Giuseppe Ranieri

Aim: Nutritional interventions might prevent hypertension–related organ damage but are far to be fully defined. Coffee is one of the most used beverages all over the world. Many studies tried to define the optimal amount of coffee to understand whether coffee has a role in cardiovascular prevention. Thus, we evaluated heart and vascular damage in well–controlled hypertensives according to coffee consumption. Methods: We evaluated 316 primary hypertensives (150F, 166M, aged 62.22±10.76) evaluated for target organ damage. The number of coffee cups per day was asked during the visit. Results: The median coffee consumption was 2 cups per day and patients were subdivided into tertiles: Group 1, 0–1 cups 112 patients (57F, 55M; 64.21±10.91 y.), Group 2, 2 cups, 101 patients (53F; 48 M; 61.95±10.10 y.), Group 3, >2 cups, 103 patients (40F; 63M; 60.32±10.95 y.). No differences were seen in BMI, systolic and diastolic BP. Group 1 had a higher left ventricular mass than the other two groups (p= 0.0008 and p=0.019 respectively) while no difference there was between group 2 and 3. Similarly, Group 1 had a significant reduction in E/e’ ratio (p=0.042 and p=0.019, respectively). No significance was found between Group 2 and 3 for left ventricular mass and diastolic function. Group 3 had an increased intima–media thickness (p=0.004 and p=0.005 vs Group 1 and 2, respectively). Prevalence of carotid stenosis was lower in Group 3 (p=0.011 and p=0.039, respectively) and was comparable in Group 1 and 2. Conclusion: Coffee consumption at least of 2 cups/day may have a role in prevention of heart remodelling and diastolic dysfunction.

Background: Obstructive Sleep Apnoea (OSA) is a common nocturnal respiratory disorder and its role as a risk factor for the development of Pulmonary Hypertension (PH) is well known. It was already demonstrated that systolic pulmonary artery pressure (PAPs) in obese patients with OSA is higher than in obese patients without OSA (Carratù P. et al, Sleep Breath 2016; 20: 613-619). Aims: to evaluate correlations between nocturnal cardiorespiratory indices, as Apnoea-Hypopnea Index (AHI), Oxygen Desaturation Index (ODI) and Total Sleep Time with oxyhemoglobin saturation below 90% (TST90), and PAPs in obese patients affected by OSA. Methods: We studied 48 consecutive patients affected by OSA, defined according to AASM guideline (Berry RB et al, J Clin Sleep Med 2012; 8 (5): 597-619). Nocturnal Respiratory failure is defined as TST90 ≥ 30%. Eight patients were excluded due to the presence of Overlap Syndrome OSA-Chronic Obstructive Pulmonary Disease (COPD). We evaluated linear correlation between hypnological parameters (AHI, ODI and TST90) and PAPs. Statistical significance: P <0.05. Results: We demonstrated that there is no correlation between severity of OSA and PAPs. Comparing AHI and ODI with PAPs, statistical significance was not obtained (respectively P: 0.20; P: 0.33). A significant direct correlation was found only between PAPs and TST90 (P: 0.03). Conclusions: Nocturnal respiratory failure could be the real determining factor for pulmonary hypertension in patients with OSA, but these preliminary results need further studies on a bigger sample to be confirmed.

Abstract:  During hemodialysis, ultrafiltration (UF) seems to affect the dialytic dose because of convective removal of urea and contraction of its distribution volume. We aimed to assess whether the adoption of a decreasing UF profile could yield a different dialytic dose from that obtained with a constant UF mode. Ten patients were randomly assigned to undergo 12 sessions with a constant UF mode (phase A) followed by 12 sessions with a decreasing UF rate (phase B), or the reverse. Kt/V and urea reduction ratio (URR) were 1.77 ± 0.26 and 70.02 ± 8.26% in phase A vs. 1.81 ± 0.36 and 71.02 ± 6.48% in phase B, respectively, showing no significant difference. Measurement of the differences in volemic variations between the two phases showed a statistically significant difference at the second hour (P < 0.001, the volemic reduction being greater in phase B than A) and at the fourth hour (P < 0.001, being greater in phase A than B). In standard bicarbonate dialysis, the adoption of a decreasing UF profile rather than a constant one does not alter the efficiency of the dialytic treatment.

