This trial is evaluating whether PP-MI Intervention will improve 1 primary outcome, 9 secondary outcomes, and 23 other outcomes in patients with Heart Failure. Measurement will happen over the course of Baseline, 12 weeks, 24 weeks, 48 weeks.
This trial requires 280 total participants across 2 different treatment groups
This trial involves 2 different treatments. PP-MI Intervention is the primary treatment being studied. Participants will all receive the same treatment. There is no placebo group. The treatments being tested are not being studied for commercial purposes.
The therapeutic effects of PP-mi intervention were mediated by the modulation of key molecular and signal transduction pathways implicated in heart failure. PP-mi can be used as an effective drug in the management of HF.
The evidence to support the notion that a cure for heart failure exists is either very weak or totally negative. The best available evidence shows that any such event will occur by chance, whereas evidence from clinical trials showing a reduction in disease and hospital stay is not statistically significant. We should then ask the question: where does all the positive evidence come from? The best estimates of the annual incidence of new heart failure in the general population is over 1% implying that all of the existing positive evidence comes from a single country -- the USA.
Patients with moderate-to-severe HF are most likely to receive beta-blockers and digoxin. ACE-I medications are administered to about two-thirds of patients, digoxin is given to about one-third of patients, and one in six patients receive diuretics. The benefit of ACE-I and beta-blockers on mortality has not been established. Digoxin is efficacious at improving symptoms in those with severe HF.
Heart failure can occur in the elderly from a variety of causes including old age, high blood pressures, valvular disease or scarring of the heart muscle (cardiac remodeling). Diagnosis and treatment of heart failure can be difficult, but treatments to improve heart strength have been shown to reduce progression of disease.
There was an estimated 1.4 million new cases of heart failure a year in the US in 2008, about one-third of the people with heart failure in the US. Many new cases of heart failure were due to coronary heart disease (50%), and half of the new cases were attributed to atrial fibrillation, ventricular tachycardia, and other arrhythmias.
I have illustrated some important clinical signs of heart failure using two patients. But what do you expect to see in a third patient in this series? Would they exhibit any signs of heart disease? I've asked myself in the recent past if one may expect any sign of heart disease from the presence of a heart failure diagnosis. My answer to my own question is not known but it isn't a pretty one either! The patient should be treated, as a common practice, for an underlying cause.
The research for both chronic and acute HF is expanding steadily, and current research guidelines are likely to be soon updated. The new guidelines will hopefully provide the optimal management for individual HF patients.
There were several new drugs and therapies that the researcher found useful in treating heart failure. The biggest new development was mexiletine, a powerful antiarrhythmic drug.
By using a rigorous analytical methodology, our study shows that there is no evidence that pp-mi affects glucose homeostasis. This is in agreement with the evidence from the large multi-center clinical trial of 3 years that also reported that the treatment did not affect weight, blood pressure, or lipid profile. Therefore, further study of PP-mi is not warranted at this time, and no clinical trial is on file with the FDA.
The risk of developing dementia is substantial after cardiovascular mortality and can be significantly lowered following a single 2-hit genotype change at -636 promoter polymorphism of the SIRT1 gene. Further studies are needed to determine whether prevention of silent cardiovascular disease in older persons with this risk factor genotype would lead to reduction in cognitive decline. Clinically silent myocardial infarction and silent sudden arrhythmic death as well as other cardiovascular events, deaths, and strokes are also important triggers for cognitive decline.
The study was not designed to show that participation in a p-mi program is efficacious in improving heart failure outcomes for the participants. There were no changes in the outcomes assessed in the participants and controls when they were enrolled or exited the study (12 months). Future, randomized clinical trials on longer length of follow up can provide the information needed to determine the true effects and benefits of the intervention.