL cholesterol target or whether patients are adherent to treatment. (See "Low-density lipoprotein cholesterol-lowering therapy in the primary prevention of cardiovascular disease", section on 'Subsequent management'.)

There are no reliable data on the optimal method of monitoring the effects of lipid-lowering therapy. We suggest that the LDL cholesterol be monitored every six weeks after the initiation of treatment until the LDL cholesterol target is achieved [1]. Thereafter, measurement every 6 to 12 months is reasonable in patients adherent to lifestyle modifications.

Triglycerides — The most common indications for measuring triglyceride levels, either as a standalone test or as part of a lipid profile, include:

Establishing the etiology of acute pancreatitis (see "Hypertriglyceridemia-induced acute pancreatitis", section on 'Pathogenesis')

Monitoring treatment of hypertriglyceridemia (see "Hypertriglyceridemia in adults: Management", section on 'Treatment goals')

Screening family members for familial hypertriglyceridemia

Non-HDL cholesterol — Non-HDL cholesterol is defined as the difference between the total cholesterol and HDL cholesterol. Non-HDL cholesterol includes all cholesterol present in lipoprotein particles that is considered atherogenic, including LDL, lipoprotein(a), intermediate-density lipoprotein (IDL), and very low-density lipoprotein (VLDL). It has been suggested that the non-HDL cholesterol fraction may be a better tool for risk assessment than LDL cholesterol [2]. We do not routinely obtain this measurement. This issue is discussed in detail elsewhere. (See "Screening for lipid disorders in adults", section on 'Choice of tests'.)

Ratios — The ratios of total cholesterol or LDL cholesterol to HDL cholesterol concentration have been evaluated in many epidemiological studies to categorize populations into high- and low-risk subgroups. We do not routinely obtain these measurements. The clinical use of these ratios are discussed elsewhere. (See "Screening for lipid disorders in adults", section on 'Choice of tests'.)

FASTING VERSUS NON-FASTING TESTS — With the exceptions of the first time a lipid profile is obtained or when the test is obtained for the purpose of following known hypertriglyceridemia, the lipid profile (or its components) do not usually require fasting [3-6]. However, many experts routinely ask their patients to fast for a follow-up lipid profile so that there is no need to repeat the test due to a concern for an inaccurate low-density lipoprotein (LDL) cholesterol due to high triglycerides.

The decision whether to have the patient fast for a subsequent lipid profile is in part dependent on patient convenience and the likelihood that the calculated LDL cholesterol value might be inaccurate due to elevated triglycerides. (See 'Measurement' below.)

Patients at increased risk for triglycerides high enough to make the calculated LDL cholesterol significantly different from a measured (direct) LDL cholesterol include those with type 2 diabetes, very obese individuals, those taking medications known to increase triglycerides, and patients with significant alcohol intake. (See "Hypertriglyceridemia in adults: Management".)

If the non-fasting plasma triglyceride component of the lipid profile returns at >400 mg/dL (>4.516 mmol/L), we obtain a fasting lipid profile.

We ask the patient to fast (8 to 12 hours without food) when we are attempting to diagnose or follow a patient with a triglyceride disorder. From a practical point of view, this means that the test will need to be obtained early in the morning (before breakfast). While mean population levels of triglycerides and calculated LDL cholesterol do not appear to vary substantially with different lengths of time since eating [7], clinically important variability in triglyceride levels in individual patients after consumption of fatty foods and drinks is likely and consistent with clinical experience. (See "Hypertriglyceridemia in adults: Management".)

The following serves to give a more detailed explanation of the potential impact of the results of a non-fasting test. If a patient has a lipid profile soon after eating a very fatty meal, chylomicrons are made to absorb the fat. The ratio of triglyceride to cholesterol in a chylomicron is about 20:1. In the fasting state, if there are no chylomicrons, then most of the triglyceride in the blood is being carried by very low-density lipoprotein (VLDL) and the triglyceride to cholesterol ratio in those particles is 5 to 1. That ratio is what most clinical laboratories use to calculate the cholesterol contribution of VLDL particles. (See 'Indirect measurement' below.)

