Assessing Long-Term Stability of Lipoprotein(a) in Frozen Blood Plasma Samples: A 14-Year Analysis from The Irish Longitudinal Study on Ageing (TILDA)

Emma Connolly; Sinéad McLoughlin; Aisling M. O'Halloran; Ann Hever; Kanika Nautiyal; Margaret McCormack; Vivion Crowley; Rose Anne Kenny

doi:10.12688/hrbopenres.14357.1

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Research Article

Assessing Long-Term Stability of Lipoprotein(a) in Frozen Blood Plasma Samples: A 14-Year Analysis from The Irish Longitudinal Study on Ageing (TILDA)

[version 1; peer review: 1 approved, 1 approved with reservations]

Emma Connolly ^1,2, Sinéad McLoughlin¹, Aisling M. O'Halloran^1-3, [...] Ann Hever¹, Kanika Nautiyal⁴, Margaret McCormack⁴, Vivion Crowley⁴, Rose Anne Kenny^1,2,5

Emma Connolly ^1,2, Sinéad McLoughlin¹, [...] Aisling M. O'Halloran^1-3, Ann Hever¹, Kanika Nautiyal⁴, Margaret McCormack⁴, Vivion Crowley⁴, Rose Anne Kenny^1,2,5

PUBLISHED 25 Mar 2026

Author details Author details

¹ The Irish Longitudinal Study on Ageing, Trinity College Dublin School of Medicine, Dublin, Leinster, D02 R590, Ireland
² Discipline of Medical Gerontology, Trinity College Dublin School of Medicine, Dublin, Leinster, D02 PN40, Ireland
³ Trinity College Dublin School of Nursing and Midwifery, Dublin, Leinster, D02 T283, Ireland
⁴ Biochemistry Department, Laboratory Medicine, St James's Hospital, Dublin, Leinster, D08 NHY1, Ireland
⁵ Mercer's Institute for Successful Ageing, St James's Hospital, Dublin, Leinster, D08 E9P6, Ireland

Emma Connolly
Roles: Investigation, Methodology, Writing – Original Draft Preparation

Sinéad McLoughlin
Roles: Investigation, Methodology, Writing – Original Draft Preparation, Writing – Review & Editing

Aisling M. O'Halloran
Roles: Conceptualization, Investigation, Writing – Review & Editing

Ann Hever
Roles: Project Administration

Kanika Nautiyal
Roles: Formal Analysis

Margaret McCormack
Roles: Formal Analysis, Writing – Review & Editing

Vivion Crowley
Roles: Formal Analysis, Resources, Writing – Review & Editing

Rose Anne Kenny
Roles: Funding Acquisition, Resources, Writing – Review & Editing

OPEN PEER REVIEW

REVIEWER STATUS

This article is included in the TILDA gateway.

Abstract

Background

Degradation of lipoprotein(a) [Lp(a)] during storage may compromise the accuracy of measurements derived from historic or biobanked samples, with implications for retrospective research and cardiovascular risk estimation. Understanding if frozen Lp(a) values reliably reflect concentrations measured in fresh plasma is essential. This study aims to assess the stability of Lp(a) by comparing fresh plasma concentrations with short- and long-term frozen samples from matched participants in a longitudinal cohort.

Method

Using data from the Irish Longitudinal study on Ageing, paired fresh and short-term frozen (4 days at -80^oC), or long-term frozen (>10years at -80^oC) were analysed using an isoform-insensitive immunoassay. Bland-Altman analyses assessed absolute and percentage differences between fresh and frozen measurements and evaluated whether degradation varied across Lp(a) concentration. Cardiovascular risk classification based on Lp(a) thresholds was compared between fresh and frozen samples.

Results

Short-term frozen samples demonstrated modest Lp(a) reduction (mean -5.8 nmol/L; 12.1% decrease), whereas long-term storage resulted in substantial loss (mean -41.1 nmol/L; 61% decrease). Percentage differences showed no proportional bias, indicating uniform degradation across concentration ranges. Storage effects altered cardiovascular risk classification in 10% of short-term samples and 49% of long-term samples. Notably, 67% of individuals with fresh Lp(a) ≥105 nmol/L were no longer above this threshold after long-term storage, with 18% misclassified as <62 nmol/L.

Conclusions

Lp(a) undergoes significant degradation during frozen storage, particularly after long-term biobanking. These changes can substantially underestimate elevated Lp(a) prevalence and cardiovascular risk. Retrospective studies relying on long-stored samples should therefore interpret Lp(a) measurements with caution.

Keywords

Lipoprotein(a); cardiovascular disease; health;

Corresponding author: Emma Connolly

Competing interests: No competing interests were disclosed.

Grant information: The author(s) declared that no grants were involved in supporting this work.

Copyright: © 2026 Connolly E et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

How to cite: Connolly E, McLoughlin S, O'Halloran AM et al. Assessing Long-Term Stability of Lipoprotein(a) in Frozen Blood Plasma Samples: A 14-Year Analysis from The Irish Longitudinal Study on Ageing (TILDA) [version 1; peer review: 1 approved, 1 approved with reservations]. HRB Open Res 2026, 9:25 (https://doi.org/10.12688/hrbopenres.14357.1) First published: 25 Mar 2026, 9:25 (https://doi.org/10.12688/hrbopenres.14357.1) Latest published: 25 Mar 2026, 9:25 (https://doi.org/10.12688/hrbopenres.14357.1)

Introduction

Lipoprotein(a) [Lp(a)] has recently emerged as a major, independent, risk factor for cardiovascular disease (CVD).^1–3 Lp(a) concentrations are largely genetically determined, affecting the size and concentration of circulating Lp(a).⁴ It is estimated that around 20% of the population have elevated Lp(a) levels which are minimally affected by diet, exercise or conventional lipid-lowering therapies. Currently, Lp(a) levels are not measured as a standard component of clinical blood panel tests, however, due to its genetic stability and its potential to identify individuals at heightened risk for CVD^5,6 the European Society of Cardiology (ESC) has recommended a one-time Lp(a) measurement for all adults with a personal or familial history of cardiovascular health issues.^7,8 This focus is particularly pertinent in countries like Ireland, where cardiovascular mortality rates are alarmingly high, with one in four deaths attributed to CVD.⁹

