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Case: 45-year-old woman comes to clinic and requests lipoprotein(a) [Lp(a)] testing. She has a family history of early coronary disease (mother age 50, sister age 48) and has hypertension with home blood pressure readings of 130-140/70-75. She had a lipid panel checked last year which showed a total cholesterol of 210 mg/dL, LDL 145 mg/dL, HDL 45 mg/dL, and triglycerides of 100 mg/dL. She does not smoke and is currently taking irbesartan, chlorthalidone, sertraline, a multivitamin, and vitamin D.
What do you recommend?
There has been a great deal of media attention on testing for Lp(a). Many of my patients are requesting testing although many of them do not need it. This patient is an exception. I think Lp(a) testing would help inform her medical care. She has a family history of early coronary disease in her mother and sister, but her own lipid profile is not worrisome.
Her 10-year cardiovascular disease risk is 2%. The cardiac risk calculator does not incorporate family history; I think this is a situation where testing for Lp(a)(as well as apolipoprotein B) can be helpful. If her Lp(a) is elevated, it helps reassess her risk and that information would be helpful in targeting aggressive interventions for other CV risk factors, including optimal blood pressure control. In her case, pushing for a goal systolic blood pressure below 120 mm Hg and making sure she is doing regular exercise and eating a heart-healthy diet. The current consensus statement on Lp(a) recommends that patients with elevated levels have aggressive lifestyle and cardiovascular risk management.1
Currently, there are no medical treatments available for high Lp(a) for primary prevention. Apheresis has been approved by the US Food and Drug Administration (FDA) for patients with familial hyperlipidemia who have LDL ≥ 100 mg/dL, Lp(a) ≥ 60 mg/dL, and coronary or other artery disease.
PCSK9 inhibitors have shown a reduction in major cardiovascular events in patients who have established coronary artery disease and high Lp(a) levels, albeit with limited data. Unlike statins, which increase Lp(a) levels, PCSK9 inhibitors reduce Lp(a) levels.2 There are promising early results in a phase 2 trial of the oral drug muvalaplin lowering Lp(a) levels by up to 85% for the highest dose, but there are no peer-reviewed articles confirming these results and no outcome trials at this time.
In patients who are already recognized as high risk, especially those with established coronary artery disease, measuring Lp(a) levels offer little benefit. These patients should already be receiving aggressive medical therapy to reach blood pressure targets if hypertensive, maximal lifestyle modifications, and statin therapy.
If these patients need more therapy because of continued coronary events, despite maximal conventional medical therapy, then adding a PCSK9 inhibitor would be appropriate whether or not a patient has a high Lp(a) level. Once Lp(a) targeted therapies are available and show clinical benefit, then the role of Lp(a) measurement and treatment in this population will be clearer.
Pearl: Most patients do not need Lp(a) testing. There are no FDA-approved treatments for high Lp(a) levels.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.
References
1. Kronenberg F et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: A European Atherosclerosis Society consensus statement. Eur Heart J. 2022;43:3925-46.
2. Ruscica M et al. Lipoprotein(a) and PCSK9 inhibition: Clinical evidence Eur Heart J Suppl 2020;Nov 18(Suppl L):L53–L56.
Case: 45-year-old woman comes to clinic and requests lipoprotein(a) [Lp(a)] testing. She has a family history of early coronary disease (mother age 50, sister age 48) and has hypertension with home blood pressure readings of 130-140/70-75. She had a lipid panel checked last year which showed a total cholesterol of 210 mg/dL, LDL 145 mg/dL, HDL 45 mg/dL, and triglycerides of 100 mg/dL. She does not smoke and is currently taking irbesartan, chlorthalidone, sertraline, a multivitamin, and vitamin D.
What do you recommend?
There has been a great deal of media attention on testing for Lp(a). Many of my patients are requesting testing although many of them do not need it. This patient is an exception. I think Lp(a) testing would help inform her medical care. She has a family history of early coronary disease in her mother and sister, but her own lipid profile is not worrisome.
Her 10-year cardiovascular disease risk is 2%. The cardiac risk calculator does not incorporate family history; I think this is a situation where testing for Lp(a)(as well as apolipoprotein B) can be helpful. If her Lp(a) is elevated, it helps reassess her risk and that information would be helpful in targeting aggressive interventions for other CV risk factors, including optimal blood pressure control. In her case, pushing for a goal systolic blood pressure below 120 mm Hg and making sure she is doing regular exercise and eating a heart-healthy diet. The current consensus statement on Lp(a) recommends that patients with elevated levels have aggressive lifestyle and cardiovascular risk management.1
Currently, there are no medical treatments available for high Lp(a) for primary prevention. Apheresis has been approved by the US Food and Drug Administration (FDA) for patients with familial hyperlipidemia who have LDL ≥ 100 mg/dL, Lp(a) ≥ 60 mg/dL, and coronary or other artery disease.
