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What To Do With Lipoprotein(a)?
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.
Does this patient have bacterial conjunctivitis?
A 54-year-old pharmacist with a history of gout, hypertension, and conjunctivitis presents for evaluation of pink eye in the summer. The morning before coming into the office, he noticed that his right eye was red and inflamed. He self-treated with saline washes and eye drops, but upon awakening the next day, he found his right eye to be crusted shut with surrounding yellow discharge. He has not had any changes to his vision but endorses a somewhat uncomfortable, “gritty” sensation. He reports no recent cough, nasal congestion, or allergies, and he has not been around any sick contacts. His blood pressure is 102/58 mm Hg, pulse is 76 bpm, and body mass index is 27.3 kg/m2. His eye exam reveals unilateral conjunctival injections but no hyperemia of the conjunctiva adjacent to the cornea. Mucopurulent discharge was neither found on the undersurface of the eyelid nor emerging from the eye. Which of the following is the best treatment for this patient’s condition?
A) Erythromycin 5 mg/gram ophthalmic ointment.
B) Ofloxacin 0.3% ophthalmic drops.
C) Antihistamine drops.
D) Eye lubricant drops.
E) No treatment necessary.
This patient is an adult presenting with presumed conjunctivitis. Because he is presenting in the summer without observed purulent discharge, his condition is unlikely to be bacterial. This patient does not need treatment, although eye lubricant drops could reduce his discomfort.
After ruling out serious eye disease, clinicians need to determine which cases of suspected conjunctivitis are most likely to be bacterial to allow for judicious use of antibiotic eye drops. This is an important undertaking as most patients assume that antibiotics are needed.
How do we know which history and clinical exam findings to lean on when attempting to categorize conjunctivitis as bacterial or not? If a patient reports purulent discharge, doesn’t that mean it is bacterial? Surprisingly, a systematic review published in 2016 by Narayana and McGee found that a patient’s self-report of “purulent drainage” is diagnostically unhelpful, but if a clinician finds it on exam, the likelihood of a bacterial etiology increases.3
Narayana and McGee analyzed three studies that enrolled a total of 281 patients with presumed conjunctivitis who underwent bacterial cultures. They then determined which findings increased the probability of positive bacterial culture. From strongest to weakest, the best indicators of a bacterial cause were found to be: complete redness of the conjunctival membrane obscuring tarsal vessels (the vessels visible on the inside of everted upper or lower eyelids) (likelihood ratio, 4.6), observed purulent discharge (LR, 3.9), matting of both eyes in the morning (LR, 3.6), and presence during winter/spring months (LR, 1.9). On the other hand, failure to observe a red eye at 20 feet (LR, 0.2), absence of morning gluing of either eye (LR, 0.3), and presentation during summer months (LR, 0.4) all decreased the probability of a bacterial cause. This review and different study by Stenson et al. unfortunately have conflicting evidence regarding whether the following findings are diagnostically helpful: qualities of eye discomfort (such as burning or itching), preauricular adenopathy, conjunctival follicles, and conjunctival papillae.3,4 Rietveld and colleagues found that a history of conjunctivitis decreased the likelihood of bacterial conjunctivitis.5
Ultimately, if the former indicators are kept in mind, primary care clinicians should be able to decrease the prescribing of topical antimicrobials to patients with non-bacterial conjunctivitis.
Pearl: The best indicators of a bacterial cause in patients with presumed conjunctivitis are complete redness of the conjunctival membrane obscuring tarsal vessels, observed purulent discharge, and matting of both eyes in the morning. Presentation during the summer months and having a history of conjunctivitis decreases the likelihood of bacterial conjunctivitis.
Ms. Momany is a fourth-year medical student at University of Washington, Seattle. Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington and serves as third-year medical student clerkship director at that university. Contact Dr. Paauw at imnews@mdedge.com.
References
1. Azari AA and Barney NP. JAMA. 2013 Oct 23; 310(16):1721-9.
2. Smith AF and Waycaster C. BMC Ophthalmol. 2009 Nov 25. doi: 10.1186/1471-2415-9-13.
3) Narayana S and McGee S. Am J Med. 2015;128(11):1220-4.e1.
4) Stenson S et al. Arch Ophthalmol. 1982;100(8):1275-7.