If a patient has a fasting triglyceride of 100 mg/dL and their postprandial, fatty meal triglyceride was 300 mg/dL, then the VLDL cholesterol calculation would be performed and the VLDL cholesterol would be estimated at 300/5 or 60 mg/dL. But if all the increased triglyceride (ie, the increase from 100 to 300 mg/dL) is due to chylomicrons, the actual VLDL plus chylomicron cholesterol is the 100/5 (from the VLDL that are present) plus 200/20 which is the cholesterol in the chylomicrons. This amounts to a total of 30 mg/dL, not 60 mg/dL. The difference between the 60 mg/dL the laboratory would calculate and the 30 mg/dL which is the correct number to be using is 30 mg/dL, and that higher value would be wrongly subtracted to give an LDL cholesterol that is 30 mg/dL lower than it actually is. If a patient comes in and their fasting triglyceride is 100 mg/dL and their non-fasting triglyceride is 120 mg/dL, then the error in using the calculated LDL cholesterol is so small as not to matter. So, the key thing is that if there is a good record of fasting triglycerides in a patient and then a non-fasting one return with a much higher value, a very significant error could be introduced into the LDL cholesterol calculation if they use that non-fasting value.

Total cholesterol and HDL cholesterol are minimally affected by fasting [8]. LDL cholesterol is typically calculated from total cholesterol, HDL cholesterol, and triglycerides using the Friedewald equation (LDL cholesterol  =  total cholesterol  -  HDL cholesterol  -  triglycerides  x  0.2) [9]. This equation is modified for those with particularly elevated levels of triglycerides (>400 mg/dL), but even with modification it is only accurate for patients who are fasting. In patients who have consumed fats prior to testing, various lipid components (eg, chylomicrons) will be elevated, which will result in a calculated LDL cholesterol that is falsely low compared with what would have been calculated in the fasting state.

The largest observational study comparing fasting and non-fasting lipid values evaluated results in over 90,000 individuals [5]. The following was noted:

The maximal mean changes at one to six hours after habitual meals were thought to be clinically insignificant at +0.3 mmol/L (26 mg/dL) for triglycerides, -0.2 mmol/L (8 mg/dL) for total cholesterol and LDL cholesterol, and -0.2 mmol/L for calculated non-HDL cholesterol.

Concentrations for HDL cholesterol, apolipoprotein A1, apolipoprotein B, and Lp(a) were unchanged.

Nonfasting lipid profiles may be used to calculate "remnant" cholesterol. Remnant cholesterol is either measured directly or calculated as: non-HDL cholesterol  -  directly measured LDL cholesterol. Remnant cholesterol has been confirmed in Mendelian randomization trials as a marker of myocardial infarction and in prospective observational studies as a predictor of initial and recurrent cardiovascular events [10,11]. (See "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Exogenous pathway of lipid metabolism' and "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Endogenous pathway of lipid metabolism'.)

MEASUREMENT — A standard serum lipid profile measures the concentration of total and high-density lipoprotein (HDL) cholesterol as well as the triglycerides. With these values, the low-density lipoprotein (LDL) cholesterol concentration can be estimated. (See 'LDL cholesterol' below.)

Total and HDL cholesterol — Serum total and HDL cholesterol are measured directly and can be obtained in fasting or nonfasting individuals; there are only small, clinically insignificant differences in these values between measurements in the fasting or non-fasting state [8]. (See 'Fasting versus non-fasting tests' above.)