The recognition of Lp(a) as an independent risk factor for CVD has been hindered by inconsistencies in measurement techniques and unit reporting.^10,11 Accurate quantification of Lp(a) is complicated by the structural heterogeneity of apolipoprotein(a) (apo(a)), which contains a variable number of kringle IV (KIV) repeats.¹² This polymorphic feature impacts the molecular weight and immunoreactivity of Lp(a), leading to assay-dependent variability and limiting comparability across studies. Early investigations explored the effects of freezing and long-term storage on Lp(a) concentration, provided evidence that sample handling could influence measured levels.^13,14 However, these observations were generated using isoform-sensitive, non-standardised assays. Re-evaluating the effects of storage and freezing using updated isoform-independent assays could more reliably evaluate the influence of storage time and freezing on Lp(a) measurement.¹⁵

Leveraging longitudinal data from The Irish Longitudinal Study on Ageing (TILDA), a nationally representative cohort study established in 2009, provides a valuable opportunity to analyse Lp(a) stability across time. This retrospective analysis, using an apo(a) size independent method to measure Lp(a) concentration in fresh and frozen blood plasma, will provide insight and clarity on the stability of Lp(a) in long-term frozen samples and the potential impact of prolonged storage on its concentration. Moreover, our findings will provide essential guidance to other cohort studies contemplating the retrospective measurement of Lp(a) in stored samples, thereby expanding the rationale and utility of such analyses in the broader context of CVD research.

Methods

Study population

The Irish Longitudinal Study on Ageing (TILDA) is a nationally representative study of community-dwelling adults aged 50 years and over living in the Republic of Ireland. TILDA’s study design and sampling method has been described previously.¹⁶ Briefly, initiated in 2009 (Wave 1), TILDA has collected longitudinal data on health, economic and social circumstances of older adults at data collection Waves occurring every two years. A comprehensive health assessment collecting biomedical data and blood sampling is collected in a dedicated research facility at every second Wave.

Ethical approval for each wave of TILDA is obtained from the Faculty of Health Sciences Research Ethics Committee at Trinity College Dublin, Ireland. Ethical approval was obtained on 02/05/2008 for Wave 1 and 31/05/2019 for Wave 6 (Ref: 190407). Written informed consent was obtained from all participants in each Wave. Participants were provided with detailed information regarding the purpose of the study, their rights as participants, and the measures taken to ensure confidentiality and data protection in advance of participation. Participation was voluntary, and participants were free to withdraw from the study at any point. TILDA adheres to the 1964 Helsinki declaration and its later amendments.

Long-term storage

Baseline blood samples were taken between November 2009 and August 2011. Written and verbal consent was obtained prior to blood draw. For participants who agreed to provide a blood sample, separate consent was requested for long-term storage for future health research. Blood draw was performed using venepuncture with a butterfly and green 21-gauge Vacutainer needle, following standard clinical guidelines on non-fasted participants. A total of 25ml of venous blood was collected into 3 vacutainers (2x 10ml K2EDTA and 1x 5ml lithium heparin tubes). The labelled blood tubes were then placed inside the specialised 3-layer blood boxes which maintained the temperature of the blood samples between 2-8 degrees Celsius (°C) for up to 48 hours until they were delivered to the central laboratory for processing. Blood samples were centrifuged and then aliquoted into up to 11 bar-coded cryovials (two lithium heparin plasma samples, seven K2EDTA plasma samples and 2 K2EDTA buffy coat samples) to protect the samples from repeated rounds of freezing and thawing in future processing and placed in storage at -80°C.¹⁶

Fresh and short-term storage

Wave 6 blood samples were collected between July and December 2023. Blood draw and laboratory processing protocols remained the same as baseline. Fresh samples were stored in a refrigerator at 4°C for up to 4 days. Short term frozen samples (N = 40) were stored at –80°C for 4 days and were not subjected to freeze/thaw cycles. Samples chosen for the validation study were equally distributed across age and sex.

Lp(a) measurement

Lp(a) was measured in an accredited laboratory within the Biochemistry Department, of the Centre for Laboratory Medicine & Molecular Pathology (LabMed) at St James’s Hospital, Dublin (ISO 15189). Lp(a) was measured using the Roche Hitachi Cobas c 502 analyser and Roche Cobas Tina-quant Lipoprotein (a) Gen.2 kit, a particle-enhanced immunoturbidimetric assay. Human Lp(a) was agglutinated with latex particles coated with anti-Lp(a) antibodies. The precipitate was determined turbidimetrically at 659 nm. This methodology, with concentration measurement in nmol/L, is not influenced by isoform size and thus provides a more accurate measurement of Lp(a). The measuring range was between 7-240 nmol/L; samples above the upper limit of detection (ULOD) were diluted and re-run with a 1:3 dilution and subsequently multiplied by 3 in accordance with the assay manufacturer guidelines. The coefficient of variation (CV) for this assay was 4.3%.

Statistical analysis

The distribution of Lp(a) values are visually presented using histograms and scatterplots where appropriate. Summary statistics, including the mean, standard deviation, minimum and maximum, and the 25^th, 50^th, 75^th percentiles of Lp(a) values are reported. The 80^th percentile was also included, as early EAS guidelines on Lp(a)-associated risk thresholds recommended that Lp(a) levels remain below the 80th percentile of the population distribution.¹ High-risk Lp(a) is reported ≥105 nmol/L, in accordance with current EAS recommendations.¹⁷ Bland-Altman analysis was used to assess the mean and percentage differences between fresh and short-term or long-term frozen samples, to evaluate potential bias or any concentration dependent effect on Lp(a) degradation. Pairwise correlation analysis is performed to examine relationships between continuous Lp(a) levels with short-term and long-term frozen samples. Wilcoxon matched pairs signed-rank test was used to assess differences in fresh and frozen samples. All statistical analyses were performed using Stata v.18.0.

Results

Fresh and short-term frozen

The first study of TILDA participants (N = 40) compared Lp(a) values in fresh plasma to 4-day frozen samples (short-term frozen) from blood drawn during the Wave 6 health assessment. Figure 1A displays the distribution of values for both measures of Lp(a), with summary statistics reported in Table 1. Mean Lp(a) levels were significantly lower in the frozen samples (p = 0.008). However, a Pearson's product-moment correlation analysis revealed a strong, positive correlation between fresh and short-term frozen samples (r(38) = 0.991, p < 0.001), as visually represented in Figure 1B.

Figure 1. Histogram (A) and scatterplot (B) of fresh and short term frozen Lp(a) plasma concentrations.

Table 1. Lp(a) concentration in Fresh plasma vs short-term frozen plasma.

