A total eclipse of the heart--and the prostate. But you can do something about it.
Q&A with Dr. Kevin McVary on the heart-prostate link.
By Howard Wolinsky
Kevin T. McVary, MD, FACS, is a professor of urology and director of the Center of Male Health Stritch School of Medicine, Stritch School of Medicine, Loyola University Medical Center in Maywood, Illinois, outside Chicago.
McVary is a rare expert on the heart and prostate gland and related issues.
He will be speaking at a fre Active Surveillance Patients webinar on Saturday, June 22, 2024, at noon Eastern. The program is entitled “Matters of the Heart—and the Prostate.” Register here: https://zoom.us/meeting/register/tJ0rdeGtrDIpEtynJ_U3A1rpWYkiCOHRMagt
Your heart is related to your prostate on many levels—biologically and symbolically. Erectile dysfunction can forecast a heart attack by years. Also, most of us who have prostate cancer will most likely die from heart disease, not prostate cancer.
Following is a Q&A The ACtive SUrveillor did with Dr. McVary:
(Dr. Kevin McVary.)
The Active Surveillor (TAS): What is the connection between the prostate and the heart?
Dr. McVary: They share many of the same age-related problems. How is that given they are so anatomically remote from one another? Both get diseases as men age. CAD [coronary artery disease] is a major cardiac one and is strongly affected by inflammation; hence, the relationship with cholesterol (the bad kind). Interestingly, the risk factors for BPH [benign prostatic hyperplasia, or enlarged prostate] and prostate cancer are also strongly influenced by high cholesterol.
Similarly, the risk for MI [myocardial infarction], etc., is strongly influenced by diabetes, obesity, smoking, and lack of exercise. Guess what? Identical for prostate disease: CaP and BPH
TAS: Should men with low-risk prostate cancer be more worried about being harmed or dying from heart disease than prostate cancer? What are the numbers?
McVary: Low-risk CaP is, by definition, one that can be safely monitored without invasive treatment. In doing so, men can be observed for many years (not ignored but retested periodically). Hence, these men, as they age, undergo cardiac risk progression. Thus, if the CaP does not progress, then they become at risk for another disease to get the “opportunity” to kill/affect them. Theyoutlive CaP only to enter other risk categories. CAD is the most likely in an aging male population
TAS: I've heard if you take care of your heart by exercising and watching your diet, your prostate health will follow? Is that true?
McVary: Yes - it relates to the above discussion.
TAS: What exercise and dietary programs are recommended for preventing or slowing prostate cancer?
McVary: Moderate exercise is enough. 20 minutes/day. It doesn't have to be Olympian exercise as there is NO ADDED risk reduction as you progress in exercise from moderate to intense.
Concerning diet - it's the same heart-healthy diet (DASH, Mediterranean diet). Pretty simple. I helped generate a cookbook for the AUA on this and used the dietician/nutritionist from the Loyola exercise center - Molly Downey. [Downloads are available here: https://www.urologyhealth.org/educational-resources/urologic-cancer-cookbook and there is also one on preventing kidney stones here: https://www.urologyhealth.org/educational-materials/kidney-cookbook }
TAS: How does erectile disorder fit in? Men typically go on AS to preserve sexual function and avoid incontinence. But what percentage of them end up with erectile disorder [ED} anyway based on age?
McVary: Those ED risks also relate to the same aging and inflammatory factors that effect cardiac and prostate health. IDENTICAL!!!
5% at age 45y, 25% at age 65y, and it gets worse from there.
The concept that ED may be related to cardiovascular risk factors and cardiovascular disease (CVD) came to the forefront with the publication of the 1994 classic article by Feldman et al. (1). ED is common, as is cardiovascular disease (CVD), as I mentioned above. As both affect similar age groups, it is not surprising that the two conditions frequently coexist. Both have a high incidence, while the prevalence of ED worldwide is currently estimated to affect up to 150 million men, and the population is aging.
By 2025, the prevalence is expected to increase to more than 00 million men (2). Although there are numerous causes of ED, including psychogenic, neurologic, endocrine, traumatic, and drug-related, the most common cause is vasculogenic (Figure below).
1. Feldman HA, Goldstein I, Hatzichristou DG, et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol 1994;151:54-61.
2. Jackson G. Erectile dysfunction and cardiovascular disease. Arab J Urol. 2012;11(3):212–6.
The findings in the Massachusetts Male Aging Study (MMAS) have stood the test of time as numerous articles published since the 1994 Feldman et al article have found similar associations between cardiovascular risk factors and the development of ED. The same vascular risk factors that contribute to coronary artery disease (CAD)- (atherosclerosis of the coronary arteries) contribute to the development of atherosclerosis in other vascular beds, including the blood vessels that supply the corpus cavernosum of the penis.
Concerning ED and heart disease:
The shared pathophysiology between CVD/heart disease and ED is well demonstrated. The medical literature has shown that heart disease and risk factors are a leading cause of ED and that ED is an early warning sign of cardiovascular disease. The fact that ED often coexists with hypertension, hyperlipidemia, and diabetes provides support for a vasculogenic etiology of ED as impaired endothelial function.
Beyond its association with vascular risk factors, vasculogenic ED has been recently recognized as a predictor of future cardiovascular events, most strikingly in men in their fifth and sixth decades. Consequently, the identification of vasculogenic ED in younger middle-aged men has potentially significant prognostic importance
TAS: Is ED the result of blockages in arteries in the area of the penis? Which patients should see the doctor about this? Is this something a urologist, a cardiologist, or both address?
McVary: The real culprit is endothelial cell dysfunction of which “blocked arteries “ is the end game.