The total cholesterol can vary by 4 to 11 percent within an individual due to multiple factors including stress, minor illness, and posture [12]. Values may also vary between different laboratories, with data suggesting that a single measurement of serum cholesterol can vary as much as 14 percent [12,13]. Thus, in an individual with a "true" serum cholesterol concentration of 200 mg/dL (5.2 mmol/L), the range of expected values is 172 to 228 mg/dL (4.5 to 5.9 mmol/L) [13,14]. These observations suggest that more than one measurement of total cholesterol should be obtained when treatment considerations demand a precise determination. Serum HDL cholesterol may demonstrate even greater variability [15].

Blood lipid levels also exhibit mild seasonal variation with a peak in total cholesterol level in the winter and a trough in the summer. One study found that the amplitude of seasonal variation of total cholesterol concentration was 3.9 mg/dL (0.10 mmol/L) in men and 5.4 mg/dL (0.14 mmol/L) in women [16].

LDL cholesterol

General approach — Measurement of LDL cholesterol does not require fasting in most cases. However, in patients who have had prior significant elevation(s) of nonfasting triglyceride, a fasting LDL cholesterol (calculated from the lipid profile) should be obtained. (See 'Fasting versus non-fasting tests' above.)

This will help to avoid miscalculation of the LDL cholesterol. An alternative approach is to obtain a direct measurement of LDL cholesterol. (See 'Direct measurement' below.)

This approach can be chosen as long as the direct method is always used to assess LDL cholesterol; switching between the calculated and direct measurements is not recommended. (See 'Causes of inaccurate results' below.)

Indirect measurement — There are multiple ways to evaluate the concentration of LDL cholesterol in plasma or serum, described below. In clinical practice, the value is usually estimated using the Friedewald equation. However, the Friedewald equation and Martin-Hopkins methods are less accurate than the Sampson/NIH method when LDL cholesterol levels are over 150 mg/dL [17].

Friedewald equation – LDL cholesterol reported in the lipid profile is generally calculated using the Friedewald formula, which states:

LDL cholesterol  =  total cholesterol  -  very low-density lipoprotein (VLDL) cholesterol  -  HDL cholesterol [18]. Stated another way, and understanding that this is an approximation, the total cholesterol in plasma or serum is the sum of cholesterol found in each of the VLDL, HDL, and LDL lipoprotein particle types. The Friedewald formula is applied to lipid values measured in the fasted state. In a non-fasting patient, the contribution of post-prandial chylomicrons to the total lipoprotein pool makes the formula much less accurate.

As mentioned above, total and HDL cholesterol are measured directly (see 'Total and HDL cholesterol' above). VLDL cholesterol is approximated by dividing the measured total triglyceride level by 5. With the measured total and HDL cholesterol and triglyceride, an approximate LDL cholesterol can be calculated. Calculators for determining LDL cholesterol are available (calculator 1 and calculator 2).

As with most laboratory measurements made on human plasma/serum, there is some sample to sample variability in the LDL cholesterol. Sources of error involved in the estimation of LDL cholesterol using the Friedewald formula include:

The formula is valid only if the total triglyceride concentration is less than 400 mg/dL (4.516 mmol/L). In patients with more pronounced hypertriglyceridemia, LDL cholesterol levels must be measured directly (direct LDL) by ultracentrifugal single spin analysis or immunoprecipitation technique [19].

The formula underestimates LDL cholesterol, particularly at low levels of LDL cholesterol (<25 mg/dL [0.6 mmol/L]) [20].

The calculation of VLDL cholesterol (from triglycerides) underestimates the cholesterol content of the atherogenic, intermediate-density lipoprotein (IDL), and VLDL remnants. (See "Lipoprotein classification, metabolism, and role in atherosclerosis".)

The estimated LDL cholesterol concentration includes cholesterol contained in other lipoproteins, such as lipoprotein(a) and lipoprotein-X. (See "Lipoprotein(a)" and "Hypercholesterolemia in primary biliary cholangitis (primary biliary cirrhosis)".)

