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Popular Erection Drug Softens a Hard Heart

Tim Boyer's picture

Researchers announce that a popular erection drug can actually soften a hard heart. Approximately 50% of patients aged 60 and over that are hospitalized because of a weakened heart, suffer from diastolic heart failure due to stiff heart muscles. An active ingredient found in a popular erection drug used primarily for penile erection difficulties may soon be used to treat some cardiac patients to soften their hard hearts.

It's Viagra

Researchers from the Ruhr University Bochum in Germany in cooperation with scientists from the Mayo Clinic in Rochester, Minnesota have recently published in the medical journal Circulation, their findings that the active ingredient in the popular erection drug Sildenafil citrate - more commonly known as Viagra - may be used to treat cardiac patients with a hard heart. This “hard heart” condition is the result of stiffened cardiac walls that manifests as diastolic heart failure - a condition in which the heart chamber does not sufficiently fill with blood.

The origins of Sildenafil citrate (Viagra), also colloquially known as "Vitamin V," "the Blue Pill,” and "Blue Diamond" among other monikers, was originally designed as a medication for treating high blood pressure and angina. The results of initial studies showed that Sildenafil citrate had little effect on treating angina, but did result in the unexpected inducing of penile erections. The drug was then marketed as a drug for treating erectile dysfunction and was dubbed “Viagra” for easy consumer identification.

However, Viagra for the penis may now become Viagra for the heart as researchers release their findings on studies using dogs as their animal model for diastolic heart failure. What they found was that the active ingredient in Viagra makes stiffened cardiac walls more elastic by activating an enzyme that causes a protein called “titin” in myocardial cells to relax.

"We have developed a therapy in an animal model that, for the first time, also raises hopes for the successful treatment of patients" says Prof. Dr. Wolfgang Linke of the RUB Institute of Physiology.

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Basically, the mechanism involves the Sildenafil citrate inhibiting a specific enzyme called phosphodiesterase 5 A, which then causes the increased formation of a messenger substance called cyclic GMP. The cyclic GMP then activates another enzyme called protein kinase G, which attaches phosphate groups to certain proteins through a phosphorylation reaction. This is a well-known mechanism that attributes to the blood vessel relaxation that gives Viagra its erection inducing properties.

What is new, however, is the researchers’ discovery that this same phosphorylation reaction also occurs in heart muscle and causes the cardiac muscle protein titin to become phosphorylated as well. When titin becomes phosphorylated it relaxes and subsequently softens the heart muscle.

"The titin molecules are similar to rubber bands," explains Professor Linke. "They contribute decisively to the stiffness of the cardiac walls. The activity of the protein kinase G causes titin to relax. This makes the cardiac walls more elastic. The effect occurs within minutes of administering the drug.”

Professor Linke explains the applicability of their findings from the dog studies to medical treatment in humans:

"Of all the patients aged over 60 who are in hospital because of a weak heart, half suffer from diastolic heart failure" explains Linke. "Although we know that the decreased distensibility of the cardiac walls is the cause, the disease cannot be treated properly with today's medicines. If, for the first time, the drug is found to have a positive effect on heart failure, we would already have a molecular mechanism on hand to explain the effect," says Linke.

Currently, clinical trials are in progress in a study called “RELAX” by the Heart Failure Network to determine the efficacy of the erection drug Sildenafil citrate in treating patients with heart failure related to a hard heart.

Reference: Circulation
Image source of Viagra: Wikipedia