Although there are numerous causes of ED in men over the age of 50 years, the most common cause is thought to be vascular. An erection can be viewed as a vascular event and factors that inhibit vasodilatation of the blood vessels to the penis inhibit this event. The risk factors affecting blood vessels, including heart disease, high cholesterol, high blood pressure, diabetes, obesity, and smoking, can all cause ED.
These can account for greater than 40% of all causes of ED. The development of endothelial dysfunction and atherosclerosis is a systemic disease; thus, when one vascular bed is affected, it is likely that other vascular beds are affected as well.
For a normal erection to occur, there must be an increase in blood supply to the corpus cavernosal, the erectile body of the penis. This process requires vasodilation of the arteries that supply the penis. For normal vasodilation to occur the endothelial cells and nerve cells in the corpus cavernosum release nitric oxide. This allows relaxation of the smooth muscle cells within the vasculature of the penis.
Cardiovascular risk factors, including hypertension, elevated cholesterol and low HDL levels, smoking, and diabetes, cause endothelial dysfunction. This results in the inability of the arteries to dilate normally to certain stimuli. This also results in increased endothelial permeability to lipids, and increased adhesion of macrophages (think inflammation as mentioned above), white blood cells, and platelets, leading to atherosclerotic plaque in the penile arterial system. In addition, damage to the endothelium leads to atherosclerotic plaques, which may lead to stenosis that physically obstructs blood flow.
Concerning who should start the evaluation: cardiology or urology? BOTH. The urologist is MOST likely to come across these men with ED and we then refer to cardiology
TAS: How would the blockages or ED be diagnosed? Ultrasound? Other imaging?
McVary: The Princeton IV Guideline references the utility of the 2019 American College of Cardiology (ACC)/American Heart Association (AHA) risk assessment guidelines using pooled cohort equations, which are based on age, sex, race, total cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, and whether the patient is receiving treatment for high blood pressure, has diabetes or smokes. This tool gives an estimate of the patient’s risk of a cardiovascular event within the next 10 years, which the Guidelines categorize as follows:
• Low risk: < 5%
• Borderline risk: 5% to <7.5%
• Intermediate risk: 7.5% to < 20%
• High risk: > or = 20%
This tool is an appropriate starting point for risk stratification in ED.
It is well known that the ACC/AHA Pooled risk ASCVD calculator is generally based on a small number of traditional CVD risk factors and thus, may be over-reliant on age. Thus, it may underestimate the risk of younger men and over-estimate the risk of older men. The Princeton IV Guidelines proposed more advanced testing for men aged 40-60, including those with borderline or intermediate risk 10-year risk (5-10%). The Princeton IV Guidelines suggest all men with this indeterminate risk receive a computed tomography (CT) coronary calcium measurement to detect the presence of subclinical CAD and the need risk factor amelioration. Based on this evaluation, further risk factor modification or statin therapy may be initiated, or a preventative cardiology consult may be obtained.
The Coronary Artery Calcium (CAC) test, also called a “heart scan,” is a CT scan of the heart done with a multidetector CT (MDCT) that takes detailed images of the arteries that supply blood to the heart muscle. The images show calcium deposits in the coronary arteries. Higher amounts of calcium are associated with more severe disease in the heart arteries. CAC scores are widely endorsed for advanced risk assessment in patients at borderline to intermediate risk in whom decisions about preventive therapy are uncertain. CAC scoring is widely accessible, fast (10-15 minutes), inexpensive (USD 75-150), and can be performed without heart rate control or intravenous contrast. One of the most common applications for CAC scoring in clinical practice is for precise risk assessment in patients with risk-enhancing factors—patients with risk conditions that place them at higher risk than expected based on traditional risk scores like pooled cohort equations.
Given the close correlation between ED and subclinical atherosclerosis as defined by CAC, and the fact that CAC scores are the single strongest predictors of CVD risk in current prevention guidelines, a strong case can be made for wider use of CAC scoring in patients with ED. In particular, in patients who would otherwise be borderline risk based on the pooled cohort equations (many young adult men), the presence of ED should be used as a rationale to conduct CAC scoring to guide earlier, personalized use of effective preventive therapies like statins, non-statin drugs, and aspirin.
TAS: What can be done about it?
If there are bad and dangerous blockages, early stenting is most common. Less bad: make changes in lifestyle, weight loss, stop the bad stuff (smoking, pot, vaping) better control diabetes.
TAS: I have heard about ultrasound being used to reduce the blockages and improve blood flow?
McVary: This is commonly done but is without good evidence. See the SMSNA [Sexual Medicine Society of North America] stance on this experimental procedure largely done for cash by MDs whose ethics should be challenged
TAS: Does ultrasound have proven benefits?
McVary: NO.
TAS: Any studies?
McVary: No good ones
TAS: How expensive is this approach?
McVary: $3,000-5,000. UP FRONT.
TAS: Do Medicare or conventional insurance cover these diagnostics and treatments?
McVary: NOPE
TAS: How successful is this approach?
McVary: No evidence that it helps
Kevin McVary, MD, is a professor of urology at Loyola Medicine outside Chicago. He joined Loyola from Southern Illinois University School of Medicine (SIU), where he was chair of the department of urology. Prior to SIU, Dr. McVary was director, Sexual Dysfunction, at Northwestern Memorial Hospital.
Dr. McVary has a long pedigree: He has served as president of the Chicago Urological Society, chair of the American Urological Association (AUA) clinical guidelines panel for benign prostate hyperplasia, a member of AUA clinical guidelines panels for erectile dysfunction and Peyronie's disease, associate editor of the Journal of Urology, co-chair of the National Comprehensive Cancer Network's Sexual Function Committee, chair of the Strategic Planning Committee of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), chair of the NIDDK urology section and advisor to the Food and Drug Administration's Center for Devices and Radiologic Health. He has published more than 290 peer-reviewed research articles.
(With apologies to Bonnie Tyler.)
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