Study Shows Statins May Help Reduce Dementia Risk in Heart Failure Patients

 

Dementia is a major concern for older individuals, affecting approximately 46.8 million people globally. Similarly, over 64 million individuals worldwide are dealing with the burden of heart failure (HF), and its prevalence is on the rise.

Heart failure and dementia share common pathological mechanisms and risk factors, with some studies suggesting that HF may play a role in the development of dementia.

As a result, the focus of research on HF outcomes has shifted towards non-cardiovascular comorbidities, placing dementia at the forefront.

However, there is a lack of studies exploring intervention strategies to address the burden of dementia in HF patients.

Several meta-analyses have shown that statin use is associated with a lower risk of all-cause dementia in a dose-response manner. Statins achieve this by lowering lipid levels, reducing inflammation, and affecting amyloid precursor proteins.

Previous studies have rarely evaluated the impact of statin use on dementia incidence among HF patients, especially in Asian patients, which could be clinically relevant.

About the Study: For this retrospective cohort study, researchers searched for all patients aged 18 years and above with HF as the primary diagnosis between 2004 and 2018, using the Clinical Data Analysis.

Out of 104,295 patients meeting the criteria, 54,004 were statin users and 50,291 were non-users after the index date, i.e., the date of the first HF diagnosis. The study analyzed the use of four types of statins and their effects on the risks of three types of dementia: Alzheimer's disease (AD), vascular dementia, and unspecified dementia.

Patients were categorized based on their low-density lipoprotein-cholesterol (LDL-C) levels to calculate their time-weighted average LDL-C level, helping researchers understand the impact of lipid control on the association between statin use and dementia risks in HF patients.

The study followed STROBE reporting guidelines, presenting variables as mean and standard deviation for continuous variables and count and percentage for categorical variables.

Results: Over an average follow-up of 9.9 years, 10,031 patients had dementia, with 2,250 having AD, 1,831 having vascular dementia, and 5,950 having unspecified dementia.

Statin users showed a 20% lower risk of dementia compared to non-users after multivariable adjustment. Statin use also lowered the risk of AD, vascular dementia, and unspecified dementia by 28%, 18%, and 20%, respectively, compared to non-users. Additionally, statin use reduced the risk of all-cause mortality by 30%.

A serum time-weighted LDL-C between 1.8 and 2.6 mmol/L or >2.6 mmol/L increased dementia risk by 21% or 51% more than a time-weighted LDL-C of <1.8 mmol/L, emphasizing the need for lipid-lowering therapies.

In subgroup analyses, statin users with less than primary education had the lowest dementia risk. The study results remained robust in sensitivity analyses.

Conclusions: This study demonstrates that statin use significantly lowers the risk of all-cause dementia and its subtypes in HF patients. Future research should focus on further validating its neuroprotective potential.