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.
In an ongoing study of heart failure patients, after adjusting for factors such as sex, age, hypertension, severity of heart failure, and comorbidities, moderate to severe depression remained a predicting factor for all-cause mortality for heart failure patients. In other words, if you’re depressed and have heart failure, you’re five times more likely to die an early death than a similar patient who isn’t depressed.
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?
English: Medical X-rays Congestive heart failure (Photo credit: Wikipedia)
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.
Body mass index (BMI) values (Photo credit: Wikipedia)
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.
Doctors have discovered that one of the medicines routinely given to end-stage heart failure patients to block the kidneys from retaining water may also be blocking reception of vital signals that tell the heart to beat more strongly. A catch-22 they can now begin to study and hopefully remedy soon.
Mesenchymal stem cells are being used successfully to reduce muscuoskeletal pain in patients with arthritic knees, regardless of past-65 age or weight. It’s also being used for “such conditions as degenerative disc disease, desiccated discs, spinal stenosis (both central and foraminal), facet arthrosis, sacroiliac joint syndrome, osteoarthritis of any joint, and sports/overuse injuries.” Exciting news. Can’t wait ’til this approach becomes a best practice for every osteo doc. Imagine potentially being able to skip that hip replacement!
We all know that breathing in traffic pollution can damage lungs. Now, in a study with rats, researchers have found the effect of breathing in smoke from combustion increased iNOS (inducible nitric oxide synthase) and other factors and resulted in damage to the olfactory bulb – inflammation, permeability and swelling. Hmmm. Wonder if this relates to why so many baby boomers have what seems like permanent excess mucus in their sinuses. Snort of fluticasone, anyone?
English: Human bone marrow. (Photo credit: Wikipedia)
Imagine a substance your doctor could inject directly into your heart soon after you have a heart attack that will prevent and/or repair some of the damage that heart attacks usually involve? AND thus possibly prevent you from developing heart failure as a result of the attack?
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 marrow stem 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.
English: A schematic showing the (laboratory) production of nitric oxide. The setup was made based on an image of the 1949 Popular Mechanics article by Kenneth M. Swezey (titled: The gas that makes you laugh). Images from http://commons.wikimedia.org/wiki/User:Rocket000/SVGs/Chemistry were used to make this image. (Photo credit: Wikipedia)
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.
One novel use for nitroxyl is as part of a nanoparticle coating for implanted medical devices that otherwise might trigger dangerous blood clots. The coating is made up of sheets of graphene integrated with two components—haemin and glucose oxidase. “Both work synergistically to catalyze the production of nitroxyl, which can be used inside the blood like nitric oxide, although it contains one less electron. Nitroxyl has been reported as being analogous to nitric oxide in its clot-preventing capability.”
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.
Shown is the back of a female patient with a doctor who is using a stethoscope to listen to her lungs. (Photo credit: Wikipedia)
It’s great to know that what a doctor can hear/feel in the physical exam of a patient with advanced heart failure is the best predictor of how well that patient will fare.
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.
English: Coronary circulation, with coronary arteries labeled in red text and other landmarks in blue text. This vector graphics image was originally created with Adobe Illustrator, and modified with Inkscape. 32px|alt=W3C|link=http://validator.w3.org/? The source code of this SVG is valid. Category:Valid SVG (Photo credit: Wikipedia)
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.
Heart Failure causes more damage than you think (Photo credit: Novartis AG)
Both Canada and the UK have recently begun large-scale human trials to test how well new approaches using stem cells and gene therapy will work for treating damage in human hearts.
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.
Just as President Obama is making a public stand to combat global warming, scientists are proving that air pollution isn’t just an inconvenience. In fact, long-term exposure even to low levels of pollution – such as living in a big city all your life -increases your risk of lung cancer, according to a study published in The Lancet Oncology journal. The pollutants mentioned in this study included “nitrogen oxides and particulate matter (including traffic, industry, and domestic heating).”
Indoor Air Pollution (Photo credit: SEDACMaps)
What’s more, another study found a “strong and consistent” relationship between exposure to pollution and hospitalizations or death from congestive heart failure. The risks increased with “exposure to air pollutants, including carbon monoxide, sulphur dioxide, and nitrogen dioxide [a big contributor to smog].” This study concluded its findings by saying, “air pollution is a pervasive public health issue with major cardiovascular and health economic consequences, and it should remain a key target for global health policy.”
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.