The low-density lipoprotein cholesterol lowering is an ineffective surrogate marker of statin responsiveness to predict cardiovascular outcomes: The 10-year experience of matched population (a STROBE-compliant article)

Myung Han Hyun, Jae Won Jang, Byoung Geol Choi, Jin Oh Na, Cheol Ung Choi, Jin Won Kim, Eung Ju Kim, Seung Woon Rha, Chang Gyu Park, Eunmi Lee, Hong Seog Seo

Research output: Contribution to journalArticle

Abstract

Statins therapy decrease both low-density lipoprotein cholesterol (LDL-C) levels and the risk of atherosclerotic cardiovascular disease (ASCVD) with considerable individual variability. Whether the amount of LDL-C lowering is a surrogate maker of statin responsiveness to ASCVD prevention has not been fully investigated. Among 2352 eligible patients with statin prescriptions in a cardiovascular center between January 2005 and February 2014, one-third of patients (33%) on statin therapy failed to achieve effective reductions in LDL-C (LDL-C level reduction of less than 15%). By using, propensity-score matched population (480 pairs, n=960), the 5-year cumulative incidences of total major adverse cardiac events (MACE) were evaluated. The 5-year total MACE did not differ between normal cholesterol responders and non-responders (15.4% vs 16.1%, respectively; P=.860). In the subgroup analysis, male sex, older age, percutaneous coronary intervention, and heart failure were positive predictors, and dyslipidemia at the beginning of statin therapy was the only negative predictor of MACE in the 5-year follow-up (all P value<.05). However, cholesterol responsiveness after statin therapy did not influence the incidence of MACE (P=.860). The amount of LDL-C lowering did not predict beneficial effect on clinical outcomes of ASCVD after statin therapy. This result supports that given statin therapy, total ASCVD risk reduction should be tailored, which may not dependent to adherence to degree of LDL-C lowering or LDL-C goal based treatment.

Original languageEnglish
Article numbere18510
JournalMedicine (United States)
Volume98
Issue number51
DOIs
Publication statusPublished - 2019 Dec 1

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Hydroxymethylglutaryl-CoA Reductase Inhibitors
LDL Cholesterol
Biomarkers
Population
Cardiovascular Diseases
Therapeutics
Cholesterol
Propensity Score
Incidence
Percutaneous Coronary Intervention
Risk Reduction Behavior
Dyslipidemias
Prescriptions
Heart Failure

Keywords

  • coronary artery disease
  • disease progression
  • low-density lipoprotein cholesterol
  • statin responsiveness

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "The low-density lipoprotein cholesterol lowering is an ineffective surrogate marker of statin responsiveness to predict cardiovascular outcomes: The 10-year experience of matched population (a STROBE-compliant article)",
abstract = "Statins therapy decrease both low-density lipoprotein cholesterol (LDL-C) levels and the risk of atherosclerotic cardiovascular disease (ASCVD) with considerable individual variability. Whether the amount of LDL-C lowering is a surrogate maker of statin responsiveness to ASCVD prevention has not been fully investigated. Among 2352 eligible patients with statin prescriptions in a cardiovascular center between January 2005 and February 2014, one-third of patients (33{\%}) on statin therapy failed to achieve effective reductions in LDL-C (LDL-C level reduction of less than 15{\%}). By using, propensity-score matched population (480 pairs, n=960), the 5-year cumulative incidences of total major adverse cardiac events (MACE) were evaluated. The 5-year total MACE did not differ between normal cholesterol responders and non-responders (15.4{\%} vs 16.1{\%}, respectively; P=.860). In the subgroup analysis, male sex, older age, percutaneous coronary intervention, and heart failure were positive predictors, and dyslipidemia at the beginning of statin therapy was the only negative predictor of MACE in the 5-year follow-up (all P value<.05). However, cholesterol responsiveness after statin therapy did not influence the incidence of MACE (P=.860). The amount of LDL-C lowering did not predict beneficial effect on clinical outcomes of ASCVD after statin therapy. This result supports that given statin therapy, total ASCVD risk reduction should be tailored, which may not dependent to adherence to degree of LDL-C lowering or LDL-C goal based treatment.",
keywords = "coronary artery disease, disease progression, low-density lipoprotein cholesterol, statin responsiveness",
author = "Hyun, {Myung Han} and Jang, {Jae Won} and Choi, {Byoung Geol} and Na, {Jin Oh} and Choi, {Cheol Ung} and Kim, {Jin Won} and Kim, {Eung Ju} and Rha, {Seung Woon} and Park, {Chang Gyu} and Eunmi Lee and Seo, {Hong Seog}",
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T1 - The low-density lipoprotein cholesterol lowering is an ineffective surrogate marker of statin responsiveness to predict cardiovascular outcomes

