Distribution of lipoprotein (a) levels in patients with lower extremity artery disease and their impact on amputation and survival: a retrospective study
Background Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the imp...
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Published in | Lipids in health and disease Vol. 24; no. 1; pp. 128 - 11 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
London
BioMed Central
02.04.2025
BioMed Central Ltd BMC |
Subjects | |
Online Access | Get full text |
ISSN | 1476-511X 1476-511X |
DOI | 10.1186/s12944-025-02542-5 |
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Abstract | Background
Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival.
Methods
Baseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30–90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed.
Results
Of 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values ≥ 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL,
p
= 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%,
p
= 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%,
p
= 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%,
p
= 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%,
p
= 0.729), amputations (4% vs. 7% vs. 0%,
p
= 0.245) and death (8% vs. 5% vs. 3%,
p
= 0.436).
Conclusions
Aggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels. |
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AbstractList | Background Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival. Methods Baseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30-90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed. Results Of 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values [greater than or equal to] 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL, p = 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%, p = 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%, p = 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%, p = 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%, p = 0.729), amputations (4% vs. 7% vs. 0%, p = 0.245) and death (8% vs. 5% vs. 3%, p = 0.436). Conclusions Aggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels. Keywords: Lipoprotein (a), Lipid-lowering therapy, Lower extremity artery disease, Low-density lipoprotein cholesterol, Revascularisation, Amputation, Death Background Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival. Methods Baseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30–90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed. Results Of 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values ≥ 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL, p = 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%, p = 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%, p = 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%, p = 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%, p = 0.729), amputations (4% vs. 7% vs. 0%, p = 0.245) and death (8% vs. 5% vs. 3%, p = 0.436). Conclusions Aggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels. Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival. Baseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30-90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed. Of 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values ≥ 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL, p = 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%, p = 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%, p = 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%, p = 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%, p = 0.729), amputations (4% vs. 7% vs. 0%, p = 0.245) and death (8% vs. 5% vs. 3%, p = 0.436). Aggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels. Abstract Background Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival. Methods Baseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30–90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed. Results Of 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values ≥ 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL, p = 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%, p = 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%, p = 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%, p = 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%, p = 0.729), amputations (4% vs. 7% vs. 0%, p = 0.245) and death (8% vs. 5% vs. 3%, p = 0.436). Conclusions Aggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels. Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival.BACKGROUNDElevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival.Baseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30-90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed.METHODSBaseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30-90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed.Of 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values ≥ 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL, p = 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%, p = 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%, p = 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%, p = 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%, p = 0.729), amputations (4% vs. 7% vs. 0%, p = 0.245) and death (8% vs. 5% vs. 3%, p = 0.436).RESULTSOf 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values ≥ 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL, p = 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%, p = 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%, p = 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%, p = 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%, p = 0.729), amputations (4% vs. 7% vs. 0%, p = 0.245) and death (8% vs. 5% vs. 3%, p = 0.436).Aggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels.CONCLUSIONSAggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels. Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality. Results regarding aggressive lipid-lowering therapies (LLT) are missing. We examined LEAD patients with Lp(a) measurement and the impact of intensive LLT on amputation and survival. Baseline characteristics of 263 LEAD patients with Lp(a) measurement treated in a tertiary hospital from 01/2017 until 01/2022 were recorded. Patients were categorized into three groups according to their Lp(a) values (< 30 mg/dL, 30-90 mg/dL and > 90 mg/dL). Lipid values and LLT were recorded at baseline and during follow-up (median 750 days). Peripheral endovascular revascularizations (EVR), amputations and death during follow-up were analysed. Of 263 patients, 75% were male, mean age was 67 ± 10 years. Elevated Lp(a) values [greater than or equal to] 30 mg/dL were found in 32%, 16% had values > 90 mg/dL. Baseline low-density lipoprotein cholesterol (LDL-C) was 89 ± 38 mg/dL, decreasing to 61 ± 30 mg/dL at follow-up, with no difference between Lp(a) groups (63 ± 32 mg/dL vs. 52 ± 23 mg/dL vs. 60 ± 25 mg/dL, p = 0.273). Statin dose was intensified more frequently in those with elevated Lp(a) (16% vs. 35% vs. 33%, p = 0.005), who also received significantly more often ezetimibe (50% vs. 58% vs. 73%, p = 0.028) and proprotein convertase subtilisin/kexin type 9 inhibitors (2% vs. 3% vs. 8%, p = 0.043). No difference was seen regarding EVR (91% vs. 95% vs. 90%, p = 0.729), amputations (4% vs. 7% vs. 0%, p = 0.245) and death (8% vs. 5% vs. 3%, p = 0.436). Aggressive LLT in high-risk LEAD patients with elevated Lp(a) levels enabled LDL-C target achievement in a majority by combination of established lipid-lowering agents. An increase in EVR, amputation or death could not be observed in patients with high Lp(a) levels. |
ArticleNumber | 128 |
Audience | Academic |
Author | Engelbertz, Christiane Malyar, Nasser M. Brix, Tobias J. Gebauer, Katrin Reinecke, Holger Varghese, Julian |
Author_xml | – sequence: 1 givenname: Katrin surname: Gebauer fullname: Gebauer, Katrin email: Katrin.Gebauer@ukmuenster.de organization: Department of Cardiology I– Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital Muenster, Cardiol, Department of Cardiology I– Coronary and Peripheral Vascular Disease, Heart Failure University Hospital Muenster – sequence: 2 givenname: Nasser M. surname: Malyar fullname: Malyar, Nasser M. organization: Department of Cardiology I– Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital Muenster, Cardiol – sequence: 3 givenname: Julian surname: Varghese fullname: Varghese, Julian organization: Institute of Medical Informatics, University of Muenster – sequence: 4 givenname: Holger surname: Reinecke fullname: Reinecke, Holger organization: Department of Cardiology I– Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital Muenster, Cardiol – sequence: 5 givenname: Tobias J. surname: Brix fullname: Brix, Tobias J. organization: Institute of Medical Informatics, University of Muenster – sequence: 6 givenname: Christiane surname: Engelbertz fullname: Engelbertz, Christiane organization: Department of Cardiology I– Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital Muenster, Cardiol |
