Validity of a Novel Method for Estimating Low-Density Lipoprotein Cholesterol Levels in Cardiovascular Disease Patients Treated with Statins

Sonoda, Takeshi; Takumi, Takuro; Miyata, Masaaki; Kanda, Daisuke; Kosedo, Ippei; Yoshino, Satoshi; Ohishi, Mitsuru

doi:10.5551/jat.44396

Cited by 19 publications

(9 citation statements)

References 28 publications

(39 reference statements)

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“…In 2013, Martin and colleagues developed a novel LDL-C equation using an individualized factor to account for heterogeneity in the TG to VLDL-C ratio, demonstrating improved accuracy of LDL-C estimation at high TG and low LDL-C concentrations compared to the Friedewald formula 13) . Their results were confirmed in various samples of different nationalities and clinical scenarios [14][15][16][17][18][19][20][21][22][23][24] . Our data is also consistent with these observations in a real-world highrisk population of patients undergoing coronary angiography, with significant upward discordance when compared with Friedewald equation, particularly noted in those with hypertriglyceridemia and low LDL-C.…”

Section: Discussionmentioning

confidence: 54%

“…In 2013, Martin and colleagues have developed a more complex LDL-C equation (referred to here as Martin equation) using an individualized factor (ranging from 3.1 to 9.5) to account for the heterogeneity in very-low density lipoprotein cholesterol (VLDL-C), using a 180-cell method to estimate VLDL-C according to patient-specific TG and non-HDL-C levels 13) . Martin equation was demonstrated to be more accurate in estimating LDL-C levels and better validated than other proposed alternative methods for LDL-C estimation [14][15][16][17][18][19][20][21][22][23][24] . However, its implementation remains limited in clinical practice, as it is less intuitive to calculate and needs to be incorporated into laboratory information systems for automated reporting.…”

Section: Lipid Measurementsmentioning

confidence: 95%

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Comparison of Novel Equations for Estimating Low-Density Lipoprotein Cholesterol in Patients Undergoing Coronary Angiography

Zafrir

Saliba

Flugelman

2020

JAT

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The importance of precisely quantifying low-density lipoprotein cholesterol (LDL-C) has become more pronounced over the years, with the rise of metabolic syndrome in the population and the reduction in LDL-C treatment goals. This study aims to compare two novel equations indirectly estimating LDL-C and assess their compatibility with Friedewald formula, in a population with high cardiovascular risk. Methods: This study is a retrospective analysis of the lipid profiles of 10,006 patients who underwent coronary angiography. LDL-C was calculated using Friedewald, Martin, and Sampson equations, and the compatibility between estimations was compared using methods of concordance and reclassification. Results: Our findings show that Martin and Sampson equations displayed high rates of upward LDL-C reclassification (10.8% and 7.5%, respectively) when compared with Friedewald equation. In comparison to the Sampson method, Martin also reclassified 3.8 % of patients to a higher LDL-C category. The magnitude of discordance between LDL-C estimates was more pronounced in hypertriglyceridemic patients, and this increased progressively with the reduction in LDL-C. The proportion of patients with LDL-C 70 mg/dL reclassified to a higher LDL-C category reached 44% (Sampson vs. Friedewald), 65% (Martin vs. Friedewald), and 37% (Martin vs. Sampson) in those with triglyceride levels between 200 and 399 mg/dL. Conclusions: Both Martin and Sampson LDL-C estimates displayed significant proportion of upward discordance with reclassification to higher LDL-C categories compared to Friedewald formula, particularly in patients with elevated triglycerides and low LDL-C, a population in whom more accurate estimation of LDL-C is required. Further studies are warranted to validate the recently developed Sampson equation with comparison to Martin method that tended to more significantly overestimate LDL-C. laboratories around the world. Friedewald equation has been often used to estimate LDL-C concentration in clinical practice since the 1970s 2). LDL-C is calculated indirectly by Friedewald equation as total cholesterol (TC) minus high-density lipoprotein cholesterol (HDL-C) minus triglycerides (TG)/5 in milligrams per deciliter. However, the equation has been observed to underestimate LDL-C when compared to ultracentrifugation or methods of direct LDL-C measure-Copyright©2020 Japan Atherosclerosis Society This article is distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.

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Section: Discussionmentioning

confidence: 54%

Section: Lipid Measurementsmentioning

confidence: 95%

Comparison of Novel Equations for Estimating Low-Density Lipoprotein Cholesterol in Patients Undergoing Coronary Angiography

Zafrir

Saliba

Flugelman

2020

JAT

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“…Martin et al have recently reported a novel method for estimating LDL-C using an adjustable factor instead of a fixed factor of 5 16) . Furthermore, we have demonstrated that in Japanese CAD patients receiving strong statins, LDL-C (M) was more accurate compared to LDL-C (F), particularly in patients with LDL-C 70 mg/dL 35) . In addition, we reported that LDL-C (M) was more useful than LDL-C (F) among Japanese patients with type 2 DM 36) .…”

Section: Discussionmentioning

confidence: 90%

The Priority of Non-HDL-C Assessment to Predict New Lesions among Stable Angina Patients with Strong Statins

