Impotence Meds Might Give Men's Hearts a Boost

But evidence isn't strong enough to routinely recommend Viagra or Cialis after heart attack, experts say

By Dennis Thompson

HealthDay Reporter

THURSDAY, March 9, 2017 (HealthDay News) -- Men taking Viagra, Levitra or Cialis to revitalize their sex life might experience a valuable side benefit: enhanced heart health, researchers say.

Those erectile dysfunction drugs, called PDE5 inhibitors, appear to reduce a man's risk of death or heart failure after a first heart attack, according to preliminary study findings.

Men taking this type of ED drug had a 33 percent reduced risk of death within three years of their first heart attack, compared to men not taking the PDE5 inhibitor, said lead researcher Dr. Daniel Andersson.

The men also experienced a 40 percent reduced risk of subsequent hospitalization for heart failure, said Andersson, a postdoctoral researcher at the Karolinska Institute in Sweden.

Further, it appeared that taking more of the drug increased the survival advantage, he added.

"We also find a dose-dependent relationship between amount of dispensed PDE5 inhibitors and increased survival," Andersson said. But, he warned that the study size was not large enough to show a definitive link between dose and benefit.

The results surprised Andersson and his colleagues because erectile dysfunction is a known risk factor for heart disease. They had expected that treatment for ED would be associated with an increased risk of death.

This should give some comfort to men who have had a heart attack but want to use these meds to improve their sex life, said Dr. Martha Gulati, chief of cardiology at the University of Arizona College of Medicine-Phoenix.

"Obviously, we do worry about the use of these medications in patients who already had a heart attack," said Gulati, who is also editor-in-chief of, the American College of Cardiology's consumer-friendly website.

"Knowing that it is relatively safe" is important, she added.

PDE5 inhibitors such as Viagra (sildenafil), Cialis (tadalafil) and Levitra (vardenafil) work by causing blood vessels to expand, improving blood flow to the penis and making it easier to achieve and maintain an erection.

To investigate the drugs' effect on heart health, the researchers used health records to identify more than 43,000 Swedish men who had suffered a first heart attack between 2007 and 2013.

A national drug register showed which ones had filled a prescription for a PDE5 inhibitor. Among the roughly 7 percent who were prescribed an erectile dysfunction drug, more than nine out of 10 received a PDE5 inhibitor.

The researchers then tracked the men for more than three years on average to see how the drugs would affect their heart health.

Taking a PDE5 inhibitor reduced a heart attack survivor's risk of early death, whether for heart-related or other reasons, researchers determined. It also reduced the chances of subsequent heart failure. (Heart failure means the heart isn't pumping blood properly.)

However, the drugs did not appear to significantly reduce risk of a follow-up heart attack or the need to have blocked arteries reopened, Andersson said.

No survival benefit was seen among men taking Muse (alprostadil), another type of erectile dysfunction drug that works through a different mechanism.

Although the results provide evidence that drugs like Viagra and Cialis may benefit heart health, the study cannot prove a direct cause-and-effect relationship, Andersson noted.

It might just be that these men are healthy enough to pursue a more active sex life than men not taking an erectile dysfunction drug, he said.

Regardless, the study does not provide enough evidence to recommend a PDE5 inhibitor as a necessary prescription for heart attack patients, Andersson said.

"We cannot recommend at this stage that all patients with previous [heart attacks] should have PDE5 inhibitors," he said.

The study is scheduled for presentation March 17 at the American College of Cardiology's annual meeting in Washington, D.C. Data presented at meetings should be considered preliminary until published in a peer-reviewed medical journal.

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SOURCES: Daniel Andersson, M.D., Ph.D., postdoctoral researcher, Karolinska Institute, Sweden; Martha Gulati, M.D., chief, cardiology, University of Arizona College of Medicine-Phoenix, and editor-in-chief,; American College of Cardiology, abstract for presentation, March 17, 2017
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