Men taking Viagra are less likely to die from cardiovascular disease

The drug is found to lower the risk of heart disease in men by up to 39 percent.
Ayesha Gulzar
Stock image of a man taking Viagra.
Stock image of a man taking Viagra.

stefanamer/iStock  

A recent study has found that men who take medication for erectile dysfunction (ED) may have a reduced risk of early death and are less likely to experience different heart problems.

ED medications, such as Viagra, Cialis, and Levitra, work by increasing blood flow to the penis. They do this by inhibiting an enzyme called phosphodiesterase type 5 (PDE5), which can interfere with the chemical signals responsible for relaxing the smooth muscles in the penis, allowing blood to flow in, and causing an erection.

The potential benefits of Viagra

To study the effect of ED medications on cardiovascular health and overall mortality, researchers looked at electronic health records for more than 23,000 American men between 2006-2020. These men had been prescribed at least one phosphodiesterase type 5 inhibitor (PDE-5i) prescription for ED, such as Viagra.

They compared them to a group of over 48,000 men with erectile dysfunction who were not prescribed an ED medicine.

The study found that men who had been taking a PDE-5i were 39 percent less likely to die from cardiovascular disease than those who had no record of a prescription. They were also 25 percent less likely to die from any cause.

The men who took a higher cumulative dose of PDE-5i were better protected against heart disease than those who took a lower dose.

These men had a 17 percent lower incidence of heart failure, a 15 percent lower incidence of getting a coronary revascularization procedure, and a 22 percent lower incidence of unstable angina.

All of those conditions could potentially be fatal if untreated — and could lead to death by heart attack down the line.

Previous studies have suggested that PDE-5i may have potential benefits for cardiovascular health. These medications have been found to improve blood flow to the heart, reduce the stiffness of blood vessels, and decrease inflammation in the body.

Some studies have also shown that PDE-5 inhibitors may positively affect platelet function, which could potentially reduce the risk of clots forming in the blood vessels.

The study leaves some unanswered questions

Before we get too excited about these results, the study has some serious limitations.

It was an observational study, meaning it can only show an association between ED medication use and reduced risk of death, not a causal relationship. Other factors, such as overall better health or frequent doctor visits, may have contributed to the reduced risk of death.

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Additionally, the study was funded by Sanofi, which sells its own PDE-5i called avanafil, so there is a potential conflict of interest.

Moreover, the study focused on ED medications paid for by insurance and did not account for those paid out of pocket. Therefore, the study may not have accurately captured who was actually taking such ED medications.

"While it is possible that Viagra may have some cardiovascular benefits, that would require further investigation, and this current study does not prove it," said Cardiologist Deepak Bhatt, the director of Mount Sinai Heart in New York, to ScienceAlert.

The next step would be to conduct a large clinical trial in a controlled environment to confirm the result. Men should always consult a healthcare professional before taking ED medication and should be aware of the potential side effects.

This study was published in the Journal of Sexual Medicine.

Study Abstract:

Background: Treatment with phosphodiesterase type 5 inhibitors (PDE-5is) is effective in treating erectile dysfunction (ED).

Aim: The objective of this study was to determine the effect of PDE-5is on the incidence of major adverse cardiovascular (CV) events (MACE; composite outcome of CV death, hospitalization for myocardial infarction, coronary revascularization, stroke, heart failure, and unstable angina pectoris) and overall mortality.

Methods: A retrospective observational cohort study was conducted in a large US claims database in men with ≥1 diagnosis of ED without prior MACE within 1 year, from January 1, 2006, to October 31, 2020. The exposed group had ≥1 claim for PDE-5i and the unexposed group had no claims for PDE-5i, and the groups were matched up to 1:4 on baseline risk variables.

Outcome: The primary outcome was MACE and the secondary outcomes were overall mortality and individual components of MACE, determined by multivariable Cox proportional hazard modeling.

Results: Matched plus multivariable analyses showed that MACE was lower by 13% in men exposed (n = 23 816) to PDE-5is (hazard ratio [HR] 0.87; 95% CI 0.79-0.95; P = .001) vs nonexposure (n = 48 682) over mean follow-up periods of 37 and 29 months, respectively, with lower incidence of coronary revascularization (HR 0.85; 95% CI 0.73-0.98; P = .029), heart failure (HR 0.83; 95% CI 0.72-0.97; P = .016), unstable angina (HR 0.78; 95% CI 0.64-0.96; P = .021), and CV death (HR 0.61; 95% CI 0.41-0.90; P = .014) with PDE-5i exposure. Phosphodiesterase type 5 inhibitor–exposed men had a 25% lower incidence of overall mortality (HR 0.75; 95% CI 0.65-0.87; P < .001). Men without coronary artery disease (CAD) but with CV risk factors at baseline showed a similar pattern. In the main study cohort, men in the highest quartile of PDE-5i exposure had the lowest incidence of MACE (HR 0.45; 95% CI 0.37-0.54; P < .001) and overall mortality (HR 0.51; 95% CI 0.37-0.71; P < .001) vs the lowest exposure quartile. In a subgroup with baseline type 2 diabetes (n = 6503), PDE-5i exposure was associated with a lower MACE risk (HR 0.79; 95% CI 0.64-0.97; P = .022).

Clinical Implications: PDE-5is may have cardioprotective effects.

Strengths and Limitations: Strengths are the large numbers of participants and consistency of the data; limitations include the retrospective nature of the study and unknown confounders.

Conclusions: In a large population of US men with ED, PDE-5i exposure was associated with lower incidence of MACE, CV death, and overall mortality risk compared to non-exposure. Risk reduction correlated with PDE-5i exposure level.

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