Endothelial dysfunction of the optic microcirculation is considered to be the main pathogenetic mechanism in nonarteritic ischemic optic neuropathy. The aim of the present work was to assess whether a clinical improvement is correlated with a reduction in the endothelial activation markers by means of LDL apheresis (LDLA). Three weekly sessions of LDLA were administered in 23 patients affected by nonarteritic ischemic optic neuropathy. Statistically significant reductions were achieved in all parameters: total cholesterol (44.6%), LDL cholesterol (54.6%), fibrinogen (60.9%), von Willebrand factor (38.6%), sE-Selectin (22.6%), sICAM-1 (14%) and sVCAM-1 (15.5%), each of which was correlated with an improvement in the mean deviation of the visual field, although statistical significance for the single parameters was not reached. However, analysis of variance between the mean deviation improvement and the set of parameters taken together yielded highly significant results (p < 0.0001). LDLA was effective in reducing the values of all evaluated endothelial activation markers, and this trend was correlated with an improvement in the visual field.

Sudden hearing loss (SHL) is a highly disabling affliction that can severely affect the subject's social and relational life. Although the etiology of the complaint is still debated, it is thought that microcirculation disturbances conditioned by an endothelial dysfunction might be the main pathogenetic mechanism. Adhesion molecules favoring interaction between leukocytes and endothelial cells are early markers of endothelial damage. In the present report, we describe a case of SHL that derived evident benefit from a single session of LDL/fibrinogen apheresis, with complete hearing recovery. In this patient, in addition to reducing LDL cholesterol and fibrinogen, the circulating adhesion molecules (sE-selectin, sVCAM-1 and sICAM-1), previously present in higher than normal concentrations, were reduced by the treatment.

Diabetic nephropathy is the most frequent cause of chronic renal failure. The onset of microalbuminuria in patients with diabetes mellitus, which seems to be related to blood pressure and the control of glycemia, is predictive of the development of true proteinuria. This multicenter, single-blind, randomized study examined the effects of benazepril and nicardipine on overnight microalbuminuria in 57 normotensive and 46 hypertensive diabetic patients. At the end of a 3-month placebo run-in period, the patients were stratified on the basis of the presence or absence of arterial hypertension and, within each stratum, randomized to receive one daily tablet of 10 mg benazepril or one tablet of 20 mg nicardipine twice daily for 6 months. Renal hemodynamics was investigated in 25 patients. Both drugs decreased overnight microalbuminuria throughout the study period, but benazepril was more effective than nicardipine (p = 0.025); in the patients with hypertension, both drugs led to a similar marked reduction in systolic and diastolic blood pressure. This study shows that benazepril was more effective than nicardipine in reducing overnight microalbuminuria in patients with diabetes mellitus, independently of their antihypertensive properties.

Summary: The aim of this study was to evaluate the efficacy of enalapril and atenolol in decreasing the severity of proteinuria in hypertensive patients suffering from insulin-dependent diabetes mellitus. We studied 20 hypertensive patients. All patients had proteinuria (<3 g/24 h) and were receiving insulin treatment. Proteinuria was measured monthly in the run-in period (3 months) and during the active drug treatment (8 months). Glomerular filtration rate, effective renal plasma flow, filtration fraction, and total renal resistance were determined after the run-in and treatment periods. The patients were randomly assigned to treatment with enalapril 20 mg/day or atenolol 100 mg/day for 8 months. In both groups blood pressure decreased significantly. After 8 months' treatment, severity of proteinuria significantly decreased both in the enal-april-treated group and in the group receiving atenolol. Glomerular filtration rate and effective renal plasma flow significantly increased, while total renal resistance decreased in the patients given enalapril, whereas glomerular filtration rate, renal plasma flow, and total renal resistance significantly decreased in the patients given atenolol. The results of this study show that enalapril and atenolol reduce proteinuria in hypertensive diabetic patients by a mechanism related to their antihypertensive effects; furthermore, the beneficial effects of enalapril might be also linked to intrarenal effects.