Stefano Taddei
@unipi.it
Department of Clinical and Experimental Medicine
University of Pisa
Stefano Taddei was born in Pisa, Italy, in 1957. He attended the State University of Pisa, where he graduated in Medicine and Surgery in 1982 and specialized in Clinical Pharmacology in 1986.
Prof. Taddei is Professor of Internal Medicine. He works currently as the Director of the Hypertension Unit of the Department of Clinical and Experimental Medicine
Prof. Taddei is a Fellow of the European Society of Cardiology, the European, International and American Society of Hypertension, the European Society of Clinical Investigation, the High Blood Pressure Council of the American Heart Association, and of the Italian Society of Hypertension. He has been a councilor of the Italian Society of Hypertension (2007-2009).
He is a member of the Editorial Boards of Hypertension, Blood Pressure, Journal of Cardiovascular Pharmacology,Current Vascular Pharmacology, Current Hypertension Reviews, High Blood Pressure and Cardiovascular Prevention and Journal of American Society of Hypertension. He is an International Associated Editor of the European Heart Journal.
His main research area is local neuro-humoral control of peripheral vessels in primary and secondary forms of hypertension, with particular emphasis on the sympathetic nervous system, the renin-angiotensin system and the endothelium.
He is also interested in the assessment of target-organ damage in hypertension, including vascular and cardiac structural alterations and the clinical pharmacology of cardiovascular drugs.
Prof. Taddei has participated in numerous clinical studies and is the authors of more than 350 original papers, reviews and editorials in international scientific journals (H index: 64; Impact Factor : >2154).
RESEARCH INTERESTS
Vascular reactivity in hypertension and cardiovascular risk factors
Scopus Publications
Scopus Publications
Diego Moriconi, Alessandro Mengozzi, Emiliano Duranti, Federica Cappelli, Stefano Taddei, Monica Nannipieri, Rosa Maria Bruno, and Agostino Virdis
Ovid Technologies (Wolters Kluwer Health)
Background: Renal hemodynamics is impaired since the early stage of cardiometabolic disease. However, in obesity, its noninvasive ultrasound assessment still fails to provide pathophysiologic and clinical meaningfulness. We aimed to explore the relationship between peripheral microcirculation and renal hemodynamics in severe obesity. Methods: We enrolled fifty severely obese patients with an indication for bariatric referring to our outpatient clinic. Patients underwent an extensive reno-metabolic examination, paired with Doppler ultrasound and measurement of the renal resistive index (RRI). On the day of the surgery, visceral fat biopsies were collected to perform an ex-vivo complete microcirculatory assessment. Media-to-lumen ratio (M/L) and vascular response to acetylcholine (ACh), alone or co-incubated with NG-nitro arginine methyl ester (L-NAME), were measured. Results: Patients were stratified according to their normotensive (NT) or hypertensive (HT) status. HT had lower estimated glomerular filtration rate and higher RRI compared to NT, while the presence and extent of albuminuria were similar between the two groups. Concerning microcirculatory assessment, there were no differences between groups as regards the microvascular structure, while the vasorelaxation to ACh was lower in HT (P = 0.042). Multivariable analysis showed a relationship between M/L and RRI (P = 0.016, St. β 0.37) and between albuminuria and the inhibitory response of L-NAME to Ach vasodilation (P = 0.036, St. β = −0.34). Notably, all these correlations were consistent also after adjustment for confounding factors. Conclusions: The RRI and albuminuria relationship with microvascular remodeling in patients affected by severe obesity supports the clinical implementation of RRI to improve risk stratification in obesity and suggests a tight pathophysiologic connection between renal haemodynamics and microcirculatory disruption.
Alessandro Sale, Marianna Noale, Simona Cintoli, Gloria Tognoni, Chiara Braschi, Nicoletta Berardi, Stefania Maggi, Lamberto Maffei, L Maffei, E Picano,et al.
Oxford University Press (OUP)
Abstract No treatment options are currently available to counteract cognitive deficits and/or delay progression towards dementia in older people with mild cognitive impairment (MCI). The ‘Train the Brain’ programme is a combined motor and cognitive intervention previously shown to markedly improve cognitive functions in MCI individuals compared to non-trained MCI controls, as assessed at the end of the 7-month intervention. Here, we extended the previous analyses to include the long-term effects of the intervention and performed a data disaggregation by gender, education and age of the enrolled participants. We report that the beneficial impact on cognitive functions was preserved at the 14-month follow-up, with greater effects in low-educated compared to high-educated individuals, and in women than in men.
