Sepsis in Internal Medicine wards: current knowledge, uncertainties and new approaches for management optimization

Sepsis represents a global health problem in terms of morbidity, mortality, social and economic costs. Although usually managed in Intensive Care Units, sepsis showed an increased prevalence among Internal Medicine wards in the last decade. This is substantially due to the ageing of population and to multi-morbidity. These characteristics represent both a risk factor for sepsis and a relative contra-indication for the admission to Intensive Care Units. Although there is a lack of literature on the management of sepsis in Internal Medicine, the outcome of these patients seems to be gradually improving. This is due to Internists’ increased adherence to guidelines and “bundles”. The routine use of SOFA score helps physicians in the definition of septic patients, even if the optimal score has still to come. Point-of-care ultrasonography, lactates, procalcitonin and beta-d-glucan are of help for treatment optimization. The purpose of this narrative review is to focus on the management of sepsis in Internal Medicine departments, particularly on crucial concepts regarding diagnosis, risk assessment and treatment.Key Messages Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. The prevalence of sepsis is constantly increasing, affecting more hospital patients than any other disease. At least half of patients affected by sepsis are admitted to Internal Medicine wards. Adherence to guidelines, routine use of clinical and lab scores and point-of-care ultrasonography are of help for early recognition of septic patients and treatment optimization

Frequency of left ventricular hypertrophy in non-valvular atrial fibrillation

Left ventricular hypertrophy (LVH) is significantly related to adverse clinical outcomes in patients at high risk of cardiovascular events. In patients with atrial fibrillation (AF), data on LVH, that is, prevalence and determinants, are inconsistent mainly because of different definitions and heterogeneity of study populations. We determined echocardiographic-based LVH prevalence and clinical factors independently associated with its development in a prospective cohort of patients with non-valvular (NV) AF. From the "Atrial Fibrillation Registry for Ankle-brachial Index Prevalence Assessment: Collaborative Italian Study" (ARAPACIS) population, 1,184 patients with NVAF (mean age 72 \ub1 11 years; 56% men) with complete data to define LVH were selected. ARAPACIS is a multicenter, observational, prospective, longitudinal on-going study designed to estimate prevalence of peripheral artery disease in patients with NVAF. We found a high prevalence of LVH (52%) in patients with NVAF. Compared to those without LVH, patients with AF with LVH were older and had a higher prevalence of hypertension, diabetes, and previous myocardial infarction (MI). A higher prevalence of ankle-brachial index 640.90 was seen in patients with LVH (22 vs 17%, p = 0.0392). Patients with LVH were at significantly higher thromboembolic risk, with CHA2DS2-VASc 652 seen in 93% of LVH and in 73% of patients without LVH (p <0.05). Women with LVH had a higher prevalence of concentric hypertrophy than men (46% vs 29%, p = 0.0003). Logistic regression analysis demonstrated that female gender (odds ratio [OR] 2.80, p <0.0001), age (OR 1.03 per year, p <0.001), hypertension (OR 2.30, p <0.001), diabetes (OR 1.62, p = 0.004), and previous MI (OR 1.96, p = 0.001) were independently associated with LVH. In conclusion, patients with NVAF have a high prevalence of LVH, which is related to female gender, older age, hypertension, and previous MI. These patients are at high thromboembolic risk and deserve a holistic approach to cardiovascular prevention

Association of kidney disease measures with risk of renal function worsening in patients with type 1 diabetes

