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Aims: Few data are available regarding the role of tricuspid annulus plane systolic excursion to pulmonary artery systolic pressure (TAPSE/PASP), a measurement of right ventricular to pulmonary artery coupling, in patients with chronic heart failure and left ventricular systolic dysfunction., Methods and Results: This retrospective single-centre study included outpatients with left ventricular systolic dysfunction (ejection fraction ≤ 50%) evaluated between January 2022 and December 2022. TAPSE/PASP was evaluated as a continuous variable and as tertiles according to its value on the first visit. The primary outcome of the study was a composite of all-cause mortality or heart failure (HF) events at the last available follow-up., Results: A total of 642 patients were included (mean age 71 ± 13 years, 78% male, mean left ventricular ejection fraction 40% [interquatile range 35-46]). Patients with lower TAPSE/PASP had more co-morbidities (i.e., atrial fibrillation, chronic kidney disease or previous cardiovascular implantable electronic device), an higher New York Heart Association class (P < 0.001), more signs of congestion (P = 0.007), and had more probability to receive intravenous furosemide during the visit (P < 0.001). After a median follow-up of 474 days [interquartile range 392-507 days], a total of 51 patients (8.0%) died (with 24 patients [3.8%] experiencing cardiovascular-related deaths), a total of 179 patients (28.1%) experienced a composite outcome, and 158 patients (24.8%) had HF events. Kaplan-Meier analysis showed that the estimated 1-year rate of the primary outcome was higher in the lowest tertile (38.0%), as compared with the intermediate (19.6%) and highest tertiles (14.9%; P-value log-rank <0.001). TAPSE/PASP ratio as a continuous variable was independently associated with the primary outcome (adjusted hazard ratio for 0.1 mm/mmHg increase 0.91, 95% CI 0.84-0.98, P = 0.009), predominantly driven by a higher risk of HF events during follow-up. Analysing the impact of TAPSE/PASP tertiles on the primary outcome, an independent associated was confirmed at multivariate analisys for the highest versus lowest tertile (adjusted hazard ratio 0.61, 95% CI 0.38-0.99, P = 0.044)., Conclusions: TAPSE/PASP was independently associated with mortality or HF events among ambulatory patients with left ventricular systolic dysfunction., (© 2024 The Author(s). ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Acute heart failure (AHF) represents a common clinical scenario that requires prompt evaluation and therapy and that is characterized by a high risk of mortality or subsequent rehospitalizations. The pathophysiology leading to AHF decompensation is still not fully understood. Significant activation of inflammatory pathways has been identified in patients with AHF, particularly in its most severe forms, and it has been hypothesized that systemic inflammation has a role in AHF pathogenesis. Several inflammatory mediators and cytokines, such as high sensitivity C-reactive protein, tumor necrosis factor-α, interleukin-6, interleukin-1, soluble suppression of tumorigenicity 2 and galectin-3, have been shown to play a role in the pathogenesis, development and worsening of this condition with an independent prediction of adverse outcomes. This manuscript reviews the prevalence and prognostic value of systemic inflammation in AHF, as well as the potential role of anti-inflammatory therapies, focusing on available evidence from clinical trials and ongoing studies., Competing Interests: MP has received personal fees from Abbot Vascular, AstraZeneca, Boehringer Ingelheim and Vifor Pharma. MA reports speaker fees from Abbott Vascular and Medtronic. MM has received consulting honoraria as a member of trial committees or advisory boards for Abbott Vascular, Actelion, Amgen, Bayer, Edwards Therapeutics, Servier, Vifor Pharma and Windtree Therapeutics. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer MM declared a past co-authorship with the authors MM, CML, RMI, DT to the handling editor., (© 2023 Garofalo, Corso, Tomasoni, Adamo, Lombardi, Inciardi, Gussago, Di Mario, Metra and Pagnesi.)

