Unlike intraurethral suppositories, intracavernosal injection (IC) injection of vasoactive agents such as PGE-1 has consistently been shown to be effective in the treatment of ED in men with diabetes. In a study of 336 men with diabetes-related ED, 83% of patients reported erections satisfactory for intercourse after IC injection of PGE-1.55 Unfortunately, 24% of these patients also reported penile pain, one of the most common side effects of IC injection therapy. Other studies have noted similar effectiveness rates.56,57
You put your penis in the cylinder and start pumping. The suction creates a vacuum, so blood rushes in to fill the spaces in the spongy tissue of the penis, creating an erection. The erection lasts only as long as the blood stays in, so you slide the band down around the base of your penis, trapping the blood. It's safe to keep the band on for up to 30 minutes.
Erectile dysfunction (ED) is commonly called impotence. It’s a condition in which a man can’t achieve or maintain an erection during sexual performance. Symptoms may also include reduced sexual desire or libido. Your doctor is likely to diagnose you with ED if the condition lasts for more than a few weeks or months. ED affects as many as 30 million men in the United States.
The blood supply to your penis starts in your heart and flows through arteries in the belly to even smaller arteries that branch off to carry blood into the penis. With sexual stimulation, these blood vessels need to rapidly increase blood flow. If these blood vessels are blocked (atherosclerosis) by coronary artery disease, you may not be able to achieve or maintain an erection.11
"The answer to the question, 'Can patients with heart disease safely have sex?' is almost always 'Yes,' unless they have such bad heart failure or severe artery disease that even a moderate amount of exertion will cause terrible chest pain," says Richard Stein, MD, who is director of preventive cardiology at New York City's Beth Israel Hospital. "And if that is the case, sex is probably the last thing on their minds anyway."
** Indeterminate risk patients include diabetics, those with mild or moderate stable angina pectoris, past myocardial infarction (2-8 wks) without intervention awaiting exercise electrocardiography, congestive heart failure (NYHA class III), and noncardiac sequelae of atherosclerotic disease (eg, peripheral artery disease and a history of stroke or transient ischemic attack); this patient with ED may require assessment for additional vascular disease using carotid intima-media thickness or ankle-brachial index and subsequent reclassification to low or high risk.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (24) | Google ScholarSee all References Erectile function relies on the arterial blood supply from the internal pudendal arteries, which are branches of the hypogastric arterial system (Figure 1). Substantial increases in internal pudendal arterial flow result in pressures within the penis that are comparable to systemic arterial levels.12x12Rampin, O and Giuliano, F. Central control of the cardiovascular and erection systems: possible mechanisms and interactions. Am J Cardiol. 2000; 86: 19F–22F
A follow-up study from the ExCEED database compared men with ED and prostate cancer to men with ED without prostate cancer and found that the prostate cancer survivors had worse erectile function but reported better quality of life than those without prostate cancer.37 The authors hypothesized that the prostate cancer survivors were able to “rationalize” away their sexual dysfunction with the knowledge that they may have been “cured” of their prostate cancer. Clearly, diabetic men could not use the same rationale.
