Heart failure is a general term that describes a variety of pathologic causes and contributing factors that result in the inability of the heart to pump sufficient oxygenated blood throughout the body to meet demands. Heart failure may develop rapidly or gradually as a as a consequence of a variety of pathological disease states including structural heart muscle defects, cardiac valve disease, pulmonary disease (eg, right-sided heart failure), coronary artery disease due to atherosclerosis, thyroid disease, and low red blood cells (anemia) to name a few (Foley 2012; Hunt 2009; Heidenreich 2013; Brum 2011; Iwanaga 2010; Ferri 2013).
Heart failure incidence is increasing. While 5.8 million people in the United States were affected by heart failure in 2009, the American Heart Association expects this number to balloon to more than 8 million individuals by 2030. Likewise, healthcare costs associated with heart failure care are projected to more than double in this timeframe, from $31 billion in 2012 to $70 billion by 2030 (Weintraub 2010; Heidenreich 2013; Hunt 2009).
These grim statistics parallel the largely unimpressive conventional medical treatment options for heart failure patients. A prospective 19-year study involving over 13 000 volunteers showed that in men and women without heart failure at baseline, more than 60% of those who subsequently went on to suffer from heart failure later in life did so as a result of atherosclerotic heart disease (He 2001). To this point, Life Extension® has identified at least 17 independent risk factors that must be actively managed if heart attack risk is to be managed optimally, which is of significant importance since prior heart attack due to atherosclerotic coronary artery disease is a major cause for subsequent heart failure. Unfortunately, mainstream medicine frequently addresses only one or two contributing factors for heart attack risk, such as high blood pressure and elevated cholesterol. This leaves aging individuals exposed to the ravages of unchecked heart attack risk factors such as excess homocysteine, insufficient vitamin D, and hormone imbalance & deficiency. This deadly oversight is a fundamental reason cardiovascular disease continues to plague so many Americans (Faloon 2009).
For example, a major gap in conventional heart failure care is neglect for the critical role that testosterone plays in cardiovascular health and the potential for testosterone replacement therapy to improve symptoms in heart failure patients. An estimated 25–30% of men with heart failure have low testosterone levels, but this easily correctable risk factor is overlooked by many mainstream physicians (Malkin 2006; Malkin 2010; Giagulli 2013). A comprehensive review of published studies revealed that testosterone replacement therapy for up to 52 weeks in men with heart failure resulted in a significant improvement in functional capacity compared to placebo (Toma 2012). These results led the researchers to remark “Given the unmet clinical needs, testosterone appears to be a promising therapy to improve functional capacity in patients with [heart failure].”
In contrast to the relatively unimpressive conventional treatment options for heart failure patients, a major breakthrough in heart failure research came in 2013 with the presentation of early results of the Q-SYMBIO coenzyme Q10 (CoQ10) trial. This groundbreaking ten-year study provides strong support for a recommendation made by Life Extension many years prior in the context of heart failure. This exciting trial showed that CoQ10 supplementation significantly improves survival even for patients with severe Class III or IV heart failure while dramatically reducing incidence of hospitalization. Specifically, heart failure patients who took 100 mg of CoQ10 three times daily were significantly less likely to have a major cardiovascular event and significantly less likely to die from any cause during the study period compared to control subjects (Mortensen 2013).
As shown by in several studies conducted by Life Extension Scientific Advisory Board Member Peter H. Langsjoen, MD, FACC, CoQ10 supplementation is especially important for individuals on cholesterol-lowering statin therapy (HMG CoA reductase inhibitors). Statin medications block the biosynthesis of both cholesterol and CoQ10, and these drugs have been shown to worsen heart muscle dysfunction in heart failure patients (PH Langsjoen, Langsjoen, 2005; P Langsjoen, Littarru, 2005; Folkers 1990; Silver 2004). In one study, diastolic dysfunction (heart muscle weakness) occurred in 70% of previously normal patients treated with 20 mg a day of Lipitor® for six months. This heart muscle dysfunction was reversible with 100 mg of CoQ10 three times daily (Silver 2004).
Although heart failure can be a frightening diagnosis, the emergence of several novel therapeutic strategies and mounting evidence for the efficacy of some natural interventions offer additional hope for those afflicted with this condition (Mortensen 2013).
This protocol will outline the biology of heart failure and how the condition is diagnosed and treated by conventional medicine. State-of-the-art treatment strategies undergoing active research will be reviewed, as will the critical need to address the numerous insidious underlying causes of heart failure. In addition to several innovative and emerging therapies, nutritional approaches to improve exercise tolerance, functional capacity, and quality of life in patients with heart failure will be presented.As heart failure is a potential endpoint for several cardiovascular and metabolic diseases, a comprehensive strategy for minimizing risk or improving outcome of heart failure should also address its underlying causes. Therefore, readers are encouraged to review additional Life Extension protocols on atherosclerosis and cardiovascular disease, high blood pressure, cardiac arrhythmia, cholesterol management, obesity and weight loss, diabetes, kidney disease, and thyroid regulation.