Low-density lipoprotein cholesterol reduction and statin intensity in myocardial infarction patients and major adverse outcomes: a Swedish nationwide cohort study
Abstract Aims Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes and statin intensity with...
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| Published in | European heart journal Vol. 42; no. 3; pp. 243 - 252 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Oxford University Press
20.01.2021
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0195-668X 1522-9645 1522-9645 |
| DOI | 10.1093/eurheartj/ehaa1011 |
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| Abstract | Abstract
Aims
Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes and statin intensity with prognosis after a myocardial infarction (MI).
Methods and results
Patients admitted with MI were followed for mortality and major CV events. Changes in LDL-C between the MI and a 6- to 10-week follow-up visit were analysed. The associations between quartiles of LDL-C change and statin intensity with outcomes were assessed using adjusted Cox regression analyses. A total of 40 607 patients were followed for a median of 3.78 years. The median change in LDL-C was a 1.20 mmol/L reduction. Patients with larger LDL-C reduction (1.85 mmol/L, 75th percentile) compared with a smaller reduction (0.36 mmol/L, 25th percentile) had lower hazard ratios (HR) for all outcomes (95% confidence interval): composite of CV mortality, MI, and ischaemic stroke 0.77 (0.70–0.84); all-cause mortality 0.71 (0.63–0.80); CV mortality 0.68 (0.57–0.81); MI 0.81 (0.73–0.91); ischaemic stroke 0.76 (0.62–0.93); heart failure hospitalization 0.73 (0.63–0.85), and coronary artery revascularization 0.86 (0.79–0.94). Patients with ≥50% LDL-C reduction using high-intensity statins at discharge had a lower incidence of all outcomes compared with those using a lower intensity statin.
Conclusions
Larger early LDL-C reduction and more intensive statin therapy after MI were associated with a reduced hazard of all CV outcomes and all-cause mortality. This supports clinical trial data suggesting that earlier lowering of LDL-C after an MI confers the greatest benefit.
Graphical Abstract |
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| AbstractList | AIMS: Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes and statin intensity with prognosis after a myocardial infarction (MI).
METHODS AND RESULTS: Patients admitted with MI were followed for mortality and major CV events. Changes in LDL-C between the MI and a 6- to 10-week follow-up visit were analysed. The associations between quartiles of LDL-C change and statin intensity with outcomes were assessed using adjusted Cox regression analyses. A total of 40 607 patients were followed for a median of 3.78 years. The median change in LDL-C was a 1.20 mmol/L reduction. Patients with larger LDL-C reduction (1.85 mmol/L, 75th percentile) compared with a smaller reduction (0.36 mmol/L, 25th percentile) had lower hazard ratios (HR) for all outcomes (95% confidence interval): composite of CV mortality, MI, and ischaemic stroke 0.77 (0.70-0.84); all-cause mortality 0.71 (0.63-0.80); CV mortality 0.68 (0.57-0.81); MI 0.81 (0.73-0.91); ischaemic stroke 0.76 (0.62-0.93); heart failure hospitalization 0.73 (0.63-0.85), and coronary artery revascularization 0.86 (0.79-0.94). Patients with ≥50% LDL-C reduction using high-intensity statins at discharge had a lower incidence of all outcomes compared with those using a lower intensity statin.