	Mean	SD	Min	25th	Median	75th	80th	Max	P value
Fresh	96.0	96.1	3.4	16.1	59.6	145.6	185.6	352.4	0.008
Short term frozen	90.2	95.5	3.3	16.6	49.0	139.7	188.2	358.4	0.008

Bland-Altman analysis for systematic bias

Bland-Altman analysis was used to assess agreement between Lp(a) levels measured in fresh plasma compared to short-term frozen samples ( Figure 2A). On average, fresh samples were 5.8 nmol/L higher than frozen samples. No proportional bias was observed (β = -0.004, p = 0.839) and variability does not change across concentrations (p = 0.888). When expressed as percentage difference (Figure 2B), we found no evidence of proportional bias (β = 03.15, p = 0.330) or concentration dependent variability, indicating that the loss in Lp(a) due to short-term storage is small with the percentage of Lp(a) degradation consistent across Lp(a) concentrations.

Figure 2. Bland -Altman plots for absolute difference (A) and percentage difference (B) between Lp(a) levels in fresh and short-term frozen plasma samples.

In clinical practice, Lp(a) thresholds are a pragmatic tool to identify values that translate into increased cardiovascular risk. In a recent consensus statement by the EAS, the risk of major cardiovascular events starts to slightly increase in individuals with Lp(a) levels of >62nmol/L with risk becoming clinically apparent in individuals with Lp(a) ≥105 nmol/L.¹⁷ To assess if potential loss of Lp(a) during storage affects participants cardiovascular risk classification, we compared the number of fresh and short-term frozen samples across defined Lp(a) cut-off points ranging from <62 nmol/L to ≥225 nmol/L. Due to the right-hand skew observed in the Lp(a) distribution in this population, a cut-off at the 80^th percentile value observed in fresh samples (186 nmol/L) was used. Outlined in Table 2, we find the distribution of samples across these cut-offs different between fresh and short-term frozen samples, with a higher proportion of frozen samples having Lp(a) levels <62 nmol/L (60.0% in frozen vs 52.5% in fresh).

Table 2. Sample distribution by Lp(a) cut-offs in fresh and short-term frozen samples.

	Fresh		Frozen
	n	%	n	%
<62 nmol/L	21	52.5	24	60.0
62-105 nmol/L	5	12.5	3	7.5
105-186 nmol/L	6	15.0	5	12.5
186-225 nmol/L	4	10.0	4	10.0
≥225 nmol/L	4	10.0	4	10.0
Total	40	100.0	40	100.0

Table 3 demonstrates how fresh samples within each Lp(a) cut-off category were reclassified following short-term storage. Overall, 10% (n = 4) of samples were reclassified based on corresponding frozen Lp(a) measurements. For participants with moderate cardiovascular risk, having Lp(a) levels within the range of 62 – 105 nmol/L, 60% (n = 3) were reclassified to <62 nmol/L and would therefore be considered lower risk. One sample above the high-risk threshold (105 – 186 nmol/L) was found to have levels between 62-105 nmol/L in corresponding frozen sample. All participants with levels above 80^th percentile (≥186 nmol/L) remained stable following short-term storage at -80^oC.

Table 3. Reclassification of fresh Lp(a) samples according to frozen Lp(a) levels across Lp(a) cut-offs.

			Short-term frozen
		Total	<62 nmol/L	62-105 nmol/L	105-186 nmol/L	186-225 nmol/L	≥225 nmol/L
		n (%)	n (%)	n (%)	n (%)	n (%)	n (%)
Fresh	<62 nmol/L	21 (100)	21 (100)	0 (0)	0 (0)	0 (0)	0 (0)
	62-105 nmol/L	5 (100)	3 (60)	2 (40)	0 (0)	0 (0)	0 (0)
	105-186 nmol/L	6 (100)	0 (0)	1 (16.7)	5 (83.3)	0 (0)	0 (0)
	186-225 nmol/L	4 (100)	0 (0)	0 (0)	0 (0)	4 (100)	0 (0)
	≥225 nmol/L	4 (100)	0 (0)	0 (0)	0 (0)	0 (0)	4 (100)
	Total	40 (100)	24 (60.0)	3(7.5)	5 (12.5)	4 (10.0)	4 (10.0)

Next, we examined the effect of long-term storage on plasma Lp(a) levels. This second study measured Lp(a) in fresh plasma collected from 100 participants during the Wave 6 health assessment and compared values to those found in plasma from the same participants collected and stored at -80^oC during the Wave 1 health assessment. The average time between blood draw and Lp(a) measurement from samples in long-term storage was 13.3 years (range 12.6-14.2 years).

Figure 3A displays an overlaid histogram for both fresh and the long term stored Lp(a) concentrations, with Table 4 displaying descriptive statistics for Lp(a) from fresh and long-term frozen samples. Overall, Lp(a) values were significantly lower in long-term frozen samples compared to matched fresh samples at Wave 6 (p < 0.001), with a mean difference of 41.1 nmol/L, corresponding to a 43% loss of Lp(a) concentration during long-term storage. However, Pearson’s product-moment correlation found a robust positive correlation between these two sample categories (r(98) = 0.876, p < 0.001), with this relationship plotted Figure 3B.

Figure 3. Histogram (A) and scatterplot (B) of fresh and long term frozen Lp(a) plasma concentrations.

Table 4. Lp(a) concentration in fresh plasma vs long-term frozen plasma.

	Mean	SD	Min	25^th	Median	75^th	80th	Max	P Value
Fresh	87.4	74.6	1.1	23.5	68.0	133.2	153.1	333.9	<0.0001
Long term frozen	46.4	44.4	0.8	12.4	30.3	66.6	86.5	192.7	<0.0001

Bland-Altman analysis

To assess the level of agreement between Lp(a) values measured in fresh and long-term frozen plasma samples, Bland-Altman analysis of the absolute difference found that fresh samples had higher Lp(a) values with an average difference of 41.1 nmol/L with a strong significant proportional bias (β = 0.54, p = 0.000) ( Figure 4A), indicating that the difference between fresh and matched long-term frozen samples increases with higher concentrations. Variability in the differences also increases with concentrations indicating heteroscedasticity (p = 0.000). To assess if this proportional bias corresponded to increased Lp(a) degradation at higher concentrations, we examined the percentage difference. Overall, Lp(a) levels in frozen-plasma samples were 61% lower than what is observed in fresh-plasma samples. There was a weak trend for the percentage difference to increase with higher Lp(a) concentration, however this was not statistically significant (β = 6.55, p = 0.063). Likewise, there was no indication of heteroscedasticity (p = 0.756) indicating that percentage loss of Lp(a) was consistent across Lp(a) concentration range ( Figure 4B).