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Cites_doi | 10.1177/1358863X221091320 10.1093/eurjpc/zwaa047 10.1016/j.ajpc.2023.100478 10.1016/j.jacc.2023.10.009 10.1016/j.lanepe.2023.100624 10.1093/eurjpc/zwab016 10.1161/CIRCULATIONAHA.105.608679 10.1016/j.ejvs.2018.01.019 10.1093/eurheartj/ehx095 10.1016/j.jcin.2022.05.050 10.1177/1526602817728068 10.1373/clinchem.2007.088013 10.1056/NEJMoa2215024 10.1024/0301-1526/a000556 10.1016/j.atherosclerosis.2018.05.033 10.1194/jlr.R083626 10.1024/0301-1526/a000834 10.1161/JAHA.119.015355 10.1016/S0140-6736(13)61249-0 10.1001/jama.2012.13415 10.1001/jamanetworkopen.2022.45720 10.1016/j.atherosclerosis.2021.11.019 10.1681/ASN.V111105 10.1016/S2213-8587(18)30290-0 10.1093/eurheartj/ehac361 10.1161/CIRCULATIONAHA.117.032235 10.1161/CIRCULATIONAHA.120.046524 10.1016/j.jacc.2019.03.013 10.3390/biom11020257 10.1093/eurheartj/ehz455 10.1016/j.atherosclerosis.2022.10.002 10.1016/j.amjcard.2023.04.017 10.1056/NEJMoa2211023 10.3390/biomedicines12061229 10.1093/eurjpc/zwae199 10.1016/j.atherosclerosis.2018.07.001 10.1016/j.amjcard.2010.01.370 10.1583/09-2733.1 10.1093/eurheartj/ehl441 10.1161/ATVBAHA.112.255521 10.1056/NEJMoa1905239 10.1161/JAHA.123.031255 10.1016/j.jacc.2013.09.042 10.3389/fcvm.2022.843602 10.1055/s-0035-1555133 10.1016/j.jacc.2024.02.013 |
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Keywords | Amputation Death Revascularisation Lipoprotein (a) Lipid-lowering therapy Lower extremity artery disease Low-density lipoprotein cholesterol |
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References_xml | – volume: 27 start-page: 385 year: 2022 ident: 2542_CR30 publication-title: Vasc Med doi: 10.1177/1358863X221091320 – volume: 28 start-page: 1279 year: 2020 ident: 2542_CR35 publication-title: Eur J Prev Cardiol doi: 10.1093/eurjpc/zwaa047 – volume: 14 start-page: 100478 year: 2023 ident: 2542_CR12 publication-title: Am J Prev Cardiol doi: 10.1016/j.ajpc.2023.100478 – volume: 82 start-page: 2265 year: 2023 ident: 2542_CR14 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2023.10.009 – volume: 29 start-page: 100624 year: 2023 ident: 2542_CR34 publication-title: Lancet Reg Health Eur doi: 10.1016/j.lanepe.2023.100624 – volume: 28 start-page: 2038 year: 2022 ident: 2542_CR32 publication-title: Eur J Prev Cardiol doi: 10.1093/eurjpc/zwab016 – volume: 113 start-page: 2623 year: 2006 ident: 2542_CR31 publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.105.608679 – volume: 55 start-page: 529 year: 2018 ident: 2542_CR5 publication-title: Eur J Vasc Endovasc Surg doi: 10.1016/j.ejvs.2018.01.019 – volume: 39 start-page: 763 year: 2018 ident: 2542_CR7 publication-title: Eur Heart J doi: 10.1093/eurheartj/ehx095 – volume: 15 start-page: 1466 year: 2022 ident: 2542_CR27 publication-title: JACC Cardiovasc Interv doi: 10.1016/j.jcin.2022.05.050 – volume: 24 start-page: 793 year: 2017 ident: 2542_CR18 publication-title: J Endovasc Ther doi: 10.1177/1526602817728068 – volume: 53 start-page: 1298 year: 2007 ident: 2542_CR39 publication-title: Clin Chem doi: 10.1373/clinchem.2007.088013 – ident: 2542_CR45 doi: 10.1056/NEJMoa2215024 – volume: 45 start-page: 403 year: 2016 ident: 2542_CR3 publication-title: Vasa doi: 10.1024/0301-1526/a000556 – volume: 275 start-page: 379 year: 2018 ident: 2542_CR2 publication-title: Atherosclerosis doi: 10.1016/j.atherosclerosis.2018.05.033 – volume: 59 start-page: 577 year: 2018 ident: 2542_CR37 publication-title: J Lipid Res doi: 10.1194/jlr.R083626 – volume: 48 start-page: 1 year: 2019 ident: 2542_CR8 publication-title: Vasa doi: 10.1024/0301-1526/a000834 – volume: 9 start-page: e015355 year: 2020 ident: 2542_CR21 publication-title: J Am Heart Assoc doi: 10.1161/JAHA.119.015355 – volume: 35 start-page: 516 year: 2015 ident: 2542_CR6 publication-title: Int Angiol – volume: 382 start-page: 1329 year: 2013 ident: 2542_CR1 publication-title: Lancet doi: 10.1016/S0140-6736(13)61249-0 – volume: 308 start-page: 1660 year: 2012 ident: 2542_CR4 publication-title: JAMA doi: 10.1001/jama.2012.13415 – volume: 5 start-page: e2245720 year: 2022 ident: 2542_CR15 publication-title: JAMA Netw Open doi: 10.1001/jamanetworkopen.2022.45720 – volume: 349 start-page: 196 year: 