Objectives Viscous and inertial components contribute to arterial distensibility and compliance in vitro. The purpose of our study was to determine whether this phenomenon is of relevance in vivo, namely, whether arterial compliance is altered by an increase in heart rate Design Arterial diameter was assessed by an echo-Doppler device in a common carotid and femoral artery, namely, in a large elastic and a muscle artery. The studies were performed in 12-week-old pentobarbitone-anaesthetized Wistar-Kyoto rats subjected to atrial pacing via a transjugular unipolar catheter at five different randomly sequenced rates (280, 310, 340, 370 and 400 beats/min). After each stage, spontaneous sinus rhythm was allowed to return. Blood pressure was measured via a catheter inserted into the carotid or femoral artery contralateral to the vessels in which the diameter was measured. Arterial compliance and distensibility values were derived according to the Langewouters formula Results A progressive increase in heart rate caused by pacing was accompanied by progressive and marked reductions in carotid artery compliance and distensibility. When quantified by the area under the distensibilitypressure or compliance-pressure curve the reduction was in the range 15-43%. Although a tendency to a similar phenomenon was observed in the femoral artery, in the latter vessel the reduction in distensibility and compliance was less marked and statistically insignificant Conclusions In the anaesthetized rat acute increases in heart rate are accompanied by reductions in arterial compliance and distensibility. The effect is greater in elastic than in muscle arteries

Uric acid (UA) is the final product of the catabolism of endogenous and exogenous purine nucleotides. While its association with articular gout and kidney disease has been known for a long time, new data have demonstrated that UA is also related to cardiovascular (CV) diseases. UA has been identified as a significant determinant of many different outcomes, such as all-cause and CV mortality, and also of CV events (mainly Acute Coronary Syndromes (ACS) and even strokes). Furthermore, UA has been related to the development of Heart Failure, and to a higher mortality in decompensated patients, as well as to the onset of atrial fibrillation. After a brief introduction on the general role of UA in CV disorders, this review will be focused on UA’s relationship with CV outcomes, as well as on the specific features of patients with ACS and Chronic Coronary Syndrome. Finally, two issues which remain open will be discussed: the first is about the identification of a CV UA cut-off value, while the second concerns the possibility that the pharmacological reduction of UA is able to lower the incidence of CV events.

Objective: The role of risk factors on the progression of arterial stiffness has not yet been extensively evaluated. The aim of the current longitudinal study was to evaluate the determinants of the PWV progression over a 4 years follow-up period in hypertensive subjects. Materials and Methods: We enrolled 333 consecutive hypertensive outpatients 18–80 aged, followed by the Hypertension Unit of St. Gerardo Hospital (Monza, Italy). At baseline anamnestic, clinical, BP, laboratory data and cfPWV were assessed. We performed a PWV follow-up examination with a median time amounting to 3.75 ± 0.53 years. Results: At baseline the mean age was 54.5 ± 12.6 years, SBP and DBP were 141.3 ± 18.6 and 86.4 ± 10.4 mmHg and PWV was 8.56 ± 1.92 m/s. Despite an improvement in BP control (from 37 to 60%), at follow-up the population showed a PWV increase (ΔPWV 0.87 ± 3.05 m/s). PWV and ΔPWV gradually increased in age decades. In patients with uncontrolled BP values at follow-up ΔPWV showed a greater increase as compared to patients with controlled BP (1.46 ± 3.67 vs 0.62 ± 2.61 m/s, p < .05). The independent predictors of ΔPWV were age, baseline PWV, baseline SBP/MBP and ΔSBP/MBP. Conclusions: the accelerated arterial aging in treated hypertensive subjects is in large measure explained by age and BP values. PWV changes over time would probably give important information that need further future research studies.

Central (aortic) systolic blood pressure (cSBP) is the pressure seen by the heart, the brain, and the kidneys. If properly measured, cSBP is closer associated with hypertension-mediated organ damage and prognosis, as compared with brachial SBP (bSBP). We investigated 24-hour profiles of bSBP and cSBP, measured simultaneously using Mobilograph devices, in 2423 untreated adults (1275 women; age, 18–94 years), free from overt cardiovascular disease, aiming to develop reference values and to analyze daytime-nighttime variability. Central SBP was assessed, using brachial waveforms, calibrated with mean arterial pressure (MAP)/diastolic BP (cSBP _MAP/DBPcal ), or bSBP/diastolic blood pressure (cSBP _SBP/DBPcal ), and a validated transfer function, resulting in 144 509 valid brachial and 130 804 valid central measurements. Averaged 24-hour, daytime, and nighttime brachial BP across all individuals was 124/79, 126/81, and 116/72 mm Hg, respectively. Averaged 24-hour, daytime, and nighttime values for cSBP _MAP/DBPcal were 128, 128, and 125 mm Hg and 115, 117, and 107 mm Hg for cSBP _SBP/DBPcal , respectively. We pragmatically propose as upper normal limit for 24-hour cSBP _MAP/DBPcal 135 mm Hg and for 24-hour cSBP _SBP/DBPcal 120 mm Hg. bSBP dipping (nighttime-daytime/daytime SBP) was −10.6 % in young participants and decreased with increasing age. Central SBP _SBP/DBPcal dipping was less pronounced (−8.7% in young participants). In contrast, cSBP _MAP/DBPcal dipping was completely absent in the youngest age group and less pronounced in all other participants. These data may serve for comparison in various diseases and have potential implications for refining hypertension diagnosis and management. The different dipping behavior of bSBP versus cSBP requires further investigation.

Heterogeneous results have been obtained in the relationship between serum uric acid (SUA) and target organ damage (TOD) in patients with hypertension. Clinic blood pressure, SUA, and cardiac, arterial (carotid and aortic), and renal TOD were assessed in 762 consecutive patients with hypertension. Hyperuricemia was defined as an SUA >7.0 in men and >6.0 mg/dL in women. Men with hyperuricemia compared with those with normal SUA showed lower estimated glomerular filtration rates and E/A ratios and a higher prevalence of carotid plaques. Women with hyperuricemia showed lower estimated glomerular filtration rates and E/A ratios and a higher intima‐media thickness. Except for pulse wave velocity, all TODs significantly correlated with SUA. However, at multivariate analysis, only estimated glomerular filtration rate was significantly determined by SUA. Our data provide evidence on the role of SUA in the development of TOD only in the case of renal alteration. It is likely that SUA may indirectly act on the other TODs through the increase in blood pressure and the decrease in glomerular filtration rate.