Background Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have demonstrated significant effects on low-density lipoprotein (LDL) cholesterol and nonhigh density lipoprotein (HDL) cholesterol. To date, there have been limited reports on the effect of PCSK9 inhibitors on remnant cholesterol. Objectives Assess the effect of PCSK9 inhibitors on nonfasting remnant cholesterol in a real world population. Identify whether pretreatment triglyceride levels are associated with PCSK9 inhibition success as indicated by changes in remnant cholesterol levels. Methods Patients in our adult lipid clinic (n = 109) receiving PCSK9 inhibition for atherosclerotic cardiovascular disease or familial hypercholesterolemia who had available pre- and post-PCSK9 inhibition standard nonfasting lipid data were, retrospectively, selected for data analysis. Remnant cholesterol was the difference between non-HDL and LDL cholesterol. LDL cholesterol was measured directly and calculated from Friedewald and Martin/Hopkins methods. Data were analyzed using repeated measures ANOVA and multivariable linear regression for differential effects on remnant and LDL cholesterol based upon pretreatment nonfasting triglyceride levels. Results Remnant cholesterol as well as total, LDL, non-HDL cholesterol, and triglycerides decreased significantly (P<0.001) after PCSK9 inhibition. Patients with higher pretreatment triglyceride levels showed greater decrease in remnant cholesterol after PCSK9 inhibition (P<0.001) than those with lower pretreatment triglycerides. Conclusions In patients receiving PCSK9 inhibitors, remnant cholesterol as determined from nonfasting blood was reduced in proportion to pretreatment triglycerides.
Background: Intolerance to the daily use of statins can be dealt with by the use of Proprotein Catylase Subtilisin Kexin Type 9 (PCSK9) inhibitors. Alternative statin dosing has previously been utilized in patients with statin intolerance. Methods: Since the introduction of PCSK9 inhibitors for clinical use in 2015, we evaluated the effectiveness of alternative statin dosing in patients with daily statin intolerance defined as the inability to tolerate the daily use of any dose of statin. Alternative statin dosing was defined as weekly, twice weekly, or every other day atorvastatin or rosuvastatin. From our lipid clinic population of 505 patients with primary hypercholesterolemia (71% with atherosclerotic cardiovascular disease), 338 (67%) had daily statin intolerance. Alternative statin dosing was agreed to by 122 patients of these 338. At the time of this analysis, 87 patients (59% with atherosclerotic cardiovascular disease) could be assessed concerning the effectiveness of alternative statin dosing to achieve their LDL-cholesterol goal. Results: Of the 87 patients undergoing alternative statin dosing with or without ezetimibe, 30 (34%) achieved their goal. An additional 22 patients had a >30% reduction in LDL-cholesterol with oral therapy alone. Twenty-nine of the 87 patients later received PCSK9 inhibition with 27 achieving either their goal or a >30% reduction in LDL cholesterol. The baseline LDL-cholesterol of those achieving their goal LDLcholesterol with alternative statin dosing (154 + 40 mg/dL) could not be distinguished (p=0.79) from those who later required PCSK9 inhibition to achieve their goal (157 + 41 mg/dL). Intolerance to alternative statin dosing was seen in 24 of the 87 (28%) patients. Conclusion: In conclusion, prior to initiating PCSK9 inhibition in patients with daily statin intolerance, a trial of alternative statin dosing should be attempted. The success of alternative statin dosing cannot be predicted by the baseline level of LDL-cholesterol.
Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have demonstrated significant lowering of low-density lipoprotein (LDL) cholesterol in patients with atherosclerotic cardiovascular disease (ASCVD) and familial hypercholesterolemia (FH). We retrospectively reviewed data concerning use of PCSK9 inhibitors from patients in our university-based adult lipid clinic. Data collected included clinical pre-treatment variables and pre-and post-treatment non-fasting lipid profiles. Of 165 candidates, 163 were approved for PCSK9 inhibition (90% ASCVD and 10% FH). A majority of patients (72%) had statin intolerance. Treatment was provided and assessed in 141 patients. After three doses of medications, LDL cholesterol fell from 170 + 58 mg/dL to 76 + 45 mg/dL (55%, P<0.001). There were no differences in efficacy according to sex, elevated lipoprotein(a), and the PCS-K9 inhibitor utilized. Continued efficacy was evaluated in 101 patients with LDL decreasing further from initial follow-up to long-term follow-up over an average of 14 months (74 ± 44 mg/dL to 68 ± 41 mg/dL). Permanent discontinuation of PCS-K9 inhibitor because of side effects occurred in 11% of patients. When strict adherence to guidelines was applied, >95% approval rate was obtained, and there was similar efficacy in LDL lowering to what has been previously reported irrespective of statin intolerance.
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