Nicola Riccardo Pugliese, Nicolò De Biase, Lavinia Del Punta, Alessio Balletti, Silvia Armenia, Simona Buralli, Alessandro Mengozzi, Stefano Taddei, Marco Metra, Matteo Pagnesi,et al.
Wiley
Limited evidence is available regarding the role of hypertensive response to exercise (HRE) in heart failure (HF). We evaluated the systolic blood pressure (SBP) to workload slope during exercise across the HF spectrum, investigating haemodynamic and prognostic correlates of HRE.
Alessio Balletti, Nicolò De Biase, Lavinia Del Punta, Francesco Filidei, Silvia Armenia, Filippo Masi, Valerio Di Fiore, Matteo Mazzola, Alessandra Bacca, Frank L. Dini,et al.
MDPI AG
Aims. We explored multiple cardiometabolic patterns, including inflammatory and congestive pathways, in patients with heart failure (HF). Methods and Results. We enrolled 270 HF patients with reduced (<50%, HFrEF; n = 96) and preserved (≥50%, HFpEF; n = 174) ejection fraction. In HFpEF, glycated hemoglobin (Hb1Ac) seemed to be relevant in its relationship with inflammation as Hb1Ac positively correlated with high-sensitivity C-reactive protein (hs-CRP; Spearman’s rank correlation coefficient ρ = 0.180, p < 0.05). In HFrEF, we found a correlation between Hb1Ac and norepinephrine (ρ = 0.207, p < 0.05). In HFpEF, we found a positive correlation between Hb1Ac and congestion expressed as pulmonary B lines (ρ = 0.187, p < 0.05); the inverse correlation, although not significant, was found in HFrEF between Hb1Ac and N-terminal pro-B-type natriuretic peptide (ρ = 0.079) and between Hb1Ac and B lines (ρ = −0.051). In HFrEF, we found a positive correlation between E/e’ ratio and Hb1Ac (ρ = 0.203, p < 0.05) and a negative correlation between tricuspid annular systolic excursion (TAPSE)/echocardiographically measured systolic pulmonary artery pressure (sPAP) (TAPSE/sPAP ratio) (ρ = −0.205, p < 0.05) and Hb1Ac. In HFpEF, we found a negative correlation between TAPSE/sPAP ratio and uric acid (ρ = −0.216, p < 0.05). Conclusion. In HF patients, HFpEF and HFrEF phenotypes are characterized by different cardiometabolic indices related to distinct inflammatory and congestive pathways. Patients with HFpEF showed an important relationship between inflammatory and cardiometabolic parameters. Conversely, in HFrEF, there is a significant relationship between congestion and inflammation, while cardiometabolism appears not to influence inflammation, instead affecting sympathetic hyperactivation.
Nicola R. Pugliese, Matteo Mazzola, Giulia Bandini, Greta Barbieri, Stefano Spinelli, Nicolò De Biase, Stefano Masi, Alberto Moggi-Pignone, Lorenzo Ghiadoni, Stefano Taddei,et al.
MDPI AG
Background: We investigated the role of the dynamic changes of pulmonary congestion, as assessed by sonographic B-lines, as a tool to stratify prognosis in patients admitted for acute heart failure with reduced and preserved ejection fraction (HFrEF, HFpEF). Methods: In this multicenter, prospective study, lung ultrasound was performed at admission and before discharge by trained investigators, blinded to clinical findings. Results: We enrolled 208 consecutive patients (mean age 76 [95% confidence interval, 70–84] years), 125 with HFrEF, 83 with HFpEF (mean ejection fraction 32% and 57%, respectively). The primary composite endpoint of cardiovascular death or HF re-hospitalization occurred in 18% of patients within 6 months. In the overall population, independent predictors of the occurrence of the primary endpoint were the number of B-lines at discharge, NT-proBNP levels, moderate-to-severe mitral regurgitation, and inferior vena cava diameter on admission. B-lines at discharge were the only independent predictor in both HFrEF and HFpEF subgroups. A cut-off of B-lines > 15 at discharge displayed the highest accuracy in predicting the primary endpoint (AUC = 0.80, p < 0.0001). Halving B-lines during hospitalization further improved event classification (continuous net reclassification improvement = 22.8%, p = 0.04). Conclusions: The presence of residual subclinical sonographic pulmonary congestion at discharge predicts 6-month clinical outcomes across the whole spectrum of acute HF patients, independent of conventional biohumoral and echocardiographic parameters. Achieving effective pulmonary decongestion during hospitalization is associated with better outcomes.