Background: Albuminuria has been classically considered a marker of kidney damage progression in diabetic patients and it is routinely assessed to monitor kidney function. However, the role of a mild GFR reduction on the development of stage 653 CKD has been less explored in type 1 diabetes mellitus (T1DM) patients. Aim of the present study was to evaluate the prognostic role of kidney disease measures, namely albuminuria and reduced GFR, on the development of stage 653 CKD in a large cohort of patients affected by T1DM. Methods: A total of 4284 patients affected by T1DM followed-up at 76 diabetes centers participating to the Italian Association of Clinical Diabetologists (Associazione Medici Diabetologi, AMD) initiative constitutes the study population. Urinary albumin excretion (ACR) and estimated GFR (eGFR) were retrieved and analyzed. The incidence of stage 653 CKD (eGFR < 60 mL/min/1.73 m2) or eGFR reduction > 30% from baseline was evaluated. Results: The mean estimated GFR was 98 \ub1 17 mL/min/1.73m2 and the proportion of patients with albuminuria was 15.3% (n = 654) at baseline. About 8% (n = 337) of patients developed one of the two renal endpoints during the 4-year follow-up period. Age, albuminuria (micro or macro) and baseline eGFR < 90 ml/min/m2 were independent risk factors for stage 653 CKD and renal function worsening. When compared to patients with eGFR > 90 ml/min/1.73m2 and normoalbuminuria, those with albuminuria at baseline had a 1.69 greater risk of reaching stage 3 CKD, while patients with mild eGFR reduction (i.e. eGFR between 90 and 60 mL/min/1.73 m2) show a 3.81 greater risk that rose to 8.24 for those patients with albuminuria and mild eGFR reduction at baseline. Conclusions: Albuminuria and eGFR reduction represent independent risk factors for incident stage 653 CKD in T1DM patients. The simultaneous occurrence of reduced eGFR and albuminuria have a synergistic effect on renal function worsening

Relationship between carotid intima-media thickness and non valvular atrial fibrillation type.

OBJECTIVE:Carotid intima-media thickness (cIMT) is a surrogate marker of subclinical atherosclerosis and it is able to predict both coronary and cerebral vascular events. No data exist on the association between cIMT and non valvular atrial fibrillation (NVAF) type. We conduct this study with the aim to analyze the association between abnormal cIMT and NVAF type.METHODS:A cross-sectional study of the "Atrial fibrillation Registry for Ankle-brachial index Prevalence Assessment-Collaborative Italian Study (ARAPACIS)" has been performed. Among 2027 patients enrolled in the ARAPACIS, 673 patients, who underwent carotid ultrasound examination to assess cIMT, were included in the study.RESULTS:Among the entire population, 478 patients (71%) had cIMT > 0.90 mm. Patients with an abnormal cIMT (>0.90 mm) were significantly older and more likely hypertensive, diabetic and with a previous history of stroke than those with normal cIMT ( 640.90 mm). These patients had more permanent/persistent NVAF and CHA2DS2-VASc score 65 2 (p < 0.0001) compared to those with cIMT <0.90 mm. Excluding all patients affected by previous cardiovascular disease, logistic regression analysis showed that independent predictors of abnormal cIMT were: age class 65-74 yrs. (p < 0.001), age class 6575 yrs. (p < 0.001), arterial hypertension (p < 0.001), calcium-channel blockers use (p < 0.001) and persistent/permanent NVAF (p = 0.001).CONCLUSION:Our findings show a high prevalence of abnormal cIMT in NVAF patients, reinforcing the concept that NVAF and systemic atherosclerosis are closely associated. Abnormal cIMT was particularly evident in persistent/permanent NVAF suggesting a more elevated atherosclerotic burden in patients with long-standing NVAF

Relationship between carotid intima-media thickness and non valvular atrial fibrillation type

OBJECTIVE: Carotid intima-media thickness (cIMT) is a surrogate marker of subclinical atherosclerosis and it is able to predict both coronary and cerebral vascular events. No data exist on the association between cIMT and non valvular atrial fibrillation (NVAF) type. We conduct this study with the aim to analyze the association between abnormal cIMT and NVAF type. METHODS: A cross-sectional study of the "Atrial fibrillation Registry for Ankle-brachial index Prevalence Assessment-Collaborative Italian Study (ARAPACIS)" has been performed. Among 2027 patients enrolled in the ARAPACIS, 673 patients, who underwent carotid ultrasound examination to assess cIMT, were included in the study. RESULTS: Among the entire population, 478 patients (71%) had cIMT > 0.90 mm. Patients with an abnormal cIMT (>0.90 mm) were significantly older and more likely hypertensive, diabetic and with a previous history of stroke than those with normal cIMT ( 640.90 mm). These patients had more permanent/persistent NVAF and CHA2DS2-VASc score 65 2 (p < 0.0001) compared to those with cIMT <0.90 mm. Excluding all patients affected by previous cardiovascular disease, logistic regression analysis showed that independent predictors of abnormal cIMT were: age class 65-74 yrs. (p < 0.001), age class 6575 yrs. (p < 0.001), arterial hypertension (p < 0.001), calcium-channel blockers use (p < 0.001) and persistent/permanent NVAF (p = 0.001). CONCLUSION: Our findings show a high prevalence of abnormal cIMT in NVAF patients, reinforcing the concept that NVAF and systemic atherosclerosis are closely associated. Abnormal cIMT was particularly evident in persistent/permanent NVAF suggesting a more elevated atherosclerotic burden in patients with long-standing NVAF. TRIAL REGISTRATION: http://clinicaltrials.gov/ct2/show/NCT01161251

