Thursday, May 9, 2019
Wednesday, May 1, 2019
Sex drug 'effective' as heart failure treatment
The British Heart Foundation funded study is a breakthrough in the treatment for the disease in which five year survival rates are lower than most common cancers.
The study of Tadalafil—which is in the same class as Viagra—proves that the drug is biologically effective as a treatment for heart failure in sheep.
However, lead author Professor Andrew Trafford argues the effect is likely to also be shown in humans. The study is published in the journal Scientific Reports.
Heart failure is a devastating condition, occurring when the heart is too weak to pump enough blood to meet the body's needs.
It also causes a build-up of fluid that backs up into the lungs, resulting in breathlessness as well fluid retention, resulting in swelling of different parts of the body.
Most current treatments are ineffective.
"This discovery is an important advance in a devastating condition which causes misery for thousands of people across the UK and beyond," said Professor Trafford.
"We do have limited evidence from human trials and epidemiological studies that show Tadalafil can be effective in treating heart failure.
"This study provides further confirmation, adds mechanistic details and demonstrates that Tadalafil could now be a possible therapy for heart failure.
"It's entirely possible that some patients taking it for er`ectile dysfunction have also unwittingly enjoyed a protective effect on their heart."
Sheep were used by the team as the physiology their hearts is similar to human hearts.
When the animals had heart failure—induced by pace makers—which was sufficiently advanced to need treatment, the team administered the drug. Within a short period the progressive worsening of the heart failure was stopped and, importantly the drug reversed the effects of heart failure.
And the biological cause of breathlessness in heart failure- the inability of the heart to respond to adrenaline was almost completely reversed.
The dose the sheep received were similar to the dose humans are given when being treated for erectile dysfunction.
Tadalafil blocks an enzyme called Phosphodiesterase 5 or PDE5S for short, which regulates how our tissue responds to hormones like adrenaline.
The research team found that in heart failure, the drug altered the signalling cascade—a series of chemical reactions in the body—to restore the hearts ability to respond to adrenaline.
And that increases the ability of the heart to force blood around the body when working harder.
Professor Trafford added: "This is a widely used and very safe drug with minimal side effects.
"However we would not advise the public to treat themselves with the drug and should always speaking to their doctor if they have any concerns or questions.
"Tadalafil is only suitable as a treatment for systolic heart failure—when the heart is not able to pump properly—and there may be interactions with other drugs patients are taking."
Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation, said:
"Viagra-type drugs were initially developed as potential treatments for heart disease before they were found to have unexpected benefits in the treatment of erectile dysfunction. We seem to have gone full-circle, with findings from recent studies suggesting that they may be effective in the treatment of some forms of heart disease—in this case, heart failure.
"We need safe and effective new treatments for heart failure, which is a cruel and debilitating condition that affects almost a million people in the UK. The evidence from this study—that a Viagra-like drug could reverse heart failure—should encourage further research in humans to determine if such drugs may help to save and improve lives."
More information:
Phosphodiesterase 5 inhibition improves contractile function
and restores transverse tubule loss and catecholamine responsiveness in
heart failure, Scientific Reports (2019).
Journal information:
Scientific Reports
Provided by
University of Manchester
User comments
14 hours ago
13 hours ago
This
is inaccurate information. This article refers to Tidalafil as being
Viagra which is incorrect, Tidalafil brand is Cialis, Viagra generic is
Sildanafil. This is significant as half life of medications and onset of
action are different, though they are both PD5's, this article fails to
distinguish which is the correct medication used in the study...the
fact that there is no author even raises more suspicion on legitimacy of
study...
8 hours ago
Grossly
irresponsible reporting. The sheep model is irrelevant to humans in
this instance. And nitric oxide's very real role in the augmentation of
neurodegenerative diseases like alzheimer's don't make it an attractive
target for heart failure treatment--unless, of course, you've got a
grant source and a crooked journal editor willing to publish your tripe.
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Monday, April 29, 2019
Tuesday, April 23, 2019
Saturday, April 20, 2019
Heart patch could limit muscle damage in heart attack aftermath: Study
indiablooms
Researchers develop adhesive patch to reduce heart attack damage
Odisha Television Ltd.
Heart patch could limit muscle damage in heart attack aftermath: Study
New York, Apr 20 (IBNS): Researchers have designed a new type of
adhesive patch that can be placed directly on the heart and may one day
help to reduce the stretching of heart muscle that often occurs after a
heart attack.
The patch, made from a water-based hydrogel material, was developed
using computer simulations of heart function in order to fine tune the
material’s mechanical properties. A study in rats showed that the patch
was effective in preventing left ventricle remodeling — a stretching of
the heart muscle that’s common after a heart attack and can reduce the
function of the heart’s main pumping chamber. The research also showed
that the computer-optimized patch outperformed patches whose mechanical
properties had been selected on an ad hoc basis.
The research, published in Nature Biomedical Engineering, was a collaboration between computer modeling and mechanics researchers in Brown University’s School of Engineering, cardiology researchers from Fudan University and material scientists from Soochow University.
“Part of the reason that it’s hard for the heart to recover after a heart attack is that it has to keep pumping,” said Huajian Gao, a professor of engineering at Brown and a co-author on the paper. “The idea here is to provide mechanical support for damaged tissue, which hopefully gives it a chance to heal.”