2022 ident: 2542_CR19 publication-title: Atherosclerosis doi: 10.1016/j.atherosclerosis.2021.11.019 – volume: 11 start-page: 105 year: 2000 ident: 2542_CR36 publication-title: J Am Soc Nephrol doi: 10.1681/ASN.V111105 – volume: 6 start-page: 934 year: 2018 ident: 2542_CR44 publication-title: Lancet Diabetes Endocrinol doi: 10.1016/S2213-8587(18)30290-0 – volume: 43 start-page: 3925 year: 2022 ident: 2542_CR9 publication-title: Eur Heart J doi: 10.1093/eurheartj/ehac361 – volume: 137 start-page: 338 year: 2018 ident: 2542_CR41 publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.117.032235 – volume: 141 start-page: 1608 year: 2020 ident: 2542_CR43 publication-title: Circulation doi: 10.1161/CIRCULATIONAHA.120.046524 – volume: 74 start-page: 1167 year: 2019 ident: 2542_CR42 publication-title: J Am Coll Cardiol doi: 10.1016/j.jacc.2019.03.013 – volume: 11 start-page: 257 year: 2021 ident: 2542_CR24 publication-title: Biomolecules doi: 10.3390/biom11020257 – volume: 41 start-page: 111 year: 2020 ident: 2542_CR28 publication-title: Eur Heart J doi: 10.1093/eurheartj/ehz455 – volume: 363 start-page: 94 year: 2022 ident: 2542_CR23 publication-title: Atherosclerosis doi: 10.1016/j.atherosclerosis.2022.10.002 – volume: 198 start-page: 47 year: 2023 ident: 2542_CR10 publication-title: Am J Cardiol doi: 10.1016/j.amjcard.2023.04.017 – volume: 387 start-page: 1855 year: 2022 ident: 2542_CR48 publication-title: N Engl J Med doi: 10.1056/NEJMoa2211023 – volume: 12 start-page: 1229 year: 2024 ident: 2542_CR13 publication-title: Biomedicines doi: 10.3390/biomedicines12061229 – volume: 31 start-page: 1792 year: 2024 ident: 2542_CR40 publication-title: Eur J Prev Cardiol doi: 10.1093/eurjpc/zwae199 – volume: 276 start-page: 10 year: 2018 ident: 2542_CR22 publication-title: Atherosclerosis doi: 10.1016/j.atherosclerosis.2018.07.001 – volume: 105 start-page: 1825 year: 2010 ident: 2542_CR20 publication-title: Am J Cardiol doi: 10.1016/j.amjcard.2010.01.370 – ident: 2542_CR29 – volume: 16 start-page: 389 year: 2009 ident: 2542_CR25 publication-title: J Endovasc Ther doi: 10.1583/09-2733.1 – volume: 28 start-page: 354 year: 2007 ident: 2542_CR17 publication-title: Eur Heart J doi: 10.1093/eurheartj/ehl441 – volume: 32 start-page: 3058 year: 2012 ident: 2542_CR16 publication-title: Arterioscler Thromb Vasc Biol doi: 10.1161/ATVBAHA.112.255521 – volume: 382 start-page: 244 year: 2020 ident: 2542_CR47 publication-title: N Engl J Med doi: 10.1056/NEJMoa1905239 – volume: 12 start-page: e031255 year: 2023 ident: 2542_CR11 publication-title: J Am Heart Assoc doi: 10.1161/JAHA.123.031255 – ident: 2542_CR46 doi: 10.1016/j.jacc.2013.09.042 – volume: 9 start-page: 843602 year: 2022 ident: 2542_CR38 publication-title: Front Cardiovasc Med doi: 10.3389/fcvm.2022.843602 – volume: 24 start-page: 278 year: 2015 ident: 2542_CR26 publication-title: Int J Angiol doi: 10.1055/s-0035-1555133 – ident: 2542_CR33 doi: 10.1016/j.jacc.2024.02.013 |
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Snippet | Background
Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and... Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and mortality.... Background Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on amputation and... Abstract Background Elevated lipoprotein (a) (Lp(a)) is an independent risk factor for lower extremity artery disease (LEAD) with equivocal effect on... |
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SubjectTerms | Aged Amputation Amputation, Surgical Amputations of leg Biomedical and Life Sciences Care and treatment Cholesterol, LDL - blood Clinical Nutrition Development and progression Female Health aspects Humans Life Sciences Lipid-lowering therapy Lipidology Lipoprotein A Lipoprotein(a) - blood Low-density lipoprotein cholesterol Lower Extremity - blood supply Lower Extremity - pathology Lower Extremity - surgery Lower extremity artery disease Male Medical Biochemistry Middle Aged Peripheral Arterial Disease - blood Peripheral Arterial Disease - mortality Peripheral Arterial Disease - surgery Peripheral vascular diseases Physiological aspects Prognosis Retrospective Studies Revascularisation Risk Factors |
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Title | Distribution of lipoprotein (a) levels in patients with lower extremity artery disease and their impact on amputation and survival: a retrospective study |
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