CONCLUSIONS: Larger early LDL-C reduction and more intensive statin therapy after MI were associated with a reduced hazard of all CV outcomes and all-cause mortality. This supports clinical trial data suggesting that earlier lowering of LDL-C after an MI confers the greatest benefit. Abstract Aims Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes and statin intensity with prognosis after a myocardial infarction (MI). Methods and results Patients admitted with MI were followed for mortality and major CV events. Changes in LDL-C between the MI and a 6- to 10-week follow-up visit were analysed. The associations between quartiles of LDL-C change and statin intensity with outcomes were assessed using adjusted Cox regression analyses. A total of 40 607 patients were followed for a median of 3.78 years. The median change in LDL-C was a 1.20 mmol/L reduction. Patients with larger LDL-C reduction (1.85 mmol/L, 75th percentile) compared with a smaller reduction (0.36 mmol/L, 25th percentile) had lower hazard ratios (HR) for all outcomes (95% confidence interval): composite of CV mortality, MI, and ischaemic stroke 0.77 (0.70–0.84); all-cause mortality 0.71 (0.63–0.80); CV mortality 0.68 (0.57–0.81); MI 0.81 (0.73–0.91); ischaemic stroke 0.76 (0.62–0.93); heart failure hospitalization 0.73 (0.63–0.85), and coronary artery revascularization 0.86 (0.79–0.94). Patients with ≥50% LDL-C reduction using high-intensity statins at discharge had a lower incidence of all outcomes compared with those using a lower intensity statin. Conclusions Larger early LDL-C reduction and more intensive statin therapy after MI were associated with a reduced hazard of all CV outcomes and all-cause mortality. This supports clinical trial data suggesting that earlier lowering of LDL-C after an MI confers the greatest benefit. Graphical Abstract Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes and statin intensity with prognosis after a myocardial infarction (MI).AIMSClinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes and statin intensity with prognosis after a myocardial infarction (MI).Patients admitted with MI were followed for mortality and major CV events. Changes in LDL-C between the MI and a 6- to 10-week follow-up visit were analysed. The associations between quartiles of LDL-C change and statin intensity with outcomes were assessed using adjusted Cox regression analyses. A total of 40 607 patients were followed for a median of 3.78 years. The median change in LDL-C was a 1.20 mmol/L reduction. Patients with larger LDL-C reduction (1.85 mmol/L, 75th percentile) compared with a smaller reduction (0.36 mmol/L, 25th percentile) had lower hazard ratios (HR) for all outcomes (95% confidence interval): composite of CV mortality, MI, and ischaemic stroke 0.77 (0.70-0.84); all-cause mortality 0.71 (0.63-0.80); CV mortality 0.68 (0.57-0.81); MI 0.81 (0.73-0.91); ischaemic stroke 0.76 (0.62-0.93); heart failure hospitalization 0.73 (0.63-0.85), and coronary artery revascularization 0.86 (0.79-0.94). Patients with ≥50% LDL-C reduction using high-intensity statins at discharge had a lower incidence of all outcomes compared with those using a lower intensity statin.METHODS AND RESULTSPatients admitted with MI were followed for mortality and major CV events. Changes in LDL-C between the MI and a 6- to 10-week follow-up visit were analysed. The associations between quartiles of LDL-C change and statin intensity with outcomes were assessed using adjusted Cox regression analyses. A total of 40 607 patients were followed for a median of 3.78 years. The median change in LDL-C was a 1.20 mmol/L reduction. Patients with larger LDL-C reduction (1.85 mmol/L, 75th percentile) compared with a smaller reduction (0.36 mmol/L, 25th percentile) had lower hazard ratios (HR) for all outcomes (95% confidence interval): composite of CV mortality, MI, and ischaemic stroke 0.77 (0.70-0.84); all-cause mortality 0.71 (0.63-0.80); CV mortality 0.68 (0.57-0.81); MI 0.81 (0.73-0.91); ischaemic stroke 0.76 (0.62-0.93); heart failure hospitalization 0.73 (0.63-0.85), and coronary artery revascularization 0.86 (0.79-0.94). Patients with ≥50% LDL-C reduction using high-intensity statins at discharge had a lower incidence of all outcomes compared with those using a lower intensity statin.Larger early LDL-C reduction and more intensive statin therapy after MI were associated with a reduced hazard of all CV outcomes and all-cause mortality. This supports clinical trial data suggesting that earlier lowering of LDL-C after an MI confers the greatest benefit.CONCLUSIONSLarger early LDL-C reduction and more intensive statin therapy after MI were associated with a