Prior research had shown that mechanical patches could be effective, the researchers say, but no one had done any research on what the optimum mechanical properties of such a patch might be. As a result, the thickness and stiffness of potential patches varies widely. And getting those properties right is important, Gao says.
“If the material is to hard or stiff, then you could confine the movement of the heart so that it can’t expand to the volume it needs to,” he said. “But if the material is too soft, then it won’t provide enough support. So we needed some mechanical principles to guide us.”
To develop those principles, the researchers developed a computer model of a beating heart, which captured the mechanical dynamics of both the heart itself and the patch when fixed to the heart’s exterior. Yue Liu, a graduate student at Brown who led the modeling work, says the model had two key components.
“One part was to model normal heart function — the expanding and contracting,” Liu said. “Then we applied our patch on the outside to see how it influenced that function, to make sure that the patch doesn’t confine the heart. The second part was to model how the heart remodels after myocardial infarction, so then we could look at how much mechanical support was needed to prevent that process.”
With those properties in hand, the team turned to the biomaterials lab of Lei Yang, a Brown Ph.D. graduate who is now a professor at Soochow University and Hebei University of Technology in China. Yang and his team developed a hydrogel material made from food-sourced starch that could match the properties from the model. The key to the material is that it’s viscoelastic, meaning it combines fluid and solid properties. It has fluid properties up to a certain amount of stress, at which point it solidifies and becomes stiffer. That makes the material ideal for both accommodating the movement of the heart and for provided necessary support, the researchers say.
The material is also cheap (a patch costs less than a penny, the researchers say) and easy to make, and experiments showed that it was nontoxic. The rodent study ultimately showed that it was effective in reducing post-heart attack damage.
“The patch provided nearly optimal mechanical supports after myocardial infarction (i.e. massive death of cardiomyocytes),” said Ning Sun, a cardiology researcher at Fudan University in China and a study co-author. “[It] maintained a better cardiac output and thus greatly reduced the overload of those remaining cardiomyocytes and adverse cardiac remodeling.”
Biochemical markers showed that the patch reduced cell death, scar tissue accumulation and oxidative stress in tissue damaged by heart attack.
More testing is required, the researchers say, but the initial results are promising for eventual use in human clinical trials.
“It remains to be seen if it will work in humans, but it’s very promising,” Gao said. “We don’t see any reason right now that it wouldn’t work.”
The research, published in Nature Biomedical Engineering, was a collaboration between computer modeling and mechanics researchers in Brown University’s School of Engineering, cardiology researchers from Fudan University and material scientists from Soochow University.
“Part of the reason that it’s hard for the heart to recover after a heart attack is that it has to keep pumping,” said Huajian Gao, a professor of engineering at Brown and a co-author on the paper. “The idea here is to provide mechanical support for damaged tissue, which hopefully gives it a chance to heal.”
Prior research had shown that mechanical patches could be effective, the researchers say, but no one had done any research on what the optimum mechanical properties of such a patch might be. As a result, the thickness and stiffness of potential patches varies widely. And getting those properties right is important, Gao says.
“If the material is to hard or stiff, then you could confine the movement of the heart so that it can’t expand to the volume it needs to,” he said. “But if the material is too soft, then it won’t provide enough support. So we needed some mechanical principles to guide us.”
To develop those principles, the researchers developed a computer model of a beating heart, which captured the mechanical dynamics of both the heart itself and the patch when fixed to the heart’s exterior. Yue Liu, a graduate student at Brown who led the modeling work, says the model had two key components.
“One part was to model normal heart function — the expanding and contracting,” Liu said. “Then we applied our patch on the outside to see how it influenced that function, to make sure that the patch doesn’t confine the heart. The second part was to model how the heart remodels after myocardial infarction, so then we could look at how much mechanical support was needed to prevent that process.”
With those properties in hand, the team turned to the biomaterials lab of Lei Yang, a Brown Ph.D. graduate who is now a professor at Soochow University and Hebei University of Technology in China. Yang and his team developed a hydrogel material made from food-sourced starch that could match the properties from the model. The key to the material is that it’s viscoelastic, meaning it combines fluid and solid properties. It has fluid properties up to a certain amount of stress, at which point it solidifies and becomes stiffer. That makes the material ideal for both accommodating the movement of the heart and for provided necessary support, the researchers say.
The material is also cheap (a patch costs less than a penny, the researchers say) and easy to make, and experiments showed that it was nontoxic. The rodent study ultimately showed that it was effective in reducing post-heart attack damage.
“The patch provided nearly optimal mechanical supports after myocardial infarction (i.e. massive death of cardiomyocytes),” said Ning Sun, a cardiology researcher at Fudan University in China and a study co-author. “[It] maintained a better cardiac output and thus greatly reduced the overload of those remaining cardiomyocytes and adverse cardiac remodeling.”
Biochemical markers showed that the patch reduced cell death, scar tissue accumulation and oxidative stress in tissue damaged by heart attack.
More testing is required, the researchers say, but the initial results are promising for eventual use in human clinical trials.
“It remains to be seen if it will work in humans, but it’s very promising,” Gao said. “We don’t see any reason right now that it wouldn’t work.”
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This is a terrible animal model and it doesn't work to further human studies. The drug is not very effective either - done that with pulmonary hypertension studies and Sildenafil.