Patients with AMI and AF/FL portend a poor prognosis in the long-term chiefly because of an excess of SD. Treatment with ACE-inhibitors and digitalis may have long-term beneficial effects on SD.

Serum uric acid (UA) has been shown to be a predictor of cardiovascular (CV) morbidity and mortality, and it may play a role in the pathogenesis of CV disease affecting vascular structure and function. However, there is limited evidence of its specific association with carotid artery stiffness and structure. The aim of our study was to evaluate whether UA is associated with early signs of atherosclerosis, namely local carotid arterial stiffness and intima-media thickening. We evaluated 698 consecutive asymptomatic patients, referred to the Cardiovascular Department for risk factors evaluation and treatment. All patients underwent carotid artery ultrasonography with measurement of common carotid intima-media thickness (IMT) and echo-tracking carotid artery stiffness index Beta. Patients with hyperuricemia (defined as serum uric acid ≥7 mg/dL in men and ≥6 mg/dL in women) had higher IMT (0.97±0.22 vs 0.91±0.18, p<0.001) and stiffness index Beta (8.3±3.2 vs 7.5±2.7, p=0.005). UA levels correlated with both IMT (r=0.225; p<0.001) and stiffness index Beta (r=0.154; p<0.001); the correlations were statistically significant in males and females. In a multivariate model which included age, arterial pressure, serum glucose and LDL-cholesterol, serum UA emerged as an independent explanatory variable of IMT and stiffness index Beta. Carotid IMT and local arterial stiffness are related to UA independently of established CV risk factors; UA may play a role in the early development of atherosclerosis.

Obesity represents a worldwide increasing health problem. Obesity, through complex and not fully understood pathogenetic mechanisms, induces different structural and functional changes of left heart chambers, right heart chambers, and arteries. Ultrasound techniques are the first choice for a comprehensive assessment of the cardiovascular adaptation to obesity. This review summarizes the up-to-date literature on the topic, with particular focus on the main clinical studies, which range over different cardiovascular adaptations to obesity, namely left ventricular mass, diastolic function, right ventricle structure and function, arterial stiffness, and intima-media thickness. Also, the importance of epicardial fat and of the degree of obesity is described. Finally, the role of weight loss and bariatric surgery and the study of cardiovascular obesity-induced abnormalities in children and adolescent are discussed.

Wave intensity (WI) is a hemodynamic index used to evaluate the interaction between the heart and the arterial system, measured with an echo-Doppler system at the level of the common carotid artery. WI has two peaks: W1 during early systole that represents left ventricular (LV) contractility, and W2 in late systole that is related to the inertia force during isovolumetric relaxation. The aim of this study was to determine whether WI parameters improve the prediction of poor outcome in patients with heart failure and reduced ejection fraction (HFrEF). Sixty-two patients (mean age 69.4 ± 11.5 years) in NYHA class II-III were followed up for 43.5 months. They underwent routine clinical work-up, transthoracic echocardiography and WI measurement. A stratified survival analysis was conducted using the Kaplan-Meier method. During follow-up, 23 patients died from cardiovascular causes. Survivors and non-survivors were similar in age, blood pressure, heart rate and echocardiographic parameters, except for LV end-diastolic volume indexed to body surface area, E/A ratio (higher in non-survivors) and deceleration time (lower in non-survivors). W2 (1950 ± 1006 vs 1117 ± 708 mmHg m/s(3), p = 0.001) was significantly lower in non-survivors, whereas W1 (6951 ± 4119 vs 5748 ± 3891 mmHg m/s(3), p = NS) was similar. At the end of follow-up, cardiovascular mortality was higher in patients with W1 ≤ 3900 mmHg m/s(3) (p = 0.02) and W2 ≤ 1000 mmHg m/s(3) (p = 0.0002). Only E/A (cut-off 1.5) was predictive of mortality (p = 0.05). In patients with HFrEF, WI parameters derived from the carotid artery better identified patients with poor prognosis and were significant predictors of cardiovascular mortality.

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