First of all, libido (sexual desire) triggers a sympathetic (adrenaline-dependent) nervous system reaction mediated through the thoracic spinal cord. Also important is tactile stimulation, the pleasurable effect of touch, which is mediated through the acetylcholine-dependent parasympathetic nervous system. Both the sympathetic and parasympathetic forces regulate the release of nitric oxide—the universal artery-relaxing agent—from the cells lining the penile arteries and all its smaller branches. Nitric oxide causes the arteries to enlarge, increasing blood flow into the penile tissues. This is followed by compression of blood-draining penile veins, which causes blood to engorge the penis and create an erection.4
Abstract | Full Text PDF | PubMed | Scopus (16) | Google ScholarSee all References These medications cause intracavernosal pressure changes in animal models, and human studies have noted deleterious effects on erectile function, decreased libido, and ejaculatory problems.42x42Weiss, RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician. 1991; 44: 2075–2082
A component of the increased risk conferred by ED could be testosterone deficiency.24 Low testosterone leads to increased levels of total and LDL cholesterol, as well as to increased production of pro-inflammatory markers and mediators.25 Endothelial dysfunction and increased arterial wall thickness, stiffening, and calcification also ensue. On this basis it has been hypothesized that chronically lowered testosterone may increase CVD risk. Indeed, androgen deficiency has emerged as a predictor of CV events, as well as of all-cause and CV mortality, both in the general population and in patients with CV risk factors, with hypertension, with established CVD, and with ED.26 Viewed from the opposite angle, higher serum testosterone showed a protective role for CV events in elderly men.27 A 2010 meta-analysis limited to studies in middle-aged men found no association between total testosterone (TT) levels and CVD risk.28 However, a more recent meta-analysis involving a larger number of studies identified significant associations between androgen deficiency and increased risk of CVD and CVD mortality.29 It should be stressed, however, that the nature of these studies cannot prove causality. The possibility that low testosterone may be an epiphenomenon, marking poor general health rather than modulating CVD risk per se has to be explored.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (58) | Google ScholarSee all References Erectile dysfunction secondary to cardiovascular disease often responds well to the standard ED treatments developed over the past few decades. Penile prosthesis implantation was developed in the 1970s, followed by intracavernosal injections of vasoactive agents, including papaverine, phentolamine, and prostaglandin E1, introduced in the 1980s.11x11Nehra, A. Intracavernosal therapy: when oral agents fail. Curr Urol Rep. 2001; 2: 468–472
Talk with your doctor about your sexual health. Do not be shy or embarrassed. Your doctor has probably dealt with this issue before. If your doctor is an older man, he might even have ED. First, your doctor will figure out what is causing your ED, which can usually be done just by talking with you. Next, your doctor will look for risk factors for atherosclerosis (the Table) by asking you questions, checking your blood pressure, and performing a few blood tests. Identifying and successfully treating atherosclerotic risk factors can reduce the chance of developing major vascular events (heart attacks and strokes).
While a widely held perception is that CVD drugs cause ED, data attest towards the contrary and some agents may be even beneficial.41 Only thiazide diuretics lead clearly to ED, while some older beta-blockers also do so, but the side-effect of ED was very low (∼3%) when the patient was blinded for the drug administration.42 In fact, the vasodilating nebivolol may even improve erectile function.35,43 ACE-inhibitors, angiotensin-receptor blockers, and calcium-channel blockers are reported to have neutral or even a positive effect on erectile function35,41,43 but more evidence is needed. Regarding statins, the largest body of evidence point towards a beneficial effect.44 A negative effect has been reported in high statin doses, possibly related to a potential reduction in serum testosterone levels, but this dose dependency warrants further investigation. In terms of patient management, when ED onset and therapy initiation are linked and a cause-and-effect association is presumed, a short period of drug withdrawal with monitoring for ED resolution for verification may be an option. In patients who developed ED long after the initiation of CV drug treatment, sexual dysfunction is less likely to be drug associated and PDE5 inhibition therapy may be initiated.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Risk of arrythmias after sexual intercourse was evaluated in 82 patients with stable coronary artery disease who were monitored with ambulatory ECG after sexual intercourse.81x81Drory, Y, Fisman, EZ, Shapira, Y, and Pines, A. Ventricular arrhythmias during sexual activity in patients with coronary artery disease. Chest. 1996; 109: 922–924
Abstract | Full Text | Full Text PDF | PubMed | Scopus (30) | Google ScholarSee all References Penile sympathetic stimulation flows through several pathways, including the sympathetic chain ganglia, which also supply such structures as the heart and vascular system. Sympathetic tone precipitates release of norepinephrine from penile adrenergic nerves, resulting in tonic contraction of cavernosal smooth muscle and its vasculature, thereby keeping the penis flaccid.9x9Andersson, K and Stief, C. Penile erection and cardiac risk: pathophysiologic and pharmacologic mechanisms. Am J Cardiol. 2000; 86: 23F–26F
ED is easily and successfully treated! If your sex drive is unaffected, but you experience problems achieving or sustaining erection for a period of four to five weeks, you may have ED. Talk to your doctor immediately. Don’t delay—erectile dysfunction doesn’t “just go away!” Additionally, ED could be a sign of a serious, even life-threatening complication, such as congestive heart failure or kidney disease. Ignoring your ED because it’s embarrassing could jeopardize your health.