Nicola Riccardo Pugliese, Stefano Masi, and Stefano Taddei
Oxford University Press (OUP)
Silvia Trifirò, Francesco Cavallin, Sabina Mangi, Lawrence Mhaluka, Silvia Maffoni, Stefano Taddei, Giovanni Putoto, and Giovanni F Torelli
African Journals Online (AJOL)
Exposure to anti-retroviral therapy in HIV infection has been associated with hypertension, but whether and to what extent HIV-related factors and anti-retroviral treatment contribute to hypertension is not well defined; in addition, data are particularly scarce in Sub-Saharan Africa.
 Aim of the study was to investigate prevalence and awareness of hypertension in a cohort of people living with HIV (PLWHIV) on anti-retroviral therapy in rural Tanzania, and to identify possible predictors of hypertension.A cross-sectional study on hypertension in PLWHIV was conducted at Tosamaganga District Hospital, Iringa Region, Tanzania. Subjects on anti-retroviral therapy, age 26-80 years and with monthly attendance to the HIV clinic, were considered eligible. A total number of 242 patients were included in the analysis. Sixty-two subjects (26%) had hypertension, the majority (77%) of them not aware of the condition and/or not on treatment. Older age, higher BMI and lower baseline T-CD4 count were predictors of hypertension at multivariate analysis. The results of the study suggest that hypertension screening should becomepart of ordinary care of PLWHIV in Tanzania, particularly in subjects with more severe immunosuppression. Leveraging already existing HIV services could be an option to prevent the burden of non-AIDS complication and related deaths.
 Keywords: HIV; Hypertension; sub-Saharan Africa.
Nicola Riccardo Pugliese, Andrea Colli, Giosuè Falcetta, Lavinia Del Punta, Carlo Puccinelli, Alessandro Fiocco, Anna Sonia Petronio, Stefano Taddei, Stefano Masi, and Laura Besola
Frontiers Media SA
ObjectivesThe present study aims to assess and describe the intracardiac blood flow dynamic in patients with mitral regurgitation (MR), repaired mitral valves (MV) and mitral valve prostheses using vector flow mapping (VFM).MethodsPatients with different MV pathologies and MV disease treatments were analysed. All patients underwent 2D transthoracic echocardiography, and images for flow visualization were acquired in VFM mode in an apical three-chamber view and four-chamber view. Vectors and vortices were qualitatively analyzed.Resultsthirty-two (32) patients underwent 2D transthoracic echocardiography (TTE) with VFM analysis. We evaluated intracardiac flow dynamics in 3 healthy subjects, 10 patients with MR (5 degenerative, 5 functional), 4 patients who underwent MV repair, 5 who underwent MV replacement (3 biological, 2 mechanical), 2 surgically implanted transcatheter heart valve (THV), 2 transcatheter edge-to-edge MV repair with MitraClip (TEER), 3 transcatheter MV replacement (TMVR) and 3 transapical off-pump MV repair with NeoChord implantation. Blood flow patterns are significantly altered in patients with MV disease and MV repair compared to control patients. MV repair is superior to replacement in restoring more physiologicalpatterns, while TMVR reproducesan intraventricular flowcloser to normal than surgical MVR and TEER.ConclusionsIntracardiac flow patterns can be clearly defined using VFM. Restoration of a physiological blood flow pattern inside the LV directly depends on the procedure used to address MV disease.
Nicola Riccardo Pugliese, Pierpaolo Pellicori, Francesco Filidei, Nicolò De Biase, Pasquale Maffia, Tomasz J Guzik, Stefano Masi, Stefano Taddei, and John G F Cleland
Oxford University Press (OUP)
Abstract Many patients with symptoms and signs of heart failure have a left ventricular ejection fraction ≥50%, termed heart failure with preserved ejection fraction (HFpEF). HFpEF is a heterogeneous syndrome mainly affecting older people who have many other cardiac and non-cardiac conditions that often cast doubt on the origin of symptoms, such as breathlessness, or signs, such as peripheral oedema, rendering them neither sensitive nor specific to the diagnosis of HFpEF. Currently, management of HFpEF is mainly directed at controlling symptoms and treating comorbid conditions such as hypertension, atrial fibrillation, anaemia, and coronary artery disease. HFpEF is also characterized by a persistent increase in inflammatory biomarkers. Inflammation may be a key driver of the development and progression of HFpEF and many of its associated comorbidities. Detailed characterization of specific inflammatory pathways may provide insights into the pathophysiology of HFpEF and guide its future management. There is growing interest in novel therapies specifically designed to target deregulated inflammation in many therapeutic areas, including cardiovascular disease. However, large-scale clinical trials investigating the effectiveness of anti-inflammatory treatments in HFpEF are still lacking. In this manuscript, we review the role of inflammation in HFpEF and the possible implications for future trials.