Relationship between carotid intima-media thickness and non valvular atrial fibrillation type

Objective: Carotid intima-media thickness (cIMT) is a surrogate marker of subclinical atherosclerosis and it is able to predict both coronary and cerebral vascular events. No data exist on the association between cIMT and non valvular atrial fibrillation (NVAF) type. We conduct this study with the aim to analyze the association between abnormal cIMT and NVAF type. Methods: A cross-sectional study of the "Atrial fibrillation Registry for Ankle-brachial index Prevalence Assessment-Collaborative Italian Study (ARAPACIS)" has been performed. Among 2027 patients enrolled in the ARAPACIS, 673 patients, who underwent carotid ultrasound examination to assess cIMT, were included in the study. Results: Among the entire population, 478 patients (71%) had cIMT>0.90mm. Patients with an abnormal cIMT (>0.90mm) were significantly older and more likely hypertensive, diabetic and with a previous history of stroke than those with normal cIMT (≤0.90mm). These patients had more permanent/persistent NVAF and CHA2DS2-VASc score ≥ 2 (p<0.0001) compared to those with cIMT <0.90mm. Excluding all patients affected by previous cardiovascular disease, logistic regression analysis showed that independent predictors of abnormal cIMT were: age class 65-74 yrs. (p<0.001), age class ≥75 yrs. (p<0.001), arterial hypertension (p<0.001), calcium-channel blockers use (p<0.001) and persistent/permanent NVAF (p=0.001). Conclusion: Our findings show a high prevalence of abnormal cIMT in NVAF patients, reinforcing the concept that NVAF and systemic atherosclerosis are closely associated. Abnormal cIMT was particularly evident in persistent/permanent NVAF suggesting a more elevated atherosclerotic burden in patients with long-standing NVAF

Prevalence of peripheral artery disease by abnormal ankle-brachial index in atrial fibrillation: implications for risk and therapy.

