A well-known side effect of statin therapy is myopathy. We report a case of statin induced necrotizing autoimmune myopathy, a rare variant of statin-induced myopathy. A 64-year-old gentleman on atorvastatin presented with muscle weakness. Initial laboratory results showed elevated liver function tests, a creatine phosphokinase (CPK) of 8200 IU/L, and positive urine myoglobin. Despite discontinuing atorvastatin, his CPK remained persistently elevated. Muscle biopsy was consistent with necrotizing myopathy. Anti-HMG CoA reductase antibody was strongly positive. Steroids followed by intravenous immunoglobulin were given. The patient's muscle weakness, CPK, and liver functions gradually improved, and he was eventually discharged on oral steroids. Statin induced necrotizing autoimmune myopathy should be considered when discontinuing statin does not lead to muscle recovery and improvement in CPK. Diagnosis is confirmed by positive anti-HMG-CoA reductase autoantibody.

Ivabradine is a heart rate-lowering agent that inhibits pacemaker funny current (I f ). It has been approved by the European Medicines Agency and the US Food and Drug Administration for patients with stable angina and heart failure (HF). AF is a common issue especially in ischaemic heart disease and HF patients. In contrast to experimental findings and a limited number of clinical trials that demonstrate the emerging role of ivabradine for heart rate control in AF or maintenance of sinus rhythm, there is accumulating contradictory data indicating that there is, in fact, an increased incidence of new-onset AF among people who are taking ivabradine in clinical practice. This article reviews the most recent evidence highlighting the diversity of data in relation to the use of ivabradine and the onset of AF and whether it has a legitimate role in AF treatment and the maintenance of sinus rhythm.