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Serum PCSK9 Levels Distinguish Individuals Who Do Not Respond to High-Dose Statin Therapy with the Expected Reduction in LDL-C.

Taylor BA, Panza G, Pescatello LS, Chipkin S, Gipe D, Shao W, White CM, Thompson PD - J Lipids (2014)

Bottom Line: The purpose of the present report was to examine whether proprotein convertase subtilisin/kexin type 9 (PCSK9) levels differ in individuals who do not exhibit expected reductions in low density lipoprotein cholesterol (LDL-C) with statin therapy.Eighteen nonresponder subjects treated with 80 mg atorvastatin treatment for 6 months without substantial reductions in LDL-C (ΔLDL-C: 2.6 ± 11.4%) were compared to age- and gender-matched atorvastatin responders (ΔLDL-C: 50.7 ± 8.5%) and placebo-treated subjects (ΔLDL-C: 9.9 ± 21.5%).Serum PCSK9 levels, both at baseline and in response to statin therapy, may differentiate individuals who do versus those who do not respond to statin treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Henry Low Heart Center, Hartford Hospital, 85 Seymour Street, Hartford, CT 06102, USA ; Department of Health Sciences, University of Hartford, 200 Bloomfield Avenue, West Hartford, CT 06117, USA.

ABSTRACT
The purpose of the present report was to examine whether proprotein convertase subtilisin/kexin type 9 (PCSK9) levels differ in individuals who do not exhibit expected reductions in low density lipoprotein cholesterol (LDL-C) with statin therapy. Eighteen nonresponder subjects treated with 80 mg atorvastatin treatment for 6 months without substantial reductions in LDL-C (ΔLDL-C: 2.6 ± 11.4%) were compared to age- and gender-matched atorvastatin responders (ΔLDL-C: 50.7 ± 8.5%) and placebo-treated subjects (ΔLDL-C: 9.9 ± 21.5%). Free PCSK9 was marginally higher in nonresponders at baseline (P = 0.07) and significantly higher in atorvastatin responders after 6 months of treatment (P = 0.04). The change in free PCSK9 over 6 months with statin treatment was higher (P < 0.01) in atorvastatin responders (134.2 ± 131.5 ng/mL post- versus prestudy) than in either the nonresponders (39.9 ± 87.8 ng/mL) or placebo subjects (27.8 ± 97.6 ng/mL). Drug compliance was not lower in the nonresponders as assessed by pill counts and poststudy plasma atorvastatin levels. Serum PCSK9 levels, both at baseline and in response to statin therapy, may differentiate individuals who do versus those who do not respond to statin treatment.

No MeSH data available.


Free PCSK9 levels (group means ± standard deviations) before (pre) and after (post) 6 months of atorvastatin 80 mg or placebo treatment in 18 individuals who did not reduce LDL-C on atorvastatin (Atorva nonrespond) versus 18 individuals who did reduce LDL-C on atorvastatin (Atorva respond) and individuals on placebo (Placebo). P values indicate group differences at each time point.
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Related In: Results  -  Collection


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fig1: Free PCSK9 levels (group means ± standard deviations) before (pre) and after (post) 6 months of atorvastatin 80 mg or placebo treatment in 18 individuals who did not reduce LDL-C on atorvastatin (Atorva nonrespond) versus 18 individuals who did reduce LDL-C on atorvastatin (Atorva respond) and individuals on placebo (Placebo). P values indicate group differences at each time point.

Mentions: Free PCSK9 (Figure 1) was marginally higher in atorvastatin nonresponders at baseline (P = 0.07) and significantly higher in atorvastatin responders after 6 months of treatment (P = 0.04). In addition, the change in free PCSK9 over 6 months with statin treatment was higher (P < 0.01) in atorvastatin responders (134.2 ± 131.5 ng/mL post- and prestudy) than in either the nonresponders (39.9 ± 87.8 ng/mL) or placebo subjects (27.8 ± 97.6 ng/mL). Total PCSK9 values at 6 months, as well as the change from baseline to 6 months, demonstrated a parallel trend (higher values and a greater change observed in atorvastatin responders), but these differences were not significant (P = 0.11 and 0.14, resp.), a finding that is likely attributable to the lower percentages of total (~30%) versus free (~70%) PCSK9 that circulate in the plasma. Finally, the change in LDL-C over 6 months was inversely correlated to the change in free PCSK9 (Pearson correlation = −0.31; P = 0.03) demonstrating that the greatest reductions in LDL-C were associated with the greatest increases in PCSK9.


