4 RRJNHS| Volume 2 | Issue 2 | June, 2016 Research & Reviews: Journal of Nursing & Health Sciences Effects of Ubiquinol in Reducing the Development of Heart Failure with Preserved Ejection Fraction and Mitochondrial Injury Qiuhua Shen 1 , John B. Hiebert 2 , Amanda R. Thimmesch 3 *, Richard L. Clancy 4 , Janet D. Pierce 5 1 Assistant Professor, University of Kansas, School of Nursing, 3901 Rainbow Blvd, Kansas City, KS 66160, USA 2 Cardiologist, University of Kansas, School of Nursing, 3901 Rainbow Blvd, Kansas City, KS 66160, USA 3 Research Associate, University of Kansas, School of Nursing, 3901 Rainbow Blvd, Kansas City, KS 66160, USA 4 Physiologist, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160, USA 5 Christine A. Hartley Endowed Professor of Nursing, University of Kansas, School of Nursing 3901 Rainbow Blvd, Kansas City, KS 66160, USA Research Article INTRODUCTION Heart failure is a progressive deteriorating disease and the leading cause of morbidity and mortality in the U.S. The prevalence of heart failure is gradually increasing and it is estimated that there will be 8.0 million US adults who have heart failure by 2030 [1] . More than 50% of heart failure patients have preserved ejection fraction (HFpEF) in which impaired cardiac muscle relaxation and diastolic flling are the hallmarks [1,2] . Many cardiovascular abnormalities and peripheral impairments contribute to the heterogeneity of HFpEF. Currently, there are no specifc treatments available for HFpEF that demonstrates effectiveness in reducing morbidity and mortality. Without suitable treatments and management, patients with HFpEF are at high risk of hospitalization and readmission resulting in signifcant suffering and healthcare costs [3] . Research has shown that left ventricular diastolic dysfunction or relaxation abnormalities contribute to the development of HFpEF, when compensatory mechanisms fail. These abnormalities are associated with, and have been attributed to hypertension. Cellular energetic impairment or decreased intracellular adenosine triphosphate (ATP) production in the heart can lead to diastolic dysfunction by affecting the disassociation ABSTRACT There is currently no effective clinical treatment for diastolic heart failure also termed heart failure with preserved ejection fraction (HFpEF) which is associated with reduced myocardial adenosine triphosphate. Ubiquinol in the electron chain is required for adenosine triphosphate synthesis. Thus, the purpose of this pilot study was to examine in a rat model the effects of ubiquinol (reduced form of Coenzyme Q10) in the development of HFpEF. Six Dahl salt-sensitive rats were randomly assigned to either control or experimental groups. Starting at the age of 7 weeks, all rats were fed 8% NaCl diet and water for 12 weeks. The rats in the experimental group were fed ubiquinol (2 mg/100 g) in the water. Blood pressures, heart rate, and echocardiographic data were obtained at baseline and at the end of experiment. Rats in the ubiquinol group had lower increases in blood pressures and left ventricular wall thickness. Heart rate variability was not signifcantly different although there was a decrease in heart rate and an increase in parasympathetic nervous system output in the ubiquinol group. There was also less cardiac mitochondrial damage in the ubiquinol group compared to the control rats. Though the sample size is small, the supplementation of ubiquinol appears to reduce blood pressure and myocardial mitochondrial injury. Received date: 20/04/2016 Accepted date: 23/05/2016 Published date: 31/05/2016 *For Correspondence University of Kansas, School of Nursing, 3901 Rainbow Blvd, Mail Stop 4043,Kansas City , Kansas 66160, United States, Tel: 913-588-4336. E-mail: athimmesch@kumc.edu Keywords: Heart failure, Coenzyme Q10, Ubiquinol, Mitochondrial damage.