MO570PULSE PRESSURE: A PREDICTOR OF CARDIOVASCULAR CALCIFICATION AND CARDIOVASCULAR MORTALITY IN HEMODIALYSIS PATIENTS

Abstract

Abstract Background and Aims The mortality rate is extremely high in chronic kidney disease (CKD), primarily due to the high prevalence of cardiovascular disease (CVD). Increased pulse pressure (PP), defined as the difference between inappropriately elevated systolic blood pressure (SBP) and reduced diastolic blood pressure (DBP) at any value of mean arterial pressure (MAP), is a surrogate measure of increased arterial stiffness of central elastic arteries (aorta and its major branches). CKD-MBD anomalies leading to calcification contribute to increased arterial stiffness and pulse pressure. This study aimed to evaluate the relationship of pulse pressure parameter with valve calcification and abdominal aortic calcification in hemodialysis patients and its impact on cardiovascular mortality. Method We performed a prospective case series study with 3 years follow- up. Plain X-ray images of the lateral lumbar spine from all subjects were studied to obtain images of the lower abdominal aorta using semiquantitative scores as described by Kauppila et al. Cardiac valve calcifications were evaluated by two-dimensional echocardiography with an HDI 5000 Sono CT echocardiographic machine with a 3.3-MHz multiphase array probe in subjects lying in the left decubitus position an according to the recommendations of the European Association of Echocardiography. The patient was evaluated as having vascular calcification if he had the presence of calcification in at least one of the site examined: a mitral valve, aortic valve or abdominal aorta. Results We studied 85 chronic stable hemodialysis patients. Mean age and meantime is therapy was 49.9±12.4 years and 51.5±28.7 months, respectively. Mean pulse pressure was 55.72±14.2 mmHg. Fifty-nine patients (69.4%) were identified with aortic abdominal calcification, and the mean Kauppila score was 4.91 ± 4.05. Sixty patients (70.5%) had at least one valve calcified, while thirty-three patients (38.8%) had both valves calcified. Univariate analysis revealed that every 1 mmHg increase in pulse pressure was associated with increased cardiovascular calcification risk p=0.020. In multivariate analysis, after adjustment for age, gender, diabetes mellitus, cholesterol, and triglyceride serum levels, the association also remained strong, where every increase of 1 mm Hg in pulse pressure was associated with increased risk for cardiovascular calcification (HR 1.02, 95% CI (1.00-1.03), p= 0.038). Besides, pulse pressure was an independent predictor for cardiovascular mortality (HR 1.03, 95% CI (1.02-1.05), p=0.002). Conclusion Pulse pressure may identify hemodialysis patients with subclinical cardiovascular calcification who need further evaluation. Wide pulse pressure is associated with increased cardiovascular mortality.