The extent of variability with calculated LDL cholesterol may be greater than with other laboratory tests since the value is influenced by the method error from each of the independent lipid measurements (total cholesterol, triglycerides, and HDL cholesterol). There is some evidence to suggest that the magnitude of the error is greater at lower LDL cholesterol levels, particularly around 70 mg/dL (1.8 mmol/L) or lower [21]. In a study of nearly 16,000 patients with fasting triglyceride concentrations <400 mg/dL (4.5 mmol/L), the 95% confidence interval for a calculated LDL cholesterol of 70 mg/dL (1.8 mmol/L) was 60 to 86 mg/dL (1.6 to 2.2 mmol/L) using LDL cholesterol measured by beta quantification (considered the gold standard) [22]. While the magnitude of variability at low LDL cholesterol values creates some clinical uncertainty, we interpret single values for LDL cholesterol in the context of prior values.

Martin/Hopkins method – Other indirect methods for deriving the LDL cholesterol level exist. One such method, Martin/Hopkins, was derived and validated in a sample of over 1.3 million lipid profiles and uses an adjustable factor for the triglyceride to VLDL cholesterol ratio [23,24]. In a large cross-sectional analysis, this method of LDL estimation was more accurate than the Friedewald equation for both fasting and nonfasting samples across a range of LDL cholesterol levels [24,25]. Among nonfasting samples, the method outperformed the Friedewald equation when LDL cholesterol was low (<70 mg/dL) or when triglyceride levels were high. The validity and utility of this method need further testing before we can recommend its routine use.

Sampson/NIH method – This LDL cholesterol equation was derived to estimate the LDL cholesterol concentrations in patients with plasma triglyceride levels up to 800 mg/dL. It is more accurate than other LDL cholesterol equations Friedewald or Martin-Hopkins for calculating LDL cholesterol levels, particularly for patients with hypertriglyceridemia [26].

Direct measurement — Assays are available to directly measure the LDL cholesterol concentration and should be considered in patients with a total triglyceride concentration >400 mg/dL (4.516 mmol/L). However, even in patients with lower triglyceride values, some direct assays may give significantly different results than the estimated LDL cholesterol, and all of the treatment guidelines for hypercholesterolemia were based upon the estimated value.

The magnitude of the difference in LDL cholesterol values between results derived from the Friedewald equation and direct measurement was evaluated in a study of 1,310,440 United States adults who underwent lipid profiling by vertical spin density gradient ultracentrifugation (2009 to 2011) and who had triglycerides <400 mg/dL (4.516 mmol/L) [27]. The broad conclusion of the research was that the LDL cholesterol, as calculated by the Friedewald equation, became progressively inaccurate as triglyceride levels increased; this was particularly apparent at LDL cholesterol values <70 mg/dL (1.81 mmol/L). For example, of patients with Friedewald LDL cholesterol <70 mg/dL, 23 percent had a direct LDL cholesterol ≥70 mg/dL (39 percent if triglycerides concurrently 150 to 199 mg/dL; 59 percent if triglycerides concurrently 200 to 399 mg/dL).

Triglycerides — Triglycerides are carried in chylomicron and VLDL particles. Triglyceride levels are influenced by recent food intake and should be measured in the fasting state when possible. (See 'Fasting versus non-fasting tests' above and "Hypertriglyceridemia in adults: Approach to evaluation".)

OTHER LIPID TESTS

LDL cholesterol particle number and size — We suggest measurement of low-density lipoprotein (LDL) particle concentration, or the surrogate measure of apolipoprotein B, in individuals with insulin resistance disorders who have not achieved their minimal acceptable LDL cholesterol targets. In such patients, this information may provide guidance as to treatment decisions, such as an increased dose of statins or combination lipid-altering therapy with statin plus either niacin or fibrate.