T2 - The 10-year experience of matched population (a STROBE-compliant article)

AU - Hyun, Myung Han

AU - Jang, Jae Won

AU - Choi, Byoung Geol

AU - Na, Jin Oh

AU - Choi, Cheol Ung

AU - Kim, Jin Won

AU - Kim, Eung Ju

AU - Rha, Seung Woon

AU - Park, Chang Gyu

AU - Lee, Eunmi

AU - Seo, Hong Seog

PY - 2019/12/1

Y1 - 2019/12/1

N2 - Statins therapy decrease both low-density lipoprotein cholesterol (LDL-C) levels and the risk of atherosclerotic cardiovascular disease (ASCVD) with considerable individual variability. Whether the amount of LDL-C lowering is a surrogate maker of statin responsiveness to ASCVD prevention has not been fully investigated. Among 2352 eligible patients with statin prescriptions in a cardiovascular center between January 2005 and February 2014, one-third of patients (33%) on statin therapy failed to achieve effective reductions in LDL-C (LDL-C level reduction of less than 15%). By using, propensity-score matched population (480 pairs, n=960), the 5-year cumulative incidences of total major adverse cardiac events (MACE) were evaluated. The 5-year total MACE did not differ between normal cholesterol responders and non-responders (15.4% vs 16.1%, respectively; P=.860). In the subgroup analysis, male sex, older age, percutaneous coronary intervention, and heart failure were positive predictors, and dyslipidemia at the beginning of statin therapy was the only negative predictor of MACE in the 5-year follow-up (all P value<.05). However, cholesterol responsiveness after statin therapy did not influence the incidence of MACE (P=.860). The amount of LDL-C lowering did not predict beneficial effect on clinical outcomes of ASCVD after statin therapy. This result supports that given statin therapy, total ASCVD risk reduction should be tailored, which may not dependent to adherence to degree of LDL-C lowering or LDL-C goal based treatment.

AB - Statins therapy decrease both low-density lipoprotein cholesterol (LDL-C) levels and the risk of atherosclerotic cardiovascular disease (ASCVD) with considerable individual variability. Whether the amount of LDL-C lowering is a surrogate maker of statin responsiveness to ASCVD prevention has not been fully investigated. Among 2352 eligible patients with statin prescriptions in a cardiovascular center between January 2005 and February 2014, one-third of patients (33%) on statin therapy failed to achieve effective reductions in LDL-C (LDL-C level reduction of less than 15%). By using, propensity-score matched population (480 pairs, n=960), the 5-year cumulative incidences of total major adverse cardiac events (MACE) were evaluated. The 5-year total MACE did not differ between normal cholesterol responders and non-responders (15.4% vs 16.1%, respectively; P=.860). In the subgroup analysis, male sex, older age, percutaneous coronary intervention, and heart failure were positive predictors, and dyslipidemia at the beginning of statin therapy was the only negative predictor of MACE in the 5-year follow-up (all P value<.05). However, cholesterol responsiveness after statin therapy did not influence the incidence of MACE (P=.860). The amount of LDL-C lowering did not predict beneficial effect on clinical outcomes of ASCVD after statin therapy. This result supports that given statin therapy, total ASCVD risk reduction should be tailored, which may not dependent to adherence to degree of LDL-C lowering or LDL-C goal based treatment.

KW - coronary artery disease

KW - disease progression

KW - low-density lipoprotein cholesterol

KW - statin responsiveness

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