Serum PCSK9 Levels Distinguish Individuals Who Do Not Respond to High-Dose Statin Therapy with the Expected Reduction in LDL-C.

Taylor BA, Panza G, Pescatello LS, Chipkin S, Gipe D, Shao W, White CM, Thompson PD - J Lipids (2014)

Free PCSK9 levels (group means ± standard deviations) before (pre) and after (post) 6 months of atorvastatin 80 mg or placebo treatment in 18 individuals who did not reduce LDL-C on atorvastatin (Atorva nonrespond) versus 18 individuals who did reduce LDL-C on atorvastatin (Atorva respond) and individuals on placebo (Placebo). P values indicate group differences at each time point.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4127223&req=5

fig1: Free PCSK9 levels (group means ± standard deviations) before (pre) and after (post) 6 months of atorvastatin 80 mg or placebo treatment in 18 individuals who did not reduce LDL-C on atorvastatin (Atorva nonrespond) versus 18 individuals who did reduce LDL-C on atorvastatin (Atorva respond) and individuals on placebo (Placebo). P values indicate group differences at each time point.
Mentions: Free PCSK9 (Figure 1) was marginally higher in atorvastatin nonresponders at baseline (P = 0.07) and significantly higher in atorvastatin responders after 6 months of treatment (P = 0.04). In addition, the change in free PCSK9 over 6 months with statin treatment was higher (P < 0.01) in atorvastatin responders (134.2 ± 131.5 ng/mL post- and prestudy) than in either the nonresponders (39.9 ± 87.8 ng/mL) or placebo subjects (27.8 ± 97.6 ng/mL). Total PCSK9 values at 6 months, as well as the change from baseline to 6 months, demonstrated a parallel trend (higher values and a greater change observed in atorvastatin responders), but these differences were not significant (P = 0.11 and 0.14, resp.), a finding that is likely attributable to the lower percentages of total (~30%) versus free (~70%) PCSK9 that circulate in the plasma. Finally, the change in LDL-C over 6 months was inversely correlated to the change in free PCSK9 (Pearson correlation = −0.31; P = 0.03) demonstrating that the greatest reductions in LDL-C were associated with the greatest increases in PCSK9.

Bottom Line: The purpose of the present report was to examine whether proprotein convertase subtilisin/kexin type 9 (PCSK9) levels differ in individuals who do not exhibit expected reductions in low density lipoprotein cholesterol (LDL-C) with statin therapy.Eighteen nonresponder subjects treated with 80 mg atorvastatin treatment for 6 months without substantial reductions in LDL-C (ΔLDL-C: 2.6 ± 11.4%) were compared to age- and gender-matched atorvastatin responders (ΔLDL-C: 50.7 ± 8.5%) and placebo-treated subjects (ΔLDL-C: 9.9 ± 21.5%).Serum PCSK9 levels, both at baseline and in response to statin therapy, may differentiate individuals who do versus those who do not respond to statin treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Henry Low Heart Center, Hartford Hospital, 85 Seymour Street, Hartford, CT 06102, USA ; Department of Health Sciences, University of Hartford, 200 Bloomfield Avenue, West Hartford, CT 06117, USA.

ABSTRACT
The purpose of the present report was to examine whether proprotein convertase subtilisin/kexin type 9 (PCSK9) levels differ in individuals who do not exhibit expected reductions in low density lipoprotein cholesterol (LDL-C) with statin therapy. Eighteen nonresponder subjects treated with 80 mg atorvastatin treatment for 6 months without substantial reductions in LDL-C (ΔLDL-C: 2.6 ± 11.4%) were compared to age- and gender-matched atorvastatin responders (ΔLDL-C: 50.7 ± 8.5%) and placebo-treated subjects (ΔLDL-C: 9.9 ± 21.5%). Free PCSK9 was marginally higher in nonresponders at baseline (P = 0.07) and significantly higher in atorvastatin responders after 6 months of treatment (P = 0.04). The change in free PCSK9 over 6 months with statin treatment was higher (P < 0.01) in atorvastatin responders (134.2 ± 131.5 ng/mL post- versus prestudy) than in either the nonresponders (39.9 ± 87.8 ng/mL) or placebo subjects (27.8 ± 97.6 ng/mL). Drug compliance was not lower in the nonresponders as assessed by pill counts and poststudy plasma atorvastatin levels. Serum PCSK9 levels, both at baseline and in response to statin therapy, may differentiate individuals who do versus those who do not respond to statin treatment.

No MeSH data available.