Morbid obesity remains most common cause of high output failure. The prevalence of the obesity is growing when two-thirds of American adults already are overweight or obese. Obesity is the risk factor for heart disease and eventually leads to heart failure. High output heart failure is common in obese patients and is characterized by high cardiac output, decreased systemic vascular resistance, and increased oxygen consumption. It often occurs in patients with chronic severe anemia, hyperthyroidism, pregnancy, arterial-venous fistulas, and liver disease. However, the pathogenesis of obesity-related high output heart failure is not fully understood. The clinical management of obesity-related high output heart failure follows conventional heart failure regimens due to lack of specific clinical recommendations. This article reviews the possible pathophysiological mechanisms and causes that contribute to obesity-related high output heart failure. This review also focuses on the implications for clinical practice and future research involved with omics technologies to explore possible molecular pathways associated with obesity-related high output heart failure.
Heart failure with preserved ejection fraction (HFpEF) currently represents approximately 50% of heart failure (HF) cases in the USA and is increasingly recognized as a leading cause of morbidity and mortality. Recent data suggest that the prevalence of HFpEF relative to HF with reduced ejection fraction (HFrEF) is increasing at a rate of 1% per year. With an aging population and increasing risk factors such as hypertension, obesity, and diabetes mellitus, HFpEF will soon be the most prevalent HF phenotype. Two-dimensional speckle-tracking echocardiography (STE) has been used to diagnose HFpEF specifically by focusing on the longitudinal systolic function of the left ventricle (LV). Yet there are many patients with HFpEF in whom there are no differences in LV global longitudinal systolic strain, but there are changes in left atrial function and structure. There are several proposed pathophysiological mechanisms for HFpEF such as endothelial dysfunction, interactions among proteins, signaling pathways, and myocardial bioenergetics. Yet only one specific therapy, mineralocorticoid receptor antagonist, spironolactone, is recommended as a treatment for patients with HFpEF. However, spironolactone does not address many of the pathophysiologic changes that occur in HFpEF, thus new novel therapeutic agents are needed. With the limited available therapies, clinicians should use STE to assess for the presence of this syndrome in their patients to provide effective diagnosis and management.
Purpose Patients with heart failure with preserved ejection fraction (HFpEF) experience fatigue due to impaired myocardial bioenergetics. Cardiomyocyte function depends on the delivery of adenosine triphosphate (ATP), yet there is no convenient bedside method to measure ATP. The purpose of this study was to develop a point-of-contact measurement of ATP that can be used in a clinical setting. Methods In a laboratory setting, digital finger punctures were conducted using 5 μl and 10 μl of capillary blood placed into various amounts of water (H2O). After mixing the solution for 10 s, a Hygiena AquaSnapTM Free ATP probe was placed into the solution for 10 s for the detection of ATP. The probe was then placed into the Hygiena luminometer for 15 s, and a value in relative light units (RLU) was obtained. Results Test samples using 10 μl of blood diluted from 50 to 500 mls of H2O produced ATP readings of 10,000-7569 RLUs. Using 5 μl of blood in 375–900 ml of H2O decreased the ATP values to 6459-4189 RLUs. Dilutional volume sparing experiments were conducted with ATP standards to determine the concentration of ATP per RLUs. Conclusion Patients with HFpEF have increased metabolic demand and impaired myocardial bioenergetics. Thus, identifying a method to measure ATP that is quick and accurate is imperative to accurately assess cellular energy production in this population. Point-of-contact measures, such as ATP, are needed for precision-guided treatment. Data from this study provides the first step toward developing evidence for health policies related to managing fatigue.
In this review article, we briefly describe the status of treatment options for HFpEF and the role of mitochondrial dysfunction in the pathogenesis of HFpEF as an alternative therapeutic target. We also examine the mechanisms of D-ribose in cellular energy production and discuss the potential disadvantages and benefits of supplemental use of D-ribose in patients with HFpEF.Background: Heart failure is a major cardiovascular disease that impacts over 6 million Americans and is one of the leading causes for morbidity and mortality. Patients with heart failure often experience shortness of breath and fatigue along with impaired physical capacity, all leading to poor quality of life. As a subtype of heart failure, heart failure with preserved ejection fraction (HFpEF) is characterized with impaired diastolic function. Currently, there are no effective treatments specifically for HFpEF, thus clinicians and researchers are searching for therapies to improve cardiac function. Emerging evidence indicate that mitochondrial dysfunction and impaired cardiac bioenergetics are among the underlying mechanisms for HFpEF. There is increased interest in investigating the use of supplements such as D-ribose to enhance mitochondrial function and improve production of adenosine triphosphate (ATP).
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