Figure 4. Bland -Altman plots for absolute difference (A) and percentage difference (B) between Lp(a) levels in fresh and long-term frozen plasma samples.

Similar to short-term analysis, to assess the impact of Lp(a) loss during long-term storage, the number of samples that fall into previously defined Lp(a) cut-offs ranging from <62 nmol/L to ≥225 nmol/L were compared between fresh and long-term frozen samples and outlined in Table 5. As previously mentioned, due to the right-hand skew observed in the Lp(a) distribution, a cut-off at the 80^th percentile value in fresh samples (153 nmol/L) was used to observe distribution across high Lp(a) values. A higher proportion of frozen samples had Lp(a) levels <62nmol/L, compared to fresh samples (68% of frozen samples compared to 46% of fresh samples). In fresh plasma, 7% of samples had levels ≥225 nmol/L of Lp(a), however, no sample contained this level of Lp(a) following long-term storage at -80^oC.

Table 5. Sample distribution by Lp(a) cut-offs in fresh and long-term frozen plasma samples.

	Fresh		Frozen
	n	%	n	%
<62 nmol/L	46	46.0	68	68.0
62-105 nmol/L	21	21.0	21	21.0
105-153 nmol/L	13	13.0	8	8.0
153-225 nmol/L	13	13.0	3	3.0
≥225 nmol/L	7	7.0	0	0.0
Total	40	100.0	40	100.0

Table 6 highlights the redistribution of participants within Lp(a) cut offs according to Lp(a) levels found in long-term frozen samples. Overall, 49% of samples were reclassified based on Lp(a) values in long-term frozen samples. In samples with fresh plasma Lp(a) values of 62 – 105 nmol/L, 81% (n = 17) measured <62 nmol/L in their corresponding frozen sample. Furthermore, of 33 samples with fresh-plasma Lp(a) levels ≥105nmol/L and therefore above the EAS-recommended elevated-risk threshold, only 11 would maintain this ‘higher risk’ status in corresponding long-term frozen samples. Indeed, 6 of these participants would be reclassified as ‘lower risk’ with levels <62 nmol/L, with the remaining 16 participants considered ‘Moderate risk’ following reclassification into the 62-105 nmol/L threshold. Strikingly, of the 7 participants with Lp(a) levels ≥225nmol/L in fresh plasma, zero maintained this levels in frozen samples following long-term storage, with 29% of these samples (n = 2) falling below the EAS recommended threshold for elevated cardiovascular risk of 105 nmol/L. These data indicating that Lp(a) levels measured in samples stored for >10 years, may not give an accurate determination of Lp(a)-associated cardiovascular risk.

Table 6. Reclassification of fresh samples according to Lp(a) cut-offs following long-term frozen storage.

		Long-term frozen
		<62 nmol/L		62-105 nmol/L		105-153 nmol/L		153-225 nmol/L		≥225 nmol/L		Total
		N	(%)	N	(%)	N	(%)	N	(%)	N	(%)	N	(%)
Fresh	<62 nmol/L	45	(98)	1	(2)	0	(0)	0	(0)	0	(0)	46	(100)
	62-105 nmol/L	17	(81)	4	(19)	0	(0)	0	(0)	0	(0)	21	(100)
	105-153 nmol/L	4	(31)	8	(61)	1	(8)	0	(0)	0	(0)	13	(100)
	153-225 nmol/L	2	(15)	6	(46)	4	(31)	1	(8)	0	(0)	13	(100)
	≥225 nmol/L	0	(0)	2	(29)	3	(43)	2	(29)	0	(0)	7	(100)
	Total	68	(68.0)	21	(21.0)	8	(8.0)	3	(3.0)	0	(0)	100	(100)

Discussion

Elevated Lp(a) is considered the most common genetically inherited risk factor for cardiovascular disease.⁸ Studies have indicated that Lp(a) remains stable across the life course and is not significantly influenced by diet and lifestyle factors. Due to this inherited stability, current guidelines support once-in-a-lifetime measurement of Lp(a) for assessment of associated cardiovascular risk.¹⁸ The potential advancement of Lp(a) research through retrospective studies relies on the knowledge that Lp(a) remains stable in storage. To reliably assess the cardiovascular risk associated with Lp(a), knowledge of its rate of degradation during freezing is crucial, as this prevents inaccurate or misleading interpretation of Lp(a) association with CVD, in retrospective analyses.

Leveraging the longitudinal design of TILDA, and the availability of archived plasma samples, this study aimed to compare Lp(a) levels in paired fresh and frozen blood plasma samples from the same participants following short-term storage (4 days at -80^oC) and long-term storage (> 10 years at -80^oC). Establishing stability of Lp(a) concentrations in frozen samples over time will inform whether retrospective assaying gives a true representation of Lp(a) concentration and corresponding cardiovascular risk association.

The findings of this study demonstrate that the process of freeze/thawing has a significant impact on Lp(a) concentration, with both absolute and relative decreases in Lp(a) over time during frozen storage. Given that Lp(a) levels are typically considered stable throughout an individual's life course, the observed differences suggest a significant degradation of the samples during the approximately 13-year period they were frozen. When compared to contemporaneous fresh plasma samples, short-term frozen samples had an average loss 5.8 nmol/L in Lp(a) concentration, with a mean percentage difference of 12.1%. However, this increases to 41.1 nmol/L (61% mean difference) in matched long-term bio-banked samples. Indicating a time dependent loss of Lp(a) during storage. These results are similar to that of Kronenberg et al., who found a statistically significant decrease in Lp(a) levels after storage,¹⁴ with a recent study from Copenhagen reporting a difference in the 80^th percentiles between frozen and fresh samples when stored for 7 years at -80^oC.³

The LPA gene determines the molecular weight of Lp(a) through the number of kringle IV (KIV) repeats that form the structure of apo(a). Low molecular weight Lp(a) with low number of KIV repeats, can be processed quickly and at higher concentration, and suggested to give rise to elevated Lp(a) levels. Whereas high molecular weight Lp(a) with a high number of KIV repeats are less concentrated in the plasma. Previous studies have suggested that baseline Lp(a) concentration, influenced by LPA genotype and apo(a) structure could influence the rate of Lp(a) degradation observed during storage.¹⁴ However, these studies were from early days of Lp(a) measurement and assays sensitive to a particular isoform of Lp(a) may influence this interpretation. Using an isoform-insensitive immunoassay, which measures the particle level of Lp(a), ensures that any measured loss of Lp(a) is not biased by isoform size. Bland-Altman analysis was also used to report the absolute difference and percentage difference of Lp(a) measured in fresh and short or long-term frozen samples. This analysis could detect if Lp(a) degradation was bias to Lp(a) concentration, and therefore Lp(a) isoform. It was found that although the absolute difference between Lp(a) measured in fresh or frozen samples increased with higher Lp(a) values, the percentage difference, which accounts for the relative change in concentration, showed no proportional bias or heteroscedasticity. Indicating that the loss in Lp(a) during storage is relatively uniform across the concentration range, and not selective to high or low molecular weight Lp(a).