LDL cholesterol does not accurately quantify LDL particles no matter how accurately the analytical techniques. This situation is most notable when the LDL particle size is small, since small LDL particles carry less cholesterol than large LDL particles. For the same amount of LDL cholesterol, the patient with smaller LDL particles may require nearly 70 percent more LDL particles to carry the same amount of cholesterol as the patient with larger LDL particles [28].

Measurement – Lipoprotein particle sizes can be measured by special laboratories that use three different analytical techniques. These laboratory methods include nuclear magnetic resonance (NMR) spectroscopy, gradient gel electrophoresis, analytical ultracentrifugation, and ion mobility (IM). Lipoprotein particle size is most often reported as an average size that takes into account the contribution of the small, intermediate, and large particles. Unlike the other methods, NMR spectroscopy reports the total concentration or blood levels of the individual LDL subclasses and then derives the average LDL particle size [29]. LDL particle concentration can be measured by NMR and IM methods.

Rationale for measurement – Strong associations between total LDL particle concentration and cardiovascular disease provide a rationale for advanced lipoprotein testing for total LDL particle numbers in cardiovascular risk assessment and treatment [30]. In high cardiometabolic risk patients, such as those with diabetes, where the disconnect between LDL cholesterol and LDL particle size is greatest, the measurement of LDL particle size may be of benefit for improving risk stratification and as a guide to titration/adjustment of lipoprotein-modifying therapy [31].

As an example, among patients with insulin resistance disorders (metabolic syndrome, type 2 diabetes), there is discordance between LDL cholesterol and LDL particle concentration/apolipoprotein B [32]. This discordance results from LDL remodeling in insulin resistance, which leads to a smaller, cholesterol-depleted LDL particle. Thus, although LDL cholesterol levels do not change with insulin resistance or with the number of metabolic risk factors, whereas the concentration of small LDL particles and total LDL particles increases progressively as the severity of insulin resistance increases and the number of metabolic risk factors increases. On statin therapy, nearly two-thirds of type 2 diabetes patients with LDL cholesterol levels less than 100 mg/dL have excess LDL particles. In patients with type 2 diabetes and LDL cholesterol levels less than 70 mg/dL on statin therapy, 41 percent have excess numbers of LDL particles.

A 2009 systematic review (of 24 studies) evaluated the association between cardiovascular outcomes and LDL subfractions or distribution (particle size; density) as well as total LDL particle number [33]. Higher LDL particle number was consistently associated with increased cardiovascular risk, independent of lipid markers. LDL subfractions/size did not add incremental risk prediction beyond that achieved with traditional risk factors.

Apolipoprotein B — Lipoprotein particles, which carry cholesterol and triglycerides, are comprised in part of apolipoproteins. For instance, each LDL particle contains one molecule of apolipoprotein B (apoB). An elevated apoB level (≥130 mg/dL) is considered an atherosclerotic cardiovascular disease risk-enhancing factor, and we suggest measuring apoB in patients with triglyceride levels over ≥200 mg/dL. This is discussed in detail elsewhere. (See "Hypertriglyceridemia in adults: Management", section on 'Treatment goals'.)

CAUSES OF INACCURATE RESULTS — In addition to the potential for variability between measurements (discussed above) of one or more component of the lipid profile, the following are two potential causes of inaccurate results:

The presence of a circulating monoclonal protein may lead to falsely low values of high-density lipoprotein (HDL) and/or low-density lipoprotein (LDL) cholesterol. (See "Laboratory methods for analyzing monoclonal proteins", section on 'Interference with laboratory tests'.)

The calculated LDL cholesterol may be inaccurate in patients with a triglyceride levels above 400 mg/dL (4.516 mmol/L). (See 'LDL cholesterol' above.)

Although the evidence is not robust, we believe that LDL cholesterol and HDL cholesterol are relatively accurate when measured in the first 24 to 48 hours after hospitalization for an ST elevation myocardial infarction (STEMI) and up to 96 hours after a non-ST elevation acute coronary syndrome (NSTEACS) [34]. Non-fasting values are acceptable. (See 'Fasting versus non-fasting tests' above.)

