Key Differences Found in Heart Failure Types Cedars-Sinai Skip to content Close Select your preferred language English عربى 简体中文 繁體中文 فارسي עִברִית 日本語 한국어 Русский Español Tagalog English English عربى 简体中文 繁體中文 فارسي עִברִית 日本語 한국어 Русский Español Tagalog Translation is unavailable for Internet Explorer Cedars-Sinai Home 1-800-CEDARS-1 1-800-CEDARS-1 Close Find a Doctor Locations Programs & Services Health Library Patient & Visitors Community My CS-Link RESEARCH clear Go Close Navigation Links Academics Faculty Development Community Engagement Calendar Research Research Areas Research Labs Departments & Institutes Find Clinical Trials Research Cores Research Administration Basic Science Research Clinical & Translational Research Center (CTRC) Technology & Innovations News & Breakthroughs Education Graduate Medical Education Continuing Medical Education Graduate School of Biomedical Sciences Professional Training Programs Medical Students Campus Life Office of the Dean Simulation Center Medical Library Program in the History of Medicine About Us All Education Programs Departments & Institutes Faculty Directory 2020 Research News Back to 2020 Research News Key Differences Found in Heart Failure Types A recent Cedars-Sinai study found fundamental differences in the cellular function of two major types of heart failure. The research, performed using laboratory rats, may help explain why existing treatments for heart failure fail to improve cardiac function in certain patients. A recent Cedars-Sinai study found fundamental differences in the cellular function of two major types of heart failure. The research, performed using laboratory rats, may help explain why existing treatments for heart failure fail to improve cardiac function in certain patients. The study, published online Aug. 23 in The Journal of Physiology, compared heart failure with preserved ejection fraction and heart failure with reduced ejection fraction. The latter is also referred to as dilated cardiomyopathy or just heart failure. Ejection fraction refers to the volume of blood that the heart can pump out to the body when it beats. "Currently there are no effective treatments for heart failure with preserved ejection fraction, which accounts for about 50% of heart failure cases," said Joshua Goldhaber, MD, Dorothy and E. Phillip Lyon Chair in Laser Research in the Smidt Heart Institute at Cedars-Sinai, professor of Cardiology and corresponding and senior author of the study. In heart failure with reduced ejection fraction, a weakened and dilated left ventricular chamber can't pump out enough blood to the body. In heart failure with preserved ejection fraction, a stiffened left ventricle can't fill up with enough blood. The latter type strikes women more than men. Both types of heart failure cause shortness of breath and fatigue. Heart failure was reported to be the contributing cause of one in eight deaths in the U.S. in 2017 by the U.S. Centers for Disease Control and Prevention. Previous studies have shown that abnormal regulation of calcium inside heart cells contributes to weak heart contraction in heart failure with reduced ejection fraction. But ,Goldhaber said, " The cellular mechanisms responsible for heart failure with preserved ejection fraction, particularly those involving regulation of cellular calcium, are not well understood. So this was a focus of our study." For the recent study, one group of an inbred strain of salt-sensitive rats was fed high-salt diets to induce high blood pressure, leading to human-type heart failure with preserved ejection fraction, and the other group underwent procedures to induce heart failure with reduced ejection fraction. Joshua Goldhaber, MD After analyzing the heart tissues of each group, the investigators found differences in how each disease affected the heart's reaction to molecules that initiate and help regulate how effectively the heart pumps and relaxes: The contraction triggered by the electrical activity of the heart was impaired in heart failure with reduced ejection fraction but enhanced in heart failure with preserved ejection fraction. Calcium movements inside the cell that link the electrical trigger to contraction were compromised in heart failure with reduced ejection fraction but were not in heart failure with preserved ejection fraction. The β-adrenergic response, which is how the body responds to the molecules that can strengthen contraction and improve relaxation, was seriously impaired in heart failure preserved ejection fraction. "The results highlight fundamental differences in how the contraction and relaxation processes work in these two types of heart failure," said Goldhaber. "Additionally, the blunted cellular response to β-adrenergic stimulation is a significant finding in the heart failure with preserved ejection fraction subjects." Eduardo Marbán, MD, PhD, executive director of the Smidt Heart Institute at Cedars-Sinai, professor of Cardiology and a co-author of the study, said the study was "very important as it rationalizes how heart failure with preserved and reduced ejection fraction differ at a cellular level. The findings may help explain why therapies that work in heart failure with reduced ejection fraction patients are ineffective in those with preserved ejection fraction heart failure." Peter J. Kilfoil, PhD, a postdoctoral scientist in Goldhaber's laboratory, was the first author of the study. The other co-authors were Eugenio Cingolani, MD, director of Cardiogenetics and assistant professor of Cardiology; Rui Zhang, MD, a project scientist in the lab; and Sabine Lotteau, PhD, a postdoctoral scientist in the lab. Funding: Research reported in this publication was supported by the Department of Defense and by the National Institutes of Health under award numbers T32 HL116273, HL048509 and HL147570. The IACUC number for animal subjects in research referenced in this article is 005280. Please ensure Javascript is enabled for purposes of website accessibility