Abstract

Purpose We established hemodynamic predictors of response to intracavernous pharmacotherapy. Materials and Methods Specific characterization and quantification of hemodynamic abnormalities of the cavernous arterial inflow and corporeal veno-occlusive mechanism associated with failure to respond to intracavernous pharmacotherapy were performed retrospectively in 69 patients with nonendocrinological impotence. We investigated atherosclerotic vascular risk factors, duplex ultrasonography peak systolic and end diastolic velocities (10 microgram prostaglandin E1), and dynamic infusion cavernosometry and cavernosography parameters (60 mg. papaverine and 6 mg. phentolamine). Results The patients were stratified by severity of the various hemodynamic parameters encountered and mean dose required for response. Response subsequently was characterized as excellent (75 percent or greater rigid erections) in 36 patients, adequate (erections sufficient for intromission) in 17 and poor or absent in 16. Psychogenic, neurogenic and mild vasculogenic causes were noted in patients with an excellent response. The adequate responses included all 3 cases with mild to moderate vascular etiologies whereas patients with a poor or no response had only severe venogenic and combined arteriogenic and venogenic etiologies. Mean flow-to-maintain values plus or minus standard deviation of 9.7 plus/minus 3.7, 10.8 plus/minus 9.5 and 59.5 plus/minus 24.2 ml. per minute were demonstrated in the excellent, adequate and poor or no response groups, respectively. There was a good correlation between mean flow-to-maintain values and mean doses of our standard vasoactive solution (r 2 = 0.88, p less than 0.0001). Pharmaco-cavernosography demonstrated diffuse or pan-cavernous corporeal veno-occlusive dysfunction in the poor or no response group. Conclusions Corporeal veno-occlusive dysfunction alone or combined with arterial disease is the specific hemodynamic abnormality causing nonresponse to intracavernous pharmacotherapy. Diffuse drainage, particularly involving the glans penis and corpus spongiosum, is greatly predictive of a poor or no response, reflecting the underlying cavernous smooth muscle myopathy and collagen degenerative alterations in these patients with end-organ failure.

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