5) Rietveld RP et al. BMJ. 2004 Jul 24;329(7459):206-10.
A 54-year-old pharmacist with a history of gout, hypertension, and conjunctivitis presents for evaluation of pink eye in the summer. The morning before coming into the office, he noticed that his right eye was red and inflamed. He self-treated with saline washes and eye drops, but upon awakening the next day, he found his right eye to be crusted shut with surrounding yellow discharge. He has not had any changes to his vision but endorses a somewhat uncomfortable, “gritty” sensation. He reports no recent cough, nasal congestion, or allergies, and he has not been around any sick contacts. His blood pressure is 102/58 mm Hg, pulse is 76 bpm, and body mass index is 27.3 kg/m2. His eye exam reveals unilateral conjunctival injections but no hyperemia of the conjunctiva adjacent to the cornea. Mucopurulent discharge was neither found on the undersurface of the eyelid nor emerging from the eye. Which of the following is the best treatment for this patient’s condition?
A) Erythromycin 5 mg/gram ophthalmic ointment.
B) Ofloxacin 0.3% ophthalmic drops.
C) Antihistamine drops.
D) Eye lubricant drops.
E) No treatment necessary.
This patient is an adult presenting with presumed conjunctivitis. Because he is presenting in the summer without observed purulent discharge, his condition is unlikely to be bacterial. This patient does not need treatment, although eye lubricant drops could reduce his discomfort.
After ruling out serious eye disease, clinicians need to determine which cases of suspected conjunctivitis are most likely to be bacterial to allow for judicious use of antibiotic eye drops. This is an important undertaking as most patients assume that antibiotics are needed.
How do we know which history and clinical exam findings to lean on when attempting to categorize conjunctivitis as bacterial or not? If a patient reports purulent discharge, doesn’t that mean it is bacterial? Surprisingly, a systematic review published in 2016 by Narayana and McGee found that a patient’s self-report of “purulent drainage” is diagnostically unhelpful, but if a clinician finds it on exam, the likelihood of a bacterial etiology increases.3
Narayana and McGee analyzed three studies that enrolled a total of 281 patients with presumed conjunctivitis who underwent bacterial cultures. They then determined which findings increased the probability of positive bacterial culture. From strongest to weakest, the best indicators of a bacterial cause were found to be: complete redness of the conjunctival membrane obscuring tarsal vessels (the vessels visible on the inside of everted upper or lower eyelids) (likelihood ratio, 4.6), observed purulent discharge (LR, 3.9), matting of both eyes in the morning (LR, 3.6), and presence during winter/spring months (LR, 1.9). On the other hand, failure to observe a red eye at 20 feet (LR, 0.2), absence of morning gluing of either eye (LR, 0.3), and presentation during summer months (LR, 0.4) all decreased the probability of a bacterial cause. This review and different study by Stenson et al. unfortunately have conflicting evidence regarding whether the following findings are diagnostically helpful: qualities of eye discomfort (such as burning or itching), preauricular adenopathy, conjunctival follicles, and conjunctival papillae.3,4 Rietveld and colleagues found that a history of conjunctivitis decreased the likelihood of bacterial conjunctivitis.5
Ultimately, if the former indicators are kept in mind, primary care clinicians should be able to decrease the prescribing of topical antimicrobials to patients with non-bacterial conjunctivitis.
Pearl: The best indicators of a bacterial cause in patients with presumed conjunctivitis are complete redness of the conjunctival membrane obscuring tarsal vessels, observed purulent discharge, and matting of both eyes in the morning. Presentation during the summer months and having a history of conjunctivitis decreases the likelihood of bacterial conjunctivitis.
Ms. Momany is a fourth-year medical student at University of Washington, Seattle. Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington and serves as third-year medical student clerkship director at that university. Contact Dr. Paauw at imnews@mdedge.com.
References
1. Azari AA and Barney NP. JAMA. 2013 Oct 23; 310(16):1721-9.
2. Smith AF and Waycaster C. BMC Ophthalmol. 2009 Nov 25. doi: 10.1186/1471-2415-9-13.
3) Narayana S and McGee S. Am J Med. 2015;128(11):1220-4.e1.
4) Stenson S et al. Arch Ophthalmol. 1982;100(8):1275-7.
5) Rietveld RP et al. BMJ. 2004 Jul 24;329(7459):206-10.
