The majority of patients who have had a heart transplant are still very severely symptomatic and are in need of ongoing treatment. In general there is great hope that with improvements in treatment of heart failure, many of these patients could be living longer, free of a transplant by good treatment of their heart failure.
In this group of patients with familial heart failure, there was a higher prevalence of left ventricular hypertrophy but no differences in ejection fraction compared to the control group. This supports the hypothesis that the development of HF does not run in families.
The cause of heart failure is not straightforward and probably involves a combination of factors. Risk factors for worsening heart failure include older age, kidney failure, diabetes and hypertension. The risk of the disease also increases with time since diagnosis. There is a clear need for prevention, with a particular emphasis on reducing smoking.
Only 3 individuals received ACEI/ARB therapy and only 17 individuals received angiotensin receptor blocker therapy. Overall, the most common treatment for CHF was β-blocker therapy, prescribed to 50-75 percent of the study population. A small percentage of individuals received digoxin.
Approximately 2.3 million Americans will have heart failure a year. Women are 4.2 times more likely to develop heart failure and are twice as likely as their male counterparts to be hospitalized for heart failure.
What are the clinical signs of heart failure? A 2016 research concluded on the fact that heart failure has no specific symptoms. Heart failure has no specific findings or abnormalities. Nevertheless, heart failure has a set of potential signs and symptoms which can vary depending on many factors that are different for each individual. The research concluded that the signs of heart failure are the clinical picture of heart failure and its severity.
HF is a disease of the heart in which the cardiac output is either too weak or can't be increased by the heart muscle. The main result is decreased exercise capacity and increased filling pressure which lead to an increase in left ventricular filling and ventricular wall fatigue. This results in inadequate cardiac output to supply the body's demands for oxygen and nutrients. The reduced cardiac capacity is the result of decreased numbers of cardiac myocytes (satellite cells), the heart's main muscle cells, and inadequate muscle perfusion and oxygen supply. Prostatic cancer may also be associated with heart failure.
Azd3427 is well tolerated in patients with CHF and is associated with a reduction in body weight (body weight decreased by 3.8% (p = 0.002) and LBM decreased (LBM decreased by 9.4% (p = 0.007). Azd3427 was well tolerated and effective in patients with mild-to-moderate CHF.
The data show that the beneficial effects of azd3427 on quality of life parameters are more pronounced than those in the placebo group, at doses recommended for clinical use. Therefore, they demonstrate its possible benefit in patients with systolic heart failure. However, the benefit of azd3427 seems to be limited. Moreover, the improvement on QoL might be only of little clinical importance to patients. Further studies are needed to clarify whether patients might have expectations.
The mortality rate for heart failure increases with age and the duration of the disease progresses similarly as age. The heart failure in the general public is most commonly present at an older age than the mean survival for patients hospitalized with heart failure.
It is clear that azd3427 has potential as a therapeutic agent for heart failure. As of the time of writing, there is no evidence that any clinical trials involving azd3427 have been completed. However, two of the researchers involved [Professor John W. MacGregor, Mr Peter I. MacIlvaine and Professor Chris Brown] received funding from Pfizer (UK) Ltd. This is likely to be of concern to many researchers. The University of Nottingham and Pfizer (UK) Ltd. provided support and advice for research at the Sir William Dunn School of Pathology and Nottingham Cardiovascular Risk Unit.