Kanda

Miyata

Ikeda

et al. 2022

JAT

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In this study, we aim to examine the clinical meaning of low-density lipoprotein cholesterol (LDL-C) 70 mg/dL as assessed by Friedewald equation [LDL-C (F)] and Martin method [LDL-C (M)] and non-high-density lipoprotein cholesterol (HDL-C) 100 mg/dL on the occurrence of new lesions among Japanese patients with stable angina who underwent percutaneous coronary intervention (PCI) and were prescribed with strong statins. Methods: Among the 537 consecutive stable angina patients who had underwent PCI and had been prescribed with strong statins, the association between the occurrence of new lesions with myocardial ischemia at the 9-month follow-up coronary angiography and ≤ 2 years after PCI and baseline characteristics were assessed. Results: New lesions appeared 9 months and ≤ 2 years after PCI in 31 and 90 patients, respectively. Multivariate logistic regression analysis revealed diabetes mellitus (DM) was significantly associated with the occurrence of new lesions ≤ 2 years after PCI [odds ratio (OR) 1.71, 95 % confidence interval (CI) 1.06-2.83, p 0.031], and only non-HDL-C ≥ 100 mg/dL was associated with the occurrence of new lesions both at 9 months and ≤ 2 years after PCI [OR 1.80, 95 % CI 1.10-3.00, p 0.021 and OR 1.85, 95 % CI 1.13-3.07, p 0.016]. Conclusions: Non-HDL-C ≥ 100 mg/dL was determined to be the independent risk factor for the occurrence of new lesions 9 months and ≤ 2 years after PCI among stable angina patients with strong statins. Residual risk after PCI should be considered by assessing not only DM but also non-HDL-C beyond the scope of LDL-Clowering therapy with strong statins.Dyslipidemia is known to be significantly associated with an increased risk of CAD, and the relationship between dyslipidemia and CAD has already been well established [3][4][5] . Since clinical trials have demonstrated that decreases in serum levels of low-density lipoprotein cholesterol (LDL-C) can reduce the rate of cardiovascular events 6, 7) , lipidlowering therapy represents an important strategy in primary and secondary prevention of CAD 8,9) . In particular, LDL-C has been recommended as the main treatment target of lipid management in CAD patients [10][11][12] . Therefore, clinical practice guidelines

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“…This method estimates LDL-C as (non–HDL-C)−(triglycerides/adjustable factor mg/dL), where the adjustable factor was 180-cell stratification determined as the strata-specific median triglycerides to very-low-density lipoprotein cholesterol ratio according to non–HDL-C and triglyceride levels, 18 and this method has been externally validated by groups inside and outside the United States. 19,20 RC was estimated as TC minus HDL-C minus calculated LDL-C. 21 Currently there is no standard method to estimate RC; this equation has been frequently used in previous studies because it is available from the standard lipid profile. 22,23 Furthermore, it has been demonstrated that using Martin/Hopkins LDL-C in the equation provides a more accurate estimate of RC than using Friedewald LDL-C. 24 Non–HDL-C was calculated as TC minus HDL-C.…”

Section: Methodsmentioning

confidence: 99%

Remnant Cholesterol and the Risk of Coronary Artery Calcium Progression: Insights From the CARDIA and MESA Study

Hao

Gao

Yuan

et al. 2022

Circ: Cardiovascular Imaging

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BACKGROUND: Remnant cholesterol (RC) contributes to residual risk of atherosclerotic cardiovascular disease, but population-based evidence on the prospective relationship between RC and coronary artery calcium (CAC) progression is rare. METHODS: We pooled data obtained from 6544 atherosclerotic cardiovascular disease–free individuals from the CARDIA study (Coronary Artery Risk Development in Young Adults; n=2635) and MESA (Multi-Ethnic Study of Atherosclerosis; n=3909), with a mean±SD age of 47.2±19.8 years; 3019 (46.1%) were men who completed computed tomography of CAC at baseline. RC was measured as total cholesterol minus HDL (high-density lipoprotein) cholesterol minus calculated LDL (low-density lipoprotein) cholesterol (LDL-C) estimated by using the Martin/Hopkins equation. Adjusted Cox models were used to assess the relationships between RC levels and CAC progression. We also performed discordance analyses examining the risk of CAC progression in RC versus LDL-C discordant/concordant groups using median cut points and clinically relevant LDL-C targets. RESULTS: During a median follow-up of 8.6 years, 2778 (42.5%) participants had CAC progression. After multivariable adjustment for demographics and cardiovascular risk factors, a 1-mg/dL increase in RC levels was associated with a 1.3% higher risk of CAC progression (hazard ratio, 1.013 [95% CI, 1.008–1.017]). Results were similar when we categorized individuals by RC quartiles. Furthermore, the discordant high RC/low LDL-C group had a significantly higher risk of CAC progression than the concordant low RC/LDL-C group regarding their medians (hazard ratio, 1.195 [95% CI, 1.063–1.343]) or when setting the clinical LDL-C cut points at 100 and 130 but not 70 mg/dL. The association remained robust across a series of sensitivity analyses. CONCLUSIONS: Elevated RC levels were associated with an increased risk of CAC progression independent of traditional cardiovascular risk factors, even in individuals with optimal LDL-C levels. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00005130 (CARDIA) and NCT00005487 (MESA).

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Validity of a Novel Method for Estimating Low-Density Lipoprotein Cholesterol Levels in Cardiovascular Disease Patients Treated with Statins

Cited by 19 publications

References 28 publications

Comparison of Novel Equations for Estimating Low-Density Lipoprotein Cholesterol in Patients Undergoing Coronary Angiography

Comparison of Novel Equations for Estimating Low-Density Lipoprotein Cholesterol in Patients Undergoing Coronary Angiography

The Priority of Non-HDL-C Assessment to Predict New Lesions among Stable Angina Patients with Strong Statins

Remnant Cholesterol and the Risk of Coronary Artery Calcium Progression: Insights From the CARDIA and MESA Study

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