A 54-year-old pharmacist with a history of gout, hypertension, and conjunctivitis presents for evaluation of pink eye in the summer. The morning before coming into the office, he noticed that his right eye was red and inflamed. He self-treated with saline washes and eye drops, but upon awakening the next day, he found his right eye to be crusted shut with surrounding yellow discharge. He has not had any changes to his vision but endorses a somewhat uncomfortable, “gritty” sensation. He reports no recent cough, nasal congestion, or allergies, and he has not been around any sick contacts. His blood pressure is 102/58 mm Hg, pulse is 76 bpm, and body mass index is 27.3 kg/m2. His eye exam reveals unilateral conjunctival injections but no hyperemia of the conjunctiva adjacent to the cornea. Mucopurulent discharge was neither found on the undersurface of the eyelid nor emerging from the eye. Which of the following is the best treatment for this patient’s condition?
A) Erythromycin 5 mg/gram ophthalmic ointment.
B) Ofloxacin 0.3% ophthalmic drops.
C) Antihistamine drops.
D) Eye lubricant drops.
E) No treatment necessary.
This patient is an adult presenting with presumed conjunctivitis. Because he is presenting in the summer without observed purulent discharge, his condition is unlikely to be bacterial. This patient does not need treatment, although eye lubricant drops could reduce his discomfort.
After ruling out serious eye disease, clinicians need to determine which cases of suspected conjunctivitis are most likely to be bacterial to allow for judicious use of antibiotic eye drops. This is an important undertaking as most patients assume that antibiotics are needed.
How do we know which history and clinical exam findings to lean on when attempting to categorize conjunctivitis as bacterial or not? If a patient reports purulent discharge, doesn’t that mean it is bacterial? Surprisingly, a systematic review published in 2016 by Narayana and McGee found that a patient’s self-report of “purulent drainage” is diagnostically unhelpful, but if a clinician finds it on exam, the likelihood of a bacterial etiology increases.3
Narayana and McGee analyzed three studies that enrolled a total of 281 patients with presumed conjunctivitis who underwent bacterial cultures. They then determined which findings increased the probability of positive bacterial culture. From strongest to weakest, the best indicators of a bacterial cause were found to be: complete redness of the conjunctival membrane obscuring tarsal vessels (the vessels visible on the inside of everted upper or lower eyelids) (likelihood ratio, 4.6), observed purulent discharge (LR, 3.9), matting of both eyes in the morning (LR, 3.6), and presence during winter/spring months (LR, 1.9). On the other hand, failure to observe a red eye at 20 feet (LR, 0.2), absence of morning gluing of either eye (LR, 0.3), and presentation during summer months (LR, 0.4) all decreased the probability of a bacterial cause. This review and different study by Stenson et al. unfortunately have conflicting evidence regarding whether the following findings are diagnostically helpful: qualities of eye discomfort (such as burning or itching), preauricular adenopathy, conjunctival follicles, and conjunctival papillae.3,4 Rietveld and colleagues found that a history of conjunctivitis decreased the likelihood of bacterial conjunctivitis.5
Ultimately, if the former indicators are kept in mind, primary care clinicians should be able to decrease the prescribing of topical antimicrobials to patients with non-bacterial conjunctivitis.
Pearl: The best indicators of a bacterial cause in patients with presumed conjunctivitis are complete redness of the conjunctival membrane obscuring tarsal vessels, observed purulent discharge, and matting of both eyes in the morning. Presentation during the summer months and having a history of conjunctivitis decreases the likelihood of bacterial conjunctivitis.
Ms. Momany is a fourth-year medical student at University of Washington, Seattle. Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington and serves as third-year medical student clerkship director at that university. Contact Dr. Paauw at imnews@mdedge.com.
References
1. Azari AA and Barney NP. JAMA. 2013 Oct 23; 310(16):1721-9.
2. Smith AF and Waycaster C. BMC Ophthalmol. 2009 Nov 25. doi: 10.1186/1471-2415-9-13.
3) Narayana S and McGee S. Am J Med. 2015;128(11):1220-4.e1.
4) Stenson S et al. Arch Ophthalmol. 1982;100(8):1275-7.
5) Rietveld RP et al. BMJ. 2004 Jul 24;329(7459):206-10.