The major impact of Lp(a) degradation during storage can be observed by reclassifying fresh plasma samples into cardiovascular risk thresholds, based on corresponding frozen Lp(a) values. This highlights the greatest challenge for retrospective studies when deciding to use historic or bio-banked samples to determine association with cardiovascular risk. Following storage at -80^oC for 4 days, 10% of samples had altered Lp(a) values resulting in reclassification of cardiovascular risk. Reclassification primarily occurred in samples below the 80^th percentile, with samples containing extremely high Lp(a) levels not being affected. The relatively small loss in Lp(a) during short-term storage, which was 5.8 nmol/L overall, resulted in these participants shifting to the next lowest cardiovascular risk category.

However, the significant Lp(a) loss observed in samples stored at -80^oC for >10 years had a substantial impact on cardiovascular risk status, with 49% of samples being reclassified. Of the seven participants who had extremely high values in fresh plasma (≥225 nmol/L), zero maintained this level in their corresponding long-term frozen samples. While this could suggest that high Lp(a) concentration, and therefore low molecular weight Lp(a), is more susceptible to degradation following long-term storage, Bland-Altman analysis of fresh vs long-term frozen samples did not find a significant differences in the percentage difference of Lp(a) loss across concentration range. In fact, 81% of Lp(a) samples between 62-105 nmol/L were also reclassified.

The most striking finding was that 67% of participants with fresh Lp(a) values over 105 nmol/L, and therefore at increased cardiovascular risk, were not above this threshold when Lp(a) was measured in corresponding long-term frozen samples. In fact, 18% of this “higher risk” group would be deemed “Lower risk” with Lp(a) values of <62 nmol/L, highlighting the potential for underestimation of cardiovascular risk when quantifying Lp(a) in archived samples.

This study reaffirms previous findings demonstrating the impact freezing can have on Lp(a)^14,19 and recommends that due to the degree of Lp(a) degradation observed following storage, the use of long-term frozen or biobanked samples in retrospective studies for Lp(a) research, should be interpreted with caution. Particularly when used in an effort to understand the prevalence of elevated Lp(a) on a population level or in association with cardiovascular outcomes. This study was unique the using Bland-Altman analysis to measure the impact freezing has on Lp(a) and found that baseline Lp(a) levels do not appear to influence the degree of Lp(a) degradation observed during storage.

Conclusions

The stability of Lp(a) in stored plasma samples remains a critical consideration for researchers and clinicians. This study emphasises the importance of considering storage conditions and sample handling when interpreting Lp(a) measurements in clinical and epidemiological studies. While Lp(a) is relatively stable within individuals over time, long-term storage can lead to significant decreases in levels. Retrospective assaying of archived plasma samples could therefore lead to an underestimation of both the prevalence of elevated Lp(a) in the population and the cardiovascular risk mediated by elevated Lp(a).

Data availability

The first six Waves of TILDA data are currently available through an application from the Irish Social Science Data Archive (ISSDA) at https://www.ucd.ie/issda/accessdata/issdadatasets/. The full TILDA dataset is held on secure severs at Trinity College Dublin. If you wish to request access to TILDA data, please contact TILDA directly at [email protected]. These requests will be evaluated on a case-by-case basis and can be facilitated through our on-site hotdesk facility. TILDA recognizes replicability as an important part of science and on application can make available all.do files and data used in this study.

Acknowledgements

The authors would like to acknowledge the commitment and cooperation of the TILDA participants and research team. This research was supported by Novartis who provided funding. Novartis had no role in study design, data collection or analysis, decision to publish or preparation of the manuscript.