In initial small studies conducted in an era before aggressive efforts to limit infarct size, clinically significant changes in components of the lipid profile (fall in LDL cholesterol and HDL cholesterol and rise in triglycerides) were observed after 24 to 48 hours after an acute myocardial infarction (and also surgical trauma or infection) with a maximal effect at seven days, and these changes persisted for approximately two months (figure 1) [35,36].

Possible causes of changes in serum lipids following an acute coronary syndrome (ACS) include tissue injury, which can reduce serum concentrations of total cholesterol, HDL cholesterol, LDL cholesterol, and apolipoproteins B and A-I [37]; hospitalization, which has been associated with significantly reduced levels of HDL cholesterol compared with values determined in the outpatient setting [38]; and stress-induced myocardial injury, which is associated with triglyceride elevation [34].

Based upon the changes in lipid profile, it has been thought to be most accurate in patients with an ACS when obtained within hours of hospitalization or in the outpatient setting after at least one month has elapsed (figure 1) [34]. The magnitude of the acute phase response is larger in STEMI than NSTEACS.

However, the 2008 LUNAR trial that included patients with unstable angina and NSTEMI had twice as many patients as all of the earlier studies combined and found that serum lipids remain relatively stable for the first 96 hours after an ACS (unstable angina, NSTEMI) [39]. The primary purpose of this randomized trial was to compare the relative efficacy of rosuvastatin and atorvastatin for LDL cholesterol lowering in patients with an ACS. Serum lipids, including direct LDL cholesterol, were measured in 507 patients on days 1, 2, and 4 after the event. The direct LDL cholesterol levels fell slightly in the 24 hours after admission from 136.2 to 133.5 mg/dL (3.52 to 3.45 mmol/L) and then rose somewhat to 141.8 mg/dL (3.67 mmol/L) over the next two days. Similar changes were noted for total cholesterol, while HDL cholesterol changes were smaller and triglyceride levels remained unchanged.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Lipid disorders and atherosclerosis in children" and "Society guideline links: Lipid disorders in adults".)

SUMMARY AND RECOMMENDATIONS

Background – The serum lipid profile measures total cholesterol and high-density lipoprotein (HDL) cholesterol as well as the triglyceride level. With these values, the low-density lipoprotein (LDL) cholesterol concentration can be estimated. (See 'Measurement' above.)

Measurements requiring fasting – Serum total and HDL cholesterol are measured directly, and there are only small, clinically insignificant differences in these values when measured in the fasting or non-fasting state. Triglyceride levels may vary after a recent meal. Thus, we generally advise that the lipid profile be measured in the fasting state. (See 'Total and HDL cholesterol' above and 'Triglycerides' above.)

LDL cholesterol measurement – The LDL cholesterol reported in the lipid profile is generally calculated from values for triglycerides, total cholesterol, and HDL cholesterol.

A directly measured LDL cholesterol concentration should be considered in patients with a total triglyceride concentration >400 mg/dL (4.516 mmol/L). (See 'LDL cholesterol' above.)

Lipid measurements we do not routinely advise – We do not advise the routine measurement of LDL particle size or concentration (number), lipoprotein levels, or the use of “ratios.” (See 'Other lipid tests' above and 'Ratios' above.)

Causes of inaccurate results – These include the presence of a circulating monoclonal protein (falsely low HDL cholesterol and/or LDL cholesterol) and triglyceride levels above 400 mg/dL (calculated LDL cholesterol). LDL cholesterol and HDL cholesterol levels are thought to be relatively accurate when measured in the first 24 to 48 hours after hospitalization for an ST elevation myocardial infarction (STEMI) and up to 96 hours after a non-ST elevation acute coronary syndrome (NSTEACS). Non-fasting values are acceptable. (See 'Causes of inaccurate results' above.)

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Topic 4556 Version 54.0

References

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