Low-dose dexamethasone reduces mortality in patients with coronavirus disease 2019 (COVID-19)-related acute respiratory distress syndrome (ARDS). We retrospectively analyzed the efficacy of high-dose dexamethasone in patients with COVID-19-related ARDS and evaluated factors affecting the composite outcome (death or invasive mechanical ventilation). From March 4th to April 1st 2020, 98 patients with COVID-19 pneumonia were included. Those who after at least 7 days from symptom onset presented a worsening of the respiratory function or of inflammatory biomarkers were started on intravenous high-dose dexamethasone (20 mg daily for 5 days, followed by 10 mg daily for 5 days). Most patients were males (62%) with a mean age of 69 years. Hypertension and cardiovascular disease (CVD) were prevalent. Following dexamethasone treatment, a significant improvement in PaO 2 /FiO 2 (277.41 [178.5-374.8] mmHg vs. 146.75 [93.62-231.16] mmHg, p < 0.001), PaO 2 (88.15 [76.62-112.0] mmHg vs. 65.65 [57.07-81.22] mmHg, p < 0.001), and SpO 2 (96 [95-98]% vs. 94 [90-96]%, p < 0.001) was observed. A concomitant decrease in C-reactive protein and ferritin levels was found (132.25 [82.27-186.5] mg/L vs. 7.3 [3.3-24.2] mg/L and 1169 [665-2056] ng/mL vs. 874.0 [569.5-1434] ng/mL, respectively; p < 0.001 for both vs. baseline). CVD was found to increase the risk of the composite outcome (RR 7.64, 95% CI 1.24-47.06, p = 0.028). In hospitalized patients with COVID-19-related ARDS, high-dose dexamethasone rapidly improves the clinical status and decreases inflammatory biomarkers. CVD was found to increase the risk of the composite outcome. These data support the importance of randomized clinical trials with high-dose dexamethasone in COVID-19 patients., (© 2021. Società Italiana di Medicina Interna (SIMI).)

Previous studies suggested that hypertensive patients with left ventricular (LV) hypertrophy display right ventricular (RV) remodelling. Few data are available about RV remodelling in naive hypertensives without severe cardiac organ damage. Our aim was to evaluate the relationship between RV and LV morpho-functional parameters in never-treated patients with grade 1 hypertension and whether central blood pressure (CBP), inflammatory and metabolic parameters are potentially associated with RV remodelling. 150 never-treated subjects without evidence of diabetes or other cardiovascular diseases were enrolled in our study. We recruited 100 patients with mild hypertension (twenty-four hours blood pressure (24 h BP) ≥ 130/80 mmHg) and 50 normotensive subjects matched for gender, age and body mass index. To estimate the LV/RV parameters, we performed echography as well as arterial tonometry to assess pulse wave analysis/velocity (PWA/PWV). We found 24 h BP, CBP and PWV were higher in hypertensive patients than in normotensives. In addition, LV mass index was higher in hypertensives, and greater RV free wall thickness was observed (5.3 ± 1.4 vs 4.6 ± 1.2 mm, P = 0.02). RV thickness correlated with interventricular septum (IVS), systolic CBP and RV E' (r = 0.50, P = 0.0001, r = 0.30, P = 0.003, r = -0.24, P = 0.015); linear regression analysis showed a correlation with only IVS (β = 0.39, P = 0.001). RV E' was correlated with IVS, LV E' and systolic CBP (r = -0.35, P = 0.0001, r = 0.25, P = 0.012, r = -0.24, P = 0.019); the correlation with IVS and LV E' (β = -0.310, P = 0.001; β = 0.27, P = 0.004) was confirmed by linear regression analysis. Our study shows RV remodelling is mostly correlated with IVS thickness, supporting the ventricular interdependence hypothesis.

Background: Soluble Receptor for Advanced Glycation End Products (sRAGE) may be considered a marker inversely related to inflammation and its participation has been established in patients with advanced atherosclerotic vascular diseases. However, it is still unknown whether sRAGE reduction could be early metabolic change in the first stage of hypertension and initial hypertension-associated cardiac damage. We sought to determine the sRAGE values in otherwise healthy, untreated and recently diagnosed mild hypertensives and evaluate their association with blood pressure (BP) values, metabolic parameters, and with subclinical initial signs of cardiac target organ damage (TOD)., Methods: sRAGE were measured in 100 hypertensive and 100 normotensive subjects matched for age, gender and body mass index (BMI), submitted to a clinic visit and both ambulatory BP monitoring and echocardiography to determine the presence of initial cardiac TOD (presence of signs of left ventricular hypertrophy: left ventricular mass indexed for height 2.7 (LVMi) > 48 g/m 2.7 for men and > 44 g/m 2.7 for women and/or increased left atrial volume 4-chamber indexed for body surface area (LAVi) > 34 ml/m 2 )., Results: sRAGE levels were similar between hypertensive and normotensive subjects and were not significantly correlated with office and 24-h BPs values. However, when subgrouping the hypertensive patients in Hyp-TOD and Hyp-withoutTOD, sRAGE was found to be different among the three groups (p = 0.030), being lower in the Hyp-TOD group than the values of both Hyp-withoutTOD (p = 0.038) and normotensives (p = 0.038). In hypertensive patients sRAGE was negatively related with both LVMi (r = - 0.239, p = 0.034) and LAVi (r = - 0.315, p = 0.005) and was independently related to cardiac TOD also in multivariable analysis., Conclusions: In this population of mild hypertensives, low circulating sRAGE may be a very early marker of initial TOD, suggesting the possible participation of oxidative stress in initial cardiac changes in human hypertension.