Stefan D. Anker, Javed Butler, Muhammad Shariq Usman, Gerasimos Filippatos, João Pedro Ferreira, Edimar Bocchi, Michael Böhm, Hans Pieter Brunner-La Rocca, Dong-Ju Choi, Vijay Chopra,et al.
Springer Science and Business Media LLC
AbstractThe EMPEROR-Preserved trial showed that the sodium–glucose co-transporter 2 inhibitor empagliflozin significantly reduces the risk of cardiovascular death or hospitalization for heart failure (HHF) in heart failure patients with left ventricular ejection fraction (LVEF) > 40%. Here, we report the results of a pre-specified analysis that separately evaluates these patients stratified by LVEF: preserved (≥ 50%) (n = 4,005; 66.9%) or mid-range (41–49%). In patients with LVEF ≥ 50%, empagliflozin reduced the risk of cardiovascular death or HHF (the primary endpoint) by 17% versus placebo (hazard ratio (HR) 0.83; 95% confidence interval (CI): 0.71–0.98, P = 0.024). For the key secondary endpoint, the HR for total HHF was 0.83 (95%CI: 0.66–1.04, P = 0.11). For patients with an LVEF of 41–49%, the HR for empagliflozin versus placebo was 0.71 (95%CI: 0.57–0.88, P = 0.002) for the primary outcome (Pinteraction = 0.27), and 0.57 (95%CI: 0.42–0.79, P < 0.001) for total HHF (Pinteraction = 0.06). These results, together with those from the EMPEROR-Reduced trial in patients with LVEF < 40%, support the use of empagliflozin across the full spectrum of LVEF in heart failure.
Martina Chiriacò, Luca Sacchetta, Giovanna Forotti, Simone Leonetti, Lorenzo Nesti, Stefano Taddei, Andrea Natali, Anna Solini, and Domenico Tricò
Wiley
To establish the long‐term prognostic value of abnormal circadian blood pressure (BP) patterns in diabetes.
Alessandro Mengozzi, Sarah Costantino, Francesco Paneni, Emiliano Duranti, Monica Nannipieri, Rudj Mancini, Michele Lai, Veronica La Rocca, Ilaria Puxeddu, Luca Antonioli,et al.
Ovid Technologies (Wolters Kluwer Health)
Background: Experimental evidence suggests a key role of SIRT1 (silent information regulator 1) in age- and metabolic-related vascular dysfunction. Whether these effects hold true in the human microvasculature is unknown. We aimed to investigate the SIRT1 role in very early stages of age- and obesity-related microvascular dysfunction in humans. Methods: Ninety-five subjects undergoing elective laparoscopic surgery were recruited and stratified based on their body mass index status (above or below 30 kg/m 2 ) and age (above or below 40 years) in 4 groups: Young Nonobese, Young Obese, Old Nonobese, and Old Obese. We measured small resistance arteries’ endothelial function by pressurized micromyography before and after incubation with a SIRT1 agonist (SRT1720) and a mitochondria reactive oxygen species (mtROS) scavenger (MitoTEMPO). We assessed vascular levels of mtROS and nitric oxide availability by confocal microscopy and vascular gene expression of SIRT1 and mitochondrial proteins by qPCR. Chromatin immunoprecipitation assay was employed to investigate SIRT1-dependent epigenetic regulation of mitochondrial proteins. Results: Compared with Young Nonobese, obese and older patients showed lower vascular expression of SIRT1 and antioxidant proteins (FOXO3 [forkhead box protein O3] and SOD2) and higher expression of pro-oxidant and aging mitochondria proteins p66 Shc and Arginase II. Old Obese, Young Obese and Old Nonobese groups endothelial dysfunction was rescued by SRT1720. The restoration was comparable to the one obtained with mitoTEMPO. These effects were explained by SIRT1-dependent chromatin changes leading to reduced p66 Shc expression and upregulation of proteins involved in mitochondria respiratory chain. Conclusions: SIRT1 is a novel central modulator of the earliest microvascular damage induced by age and obesity. Through a complex epigenetic control mainly involving p66 Shc and Arginase II, it influences mtROS levels, NO availability, and the expression of proteins of the mitochondria respiratory chain. Therapeutic modulation of SIRT1 restores obesity- and age-related endothelial dysfunction. Early targeting of SIRT1 might represent a crucial strategy to prevent age- and obesity-related microvascular dysfunction.
