Higher pulse pressure and risk for cardiovascular events in patients with essential hypertension: The Campania Salute Network.

Abstract

Background Increased pulse pressure is associated with structural target organ damage, especially in elderly patients, increasing cardiovascular risk. Design In this analysis, we investigated whether high pulse pressure retains a prognostic effect also when common markers of target organ damage are taken into account. Methods We analysed an unselected cohort of treated hypertensive patients from the Campania Salute Network registry ( n = 7336). Participants with available cardiac and carotid ultrasound were required to be free of prevalent cardiovascular disease, with ejection fraction ≥50%, and no more than stage III Chronic Kidney Disease. The median follow-up was 41 months and end-point was occurrence of major cardiovascular events (i.e. fatal and non-fatal stroke or myocardial infarction and sudden death). Based on current guidelines, pulse pressure ≥60 mm Hg was classified as high pulse pressure ( n = 2356), at the time of the initial visit, whereas pulse pressure <60 mm Hg was considered normal ( n = 4980). Results High pulse pressure patients were older, more likely to be women and diabetic, while receiving more antihypertensive medications than normal pulse pressure (all p < 0.0001). High pulse pressure exhibited greater prevalence of left ventricular hypertrophy, and carotid plaque than normal pulse pressure (all p < 0.0001). In Cox regression, high pulse pressure patients had 57% increased hazard of major cardiovascular events, compared to normal pulse pressure (hazard ratio = 1.57; 95% confidence interval: 1.12-2.22, p = 0.01), an effect that was independent of significant prognostic impact of older age, male sex, diabetes, left ventricular hypertrophy, carotid plaque and less prescription of anti-renin-angiotensin system therapy. Conclusions High pulse pressure is a functional marker of target organ damage, predicting cardiovascular events in hypertensive patients, even independently of well-known structural markers of target organ damage.