Case Presentation: A 71-year-old female patient with a medical history of coronary artery disease (CAD), hypertension (HTN), and mixed hyperlipidemia presented to our medical facility, reporting chest pain. She underwent a left heart catheterization, revealing significant stenosis in the proximal right coronary artery (RCA), which was successfully treated with percutaneous transluminal coronary angioplasty (PTCA) and the placement of a drug-eluting stent. Additionally, during the procedure, she was found to have 50-70% ostial diagonal artery stenosis and opted for medical management. Her medication regimen included Aspirin 81 mg, Clopidogrel 75 mg, and a low dose of Atorvastatin 10 mg.The patient had previously tried Atorvastatin in 2018 at a higher dose of 80 mg but experienced myalgia and discontinued it after three weeks. Therefore, this time, a lower dose of 10 mg was prescribed. After three weeks on this medication, she reported experiencing the same symptoms she had encountered a few years prior. She ceased taking the statin after this period. Initially, she developed generalized myalgia, which did not improve upon discontinuation but instead progressed. Consequently, she was referred to rheumatology for further evaluation to rule out other potential causes of myopathy. During the evaluation process, her condition deteriorated to the point where she became generally weak and reliant on a cane for mobility, ultimately losing the ability to walk. Initial creatine kinase (CK) levels were elevated at 7528 and increased to 9492 despite discontinuing Atorvastatin. Aldolase levels were measured at 90.7. A comprehensive workup for alternative causes of myositis was conducted, which was negative and only HMG-CoA reductase antibody (HMGCR Ab) was positive.
Discussion: In our specific case, the patient had previously been prescribed statins a few years before her current presentation. When she experienced proximal muscle weakness, she discontinued the statin medication, resulting in the resolution of her muscle weakness. Subsequently, after encountering an atherosclerotic event and undergoing stent placement, an attempt was made to use a lower dose of atorvastatin. However, while on atorvastatin, she developed myalgias and muscle weakness, which progressed to a severe decline in her ability to walk, almost reaching a state of paralysis. Extensive diagnostic investigations were undertaken, encompassing muscle biopsy and autoimmune testing, revealing a positive result for HMG-CoA receptor antibodies. Notably, the patient’s creatine phosphokinase (CPK) levels were initially elevated and continued to rise, even after discontinuing statins. The CPK levels reached their peak within three weeks but returned to a normal range over the course of three months.
Conclusions: Immediate clinical assessment is imperative when a patient presents with complaints of proximal muscle weakness while undergoing statin therapy, and it is crucial to promptly measure their creatine phosphokinase (CPK) levels. Furthermore, we conclude that for patients who have previously experienced intolerance to statins, rather than attempting an alternative statin class or a reduced dosage.