Diego Moriconi, Luca Antonioli, Stefano Masi, Rosario Bellini, Carolina Pellegrini, Eleni Rebelos, Stefano Taddei, and Monica Nannipieri
Wiley
Obesity is associated with glomerular hyperfiltration which may precede the development of overt renal damage. Few studies evaluated the link between inflammasome signalling and hyperfiltration. The aim is to evaluate the relationship between IL1‐β/Caspase‐1, insulin sensitivity and hyperfiltration in subjects with severe obesity, before and after weight loss.
Iacopo Fabiani, Giorgia Panichella, Alberto Aimo, Chrysanthos Grigoratos, Giuseppe Vergaro, Nicola Riccardo Pugliese, Stefano Taddei, Daniela Maria Cardinale, Claudio Passino, Michele Emdin,et al.
Springer Science and Business Media LLC
AbstractCancer and cardiovascular diseases, including heart failure (HF), are the main causes of death in Western countries. Several anticancer drugs and radiotherapy have adverse effects on the cardiovascular system, promoting left ventricular dysfunction and ultimately HF. Nonetheless, the relationship between cancer and HF is likely not unidirectional. Indeed, cancer and HF share common risk factors, and both have a bidirectional relationship with systemic inflammation, metabolic disturbances, and neurohormonal and immune activation. Few studies have assessed the impact of untreated cancer on the heart. The presence of an active cancer has been associated with elevated cardiac biomarkers, an initial impairment of left ventricular structure and function, autonomic dysfunction, and reduced exercise tolerance. In turn, these conditions might increase the risk of cardiac damage from chemotherapy and radiotherapy. HF drugs such as beta-blockers or inhibitors of the renin–angiotensin–aldosterone system might exert a protective effect on the heart even before the start of cancer therapies. In this review, we recapitulate the evidence of cardiac involvement in cancer patients naïve from chemotherapy and radiotherapy and no history of cardiac disease. We also focus on the perspectives for an early diagnosis and treatment to prevent the progression to cardiac dysfunction and clinical HF, and the potential benefits of cardioactive drugs on cancer progression.
Federica Poli, Catherine Fortier, Hakim Khettab, Francesco Faita, Saverio Vitali, Giacomo Aringhieri, Lorenzo Ghiadoni, Stefano Taddei, Laurence Amar, Aurelien Lorthioir,et al.
Elsevier BV
Subodh Verma, Nitish K Dhingra, Javed Butler, Stefan D Anker, Joao Pedro Ferreira, Gerasimos Filippatos, James L Januzzi, Carolyn S P Lam, Naveed Sattar, Barbara Peil,et al.
Elsevier BV
Agnieszka Latosinska, Rosa Maria Bruno, Marco Pappaccogli, Alessandra Bacca, Christophe Beauloye, Pierre Boutouyrie, Hakim Khettab, Jan A Staessen, Stefano Taddei, Laurent Toubiana,et al.
Ovid Technologies (Wolters Kluwer Health)
Fibromuscular dysplasia (FMD), a nonatherosclerotic, noninflammatory disease of medium-sized arteries, is an underdiagnosed disease. We investigated the urinary proteome and developed a classifier for discrimination of FMD from healthy controls and other diseases. We further hypothesized that urinary proteomics biomarkers may be associated with alterations in medium-sized, but not large artery geometry and mechanics. The study included 33 patients with mostly multifocal, renal FMD who underwent in depth arterial exploration using ultra-high frequency ultrasound. The cohort was separated in a training set of 23 patients with FMD from Belgium and an independent test set of 10 patients with FMD from Italy. For each set, controls matched 2:1 were selected from the Human Urinary Proteome Database. The specificity of the classifier was tested in 700 additional controls from general population studies, patients with chronic kidney disease (n=66) and coronary artery disease (n=31). Three hundred thirty-five urinary peptides, mostly related to collagen turnover, were identified in the training cohort and combined into a classifier. When applying in the test cohort, the area under the receiver operating characteristic curve was 1.00, 100% specificity at 100% sensitivity. The classifier maintained a high specificity in additional controls (98.3%), patients with chronic kidney (90.9%) and coronary artery (96.8%) diseases. Furthermore, in patients with FMD, the proteomic score was positively associated with radial wall thickness and wall cross-sectional area. In conclusion, a proteomic score has the potential to discriminate between patients with FMD and controls. If confirmed in a wider and more diverse cohort, these findings may pave the way for a noninvasive diagnostic test of FMD.
