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Heart Health

Viagra for Heart Failure? Works Better for the Guys

Clear-cut gender differences stand out in measuring impact of Viagra as therapy for heart failure, according to a study done at Johns Hopkins and posted online May 16th 2014 in The Journal of Clinical Investigation. Specifically, in female mice modeling human heart failure, the benefits of sildenafil, the generic name for Viagra, ranged from robust to practically nonexistent depending on the animals' levels of the hormone estrogen. Yet in male mice, sildenafil generally appears to work well because it targets a different biological process independent of estrogen. Estrogen is present in both male and female mammals, although in different amounts.

A release from the university quotes lead scientist Eiki Takimoto, M.D., Ph.D. as saying, "The research is especially significant because it offers a mechanism to explain how estrogen affects sildenafil's efficacy. That's the first time the actual pathway of a hormone's cause and effect on a drug has been mapped out."

Takimoto explains that the results of the team’s investigations in varied male and female mouse models of heart failure are so clear that physicians may need to take gender into consideration when prescribing certain medications and that drug developers would be wise to take them into careful account when setting protocols for clinical trials of the medication in people.  

The release notes that sildenafil, the generic compound used to initiate and strengthen male erections, works by encouraging blood vessels to dilate and increase blood flow to the penis. The effects are similar to some drugs, such as nitrates, already used to increase blood flow to failing hearts. Besides these effects, beneficial direct effects on heart muscles have been suggested by recent experimental studies, which is why researchers believe the drug could help patients with heart failure.

Heart failure is the most common reason for hospital admissions in the Medicare population, according to heart experts, and is the leading cause of death in Americans. Useful drugs such as beta-blockers and ACE inhibitors help to increase the blood-pumping efficiency of the heart, "yet they don't fully address the ongoing pathology," says Takimoto.

Whether due to a heart attack, hypertension, arteriosclerosis or other reasons, even moderate injury to heart muscle cells can initiate a downhill remodeling of broad areas of heart tissue, including enlargement of the heart and stiffening of heart chambers as fibrous proteins replace more flexible ones in muscle cells. The weakened and altered heart muscle compromises circulation, a hallmark of heart failure.

"Because cardiac remodeling is an underlying mechanism," Takimoto says, "we've put more than a decade of research into understanding it enough to stop or reverse it."

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