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Do you have any safety concerns about driving LDL-C levels to less than 50 mg/dL with PCSK9 inhibitors?

Do you have any safety concerns about driving LDL-C levels to less than 50 mg/dL with PCSK9 inhibitors?

You have introduced the concept of progressive atherosclerotic burden to characterize the multiplicity of biologic, metabolic, and clinical markers in a CV risk profile. How do you apply this aggregated risk to patient selection for PCSK9 inhibitors?

How large is the subgroup of diabetic patients who you feel are likely to appropriate candidates for PCSK9 inhibition to optimize CV risk reduction? And how does the lack of a safety signal influence your recommendations for this group?

How large is the subgroup of diabetic patients who you feel are likely to appropriate candidates for PCSK9 inhibition to optimize CV risk reduction? And how does the lack of a safety signal influence your recommendations for this group?

Since ESC and ACC/AHA are examining hard LDL-C targets for patients at risk for ASCVD, how does ODYSSEY Outcomes help inform cardiologists about the rationale for PCSK9-mediated lowering to achieve ultra-low levels (i.e. <50 mg/dL) of LDL-C?

Since ESC and ACC/AHA are examining hard LDL-C targets for patients at risk for ASCVD, how does ODYSSEY Outcomes help inform cardiologists about the rationale for PCSK9-mediated lowering to achieve ultra-low levels (i.e. <50 mg/dL) of LDL-C?

How should the fact that CV risk is not binary, but progressive, influence the decision to use a PCSK9 inhibitor?

How should the fact that CV risk is not binary, but progressive, influence the decision to use a PCSK9 inhibitor?

Although the AHA Guidelines emphasize CV risk and mortality reductions with statins, ODYSSEY Outcomes provides comparable evidence for alirocumab. How compelling is the evidence for PCSK9 inhibition as a mediator of CV risk and mortality reduction?

Although the AHA Guidelines emphasize CV risk and mortality reductions with statins, ODYSSEY Outcomes provides comparable evidence for alirocumab. How compelling is the evidence for PCSK9 inhibition as a mediator of CV risk and mortality reduction?

How do you see the benefit/safety risk equation shaping up for PCSK9 inhibitors based on the FOURIER and, most recently, the ODYSSEY Outcomes Trial?

How do you see the benefit/safety risk equation shaping up for PCSK9 inhibitors based on the FOURIER and, most recently, the ODYSSEY Outcomes Trial?

In the setting of secondary prevention for patients with diabetes, the role of LDL-C has special significance. How do you view the importance for the of PCSK9 inhibitors, therefore, specifically for reducing residual CV risk in the T2D population?

In the setting of secondary prevention for patients with diabetes, the role of LDL-C has special significance. How do you view the importance for the of PCSK9 inhibitors, therefore, specifically for reducing residual CV risk in the T2D population?

In the setting of a medical cardiology practice, to what extent is statin-induced muscle intolerance an important cause of poor statin adherence, increased healthcare costs, and increased cardiac event rates?

In the setting of a medical cardiology practice, to what extent is statin-induced muscle intolerance an important cause of poor statin adherence, increased healthcare costs, and increased cardiac event rates?

Based on ODYSSEY Outcomes and FOURIER, what are the findings and/or biologic risk features—Lp(a), for example—in patients managed in an interventional cardiology setting that would make you advocate for the use of PCSK9 inhibitors?

Based on ODYSSEY Outcomes and FOURIER, what are the findings and/or biologic risk features—Lp(a), for example—in patients managed in an interventional cardiology setting that would make you advocate for the use of PCSK9 inhibitors?

As the Director of the Center for Cardiovascular Disease Prevention, what patient types on the risk landscape of ASCVD do you believe deserve special attention because they are likely to be eligible candidates for PCSK9-mediated LDL-C reduction?

As the Director of the Center for Cardiovascular Disease Prevention, what patient types on the risk landscape of ASCVD do you believe deserve special attention because they are likely to be eligible candidates for PCSK9-mediated LDL-C reduction?

What should the ideal target LDL-C be in the Type 2 diabetes population? And what is the advantage of the treat-to-target strategy employed in ODYSSEY Outcomes and what did we learn about associated, all-cause mortality with alirocumab in that trial?

What should the ideal target LDL-C be in the Type 2 diabetes population? And what is the advantage of the treat-to-target strategy employed in ODYSSEY Outcomes and what did we learn about associated, all-cause mortality with alirocumab in that trial?

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