Alessandro Mengozzi, Nicola Riccardo Pugliese, Martina Chiriacò, Stefano Masi, Agostino Virdis, and Stefano Taddei
Ovid Technologies (Wolters Kluwer Health)
ABSTRACT
Longer life span and increased prevalence of chronic, non-communicable, inflammatory diseases fuel cardiovascular mortality. The microcirculation is central in the crosstalk between ageing, inflammation, cardiovascular and metabolic diseases. Microvascular dysfunction, characterized by alteration in the microvascular endothelial function and wall structure, is described in an increasing number of chronic, age-associated diseases, suggesting it might be a marker of ageing superior to chronological age. The aim of this review is to thoroughly explore the connections between microvascular dysfunction, ageing and metabolic disorders by detailing the major role played by inflammation and oxidative stress in their evolution. Older age, hypertension, nutrient abundance and hyperglycaemia concur in the induction of a persistent low-grade inflammatory response, defined as meta-inflammation or inflammageing. This increases the local generation of reactive oxygen species that further impairs endothelial function and amplifies the local inflammatory response. Mitochondrial dysfunction is a hallmark of many age-related diseases. The alterations of mitochondrial function promote irreversible modification in microvascular structure. The interest in the hypothesis of chronic inflammation at the centre of the ageing process lies in its therapeutic implications. Inhibition of specific inflammatory pathways has been shown to lower the risk of many age-related diseases, including cardiovascular disease. However, the whole architecture of the inflammatory response underpinning the ageing process and its impact on the burden of age-related diseases remain to be fully elucidated. Additional studies are needed to unravel the connection between these biological pathways and to address their therapeutic power in terms of cardiovascular prevention.
Maria Agata Miselli, Francesco Cavallin, Samwel Marwa, Bruno Ndunguru, Rehema John Itambu, Katunzi Mutalemwa, Monica Rizzi, Giulia Ciccarelli, Simone Conte, Stefano Taddei,et al.
MDPI AG
Morbidity and mortality due to noncommunicable diseases (NCDs) are growing exponentially across Tanzania. The limited availability of dedicated services and the disparity between rural and urban areas represent key factors for the increased burden of NCDs in the country. From March 2019, an integrated management system was started in the Iringa District Council. The system implements an integrated management of hypertension and diabetes between the hospital and the peripheral health centers and introduces the use of paper-based treatment cards. The aim of the study was to present the results of the first 6 months’ roll-out of the system, which included 542 patients. Data showed that 46.1% of patients returned for the reassessment visit (±1 month), more than 98.4% of patients had blood pressure measured and were checked for complication, more than 88.6% of patients had blood sugar tested during follow-up visit, and blood pressure was at target in 42.8% of patients with hypertension and blood sugar in 37.3% of diabetic patients. Most patients who were lost to follow-up or did not reach the targets were those without medical insurance or living in remote peripheries. Our findings suggest that integrated management systems connecting primary health facilities and referral hospitals may be useful in care and follow-up of patients with hypertension and diabetes.
Stefan D. Anker, Javed Butler, Gerasimos Filippatos, João P. Ferreira, Edimar Bocchi, Michael Böhm, Hans-Peter Brunner–La Rocca, Dong-Ju Choi, Vijay Chopra, Eduardo Chuquiure-Valenzuela,et al.
Massachusetts Medical Society
BACKGROUND
Sodium-glucose cotransporter 2 inhibitors reduce the risk of hospitalization for heart failure in patients with heart failure and a reduced ejection fraction, but their effects in patients with heart failure and a preserved ejection fraction are uncertain.
