Our study demonstrated a higher prevalence of ED in hypertensive patients than in normotensive individuals (32.1% vs. 16.0%). This finding is consistent with reports from previous studies in Nigeria.[5
] However, the prevalence of ED is lower than findings in some Caucasian studies.[6
] For instance, Aranda et al
] reported a prevalence of ED among hypertensive patients of 46% in Spain where patients with diabetes mellitus were included in the study. In this study, diabetes mellitus was an exclusion criterion and only newly diagnosed hypertensive patients were used. Thus, the difference in prevalence may be due to study methodology including the selection of patients.
Hypertensive patients with ED have significantly higher cardiovascular risk factors when compared to their counterparts without ED and to the normotensive controls. This is consistent with findings in previous studies.[5
] These cardiovascular factors have been implicated in the pathogenesis of ED in HBP.[25
] MA was found in 37% of the hypertensive patients as against 6.7% in the controls. This finding is higher than that of Akinsola et al
. who reported 17.4% prevalence of MA in HT. The difference may be attributed to patient selection as we recruited hypertensive patients who had never been treated previously for the study. Treatment of HBP with antihypertensive medications, particularly angiotensin-converting-enzyme (ACE) inhibitors, has been found to improve MA.[27
] In our study, MA, a cardiovascular risk factor and marker of endothelial damage, is also significantly more common in hypertensives with ED than in hypertensives without ED. That is, patients with ED are more likely to have endothelial damage and dysfunction than their counterparts without ED. The study also revealed that ED may also be related to cardiac damage as significantly more hypertensive patients with ED have ECG LVH.
ED is often a sentinel manifestation of damage to the vascular endothelium.[28
] The main link between ED and cardiovascular disease is the vascular endothelium, which has a fundamental role in the regulation of circulation. The formation of nitric oxide is a fundamental link between the endothelium and ED.[25
] Nitric oxide is produced in the endothelial cells by nitric oxide synthase. Its release stimulates the relaxation of smooth muscle cells of the corpus carvernosum. Thus, once the ability to generate nitric oxide has been compromised, ED may ensue.[25
] The study shows that MAL and ED might represent different variables with a common pathological process such as vascular damage. This hypothesis is consistent with the finding of Pedrinelli et al
] who reported that MA was strongly associated with C-reactive protein (CRP) which is an evidence of subclinical inflammation. CRP is also a cardiovascular risk factor and predicts cardiovascular prognosis independent of conventional risk factors.[32
] Thus, vascular damage with possible atherosclerosis and the resultant inadequate blood flow to the erectile tissue might cause ED.
There are conflicting reports on the role of cigarette smoking in the etio-pathogenesis of ED. Moreira et al
] showed a 2.5-fold increased risk of ED among smokers in contrast to the study by Doumas et al
] and the Massachusetts Male Aging Study[34
] where smoking was found not to be associated with ED. This notwithstanding, long-term cigarette smoking is a major risk factor for vasculogenic ED because of its effects on the vascular endothelium.[34
] Cigarette smoking decreases the nitric oxide synthase activity in the penis. It also causes nicotine-induced vasoconstriction of the cavernous smooth muscle.[34
] In our study, patients with ED were significantly more likely to be cigarette smokers than those without ED. This is consistent with the report of a Nigerian study by Opadijo.[5
] The effect of alcohol on penile erection depends on the volume and the duration of consumption. Although small quantities of alcohol may improve erection and enhance libido, large amounts result in central sedation, depression of libido, and ED.[35
] Polyneuropathy from chronic alcoholic intake may also cause or worsen ED.[35
] In our study, we found no association between alcohol ingestion and ED. However, one of the limitations of the study is that the alcohol ingestion was not quantified.