To the Editor: Nonvalvular atrial fibrillation (NVAF) is the most common sustained arrhythmia encountered in clinical practice and is associated with a 5-fold increased risk for stroke (1). Moreover, patients with NVAF often suffer from atherosclerotic complications such as acute myocardial infarction (AMI) (2). Peripheral artery disease (PAD) is an established marker of systemic atherosclerosis but its prevalence in NVAF is still unclear. We reasoned that inclusion of ankle-brachial index (ABI), which is an established tool for diagnosis of PAD (3), in the CHA2DS2-VASc (4) score would better define the prevalence of vascular disease. To address this issue, the Italian Society of Internal Medicine (SIMI) established an Italian registry documenting ABI in NVAF patients. The Atrial Fibrillation Registry for the ARAPACIS (Ankle-brachial Index Prevalence Assessment: Collaborative Italian Study) study is an independent research project involving all Regional Councils of SIMI. The first objective of the study was to estimate the prevalence of ABI 640.90 in NVAF patients. Consecutive patients with NVAF referred to internal medicine wards were eligible for the enrollment. Enrollment started in October 2010 and continued until October 30, 2012. Patients were enrolled if they were 18 years or older and had a diagnosis of NVAF, recording during the qualifying admission/consultation or in the preceding 12 months, and if it was possible to obtain the ABI measurement. Exclusion criteria included the following: acquired or congenital valvular AF, active cancer, disease with life expectancy <3 years, hyperthyroidism and pregnancy. We initially planned to include 3,000 patients. The Data and Safety Monitoring Board (Online Appendix) decided to perform an interim analysis to assess the prevalence of ABI in the enrolled populations\u2014as a higher than expected prevalence of low ABI was detected\u2014and decided to interrupt the patients' enrollment. The sample size was amended as follows: a sample of 2,027 patients leads to the expected prevalence of 21% with a 95% confidence interval width of 3.5% (StataCorp LP, College Station, Texas). Among the 2,027 NVAF patients included in the study, hypertension was detected in 83%, diabetes mellitus in 23%, dyslipidemia in 39%, metabolic syndrome in 29%, and smoking in 15%. At least 1 atherosclerotic risk factor was detected in 90% of patients. The NVAF population was at high risk for stroke, with only 18% having a CHA2DS2-VASc score of 0 to 1, while 82% had a risk 652. Despite this, 16% were untreated with any antithrombotic drug, 19% were treated with antiplatelet drugs (APs), and 61% with oral anticoagulants (OAC); 4% of patients were treated with both APs and OAC. Among the AF population, 428 patients (21%) had ABI 640.90 compared with 1,381 patients, who had an ABI of 0.91 to 1.39 (69%); 204 patients (10%) had ABI 651.40 (Fig. 1). ABI recorded only in 1 leg was excluded from the analysis (n = 14). ABI 640.90 progressively increased from paroxysmal to permanent NVAF (18%, 21%, 24%; p = 0.0315). Figure 1. ABI Distribution of Any Category and CHA2DS2-VASc Score Including ABI 640.90 C = congestive heart failure (or left ventricular systolic dysfunction) (Points: 1), H = hypertension (Points: 1), A2 = Age 6575 years (Points: 2), D = diabetes mellitus (Points: 1), S2 = prior stroke or transient ischemic attack or thromboembolism (Points: 2); V = vascular disease (previous acute myocardial infarction, peripheral arterial disease, or aortic plaque) (Points: 1); A = age 65 to 74 years (Points: 1); Sc = sex category (female) (Points: 1). ABI = ankle brachial index. Figure optionsDownload full-size imageDownload high-quality image (447 K)Download as PowerPoint slide NVAF patients with ABI 640.90 were more likely to be hypertensive (88% vs. 82%; p = 0.032), diabetic (34% vs. 20%; p 0.90 (93% vs. 82%; p < 0.0001). Logistic regression analysis demonstrated that ABI 640.90 was significantly associated with a smoking habit (odds ratio [OR]: 1.99; 95% confidence interval [CI]: 1.48 to 2.66; p < 0.0001), diabetes (OR: 1.93; 95% CI: 1.51 to 2.46; p < 0.0001), age class 65 to 74 years (OR: 2.05; 95% CI: 1.40 to 3.07; p < 0.0001), age class 6575 years (OR: 3.12; 95% CI: 2.16 to 4.61; p < 0.0001), and history of previous transient ischemic attack/stroke (OR: 1.64; 95% CI: 1.20 to 2.24; p = 0.002). Vascular disease, as assessed by the history elements of CHA2DS2VASc score, was recorded in 17.3% of patients; inclusion of ABI 640.90 in the definition of vascular disease yielded a total prevalence of 33%. A higher prevalence of vascular disease was detected if ABI 640.90 was included in the CHA2DS2VASc score (Fig. 1). CHA2DS2VASc including ABI 640.90 was more associated with previous stroke (43%; OR: 1.85; 95% CI: 1.41 to 2.44; p < 0.0001) compared to CHA2DS2VASc with ABI 0.91 to 1.39 (23%; OR: 1.52; 95% CI: 1.10 to 2.11; p = 0.0117). To the best of our knowledge, there is no large-scale study that specifically examined the prevalence of ABI 640.90 in NVAF. In our population, 21% had ABI 640.90 indicating that NVAF is often associated with systemic atherosclerosis. The CHADS2 has been recently refined with the CHA2DS2-VASc score, which includes vascular disease as documented by a history of AMI, symptomatic PAD, or detection of atherosclerotic plaque in the aortic arch (4). Comparison of vascular prevalence as assessed by CHA2DS2-VASc score and/or ABI 640.90 is of interest to define the potentially positive impact of measuring ABI in the management of NVAF patients. Inclusion of ABI 640.90 in the definition of vascular disease greatly increased the prevalence of vascular disease, which increased from 17.3% (based on history alone) to 33% (based on ABI) in the entire population. If ABI 640.90 was encompassed in the definition of vascular disease of CHA2DS2-VASc score the prevalence of vascular disease increased in every risk class. Inclusion of ABI 640.90 in the CHA2DS2-VASc score allowed us to better define the risk profile of NVAF patients with an up-grading of the risk score in each CHA2DS2-VASc score category. This may have important therapeutic implications if the new score could be tested prospectively, as a higher number of NVAF patients would potentially be candidates for an anticoagulant treatment by measuring ABI. A prospective study is, therefore, necessary to validate the risk score of this new definition of vascular disease. In conclusion, this study provides the first evidence that one-fifth of NVAF patients had an ABI 640.90, indicating that it may represent a simple and cheap method to better define the prevalence of vascular disease in NVAF

