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Motivational Change for the Management of Male Sexual Health Concerns
Goals are collaboratively set, and the patient is given a menu of options. Change is seen as a continuum, and small steps are validated.
This is not easy, and sounds a bit superficial. Yet, it is often necessary to reframe, reflect, and note ambivalence when discussing behavior change. It is important to summarize to recap major points. I often leave patients with a memo stickie or notepad with a handwritten note detailing the goals of our compromise and plan: 1. 20 minutes of brisk walking till you sweat 3 days each week, with spouse if possible 2. No more than 6 cigarettes each day at planned intervals. 3. Cheating on one day a week when going out to dinner. 4. Yogurt smoothie for breakfast including fresh or frozen fruit ...
Finally, the focus for this is the rationale for intervention to reduce the risk of CAD. As an advocate for the emerging field of men’s health, and noting the nonmodifiable risk factor of gender and the Framingham data describing that men have the onset of symptoms of CHD ten years earlier than women, I look toward ways of intervening to reduce this risk particularly in men. Men, as noted in the Commonwealth Study of 2000, are less hesitant to seek medical care early or for prevention. In this regard, it should be noted that one of the most significant emerging risk factors for early or sentinel CAD in men is the presence of erectile dysfunction.
In an article published by Min in the Archives of Internal Medicine this January in 2006, 221 men referred for stress myocardial perfusion testing were assessed for the prevalence of ED, and the prevalence of severe coronary heart disease, and left ventricular dysfunction. ED was present in 54% of patients, and men with ED had significantly more severe CAD and LVD (Ejection fraction of <50%). ED was associated with a shorter exercise time and lower Duke treadmill score.
From this study it can be concluded that ED is a stronger predictor of both CAD and high-risk findings than traditional office based CV risk factors even without established CAD e.g. primary prevention.. Therefore, in the cascade of atherosclerosis as presented by Dr. Rippe and others, those men with CV risk factors including: age, gender, lipids, hypertension, diabetes, obesity, inactivity, smoking and poor diet result in subclinical disease burden such as LVH, coronary calcification, carotid stenosis, inflammation, arterial endothelial dysfunction, and procoagulant milieu. This in turn leads to the expression of clinical disease such as stroke, PVD, angina, MI, sudden death and heart failure. In a new diagnostic model for ED and CVD, cardiovascular risk factors lead to arteriole oxidative stress, endothelial cell compromise and smooth muscle dysfunction, inflammation, all leading to atherosclerosis and progression of occlusive vascular disease, thereby leading to the vascular events of CAD, MI, CVA, PVD and ED. Perhaps ED is the sentinel event. Thus, if we had a means to identify those men at greatest risk for CAD, we could aggressively partner with these individuals to modify risk.
In men, the penis can be a barometer of early vascular disease, and perhaps yield early detection. This is due to several factors: the small size of the penile arteries; the percentage of endothelial and smooth muscle cells per unit volume; and lastly, the fact that penis is an external organ and ED is easily recognized by men.
The article that established ED as an emerging risk factor for atherosclerosis and CVD was published by Dr. Ian Thompson and his group in JAMA this past December of 2005. In this article the 9,457 men aged 55 or older randomized to the placebo group in the Prostate Cancer Prevention Trial were evaluated every three months for ED and CVD between 1994 and 2003. A prospective assessment of incident ED was examined.
At study entry, 4,247 men had no ED or CVD. Yet, 57% of these men developed incident ED after 5 years; 67% developed ED by 7 years. Men with incident ED had a significantly increased risk of MI or angina compared to men with no ED. The study concluded that incident ED has a risk similar to family history of CAD, cigarette smoking, or dyslipidemia. It suggests that erectile function could serve as a surrogate measure of treatment efficacy in preventative interventions for cardiac disease. This is consistent with findings of an earlier study by Kaiser noting that impaired brachial artery endothelium was discovered in men with ED as compared to age-matched controls. ED appears to occur before the development of overt structural or functional vascular disease, and abnormalities in perpheral vascualr NO/cGMP vasodilator system may result in ED as an early clinical manifestation of CVD.
In summary, add ED to one of the modifiable risk factors for CVD. “A flagging penis” should raise the red flag of warning to evaluate the patient for arterial disease elsewhere. To paraphrase Drs. Solomon and Jackson, the advances in the field of research for ED include the increasing awareness of its high prevalence among men with CVD. An emphasis on this strong correlation with CVD would not only open the door to men to admit more feely to having ED, but would also bring about opportunities for health care systems to address the increasing prevalence of this distressing condition through cardiovascular risk assessment and modification. ED equals “early detection” equals “endothelial dysfunction” equals “early treatment” equals “education”.
Borrelli B. Using Motivational Interviewing to Promote Patient Behavior Change and Enhance Health. Medscape.com. August, 2006.
Min JK, Williams KA, Okwuosa TM, Bell GW, Panutich MS and Ward RP. Prediction of Coronary Heart Disease by Erectile Dysfunction in Men Referred for Nuclear Stress Testing. Arch Intern Med. 2006;166:201-206.
Kaiser DR, Billups KL, Bank AL. Impaired brachial artery endothelium dependent and independent vasodilation in men with erectile dysfunction and no other clinical cardiovascular disease. J. Am Coll Cardiol. 2004;43:179-184.
Solomon H, Man JW, Jackson G. Erectile dysfunction and the cardiovascular patient: endothelial dysfunction is the common denominator. Heart. 2003;89:251-254.
Thompson IM, Tangen CM, Goodman PJ, Probstfield JL, Moinpour CM, and Coltman CA. JAMA. 2005;294:2996-3002.
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