Statins, Muscle Disease and Mitochondria.

Area of Science:

• Cardiology and Pharmacology
• Biochemistry and Molecular Biology

Background:

• Cardiovascular disease (CVD) causes millions of deaths annually, with dyslipidemia a key factor in atherosclerosis.
• Statins are primary treatments for dyslipidemia, offering significant benefits despite potential adverse events.
• Statin-associated muscle disease (SAMS) is the most frequent reason for statin discontinuation, with varying reported incidences.

Purpose of the Study:

• To review the current understanding of the pathophysiology and mechanisms behind statin-associated muscle disease (SAMS).
• To focus on etiological hypotheses related to mitochondrial dysfunction as the likely cause of SAMS.

Main Methods:

• Literature review of studies investigating statin-associated muscle disease (SAMS).
• Analysis of proposed etiological hypotheses, with a focus on mitochondrial dysfunction.

Main Results:

• Statin-associated muscle disease (SAMS) incidence ranges from 5% to 29%, with severe rhabdomyolysis being rare (approx. 1 in 10,000).
• Mitochondrial dysfunction is implicated as the most probable cause of SAMS.
• The precise mechanisms leading to statin-induced mitochondrial dysfunction remain under investigation.

Conclusions:

• Understanding the mechanisms of SAMS is crucial for optimizing statin therapy.
• Further research into statin-induced mitochondrial dysfunction is needed to elucidate SAMS pathophysiology.
• This review highlights key hypotheses regarding mitochondrial dysfunction in SAMS development.