Erectile dysfunction and heart disease: What’s the connection?

Erectile dysfunction may be an early sign of cardiovascular disease

Even if your doctor has given you a clean bill of health, beware: problems getting or keeping an erection firm enough for sexual intercourse may signal trouble, especially cardiovascular disease, down the road.

The connection between erectile dysfunction (ED) and cardiovascular disease (CVD) isn’t as far-fetched as it may seem. Both follow the same age-related trajectory and become increasingly common from age 45 onward. They even share common causes. A study of 570 middle-aged California men begun in 1972 shows that smoking, overweight, and high cholesterol or high triglycerides — all risk factors for heart disease — were linked with erection difficulties 25 years later. That report appeared in The Journal of the American College of Cardiology in 2004.

But until a landmark study based on data from the Prostate Cancer Prevention Trial was published in The Journal of the American Medical Association the following year, researchers did not have evidence of a strong association between ED and CVD. That study was a randomized, controlled trial — the gold standard of scientific inquiry — designed to test the hypothesis that taking the drug finasteride (Proscar) would reduce the risk of developing prostate cancer. Beginning in 1994, 18,882 men ages 55 or older were randomly assigned to receive either finasteride or a placebo for seven years. Because participants might experience adverse sexual side effects, they completed yearly surveys asking whether they had erections, experienced a drop in libido, or noticed a decrease in ejaculate. Study coordinators also recorded any cardiovascular complications, such as heart attack, surgical treatment for coronary artery disease, recurrent chest pain, stroke, congestive heart failure, abnormal heart rhythms, or cardiac arrest.

To evaluate a possible link between the two conditions, researchers at the University of Texas examined data only on the 8,063 men who were taking a placebo and did not have a history of cardiovascular problems. After seven years, 65% of the men without ED at the start of the Texas study had developed erectile troubles, and many subsequently experienced recurrent chest pain, heart attacks, and stroke. In fact, older men with ED had nearly twice the risk of developing cardiovascular disease as those without it. Put another way, ED had about the same effect on CVD risk as smoking, having high cholesterol, or having a family history of heart attack.

A 2007 Dutch study of 1,248 men came to similar conclusions. Those with ED were approximately 1.5 to 2.5 times more likely to develop CVD, defined as heart attack, stroke, or sudden death, than men without ED. The chances of developing CVD were greatest among men with severe ED, defined as having erections with severely reduced rigidity or not having erections at all. Even after factors such as age, cholesterol levels, blood pressure, diabetes, and smoking were taken into account, the increased risk of CVD was still statistically significant. Researchers also estimated that nearly 12% of “cardiovascular events,” such as heart attacks, might have been avoided if the men had been more aggressive about CVD prevention after they began having erectile troubles. (To read these and other related studies on your own, see “A link between ED and CVD,” below.)

Rather than follow men over several years to see if they developed CVD, a Johns Hopkins study of 2,126 adult males in the National Health and Nutrition Examination Survey (NHANES) looked at risk factors for CVD among men with and without ED. Researchers found that almost 90% of men with ED had at least one major CVD risk factor — high blood pressure, high cholesterol, diabetes, or smoking. They also queried participants, who were ages 20 or older, about physical activity and found that men with ED were much less likely to exercise.

A second group of researchers using NHANES data came to slightly different conclusions. Men who had urinary difficulties or diabetes, as well as men who were taking antidepressants and certain medications for high blood pressure, had an increased risk of ED, while men with a history of cardiovascular disease and those with untreated high blood pressure had a small, statistically insignificant risk of erectile trouble. (See “Hypertension, drugs, and erections,” below.) Unlike the Johns Hopkins researchers, these investigators excluded men under age 40. They also incorporated different variables, such as urinary function and use of medications, into their analysis.

Both NHANES studies hint at proverbial chicken-or-egg questions: Does ED cause CVD? Is ED the first sign of unrecognized, occult CVD? Or is ED by itself simply another risk factor for CVD? Neither study comes to a definitive conclusion. Nor do the other studies, although far more men in the Texas study had ED prior to developing CVD than vice versa. That leaves the exact nature of the ED-CVD connection unclear.

But given that cardiovascular disease is the leading cause of death in the United States, and that 50% of deaths due to heart disease occur in men with no history of the disease, most of the researchers recommended cardiovascular screening for men seeking help for ED. Doing so, they wrote, would allow for earlier intervention, potentially reducing the number of people who die of CVD.