METHODS
In this double-blind trial, we randomly assigned 5988 patients with class II-IV heart failure and an ejection fraction of more than 40% to receive empagliflozin (10 mg once daily) or placebo, in addition to usual therapy. The primary outcome was a composite of cardiovascular death or hospitalization for heart failure.
RESULTS
Over a median of 26.2 months, a primary outcome event occurred in 415 of 2997 patients (13.8%) in the empagliflozin group and in 511 of 2991 patients (17.1%) in the placebo group (hazard ratio, 0.79; 95% confidence interval [CI], 0.69 to 0.90; P<0.001). This effect was mainly related to a lower risk of hospitalization for heart failure in the empagliflozin group. The effects of empagliflozin appeared consistent in patients with or without diabetes. The total number of hospitalizations for heart failure was lower in the empagliflozin group than in the placebo group (407 with empagliflozin and 541 with placebo; hazard ratio, 0.73; 95% CI, 0.61 to 0.88; P<0.001). Uncomplicated genital and urinary tract infections and hypotension were reported more frequently with empagliflozin.
CONCLUSIONS
Empagliflozin reduced the combined risk of cardiovascular death or hospitalization for heart failure in patients with heart failure and a preserved ejection fraction, regardless of the presence or absence of diabetes. (Funded by Boehringer Ingelheim and Eli Lilly; EMPEROR-Preserved ClinicalTrials.gov number, NCT03057951).
Myrthe van der Bruggen, Bart Spronck, Siske Bos, Maarten H G Heusinkveld, Stefano Taddei, Lorenzo Ghiadoni, Tammo Delhaas, Rosa Maria Bruno, and Koen D Reesink
Oxford University Press (OUP)
Abstract Background Conventional measures for assessing arterial stiffness are inherently pressure dependent. Whereas statistical pressure adjustment is feasible in (larger) populations, it is unsuited for the evaluation of an individual patient. Moreover, statistical “correction” for blood pressure may actually correct for: (i) the acute dependence of arterial stiffness on blood pressure at the time of measurement; and/or (ii) the remodeling effect that blood pressure (hypertension) may have on arterial stiffness, but it cannot distinguish between these processes. METHODS We derived—assuming a single-exponential pressure–diameter relationship—3 theoretically pressure-independent carotid stiffness measures suited for individual patient evaluation: (i) stiffness index β0, (ii) pressure-corrected carotid pulse wave velocity (cPWVcorr), and (iii) pressure-corrected Young’s modulus (Ecorr). Using linear regression analysis, we evaluated in a sample of the CATOD study cohort changes in mean arterial pressure (ΔMAP) and comparatively the changes in the novel (Δβ0, ΔcPWVcorr, and ΔEcorr) as well as conventional (ΔcPWV and ΔE) stiffness measures after a 2.9 ± 1.0-year follow-up. RESULTS We found no association between ΔMAP and Δβ0, ΔcPWVcorr, or ΔEcorr. In contrast, we did find a significant association between ΔMAP and conventional measures ΔcPWV and ΔE. Additional adjustments for biomechanical confounders and traditional risk factors did neither materially change these associations nor the lack thereof. Conclusions Our newly proposed pressure-independent carotid stiffness measures avoid the need for statistical correction. Hence, these measures (β0, cPWVcorr, and Ecorr) can be used in a clinical setting for (i) patient-specific risk assessment and (ii) investigation of potential remodeling effects of (changes in) blood pressure on intrinsic arterial stiffness.
Marijana Tadic, Carla Sala, Guido Grassi, Giuseppe Mancia, Stefano Taddei, Wolfgang Rottbauer, and Cesare Cuspidi
MDPI AG
Studies show that patients with elevated triglycerides and well-controlled LDL levels under statin therapy still have a significant residual risk of cardiovascular (CV) events. Despite many attempts to reduce triglycerides with different hypolipidemic drugs, no therapeutic option has given satisfactory results so far. The initial enthusiasm that omega-3 fatty acids can effectively reduce triglycerides and CV risk was replaced with skepticism when the first large clinical trials failed to show any benefit in primary or secondary prevention. However, the latest studies succeeded in showing a positive effect of omega-3 fatty acids on CV outcome in patients with hypertriglyceridemia. The largest benefit was reported in secondary but not primary prevention. Interestingly, the reduction in triglycerides in some of these studies was disproportionately low to the relatively high CV risk reduction, which could indicate some other effects of omega-3 fatty acids that go well beyond hypotriglyceridemic action. This includes blood pressure reduction, antithrombotic effect, improvement of inflammatory status, endothelial function, and insulin resistance. Investigations also reported a significant and positive influence of omega-3 fatty acids on the composition and stabilization of coronary atherosclerotic plaques in patients with and without previous CV events. In addition to insufficiently known mechanisms of action and conflicting results about the effectiveness of omega-3 fatty acids, the safety problems, which include increased prevalence of atrial fibrillation and hemorrhage, were also reported. The aim of this clinical review was to summarize the current knowledge regarding the use of omega-3 fatty acids in CV patients, particularly those with coronary artery disease, and to present an overview of key clinical trial data.