reduced hazard of all CV outcomes and all-cause mortality. This supports clinical trial data suggesting that earlier lowering of LDL-C after an MI confers the greatest benefit. Aims: Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes and statin intensity with prognosis after a myocardial infarction (MI). Methods and results: Patients admitted with MI were followed for mortality and major CV events. Changes in LDL-C between the MI and a 6-to 10-week follow-up visit were analysed. The associations between quartiles of LDL-C change and statin intensity with outcomes were assessed using adjusted Cox regression analyses. A total of 40 607 patients were followed for a median of 3.78 years. The median change in LDL-C was a 1.20 mmol/L reduction. Patients with larger LDL-C reduction (1.85 mmol/L, 75th percentile) compared with a smaller reduction (0.36 mmol/L, 25th percentile) had lower hazard ratios (HR) for all outcomes (95% confidence interval): composite of CV mortality, MI, and ischaemic stroke 0.77 (0.70-0.84); all-cause mortality 0.71 (0.63-0.80); CV mortality 0.68 (0.57-0.81); MI 0.81 (0.73-0.91); ischaemic stroke 0.76 (0.62-0.93); heart failure hospitalization 0.73 (0.63-0.85), and coronary artery revascularization 0.86 (0.79-0.94). Patients with ≥50% LDL-C reduction using high-intensity statins at discharge had a lower incidence of all outcomes compared with those using a lower intensity statin. Conclusions: Larger early LDL-C reduction and more intensive statin therapy after MI were associated with a reduced hazard of all CV outcomes and all-cause mortality. This supports clinical trial data suggesting that earlier lowering of LDL-C after an MI confers the greatest benefit. Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not yet been shown in a real-world setting. We aimed to investigate the association between LDL-C changes and statin intensity with prognosis after a myocardial infarction (MI). Patients admitted with MI were followed for mortality and major CV events. Changes in LDL-C between the MI and a 6- to 10-week follow-up visit were analysed. The associations between quartiles of LDL-C change and statin intensity with outcomes were assessed using adjusted Cox regression analyses. A total of 40 607 patients were followed for a median of 3.78 years. The median change in LDL-C was a 1.20 mmol/L reduction. Patients with larger LDL-C reduction (1.85 mmol/L, 75th percentile) compared with a smaller reduction (0.36 mmol/L, 25th percentile) had lower hazard ratios (HR) for all outcomes (95% confidence interval): composite of CV mortality, MI, and ischaemic stroke 0.77 (0.70-0.84); all-cause mortality 0.71 (0.63-0.80); CV mortality 0.68 (0.57-0.81); MI 0.81 (0.73-0.91); ischaemic stroke 0.76 (0.62-0.93); heart failure hospitalization 0.73 (0.63-0.85), and coronary artery revascularization 0.86 (0.79-0.94). Patients with ≥50% LDL-C reduction using high-intensity statins at discharge had a lower incidence of all outcomes compared with those using a lower intensity statin. Larger early LDL-C reduction and more intensive statin therapy after MI were associated with a reduced hazard of all CV outcomes and all-cause mortality. This supports clinical trial data suggesting that earlier lowering of LDL-C after an MI confers the greatest benefit. |
| Author | Renlund, Henrik Yari, Ali Hamer, Andrew W Schubert, Jessica Lindahl, Bertil Hagström, Emil Ueda, Peter James, Stefan Jernberg, Tomas Reading, Stephanie R Melhus, Håkan Leosdottir, Margrét Dluzniewski, Paul J |
| AuthorAffiliation | ehaa1011-aff1 Department of Medical Sciences, Uppsala University , Uppsala, Sweden ehaa1011-aff5 Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital , Stockholm, Sweden ehaa1011-aff4 Department of Clinical Sciences, Faculty of Medicine, Lund University , Malmö, Sweden ehaa1011-aff6 Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet , Stockholm, Sweden ehaa1011-aff7 Amgen, Inc , Thousand Oaks, CA, USA ehaa1011-aff3 Department of Cardiology, Skåne University Hospital, Malmö , Sweden ehaa1011-aff2 Uppsala Clinical Research Center , Uppsala, Sweden |
| AuthorAffiliation_xml | – name: ehaa1011-aff5 Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital , Stockholm, Sweden – name: ehaa1011-aff4 Department of Clinical Sciences, Faculty of Medicine, Lund University , Malmö, Sweden – name: ehaa1011-aff2 Uppsala Clinical Research Center , Uppsala, Sweden – name: ehaa1011-aff6 Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet , Stockholm, Sweden – name: ehaa1011-aff7 Amgen, Inc , Thousand Oaks, CA, USA – name: ehaa1011-aff1 Department of Medical Sciences, Uppsala University , Uppsala, Sweden – name: ehaa1011-aff3 Department of Cardiology, Skåne University Hospital, Malmö , Sweden |
