Introduction: It has been proposed that increased sympathetic nerve play a role in pathogenesis of HFpEF. Recent study suggests that statin use is associated with improved mortality rates in HFpEF patients. Accumulating evidence revealed that lipophilic statins reduced sympathetic nerve activity by crossing the blood-brain barrier in patients with HT and HF with reduced ejection fraction. However, it remains unclear whether hydrophilic statins exert the same effect on sympathetic nerve activity.
Hypothesis: In this study, we evaluated whether atorvastatin inhibited sympathetic nerve activity, compared to rosuvastatin, in HFpEF patients.
Methods: This study was designed as a prospective randomized open-label crossover trial. Fifteen HFpEF (left ventricular ejection fraction (LVEF) >50%, E/E’>10) patients with dyslipidemia, participated in this study. A randomization schedule was used to assign subjects to either the atorvastatin (10 mg) or rosuvastatin group (2.5 mg) with each drug administered as 1 tablet daily for 8 weeks. After the first 8 weeks, the subjects underwent 1-week washout period, followed by taking the alternative drug daily for another 8 weeks. We measured the patients’ blood pressure (BP), heart rate (HR), LVEF, E/E’, low-density lipoprotein cholesterol (LDL), high-density lipoprotein (HDL), triglycerides (TG), and directly recorded muscle sympathetic nerve activity (MSNA), via microneurography.
Results: Atorvastatin and rosuvastatin produced similar reduction of LDL (–51.2±10.5 vs. –42.8±10.5mg/dL; P=0.7, respectively). MSNA was significantly reduced in the atorvastatin compared with the rosuvastatin group (–9.8±3.9 vs. –6.2±3.9 bursts per minute, P<0.05). However, reduction of MSNA did not have a correlation with reduction of LDL (r=0.04, 0.02). No significant difference was observed in terms of the baroreflex control of HR, or MSNA, between the two groups.
Conclusions: Our data show that atorvastatin, compared with rosuvastatin, exerts a favorable effect on sympathetic nerve activity, without affecting baroreflex sensitivity, in HFpEF patients. These results indicate that lipophilic statin, but not hydrophilic statin, might reduce sympathetic nerve activity in HFpEF.