Correction to: Major adverse cardiovascular events in non-valvular atrial fibrillation with chronic obstructive pulmonary disease: the ARAPACIS study (Internal and Emergency Medicine, (2018), 13, 5, (651-660), 10.1007/s11739-018-1835-9)

In the original publication, one of the ARAPACIS collaborators Dr. “Leonardo Di Gennaro” name has been erroneously mentioned as “Leonardo De Gennaro”

Major adverse cardiovascular events in non-valvular atrial fibrillation with chronic obstructive pulmonary disease : the ARAPACIS study

Chronic obstructive pulmonary disease (COPD) increases the risk of mortality in non-valvular atrial fibrillation (NVAF) patients. Data on the relationship of COPD to major cardiovascular events (MACE) in AF have not been defined. The aim of the study is to assess the predictive value of COPD on incident MACE in NVAF patients over a 3-year follow-up. In the Atrial Fibrillation Registry for Ankle-Brachial Index Prevalence Assessment-Collaborative Italian Study (ARAPACIS) cohort, we evaluate the impact of COPD on the following clinical endpoints: MACE (including vascular death, fatal/non-fatal MI and stroke/TIA), cardiovascular (CV) death and all-cause mortality. Among 2027 NVAF patients, patients with COPD (9%) are more commonly male, elderly and at higher thromboembolic risk. During a median 36.0&nbsp;months follow-up, 186 patients experienced MACE: vascular death (n\u2009=\u200972), MI (n\u2009=\u200957), stroke/TIA (n\u2009=\u200957). All major outcomes (including stroke/TIA, MI, vascular death, and all-cause death) are centrally adjudicated. Kaplan-Meier curves show that NVAF patients with COPD are at higher risk for MACE (p\u2009&lt;\u20090.001), CV death (p\u2009&lt;\u20090.001) and all-cause death (p\u2009&lt;\u20090.001). On Cox proportional hazard analysis, COPD is an independent predictor of MACE (Hazard ratio [HR] 1.77, 95% Confidence Intervals [CI] 1.20-2.61; p\u2009=\u20090.004), CV death (HR 2.73, 95% CI 1.76-4.23; p\u2009&lt;\u20090.0001) and all-cause death (HR 2.16, 95% CI 1.48-3.16; p\u2009&lt;\u20090.0001). COPD is an independent predictor of MACE, CV death and all-cause death during a long-term follow-up of NVAF patients

Correction to: Major adverse cardiovascular events in non-valvular atrial fibrillation with chronic obstructive pulmonary disease: the ARAPACIS study

