Higher rate of cardiovascular disease seen in men with CP/CPPS

May 18, 2011

Men with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) are associated with a higher rate of arterial stiffness and vascular endothelial dysfunction than those without the condition, say researchers from Cleveland Clinic.

Men with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) show a higher rate of arterial stiffness and vascular endothelial dysfunction than those without the condition, say researchers from Cleveland Clinic.

In a pilot cohort of men with CPPS, there was a higher incidence of peripheral arterial tone abnormalities than in a group of similarly aged asymptomatic controls. These abnormalities have been linked to the development of cardiovascular disease (ie, myocardial infarction, heart failure, and stroke).

"If confirmed, CPPS may emerge as an associated risk factor for cardiovascular disease and, much like in the young endothelial dysfunction population, could prompt early referral to an internist for preventative cardiology measures," said first author Daniel A. Shoskes, MD.

Dr. Shoskes and colleagues used the EndoPAT machine (Itamar Medical, Caesarea, Israel) to assess two endpoints: the augmentation index (AI), a measure of arterial stiffness; and the reactive hyperemia index (RHI), a measure of nitric oxide-mediated endothelial vasodilatation. Both elevated AI and diminished RHI suggest vascular and endothelial disease.

Twenty-one men with symptomatic, untreated CP/CPPS and 14 asymptomatic patients were tested with the EndoPAT machine. Symptom severity in patients was measured by the NIH Chronic Prostatitis Symptom Index (CPSI) and by the UPOINT system, a system developed by Dr. Shoskes that classifies patients with chronic pelvic pain syndrome.

Ages were similar in the CP/CPPS group and controls (median, 40 years). Patients had median symptom duration of 24 months (range, 3-440), mean CPSI score of 24.7±5.1 (range, 18-37) and mean UPOINT domains of 2.9±1.1 (range, 1-5).

AI was significantly higher (greater arterial stiffness) in CPPS patients versus controls (5.0%±2.3 vs. –6.0%±3.0, p=.006). RHI was significantly lower (more endothelial dysfunction) in CPPS patients (1.76±1.2 vs. 2.21±1.7, p=.03). Age had a negative correlation to RHI (Spearman R –0.48, p=.03) but not AI. There was no correlation between symptom duration, severity, or phenotype (number or type of UPOINT domains) and RHI or AI.