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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.

The role of resting Heart Rate on the progression of arterial stiffness has not yet been extensively evaluated. The aim of this study is to investigate the relationship between resting HR and baseline arterial stiffness (evaluated by cfPWV) as well as its progression in a population of hypertensive patients over a 3.7 years follow-up period.

Background Heterogeneous results have been obtained regarding the presence of Target Organe Damage (TOD) in subjects with high-normal Blood Pressure (BP) value (sistoly 130–139, diastolic 85–89 mmHg). Purpose Aim of our study was to assess the prevalence of TOD in healthy subjects with high-normal BP comparing them with subjects with BP values that are considered normal (<130/85 mmHg) or indicative of hypertension (≥140/90 mmHg). Methods 755 otherwise healthy subjects participated at the present analysis. TOD was evaluated as Pulse Wave Velocity (PWV), Left Ventricular Mass Index (LVMI) and carotid Intima-Media Thickness (IMT) and plaque. Results When subjects were classified according to BP levels we found that high-normal BP group showed intermediate values of PWV and LMVI with higher value of IMT. This corresponds to intermediate prevalence of arterial stiffness (PWV>10 m/s: 3.4% vs 2.3% for normal and 9.6% for high BP groups, p=0.0014), Left Ventricular Hypertrophy – LVH (32.4% vs 25.7% for normal and 46.6% for high BP groups, p=0.0001) while there were no differences for IMT>0.9 or carotid plaque. At multivariable analysis the odds of having a PWV>10 m/s (OR=1.75, 95% C.I. 0.59–5.16), an IMT>0.9 mm (OR=1.81, 95% C.I. 0.60–5.00) or a LVH (OR=1.1, 95% C.I. 0.72–1.67) in the high-normal group resulted not different to the normal group. Conclusions In our otherwise healthy population, high-normal BP values were not related to aortic, carotid or cardiac TOD.

SARS-CoV-2 infection determines a disease that predominantly affects lungs. However the cytokines storms, determined by the huge immune response to the infection, could affect also other organs and apparatus such as heart and vessels. Beyond the acute inflammation itself also hypercoagulative status has been linked to SARSCoV-2 infection and this surely relates to the increase seen in prevalence of pulmonary embolism and myocardial infarction. A number of cardiac abnormalities and pathologies have been observed, with special attention to cardiac arrhythmias and myocardial involvement. Furthermore, indirect damages determined by the reduction in acute and chronic cardiovascular care, results in a strong mortality and morbidity outcomes in cardiological patients. In this review we will summarise current knowledge on both direct and indirect cardiovascular damages determined by the SARS-CoV-2 pandemia.