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1. Nordestgaard BG, Chapman MJ, Ray K, et al.: Lipoprotein(a) as a cardiovascular risk factor: current status. Eur. Heart J. 2010; 31(23): 2844–2853. PubMed Abstract | Publisher Full Text
2. Orsó E, Schmitz G: Lipoprotein(a) and its role in inflammation, atherosclerosis and malignancies. Clin. Res. Cardiol. Suppl. 2017; 12(1): 31–37.
3. Kamstrup PR: Lipoprotein(a) and Cardiovascular Disease. Clin. Chem. 2021; 67(1): 154–166. PubMed Abstract | Publisher Full Text
4. Kronenberg F, Utermann G: Lipoprotein(a): resurrected by genetics. J. Intern. Med. 2013; 273(1): 6–30. PubMed Abstract | Publisher Full Text
5. Kronenberg F, Mora S, Stroes ESG, et al.: Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur. Heart J. 2022; 43(39): 3925–3946. PubMed Abstract | Publisher Full Text
6. Stürzebecher PE, Schorr JJ, Klebs SHG, et al.: Trends and consequences of lipoprotein(a) testing: Cross-sectional and longitudinal health insurance claims database analyses. Atherosclerosis. 2023; 367: 24–33. PubMed Abstract | Publisher Full Text
7. Mach F, Baigent C, Catapano AL, et al.: 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk: The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS). Eur. Heart J. 2019; 41(1): 111–188.
8. Cegla J, Neely RDG, France M, et al.: HEART UK consensus statement on Lipoprotein(a): A call to action. Atherosclerosis. 2019; 291: 62–70. PubMed Abstract | Publisher Full Text
9. NIPC NIfPaCH: Advancing a Prevention Agenda for Cardiovascular Care in Ireland. Report.2023.
10. Erqou S, Kaptoge S, Perry PL, et al.: Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA. 2009; 302(4): 412–423. PubMed Abstract | Publisher Full Text
11. Tsimikas S, Fazio S, Viney NJ, et al.: Relationship of lipoprotein(a) molar concentrations and mass according to lipoprotein(a) thresholds and apolipoprotein(a) isoform size. J. Clin. Lipidol. 2018; 12(5): 1313–1323. PubMed Abstract | Publisher Full Text
12. Marcovina SM, Albers JJ: Lipoprotein (a) measurements for clinical application. J. Lipid Res. 2016; 57(4): 526–537. PubMed Abstract | Publisher Full Text
13. Kronenberg F, Lobentanz EM, König P, et al.: Effect of sample storage on the measurement of lipoprotein [a], apolipoproteins B and A-IV, total and high density lipoprotein cholesterol and triglycerides. J. Lipid Res. 1994; 35(7): 1318–1328. PubMed Abstract
14. Kronenberg F, Trenkwalder E, Dieplinger H, et al.: Lipoprotein(a) in Stored Plasma Samples and the Ravages of Time. Arterioscler. Thromb. Vasc. Biol. 1996; 16(12): 1568–1572. PubMed Abstract
15. Kronenberg F: Lipoprotein(a) measurement issues: Are we making a mountain out of a molehill?. Atherosclerosis. 2022; 349: 123–135. PubMed Abstract | Publisher Full Text
16. Whelan BJ, Savva GM: Design and Methodology of The Irish Longitudinal Study on Ageing. J. Am. Geriatr. Soc. 2013; 61(s2): S265–S268. Publisher Full Text
17. Mach F, Koskinas KC, Roeters van Lennep JE, et al.: 2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias. Eur. Heart J. 2025; 409: 120479. Publisher Full Text
18. Kronenberg F, Bedlington N, Ademi Z, et al.: The Brussels International Declaration on Lipoprotein(a) Testing and Management. Atherosclerosis. 2025; 406: 119218. Publisher Full Text
19. Simó JM, Camps J, Vilella E, et al.: Instability of lipoprotein(a) in plasma stored at -70 degrees C: effects of concentration, apolipoprotein(a) genotype, and donor cardiovascular disease. Clin. Chem. 2001; 47(9): 1673–1678. PubMed Abstract

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¹ The Irish Longitudinal Study on Ageing, Trinity College Dublin School of Medicine, Dublin, Leinster, D02 R590, Ireland
² Discipline of Medical Gerontology, Trinity College Dublin School of Medicine, Dublin, Leinster, D02 PN40, Ireland
³ Trinity College Dublin School of Nursing and Midwifery, Dublin, Leinster, D02 T283, Ireland
⁴ Biochemistry Department, Laboratory Medicine, St James's Hospital, Dublin, Leinster, D08 NHY1, Ireland
⁵ Mercer's Institute for Successful Ageing, St James's Hospital, Dublin, Leinster, D08 E9P6, Ireland

Emma Connolly
Roles: Investigation, Methodology, Writing – Original Draft Preparation

Sinéad McLoughlin
Roles: Investigation, Methodology, Writing – Original Draft Preparation, Writing – Review & Editing

Aisling M. O'Halloran
Roles: Conceptualization, Investigation, Writing – Review & Editing

Ann Hever
Roles: Project Administration

Kanika Nautiyal
Roles: Formal Analysis

Margaret McCormack
Roles: Formal Analysis, Writing – Review & Editing

Vivion Crowley
Roles: Formal Analysis, Resources, Writing – Review & Editing

Rose Anne Kenny
Roles: Funding Acquisition, Resources, Writing – Review & Editing

Competing interests

No competing interests were disclosed.

Grant information

The author(s) declared that no grants were involved in supporting this work.

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Connolly E, McLoughlin S, O'Halloran AM et al. Assessing Long-Term Stability of Lipoprotein(a) in Frozen Blood Plasma Samples: A 14-Year Analysis from The Irish Longitudinal Study on Ageing (TILDA) [version 1; peer review: 1 approved, 1 approved with reservations]. HRB Open Res 2026, 9:25 (https://doi.org/10.12688/hrbopenres.14357.1)

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Reviewer Report 21 Apr 2026

Terry Gbaa, Benue State University Teaching Hospital, Makurdi, Benue, Nigeria; DemyHealth Group, Abuja, FCT Abuja, Nigeria

Approved

https://doi.org/10.21956/hrbopenres.15813.r54447

The manuscript was insightful in understanding the effectiveness and interpretation of stored Lp(a) samples.
The study was well thought out and carried out in a simple, systematic way using simple analysis and also reclassification of cardiovascular risk, which is ... Continue reading

The manuscript was insightful in understanding the effectiveness and interpretation of stored Lp(a) samples.
The study was well thought out and carried out in a simple, systematic way using simple analysis and also reclassification of cardiovascular risk, which is dependent on sample age.
The literature review was accurately referenced for this study.

Is the work clearly and accurately presented and does it cite the current literature?

Yes
Is the study design appropriate and is the work technically sound?

Yes
Are sufficient details of methods and analysis provided to allow replication by others?

Yes
If applicable, is the statistical analysis and its interpretation appropriate?

Yes
Are all the source data underlying the results available to ensure full reproducibility?

Yes
Are the conclusions drawn adequately supported by the results?

Yes

Competing Interests: No competing interests were disclosed.

Reviewer Expertise: Lipids, Cardiovascular, pathology

I confirm that I have read this submission and believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard.

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Reviewer Report 07 Apr 2026

Anton Gisterå, Karolinska Institutet, Stockholm, Stockholm County, Sweden

Approved with Reservations

https://doi.org/10.21956/hrbopenres.15813.r54451

This is a relevant and useful study by Connolly et al., examining the long‑term stability of Lp(a) in stored TILDA samples. The work raises important considerations for retrospective analyses of Lp(a) as a cardiovascular biomarker. The manuscript would be strengthened if the ... Continue reading

This is a relevant and useful study by Connolly et al., examining the long‑term stability of Lp(a) in stored TILDA samples. The work raises important considerations for retrospective analyses of Lp(a) as a cardiovascular biomarker. The manuscript would be strengthened if the authors addressed whether changes in Lp(a) over time in the long-term cohort could be influenced by sex, kidney function, or inflammatory status. Given the established effects of estrogen on Lp(a), it would also be helpful to clarify whether female participants were post‑menopausal at enrolment.

