ERECTILE DYSFUNCTION (ED) AS EARLY MARKER OF CEREBRAL ISCHAEMIC DEMAGE. IS IT USEFUL PERFORMING NEUROLOGICAL INVESTIGATIONS?

Title: Erectyle dysfunction as early marker of cerebral ischemic damage. Is it useful performing neurological investigations? Introduzione e obiettivi: Erectile dysfunction (ED) is not only an evidence of diffuse atherosclerosis, but it’s also an index of early endothelial damage. Many authors demonstrated the association with cardiovascular events and coronary artery diseases (CAD); the severity of ED was correlated with the angiographic extension of coronary atherosclerotic process. However, to date, few studies have given information about association between ED and subclinical cerebral ischaemic damage. The primary aim of this explorative study was to test the hypothesis that patients with isolated ED, without signs of systemic and carotid atherosclerosis, compared to healthy population, have a reduced cerebral vasoreactivity ( CVR) as a marker of endothelial damage. Materials and methods: 15 patients with erectile dysfunction ( ED+) and 15 without erectile dysfunction (ED-) subjects, matched for age and vascular risk factors, were submitted to andrological and neurolological screening. Ecocolordoppler of cavernous arteries and nocturnal penil tumescence rigidometry were performed. Neurological assessment was performed by carotid duplex ultrasound and Transcranial Doppler and by assessing cerebrovascular reserve on both middle cerebral arteries simultaneously calculating Vasomotor Reserve (VMR), measured after breath holding and hyperventilation and Breath Holding index.). Results:Carotid Duplex scanning showed a light carotid stenosis only in 3 patients (2 in the ED+ and 1 in the ED- group). No differences were observed in intima-media thickness between ED+ and ED. Slight slower mean middle cerebral arteries (MCA) flow velocities were observed in ED+ in respect to ED -. ED + patients showed a reduced VMR and a slower VMR rate of change in respect to ED. Conclusions: The reduced reactivity in patients with isolated ED may represent a marker of early cerebral vasomotor dysfunction due to subclinical endothelial damage. In our opinion performing neurological investigations is an unnecessary screening, even if our data encourage further studies about the relation between ED and cerebral ischaemic damage.