PCSK9 inhibitors have shown a reduction in major cardiovascular events in patients who have established coronary artery disease and high Lp(a) levels, albeit with limited data. Unlike statins, which increase Lp(a) levels, PCSK9 inhibitors reduce Lp(a) levels.2 There are promising early results in a phase 2 trial of the oral drug muvalaplin lowering Lp(a) levels by up to 85% for the highest dose, but there are no peer-reviewed articles confirming these results and no outcome trials at this time.
In patients who are already recognized as high risk, especially those with established coronary artery disease, measuring Lp(a) levels offer little benefit. These patients should already be receiving aggressive medical therapy to reach blood pressure targets if hypertensive, maximal lifestyle modifications, and statin therapy.
If these patients need more therapy because of continued coronary events, despite maximal conventional medical therapy, then adding a PCSK9 inhibitor would be appropriate whether or not a patient has a high Lp(a) level. Once Lp(a) targeted therapies are available and show clinical benefit, then the role of Lp(a) measurement and treatment in this population will be clearer.
Pearl: Most patients do not need Lp(a) testing. There are no FDA-approved treatments for high Lp(a) levels.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.
References
1. Kronenberg F et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: A European Atherosclerosis Society consensus statement. Eur Heart J. 2022;43:3925-46.
2. Ruscica M et al. Lipoprotein(a) and PCSK9 inhibition: Clinical evidence Eur Heart J Suppl 2020;Nov 18(Suppl L):L53–L56.
Case: 45-year-old woman comes to clinic and requests lipoprotein(a) [Lp(a)] testing. She has a family history of early coronary disease (mother age 50, sister age 48) and has hypertension with home blood pressure readings of 130-140/70-75. She had a lipid panel checked last year which showed a total cholesterol of 210 mg/dL, LDL 145 mg/dL, HDL 45 mg/dL, and triglycerides of 100 mg/dL. She does not smoke and is currently taking irbesartan, chlorthalidone, sertraline, a multivitamin, and vitamin D.
What do you recommend?
There has been a great deal of media attention on testing for Lp(a). Many of my patients are requesting testing although many of them do not need it. This patient is an exception. I think Lp(a) testing would help inform her medical care. She has a family history of early coronary disease in her mother and sister, but her own lipid profile is not worrisome.
Her 10-year cardiovascular disease risk is 2%. The cardiac risk calculator does not incorporate family history; I think this is a situation where testing for Lp(a)(as well as apolipoprotein B) can be helpful. If her Lp(a) is elevated, it helps reassess her risk and that information would be helpful in targeting aggressive interventions for other CV risk factors, including optimal blood pressure control. In her case, pushing for a goal systolic blood pressure below 120 mm Hg and making sure she is doing regular exercise and eating a heart-healthy diet. The current consensus statement on Lp(a) recommends that patients with elevated levels have aggressive lifestyle and cardiovascular risk management.1
Currently, there are no medical treatments available for high Lp(a) for primary prevention. Apheresis has been approved by the US Food and Drug Administration (FDA) for patients with familial hyperlipidemia who have LDL ≥ 100 mg/dL, Lp(a) ≥ 60 mg/dL, and coronary or other artery disease.
PCSK9 inhibitors have shown a reduction in major cardiovascular events in patients who have established coronary artery disease and high Lp(a) levels, albeit with limited data. Unlike statins, which increase Lp(a) levels, PCSK9 inhibitors reduce Lp(a) levels.2 There are promising early results in a phase 2 trial of the oral drug muvalaplin lowering Lp(a) levels by up to 85% for the highest dose, but there are no peer-reviewed articles confirming these results and no outcome trials at this time.
In patients who are already recognized as high risk, especially those with established coronary artery disease, measuring Lp(a) levels offer little benefit. These patients should already be receiving aggressive medical therapy to reach blood pressure targets if hypertensive, maximal lifestyle modifications, and statin therapy.
If these patients need more therapy because of continued coronary events, despite maximal conventional medical therapy, then adding a PCSK9 inhibitor would be appropriate whether or not a patient has a high Lp(a) level. Once Lp(a) targeted therapies are available and show clinical benefit, then the role of Lp(a) measurement and treatment in this population will be clearer.
Pearl: Most patients do not need Lp(a) testing. There are no FDA-approved treatments for high Lp(a) levels.
Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.
References
1. Kronenberg F et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: A European Atherosclerosis Society consensus statement. Eur Heart J. 2022;43:3925-46.
2. Ruscica M et al. Lipoprotein(a) and PCSK9 inhibition: Clinical evidence Eur Heart J Suppl 2020;Nov 18(Suppl L):L53–L56.