The findings show that differences in sample processing influence measured concentrations. In routine clinical practice, Lp(a) is almost always measured in fresh samples, so these storage‑related effects are unlikely to affect clinical decision‑making. The cutoffs used here may be reasonable for contemporary risk stratification but are less reliable when applied to historical biobank material. The small size of the short‑term cohort (n=40) introduces uncertainty in the reclassification estimates, and this is not entirely clear from the abstract. Although it may be possible to establish reference intervals for stored samples using identical handling procedures, continuous values generally offer greater statistical power than categorical cut points at the cohort level, which may limit the practical impact of misclassification.

It would also be informative to know whether any long‑stored samples fell below the assay’s detection limit, as this would suggest the need for more sensitive assays when analysing older specimens. The preprocessing procedures appear consistent, but confirmation that the short‑term cohort was also non‑fasted would be helpful. It should also be stated whether there was participant overlap between the short‑term and long‑term cohorts.

Fresh samples were refrigerated for four days before analysis. It would be useful for the authors to comment on whether this storage period could itself alter Lp(a) concentrations, for instance by evaporation or other artefacts, and whether such effects can be ruled out.

The statistical analysis addresses the possibility that apo(a) isoform size contributes to stability differences, as suggested previously. It would be valuable to discuss other plausible biological mechanisms behind the observed long‑term degradation. For example, oxidised phospholipids may influence particle integrity, and adjusting for apoB or LDL particle concentrations might provide insight. LDL‑like particle aggregation during frozen storage is another potential mechanism worth considering.

Specific comments:
• The grant information states that no grants were involved, yet the text later notes that Novartis funded the study.
• Please add g‑force values for plasma preparation.
• Use past tense consistently (e.g., “did” instead of “does” in paragraph 5 on page 4, and “increased” instead of “increases” in paragraph 3 on page 9).
• A blank space appears to be missing in page 6, paragraph 1.

Is the work clearly and accurately presented and does it cite the current literature?

Yes
Is the study design appropriate and is the work technically sound?

Yes
Are sufficient details of methods and analysis provided to allow replication by others?

Yes
If applicable, is the statistical analysis and its interpretation appropriate?

Yes
Are all the source data underlying the results available to ensure full reproducibility?

Yes
Are the conclusions drawn adequately supported by the results?

Yes

Competing Interests: No competing interests were disclosed.

Reviewer Expertise: Cardiovascular immunology

I confirm that I have read this submission and believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard, however I have significant reservations, as outlined above.

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Version 1 25 Mar 26	read	read

Anton Gisterå, Karolinska Institutet, Stockholm, Sweden
Terry Gbaa, Benue State University Teaching Hospital, Makurdi, Nigeria; DemyHealth Group, Abuja, Nigeria

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Reviewer Report

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21 Apr 2026 | for Version 1

Terry Gbaa, Benue State University Teaching Hospital, Makurdi, Benue, Nigeria; DemyHealth Group, Abuja, FCT Abuja, Nigeria

12 Views Cite this report Responses(0)

Approved

The manuscript was insightful in understanding the effectiveness and interpretation of stored Lp(a) samples.
The study was well thought out and carried out in a simple, systematic way using simple analysis and also reclassification of cardiovascular risk, which is dependent on sample age.
The literature review was accurately referenced for this study.

Is the work clearly and accurately presented and does it cite the current literature?

Yes
Is the study design appropriate and is the work technically sound?

Yes
Are sufficient details of methods and analysis provided to allow replication by others?

Yes
If applicable, is the statistical analysis and its interpretation appropriate?

Yes
Are all the source data underlying the results available to ensure full reproducibility?

Yes
Are the conclusions drawn adequately supported by the results?

Yes

Competing Interests

No competing interests were disclosed.

Reviewer Expertise

Lipids, Cardiovascular, pathology

I confirm that I have read this submission and believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard.

Respond to this report

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Reviewer Report

15 Views

07 Apr 2026 | for Version 1

Anton Gisterå, Karolinska Institutet, Stockholm, Stockholm County, Sweden

15 Views Cite this report Responses(0)

Approved With Reservations

This is a relevant and useful study by Connolly et al., examining the long‑term stability of Lp(a) in stored TILDA samples. The work raises important considerations for retrospective analyses of Lp(a) as a cardiovascular biomarker. The manuscript would be strengthened if the authors addressed whether changes in Lp(a) over time in the long-term cohort could be influenced by sex, kidney function, or inflammatory status. Given the established effects of estrogen on Lp(a), it would also be helpful to clarify whether female participants were post‑menopausal at enrolment.

The findings show that differences in sample processing influence measured concentrations. In routine clinical practice, Lp(a) is almost always measured in fresh samples, so these storage‑related effects are unlikely to affect clinical decision‑making. The cutoffs used here may be reasonable for contemporary risk stratification but are less reliable when applied to historical biobank material. The small size of the short‑term cohort (n=40) introduces uncertainty in the reclassification estimates, and this is not entirely clear from the abstract. Although it may be possible to establish reference intervals for stored samples using identical handling procedures, continuous values generally offer greater statistical power than categorical cut points at the cohort level, which may limit the practical impact of misclassification.

It would also be informative to know whether any long‑stored samples fell below the assay’s detection limit, as this would suggest the need for more sensitive assays when analysing older specimens. The preprocessing procedures appear consistent, but confirmation that the short‑term cohort was also non‑fasted would be helpful. It should also be stated whether there was participant overlap between the short‑term and long‑term cohorts.

Fresh samples were refrigerated for four days before analysis. It would be useful for the authors to comment on whether this storage period could itself alter Lp(a) concentrations, for instance by evaporation or other artefacts, and whether such effects can be ruled out.

The statistical analysis addresses the possibility that apo(a) isoform size contributes to stability differences, as suggested previously. It would be valuable to discuss other plausible biological mechanisms behind the observed long‑term degradation. For example, oxidised phospholipids may influence particle integrity, and adjusting for apoB or LDL particle concentrations might provide insight. LDL‑like particle aggregation during frozen storage is another potential mechanism worth considering.

Specific comments:
• The grant information states that no grants were involved, yet the text later notes that Novartis funded the study.
• Please add g‑force values for plasma preparation.
• Use past tense consistently (e.g., “did” instead of “does” in paragraph 5 on page 4, and “increased” instead of “increases” in paragraph 3 on page 9).
• A blank space appears to be missing in page 6, paragraph 1.

Is the work clearly and accurately presented and does it cite the current literature?

Yes
Is the study design appropriate and is the work technically sound?

Yes
Are sufficient details of methods and analysis provided to allow replication by others?

Yes
If applicable, is the statistical analysis and its interpretation appropriate?

