Aims We investigated the prevalence and risk factors for developing erectile dysfunction (ED) in 1312 Korean men with diabetes in a multicentre study. MethodsWe used the modified International Index for Erectile Function-5 criteria to identify mild, moderate and complete ED. A standardized face-toface questionnaire was used by trained interviewers, and validated against telephone interviews. We recorded the duration of diabetes, level of glycaemic control, vital signs, complications, exercise and alcohol and smoking habits, and diabetes treatments used. ResultsThe mean age and median duration of diabetes were 53.8 ± 6.65 and 6 years (range 1-43), respectively. The mean HbA 1c and fasting glucose levels were 7.9 ± 1.65% and 8.6 ± 2.82 mmol/l, respectively. The overall prevalences of mild, moderate, complete ED and all ED (mild-to-complete) were 20.1, 19.5, 25.8 and 65.4%, respectively. ED was more common with age, reaching 79.3% in men aged > 60 years. Subjects aged > 60 years and with a duration of diabetes > 10 years were at greatest risk for all ED (OR = 10.4, 95% CI 5.8-18.5, P < 0.001) and complete ED (OR = 13.2, 95% CI 7.3-23.9, P < 0.001) when compared with the reference group (age 40-50 years with duration < 6 years). Age, duration of diabetes, HbA 1c , insulin use, neuropathy and macrovascular complications were positively associated with ED, but alcohol consumption and exercise habits were negatively associated. ConclusionsThe prevalence of complete ED was approximately six times higher than in the general population.

Vardenafil 10 mg did not impair the ability of patients with stable CAD to exercise at levels equivalent or greater than that attained during sexual intercourse (average of 2.5 to 3.3 METS).

Herpesviruses have been implicated as etiologic factors in the pathogenesis of human arteriosclerosis. We have examined the pathobiological effects of human herpes simplex virus (HSV-1) infection in influencing lipid accumulation and metabolism in human and bovine arterial smooth muscle cells (SMC). Significantly greater amounts of saturated cholesteryl esters (CE) and triacylglycerols (TG) accumulate in HSV-Iinfected human and bovine arterial SMC than uninfected cells. This CE accumulation results, in part, from decreased CE hydrolysis. Furthermore, arachidonate-stimulated, HSV-1-infected arterial SMC have a reduced capacity to produce prostacyclin (an agonist of intracellular CE hydrolytic activity) than uninfected, stimulated SMC. It appears that HSV-1 may induce lipid accumulation in arterial SMC similar, in part, to the lipid accumulation observed in vivo during human atherogenesis. Thus, herpesviruses may contribute to lipid accumulation, which is a characteristic feature of atherosclerosis.

Atherosclerosis can be defined in broad terms as a vascular disease accompanied by dysregulation of cholesterol metabolism and the accumulation of smooth muscle cells and macrophages within the vessel wall. At the interface of the blood and the vessel wall is the endothelium, which actively participates in a plethora of critical homeostatic functions in addition to affecting cholesterol trafficking in the underlying smooth muscle cell and macrophage. These events include: 1) inflammation resulting in release of cytokines, 2) changes in vascular reactivity causing release of endothelial cell derived relaxing factor (EDRF) and PGI2, and 3) control of vascular smooth cell proliferation via release of growth factors and growth suppressor molecules. Each process has been linked to the regulation of cholesterol accretion in the arterial cell. Furthermore, each homeostatic process is regulated by transmembrane signaling mechanisms at the lipid-protein interface of the membrane. Data have emerged recently indicating that biological response modifiers that trigger transmembrane signaling work in a sequential manner to control cell function. We review studies of the regulatory mechanisms of transmembrane signal transduction that advance the concept that phosphorylation of the specific protein components of the receptor machinery may result in a cooperative cellular response to ligands that will ultimately affect cholesterol delivery and trafficking within cells. We review recent data demonstrating that eicosanoids and cytokines released from one cell activate their receptors on neighboring cells, and interact with each other during this "cross-talk phenomenon." Cross-talking among phosphorylation reactions involving, for example, protein kinases A and C and tyrosine protein kinase, coupled with the highly regulated eicosanoid pathways and the diacylglycerol-phosphatidyl inositol (DG-PI) system, are discussed in terms of their metabolic impact on cholesterol delivery, intracellular processing, and efflux.

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