Erectile dysfunction and heart disease are very serious medical conditions that requires prompt treatment. In addition to being a symptom of heart disease; ED is linked to many other physical and psychological problems. Men with ED can be withdrawn from their partner and even avoid romantic relationships. It may be difficult for men with erectile dysfunction to reproduce and can lead to low self-esteem, depression and poor work performance. Frequent medical check ups for patients with erectile dysfunction and high blood pressure is recommended.
Some research even suggests the effect of blood pressure drugs may be more psychological than physical. When ED occurs after a man begins to take a new medication, it's possible that anxiety about his health, rather than the medication, may trigger the problem. And being aware of possible side effects may make a man more likely to recognize them as abnormal.
How common is impotence? According to findings from several studies, including “The Massachusetts Male Aging Study,” overall prevalence for men between 40–70 years old is around 52 percent (or around 30 percent of all men between 18–60 years old). That’s right — nearly half of all men over 40 experience erectile dysfunction symptoms at some point. Not surprisingly, research demonstrates that impotence is increasingly prevalent with age. Around 40 percent of men in their 40s experience sexual dysfunction. Up to 70 percent of men in their 70s experience ED. (1) Every year more than 617,000 new cases of impotence occur in the United States alone.
The recommended dosage of sildenafil is 50 mg/day, usually taken 1 hour before sexual activity. This dose may be increased to 100 mg or decreased to 25 mg based on side effects.6 PDE5 inhibitors also have a beneficial effect in the treatment of heart failure with reduced ejection fraction as well as pre- and post-capillary pulmonary hypertension. The use of PDE5 inhibitors in the treatment of right heart failure and left ventricular failure associated with combined pre- and post-capillary pulmonary hypertension has been well studied.71,72
Erectile dysfunction (ED) is defined as the inability to achieve or maintain an erection for satisfactory sexual performance. The prevalence of ED has been estimated as nearly 40% of men >40 years of age1 although these figures are contested.2 ED increases in frequency with age and is estimated to affect 15% of men aged 40–50 years, 45% of men in their 60s and 70% of men older than 70 years.3 Successful erection is a complex system involving reflex action (peripheral nerves and spinal cord), the limbic system (psychogenic stimuli) and the release of nitric oxide. Adequate levels of testosterone are required, and hence an intact hypothalamic/pituitary/testicular axis. Hence, ED can result from disease or treatment that produces hormonal deficiency, neurological impairment, problems with penile blood flow, disorders of tissue mechanics, psychological factors or any combination of these.
Penile implants - are generally used if physical damage (like an accident) makes the anatomical parts needed for an erection not work. These are inserted by surgery and can provide a permanent treatment choice if others fail to work. The implants can be semi-rigid or inflatable. They can be pretty expensive and are not usually available on the NHS.
But recently Brandon had some troubles keeping it up. At first, Kayla just thought it was her and that he needed some kind of a change to what they usually did, but later Brandon admitted that as of late, he just couldn’t seem to maintain an erection, and that it took way too much effort to go long. It wasn’t that he wasn’t aroused; his body just wasn’t keeping up.
Erectile dysfunction is an accurate predictor of heart attacks and strokes in the future. Psychogenic components play a role in erectile dysfunction, but the most common and primary cause in most men is organic vascular insufficiency, meaning not enough blood gets to the penis. Erectile dysfunction usually occurs one to five years before a male manifests overt signs of cardiovascular disease. The first sign may be death.
PubMed | Google ScholarSee all References A dose-related phenomenon with propranolol use was suggested by another study, which showed that patients receiving propranolol dosages exceeding 120 mg/d developed ED at a higher rate than patients who received lower dosages of the same medication.43x43Warren, SC and Warren, SG. Propranolol and sexual impotence [letter]. Ann Intern Med. 1977; 86: 112
David F. Penson, MD, MPH, is an associate professor of urology and preventive medicine in the Keck School of Medicine at the University of Southern California, in Los Angeles. Hunter Wessells, MD, is an associate professor of urology at the University of Washington School of Medicine and chief of urology at Harborview Medical Center in Seattle, Wash.
Beta-blockers: A popular blood pressure medication that affects part of the nervous system in an attempt to slow and regulate heartbeats, helping reduce blood pressure. Unfortunately, this same part of the nervous system is also responsible for causing erections, and when beta blockers are used, it indirectly reduces the amount of blood flow to the penis.
The common associations between cardiovascular disease and ED have led some researchers to explore whether onset of ED can be an effective predictor of the presence of cardiovascular disease. A study of 40 patients with cardiac disease found an association between sexual dysfunction and the presence of cardiovascular disease, as well as a correlation between the severity of ED and the number of coronary arteries with extensive atherosclerosis.16x16Greenstein, A, Chen, J, Miller, H, Matzkin, H, Villa, Y, and Braf, Z. Does severity of ischemic coronary disease correlate with erectile function?. Int J Impot Res. 1997; 9: 123–126
The vascular endothelium has an important role in angiogenesis and vascular repair by producing regulatory substances, including NO, prostaglandin, endothelins, prostacyclin and angiotensin II. These regulatory factors regulate the blood flow to the penis by controlling smooth muscle contractility and subsequent vasoconstriction and vasodilatation. Generally, in erectile tissue, increased blood flow through the cavernosal artery increases shear stress and produces NO, which further relaxes the vascular smooth muscles and increases blood flow in the corpora cavernosa.54 These events cause penile erection. However, in ED, endothelial NO synthesis is reduced and there is increased endothelial cell death (Figure 2).55
Experimental hyperglycemia may also affect cavernosal smooth muscle cell contractile responses. In experimental diabetes, penile smooth muscle has augmented force responses to vaconstrictors, possibly mediated by changes in expression of protein kinase C and the RhoA-Rho kinase Ca2+-sensitization pathway.32 These changes may promote flaccidity and alter the relaxation responses to nitric oxide. End-stage penile dysfunction may occur as a result of diabetes, with progressive loss of normal cavernosal endothelium and smooth muscle cells from the corpus cavernosum.33 Replacement by fibrotic tissue may lead to complete erectile failure.34
Neurological (nerve and brain) diseases: The nervous system plays a vital part in achieving and maintaining an erection. It is common for men with conditions such as stroke, multiple sclerosis (MS), Alzheimer’s disease, Parkinson’s disease, and spinal cord injuries to experience ED. This is due to an interruption in the transmission of nerve impulses between the brain and the penis.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References Phosphodiesterase type 5 is found predominantly in the smooth muscle of the corpora cavernosa but can be found in smaller quantities in platelets and other vascular smooth muscle.56x56Wallis, RM, Corbin, JD, Francis, SH, and Ellis, P. Tissue distribution of phosphodiesterase families and the effects of sildenafil on tissue cyclic nucleotides, platelet function, and the contractile responses of trabeculae carneae and aortic rings in vitro. Am J Cardiol. 1999; 83: 3C–12C