Yes
Are all the source data underlying the results available to ensure full reproducibility?

Yes
Are the conclusions drawn adequately supported by the results?

Yes

Competing Interests

No competing interests were disclosed.

Reviewer Expertise

Cardiovascular immunology

I confirm that I have read this submission and believe that I have an appropriate level of expertise to confirm that it is of an acceptable scientific standard, however I have significant reservations, as outlined above.

Respond to this report

Responses (0)

[1] 1. Nordestgaard BG, Chapman MJ, Ray K, et al.: Lipoprotein(a) as a cardiovascular risk factor: current status. Eur. Heart J. 2010; 31(23): 2844–2853. PubMed Abstract | Publisher Full Text

[2] 2. Orsó E, Schmitz G: Lipoprotein(a) and its role in inflammation, atherosclerosis and malignancies. Clin. Res. Cardiol. Suppl. 2017; 12(1): 31–37.

[3] 3. Kamstrup PR: Lipoprotein(a) and Cardiovascular Disease. Clin. Chem. 2021; 67(1): 154–166. PubMed Abstract | Publisher Full Text

[4] 4. Kronenberg F, Utermann G: Lipoprotein(a): resurrected by genetics. J. Intern. Med. 2013; 273(1): 6–30. PubMed Abstract | Publisher Full Text

[5] 5. Kronenberg F, Mora S, Stroes ESG, et al.: Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. Eur. Heart J. 2022; 43(39): 3925–3946. PubMed Abstract | Publisher Full Text

[6] 6. Stürzebecher PE, Schorr JJ, Klebs SHG, et al.: Trends and consequences of lipoprotein(a) testing: Cross-sectional and longitudinal health insurance claims database analyses. Atherosclerosis. 2023; 367: 24–33. PubMed Abstract | Publisher Full Text

[7] 7. Mach F, Baigent C, Catapano AL, et al.: 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk: The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS). Eur. Heart J. 2019; 41(1): 111–188.

[8] 8. Cegla J, Neely RDG, France M, et al.: HEART UK consensus statement on Lipoprotein(a): A call to action. Atherosclerosis. 2019; 291: 62–70. PubMed Abstract | Publisher Full Text

[9] 9. NIPC NIfPaCH: Advancing a Prevention Agenda for Cardiovascular Care in Ireland. Report.2023.

[10] 10. Erqou S, Kaptoge S, Perry PL, et al.: Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA. 2009; 302(4): 412–423. PubMed Abstract | Publisher Full Text

[11] 11. Tsimikas S, Fazio S, Viney NJ, et al.: Relationship of lipoprotein(a) molar concentrations and mass according to lipoprotein(a) thresholds and apolipoprotein(a) isoform size. J. Clin. Lipidol. 2018; 12(5): 1313–1323. PubMed Abstract | Publisher Full Text

[12] 12. Marcovina SM, Albers JJ: Lipoprotein (a) measurements for clinical application. J. Lipid Res. 2016; 57(4): 526–537. PubMed Abstract | Publisher Full Text

[13] 13. Kronenberg F, Lobentanz EM, König P, et al.: Effect of sample storage on the measurement of lipoprotein [a], apolipoproteins B and A-IV, total and high density lipoprotein cholesterol and triglycerides. J. Lipid Res. 1994; 35(7): 1318–1328. PubMed Abstract

[14] 14. Kronenberg F, Trenkwalder E, Dieplinger H, et al.: Lipoprotein(a) in Stored Plasma Samples and the Ravages of Time. Arterioscler. Thromb. Vasc. Biol. 1996; 16(12): 1568–1572. PubMed Abstract

[15] 15. Kronenberg F: Lipoprotein(a) measurement issues: Are we making a mountain out of a molehill?. Atherosclerosis. 2022; 349: 123–135. PubMed Abstract | Publisher Full Text

[16] 16. Whelan BJ, Savva GM: Design and Methodology of The Irish Longitudinal Study on Ageing. J. Am. Geriatr. Soc. 2013; 61(s2): S265–S268. Publisher Full Text

[17] 17. Mach F, Koskinas KC, Roeters van Lennep JE, et al.: 2025 Focused Update of the 2019 ESC/EAS Guidelines for the management of dyslipidaemias. Eur. Heart J. 2025; 409: 120479. Publisher Full Text

[18] 18. Kronenberg F, Bedlington N, Ademi Z, et al.: The Brussels International Declaration on Lipoprotein(a) Testing and Management. Atherosclerosis. 2025; 406: 119218. Publisher Full Text

[19] 19. Simó JM, Camps J, Vilella E, et al.: Instability of lipoprotein(a) in plasma stored at -70 degrees C: effects of concentration, apolipoprotein(a) genotype, and donor cardiovascular disease. Clin. Chem. 2001; 47(9): 1673–1678. PubMed Abstract

Assessing Long-Term Stability of Lipoprotein(a) in Frozen Blood Plasma Samples: A 14-Year Analysis from The Irish Longitudinal Study on Ageing (TILDA)

Abstract

Background

Method

Results

Conclusions

Keywords

Introduction

Methods

Study population

Long-term storage

Fresh and short-term storage

Lp(a) measurement

Statistical analysis

Results

Fresh and short-term frozen

Figure 1. Histogram (A) and scatterplot (B) of fresh and short term frozen Lp(a) plasma concentrations.

Table 1. Lp(a) concentration in Fresh plasma vs short-term frozen plasma.

Bland-Altman analysis for systematic bias

Figure 2. Bland -Altman plots for absolute difference (A) and percentage difference (B) between Lp(a) levels in fresh and short-term frozen plasma samples.

Table 2. Sample distribution by Lp(a) cut-offs in fresh and short-term frozen samples.

Table 3. Reclassification of fresh Lp(a) samples according to frozen Lp(a) levels across Lp(a) cut-offs.

Figure 3. Histogram (A) and scatterplot (B) of fresh and long term frozen Lp(a) plasma concentrations.

Table 4. Lp(a) concentration in fresh plasma vs long-term frozen plasma.

Bland-Altman analysis

Figure 4. Bland -Altman plots for absolute difference (A) and percentage difference (B) between Lp(a) levels in fresh and long-term frozen plasma samples.

Table 5. Sample distribution by Lp(a) cut-offs in fresh and long-term frozen plasma samples.

Table 6. Reclassification of fresh samples according to Lp(a) cut-offs following long-term frozen storage.

Discussion

Conclusions

Data availability

Acknowledgements

References

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