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Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.
Statins Are Not Bad For the Liver
When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.
But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).1 A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.2 Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.
In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.3 The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.4
Statins Do Not Cause Muscle Pain in Most Patients
Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.5 Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.
Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.6 Muscle-related side effects were reported by 60% of former statin users and 25% of current users.
Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.7 Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.
Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.8 Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
Statins Are Likely Helpful In the Very Elderly
Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.
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. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.
2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.
3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.
4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.
5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.
6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.
7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.
8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.
9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.
Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.
Statins Are Not Bad For the Liver
When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.
But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).1 A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.2 Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.
In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.3 The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.4
Statins Do Not Cause Muscle Pain in Most Patients
Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.5 Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.
Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.6 Muscle-related side effects were reported by 60% of former statin users and 25% of current users.
Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.7 Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.
Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.8 Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
Statins Are Likely Helpful In the Very Elderly
Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.
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. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.
2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.
3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.
4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.
5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.
6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.
7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.
8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.
9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.
Recently, a patient of mine was hospitalized with chest pain. She was diagnosed with an acute coronary syndrome and started on a statin in addition to a beta-blocker, aspirin, and clopidogrel. After discharge, she had symptoms of dizziness and recurrent chest pain and her first thought was to stop the statin because she believed that her symptoms were statin-related side effects. I will cover a few areas where I think that there are some misunderstandings about statins.
Statins Are Not Bad For the Liver
When lovastatin first became available for prescription in the 1980s, frequent monitoring of transaminases was recommended. Patients and healthcare professionals became accustomed to frequent liver tests to monitor for statin toxicity, and to this day, some healthcare professionals still obtain liver function tests for this purpose.
But is there a reason to do this? Pfeffer and colleagues reported on the results of over 112,000 people enrolled in the West of Scotland Coronary Protection trial and found that the percentage of patients with any abnormal liver function test was similar (> 3 times the upper limit of normal for ALT) for patients taking pravastatin (1.4%) and for patients taking placebo (1.4%).1 A panel of liver experts concurred that statin-associated transaminase elevations were not indicative of liver damage or dysfunction.2 Furthermore, they noted that chronic liver disease and compensated cirrhosis were not contraindications to statin use.
In a small study, use of low-dose atorvastatin in patients with nonalcoholic steatohepatitis improved transaminase values in 75% of patients and liver steatosis and nonalcoholic fatty liver disease activity scores were significantly improved on biopsy in most of the patients.3 The US Food and Drug Administration (FDA) removed the recommendation for routine regular monitoring of liver function for patients on statins in 2012.4
Statins Do Not Cause Muscle Pain in Most Patients
Most muscle pain occurring in patients on statins is not due to the statin although patient concerns about muscle pain are common. In a meta-analysis of 19 large statin trials, 27.1% of participants treated with a statin reported at least one episode of muscle pain or weakness during a median of 4.3 years, compared with 26.6% of participants treated with placebo.5 Muscle pain for any reason is common, and patients on statins may stop therapy because of the symptoms.
Cohen and colleagues performed a survey of past and current statin users, asking about muscle symptoms.6 Muscle-related side effects were reported by 60% of former statin users and 25% of current users.
Herrett and colleagues performed an extensive series of n-of-1 trials involving 200 patients who had stopped or were considering stopping statins because of muscle symptoms.7 Participants received either 2-month blocks of atorvastatin 20 mg or 2-month blocks of placebo, six times. They rated their muscle symptoms on a visual analogue scale at the end of each block. There was no difference in muscle symptom scores between the statin and placebo periods.
Wood and colleagues took it a step further when they planned an n-of-1 trial that included statin, placebo, and no treatment.8 Each participant received four bottles of atorvastatin 20 mg, four bottles of placebo, and four empty bottles. Each month they used treatment from the bottles based on a random sequence and reported daily symptom scores. The mean symptom intensity score was 8.0 during no-tablet months, 15.4 during placebo months (P < .001, compared with no-tablet months), and 16.3 during statin months (P < .001, compared with no-tablet months; P = .39, compared with placebo).
Statins Are Likely Helpful In the Very Elderly
Should we be using statins for primary prevention in our very old patients? For many years the answer was generally “no” on the basis of a lack of evidence. Patients in their 80s often were not included in clinical trials. The much used American Heart Association risk calculator stops at age 79. Given the prevalence of coronary artery disease in patients as they reach their 80s, wouldn’t primary prevention really be secondary prevention? Xu and colleagues in a recent study compared outcomes for patients who were treated with statins for primary prevention with a group who were not. In the patients aged 75-84 there was a risk reduction for major cardiovascular events of 1.2% over 5 years, and for those 85 and older the risk reduction was 4.4%. Importantly, there were no significantly increased risks for myopathies and liver dysfunction in either age group.
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. He is a member of the editorial advisory board of Internal Medicine News. Dr. Paauw has no conflicts to disclose. Contact him at imnews@mdedge.com.
References
1. Pfeffer MA et al. Circulation. 2002;105(20):2341-6.
2. Cohen DE et al. Am J Cardiol. 2006;97(8A):77C-81C.
3. Hyogo H et al. Metabolism. 2008;57(12):1711-8.
4. FDA Drug Safety Communication: Important safety label changes to cholesterol-lowering statin drugs. 2012 Feb 28.
5. Cholesterol Treatment Trialists’ Collaboration. Lancet. 2022;400(10355):832-45.
6. Cohen JD et al. J Clin Lipidol. 2012;6(3):208-15.
7. Herrett E et al. BMJ. 2021 Feb 24;372:n1355.
8. Wood FA et al. N Engl J Med. 2020;383(22):2182-4.
9. Xu W et al. Ann Intern Med. 2024;177(6):701-10.