Millions of Americans suffer from heart failure, and it’s the leading cause of hospitalization for people over 65. It comes in four stages, from mild to severe, and is a progressive and always eventually fatal disease. But the course of the disease can be profoundly affected by other factors.
Now, add that fact to this one: heart failure patients who exercise more have fewer hospitalizations and better outcomes on all scores. Another recent study examined how levels of social support and barriers to exercise affected heart failure patients’ willingness to keep up with exercise programs. Not surprisingly, when patients completed surveys about the types of support they received and their barriers to exercise, those who had worse situations in regard to finances, weather, transportation, and/or childcare had less success in adhering to exercise regimens. And those with reduced barriers did, in fact, exercise more and have better outcomes.
Medical experts can only surmise why exercise helps depression, but there’s clear evidence that it does. So, what is the cost of having millions of heart failure patients regularly re-hospitalized versus helping reduce those social barriers and giving them the chance to experience longer and better-quality lives?
Heart attack and heart failure are major causes of death and disability around the world. And although when we are brand new babies, our hearts can regenerate themselves–just like our blood and skin do throughout our lives–but once we’re past infancy, this ability to automatically regenerate new heart cells disappears. That’s why the only “cure” for advanced heart failure is a heart transplant.
Now a team of Australian and Israeli researchers at the Sydney Victor Change Cardiac Research Institute and the Weizmann Institute of Science has proven a method of getting murine (mouse) heart cells (cardiomyocytes) to recharge their ability to regrow. Invoking the neonatal process, researchers developed a strategy for administering Neuregulin-1 (NRG1) and inducing co-receptor ERGG2 expression, thereby encouraging hypertrophy, then dedifferentiation and growth of the mouse heart cells. Although it’s still early days and much more research is needed, this study is extremely promising for future sufferers of heart attack and heart failure.
If they can get mice hearts to regrow their damaged cells, it’s highly likely that one day they’ll be able to get ours to do the same. Too bad most of us won’t be around for it.
They discovered a while ago that patients who were obese before they were diagnosed with heart failure tended to live significantly longer than patients who were just overweight or of normal weight. You know how many doctors automatically tell you to lose weight, no matter what condition you’re dealing with? Accordingly they’ve named this the “obesity paradox.” And now another study has solidly confirmed this apparent contradiction in regard to heart failure. The conclusion is so sure that at this point some researchers are even suggesting they ought to start considering how to identify an ideal BMI and potentially begin suggesting to patients ways to maintain that BMI.
Just imagine. Doctors telling you to gain weight and advising you what to eat to keep the weight on. Almost inconceivable. But hey, don’t most people – with many exceptions of course – start putting on significant weight when they hit a certain age? Most baby boomers will be nodding their heads vigorously at this point.
Makes me wonder if Nature doesn’t know something we don’t know about weight in older people – or something we simply haven’t been willing to consider before.
Yep. They’ve done it in a recent study with 40 patients in Japan – half got a protein drip called G-CSF and the rest a saline solution (placebo).
…researchers from the Gunma Prefectural Cardiovascular Center in Maebashi, Japan, have found that a protein called G-CSF—when injected into the hearts of patients who recently suffered an attack—can actually spur a type of bone marrowstem cells to migrate to the heart and curb the spread of cellular death that normally takes place.
Clinical trials are in the works to confirm these dramatic preliminary promises.
The substance nitric oxide (NO), one of my favorite topics, is now known to be break-downable into components, one of which has one less electron. It’s known as NO(-) or HNO or nitroxyl, and researchers are finding some exciting new applications for it.
The other use for nitroxyl (HNO) involves its use in treating heart failure. Researchers normally write in very reserved terms about their discoveries, but the author of the passage below seems pretty excited about the implications of the research. Basically it’s saying that HNO donors can do things that regular NO donors cannot do and may be dramatically more useful in treating cardiovascular disease.
Thus, unlike NO*, HNO can target cardiac sarcoplasmic ryanodine receptors to increase myocardial contractility, can interact directly with thiols and is resistant to both scavenging by superoxide (*O2-) and tolerance development. HNO donors are protective in the setting of heart failure in which NO donors have minimal impact.
It’s cool to see this showing three of my favorite topics coming together: nitric oxide, nanotechnology and heart failure. But then, when all is said and done someday, everything in bioscience will undoubtedly coalesce in one way or another.
Despite the development of continually more sophisticated diagnostic tools, it’s comforting to know that the best guide to a patient’s prognosis is the doctor’s careful listening to and observation of four important indicators: 1) distended jugular venous distention, 2) a third heart sound, 3) rales (crackles) in the lungs, and 4) peripheral edema (swelling in the legs and ankles).
I am grateful that most doctors have some training in how to present bad news to a patient. As one of their duties, that’s gotta suck. But the hope is that patient and doctor have developed a respectful, caring relationship along the way.
Researchers at Saint Louis University have had such promising results from a small (40 patients) earlier study using gene therapy for repairing heart failure damage that they’re now instituting a clinical trial. The trial will use a genetically targeted regulatory protein replacement therapy to see how well it can repair damage in 200 patients who’ve either had a prior heart attack or have cardiomyopathy or advanced heart failure.
The therapy involves infusing a gene – a type of regulatory protein called SERCA-2a – down the coronary arteries that may help heart cells utilize calcium better, which is similar to an engine getting better gas mileage. This outpatient procedure is performed in a cardiac catheterization lab and aims to increase the level of SERCA-2a, which is reduced in the individual heart muscle cells in patients with heart failure and can thereby change the way those cells function.
Worldwide 52 sites will participate in the trial, 33 in the U.S. To participate in the trial, please contact the Cardiology Research Office at Saint Louis University at 314-577-8876. Read the original article here.
The idea of the Canadian study is that a patient’s own stem cells are the most direct and effective way to repair damage and rebuild function in the heart. But because the stem cells from a damaged heart are not working up to normal capacity, scientists tested and found that adding extra copies of a gene that “stimulates blood vessel growth and improves tissue healing, known as endothelial nitric oxide synthase,” improves that function.
In other words, the gene stimulates the patient’s stem cells to reproduce more quickly and do their magic to help the heart heal itself. The Canadian trial is for post-heart-attack patients.The UK trial will be using a carrier virus to insert a gene into heart failure patients to help their hearts pump better.
Nothing but good news here – except that it will be two and three years before results are in. Stay tuned.
I read a news item about these studies the other day when the early morning temp was 80 degrees and the humidity was 81%. I have never been inclined to go out walking in weather like that, but now there’s a stronger reason beyond simple discomfort to stay home. For a person living with heart failure, taking a walk in those conditions could be considered suicidal.
Looking at how bioscience news affects business, higher education, government – and you and me