Franz H Messerli, Jana Brguljan, Emrush Rexhaj, Peter Sever, Stuart Pocock, and Stefano Taddei
Oxford University Press (OUP)
Simona Cintoli, , Claudia Radicchi, Marianna Noale, Stefania Maggi, Giuseppe Meucci, Gloria Tognoni, Ubaldo Bonuccelli, Alessandro Sale, Nicoletta Berardi,et al.
Springer Science and Business Media LLC
Cognitive impairments associated with aging and dementia are major sources of neuropsychiatric symptoms (NPs) and deterioration in quality of life (QoL). Preventive measures to both reduce disease and improve QoL in those affected are increasingly targeting individuals with mild cognitive impairment (MCI) at early disease stage. However, NPs and QoL outcomes are too commonly overlooked in intervention trials. The purpose of this study was to test the effects of physical and cognitive training on NPs and QoL in MCI. Baseline data from an MCI court (N = 93, mean age 74.9 ± 4.7) enrolled in the Train the Brain (TtB) study were collected. Subjects were randomized in two groups: a group participated to a cognitive and physical training program, while the other sticked to usual standard care. Both groups underwent a follow-up re-evaluation after 7 months from baseline. NPs were assessed using the Neuropsychiatric Inventory (NPI) and QoL was assessed using Quality of Life-Alzheimer’s Disease (QOL-AD) scale. After 7 months of training, training group exhibited a significant reduction of NPs and a significant increase in QOL-AD with respect to no-training group (p = 0.0155, p = 0.0013, respectively). Our preliminary results suggest that a combined training can reduce NPs and improve QoL. Measuring QoL outcomes is a potentially important factor in ensuring that a person with cognitive deficits can ‘live well’ with pathology. Future data from non-pharmacological interventions, with a larger sample and a longer follow-up period, could confirm the results and the possible implications for such prevention strategies for early cognitive decline.
Marco Pappaccogli, Silvia Di Monaco, Ewa Warchoł-Celińska, Aurélien Lorthioir, Laurence Amar, Lucas S Aparicio, Christophe Beauloye, Rosa Maria Bruno, Patrick Chenu, Peter de Leeuw,et al.
Oxford University Press (OUP)
Abstract Aims Since December 2015, the European/International Fibromuscular Dysplasia (FMD) Registry enrolled 1022 patients from 22 countries. We present their characteristics according to disease subtype, age and gender, as well as predictors of widespread disease, aneurysms and dissections. Methods and results All patients diagnosed with FMD (string-of-beads or focal stenosis in at least one vascular bed) based on computed tomography angiography, magnetic resonance angiography, and/or catheter-based angiography were eligible. Patients were predominantly women (82%) and Caucasians (88%). Age at diagnosis was 46 ± 16 years (12% ≥65 years old), 86% were hypertensive, 72% had multifocal, and 57% multivessel FMD. Compared to patients with multifocal FMD, patients with focal FMD were younger, more often men, had less often multivessel FMD but more revascularizations. Compared to women with FMD, men were younger, had more often focal FMD and arterial dissections. Compared to younger patients with FMD, patients ≥65 years old had more often multifocal FMD, lower estimated glomerular filtration rate and more atherosclerotic lesions. Independent predictors of multivessel FMD were age at FMD diagnosis, stroke, multifocal subtype, presence of aneurysm or dissection, and family history of FMD. Predictors of aneurysms were multivessel and multifocal FMD. Predictors of dissections were age at FMD diagnosis, male gender, stroke, and multivessel FMD. Conclusions The European/International FMD Registry allowed large-scale characterization of distinct profiles of patients with FMD and, more importantly, identification of a unique set of independent predictors of widespread disease, aneurysms and dissections, paving the way for targeted screening, management, and follow-up of FMD.