Just say NO

At its most basic level, an erection is a matter of hydraulics. Blood fills the penis, causing it to swell and become firm. But getting to that stage requires extraordinary orchestration of body mechanisms. Chemical messengers, blood vessels, nerves, hormones, and the psyche must work together.

When a touch, a look, even a thought nudges the brain to send signals of arousal down the spinal cord and into the nerves in the penis, the nerves “talk” to one another by releasing nitric oxide (NO) and other chemical messengers. These messengers boost the production of other important chemicals, including cyclic guanosine monophosphate (GMP), prostaglandins, and vasoactive intestinal polypeptide. These chemicals initiate the erection by relaxing the smooth muscle cells lining the tiny arteries that lead to the corpora cavernosa, a side-by-side pair of flexible cylinders that run the length of the penis. (See Figure 1.)

As the arteries relax, the thousands of tiny caverns inside these cylinders fill with blood. Blood floods the penis through two central arteries that run through the corpora cavernosa and branch off into smaller arteries. The amount of blood in the penis increases sixfold during an erection. The blood in the corpora cavernosa compresses and then closes off the openings to the veins that normally drain blood away from the penis. Temporarily trapped, the blood filling the arteries sustains the erection. (See Figure 2.)

Some signal — usually an orgasm, but possibly a distraction, interruption, or even cold temperature — brings an erection to an end. This process, called detumescence, occurs when the chemical messengers that started and maintained the erection stop being produced, and other chemicals, such as the enzyme phosphodiesterase 5 (PDE5), destroy the remaining messengers. Blood seeps out of the passages in the corpora cavernosa. Once this happens, the veins in the penis begin to open and the blood drains out. The penis returns to its limp, or flaccid, state.

Since erections depend on the blood vessels that serve the penis, it’s not surprising that vascular disease is the leading cause of ED. The most common type of vascular disease is atherosclerosis, which occurs when fatty deposits build up on artery walls, narrowing and clogging them. (See Figure 3.) The accumulation of these fatty plaques also interferes with NO production. A lack of NO in the arteries leading to or inside the penis can weaken or prevent an erection. High blood pressure, high cholesterol, diabetes, and smoking all lead to atherosclerosis. (See “What’s blood sugar got to do with it?” below, for more information on diabetes and ED.)

Many people think of atherosclerosis as occurring mainly in the heart’s arteries. But in fact, it can occur in arteries throughout the body — including those in the penis. Some researchers have hypothesized that because the penile arteries are smaller in diameter than the coronary arteries, plaques in the penile arteries may obstruct blood flow to a greater degree than in the coronaries. That’s why ED may occur before other symptoms of heart disease, such as chest pain.

Studies have also shown that damage to the endothelium, the thin layer of cells that lines blood vessels, plays a role in ED. Malfunctioning endothelial cells seem to interfere with the production of NO, but other cells continue to produce PDE5 and other enzymes that break down cyclic GMP. That limits the ability of vessels to dilate and admit the increased blood needed for an erection. Stress on vessels can also affect blood flow, the stiffness or elasticity of vessels, and the likelihood that blood platelets will stick to the endothelium, further restricting blood flow. (For a list of scientific papers on atherosclerosis and endothelial function, see “Vascular disorders and ED,” below.)

Making the connection

The idea that ED is a vascular condition isn’t particularly new. So why have doctors only recently made the connection between ED and CVD? Thank Viagra. Before its introduction, most men were too embarrassed to mention ED. And doctors didn’t ask because there wasn’t much they could do to help. Sildenafil (Viagra) helped transform ED from a deep, dark secret into grist for talk shows and fair game for questions in the doctor’s office. Such openness made it possible to gauge the extent of erection problems, which affect 15 million to 30 million Americans, depending on whom you ask and how you define ED. This, in turn, has allowed researchers and clinicians to see links between ED, CVD, and other conditions.

ED warrants a thorough check-up for signs of heart disease. This includes testing for high cholesterol, high blood pressure, and diabetes; a discussion about smoking and other risk factors; and a conversation about symptoms that might suggest atherosclerosis elsewhere in the body, such as chest pressure, episodes of weakness or numbness, or pain in the calf muscles while walking.

Similarly, heart disease should, at some point, prompt a man-to-doctor conversation about sexual function. Heart trouble shouldn’t stand in the way of a satisfying sex life or the use of drugs to combat ED. (See “Are erection drugs safe for men with heart disease?” below.) If your doctor brushes off your questions or seems uncomfortable answering them, ask for a referral to a clinician who specializes in sexual function.

Originally published Jan. 1, 2008; last reviewed April 22, 2011.