| Author_xml | – sequence: 1 givenname: Jessica orcidid: 0000-0002-1917-5885 surname: Schubert fullname: Schubert, Jessica email: jessica.schubert@medsci.uu.se organization: Department of Medical Sciences, Uppsala University, Uppsala, Sweden – sequence: 2 givenname: Bertil orcidid: 0000-0002-5795-0061 surname: Lindahl fullname: Lindahl, Bertil organization: Department of Medical Sciences, Uppsala University, Uppsala, Sweden – sequence: 3 givenname: Håkan orcidid: 0000-0002-6857-5973 surname: Melhus fullname: Melhus, Håkan organization: Department of Medical Sciences, Uppsala University, Uppsala, Sweden – sequence: 4 givenname: Henrik orcidid: 0000-0002-2141-6086 surname: Renlund fullname: Renlund, Henrik organization: Uppsala Clinical Research Center, Uppsala, Sweden – sequence: 5 givenname: Margrét orcidid: 0000-0003-1677-1566 surname: Leosdottir fullname: Leosdottir, Margrét organization: Department of Cardiology, Skåne University Hospital, Malmö, Sweden – sequence: 6 givenname: Ali orcidid: 0000-0002-0196-4894 surname: Yari fullname: Yari, Ali organization: Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden – sequence: 7 givenname: Peter orcidid: 0000-0002-3275-8743 surname: Ueda fullname: Ueda, Peter organization: Clinical Epidemiology Division, Department of Medicine, Karolinska Institutet, Stockholm, Sweden – sequence: 8 givenname: Stefan orcidid: 0000-0003-4413-9736 surname: James fullname: James, Stefan organization: Department of Medical Sciences, Uppsala University, Uppsala, Sweden – sequence: 9 givenname: Stephanie R orcidid: 0000-0003-0494-7448 surname: Reading fullname: Reading, Stephanie R organization: Amgen, Inc, Thousand Oaks, CA, USA – sequence: 10 givenname: Paul J surname: Dluzniewski fullname: Dluzniewski, Paul J organization: Amgen, Inc, Thousand Oaks, CA, USA – sequence: 11 givenname: Andrew W surname: Hamer fullname: Hamer, Andrew W organization: Amgen, Inc, Thousand Oaks, CA, USA – sequence: 12 givenname: Tomas orcidid: 0000-0003-1695-379X surname: Jernberg fullname: Jernberg, Tomas organization: Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden – sequence: 13 givenname: Emil surname: Hagström fullname: Hagström, Emil organization: Department of Medical Sciences, Uppsala University, Uppsala, Sweden |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33367526$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-430124$$DView record from Swedish Publication Index http://kipublications.ki.se/Default.aspx?queryparsed=id:146014324$$DView record from Swedish Publication Index |
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| ContentType | Journal Article |
| Copyright | The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology. 2020 The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology. |
| Copyright_xml | – notice: The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology. 2020 – notice: The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology. |
| CorporateAuthor | Lunds universitet Profile areas and other strong research environments Department of Clinical Sciences, Malmö Lund University Strategiska forskningsområden (SFO) EpiHealth: Epidemiology for Health Faculty of Medicine Internmedicin - epidemiologi Strategic research areas (SRA) Medicinska fakulteten Profilområden och andra starka forskningsmiljöer Internal Medicine - Epidemiology Institutionen för kliniska vetenskaper, Malmö |
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| Keywords | Myocardial infarction Cardiovascular outcomes Secondary prevention Statin LDL-C Cardiovascular mortality |
| Language | English |
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Aims
Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has,... Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however, not... AIMS: Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however,... Aims: Clinical trials have demonstrated that a reduction in low-density lipoprotein cholesterol (LDL-C) reduces cardiovascular (CV) events. This has, however,... |
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| SubjectTerms | Cardiology and Cardiovascular Disease Cardiovascular mortality Cardiovascular outcomes Clinical Medicine Clinical Research Kardiologi och kardiovaskulära sjukdomar Klinisk medicin LDL-C Medical and Health Sciences Medicin och hälsovetenskap Myocardial infarction Secondary prevention Statin |
| Title | Low-density lipoprotein cholesterol reduction and statin intensity in myocardial infarction patients and major adverse outcomes: a Swedish nationwide cohort study |
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