none372In the original publication, one of the ARAPACIS collaborators Dr. “Leonardo Di Gennaro” name has been erroneously mentioned as “Leonardo De Gennaro”.noneRaparelli V.; Pastori D.; Pignataro S.F.; Vestri A.R.; Pignatelli P.; Cangemi R.; Proietti M.; Davi G.; Hiatt W.R.; Lip G.Y.H.; Corazza G.R.; Perticone F.; Violi F.; Basili S.; Alessandri C.; Serviddio G.; Palange P.; Greco E.; Bruno G.; Averna M.; Giammanco A.; Sposito P.; DeCristofaro R.; Carulli L.; DiGennaro L.; Pellegrini E.; Cominacini L.; Mozzini C.; Pasini A.F.; Sprovieri M.; Spagnuolo V.; Cerqua G.; Cerasola G.; Mule G.; Barbagallo M.; Lo Sciuto S.; Monteverde A.; Saitta A.; Lo Gullo A.; Malatino L.; Cilia C.; Terranova V.; Pisano M.; Pinto A.; DiRaimondo D.; Tuttolomondo A.; Conigliaro R.; Signorelli S.; DePalma D.; Galderisi M.; Cudemo G.; Galletti F.; Fazio V.; DeLuca N.; Meccariello A.; Caputo D.; DeDonato M.T.; Iannuzi A.; Bresciani A.; Giunta R.; Utili R.; Iorio V.; Adinolfi L.E.; Sellitto C.; Iuliano N.; Bellis P.; Tirelli P.; Sacerdoti D.; Vanni D.; Iuliano L.; Ciacciarelli M.; Pacelli A.; Palazzuoli A.; Cacciafesta M.; Gueli N.; Lo Iacono C.; Brusco S.; Verrusio W.; Nobili L.; Tarquinio N.; Pellegrini F.; Vincentelli G.M.; Ravallese F.; Santini C.; Letizia C.; Petramala L.; Zinnamosca L.; Minisola S.; Cilli M.; Colangelo L.; Falaschi P.; Martocchia A.; Pastore F.; Bertazzoni G.; Attalla El Halabieh E.; Paradiso M.; Lizzi E.M.; Timmi S.; Battisti P.; Cerci S.; Ciavolella M.; DiVeroli C.; Malci F.; DeCiocchis A.; Abate D.; Castellino P.; Zanoli L.; Fidone F.; Mannarino E.; Pasqualini L.; Oliverio G.; Pende A.; Artom N.; Ricchio R.; Fimognari F.L.; Alletto M.; Messina S.; Sesti G.; Arturi F.; Succurro E.; Fiorentino T.V.; Pedace E.; Scarpino P.E.; Carullo G.; Maio R.; Sciacqua A.; Frugiuele P.; Battaglia G.; Atzori S.; Delitala G.; Angelucci E.; Sestili S.; Traisci G.; DeFeudis L.; DiMichele D.; Fava A.; Balsano C.; DeCiantis P.; Desideri G.; Camerota A.; Mezzetti M.; Gresele P.; Vedovati C.; Fierro T.; Puccetti L.; Bertolotti M.; Mussi C.; Boddi M.; Savino A.; Contri S.; Degl'Innocenti G.; Saller A.; Fabris F.; Pesavento R.; Filippi L.; Vedovetto V.; Puato M.; Treleani M.; DeLuca E.; DeZaiacomo F.; Giantin V.; Semplicini A.; Minuz P.; Romano S.; Fantin F.; Manica A.; Stockner I.; Pattis P.; Gutmann B.; Catena C.; Colussi G.; Sechi L.A.; Annoni G.; Bruni A.A.; Castagna A.; Spinelli D.; Miceli E.; Padula D.; Schinco G.; Spreafico S.; Secchi B.; Vanoli M.; Casella G.; Pulixi E.A.; Sansone L.; Serra M.G.; Longo S.; Antonaci S.; Belfiore A.; Frualdo M.; Palasciano G.; Ricci L.; Ventrella F.; Bianco C.; Santovito D.; Cipollone F.; Nicolai S.; Salvati F.; Rini G.B.; Scozzari F.; Muiesan M.L.; Salvetti M.; Bazza A.; Picardi A.; Vespasiani-Gentilucci U.; DeVincentis A.; Cosio P.; Terzolo M.; Madaffari B.; Parasporo B.; Fenoglio L.; Bracco C.; Melchio R.; Gentili T.; Salvi A.; Nitti C.; Gabrielli A.; Martino G.P.; Capucci A.; Brambatti M.; Sparagna A.; Tirotta D.; Andreozzi P.; Ettorre E.; Viscogliosi G.; Servello A.; Musumeci M.; Delfino M.; Giorgi A.; Glorioso N.; Melis G.; Marras G.; Matta M.; Sacco A.; Stellitano E.; Scordo A.; Russo F.; Caruso A.A.; Porreca E.; Tana M.; Ferri C.; Cheli P.; Portincasa P.; Muscianisi G.; Giordani S.; Stanghellini V.; Sabba C.; Mancuso G.; Bartone M.; Calipari D.; Arcidiacono G.; Bellanuova I.; Ferraro M.; Marigliano G.; Cozzolino D.; Lampitella A.; Acri V.; Galasso D.; Mazzei F.; Buratti A.; Galasso S.; Porta M.; Brizzi M.F.; Fattorini A.; Sampietro F.; D'Angelo A.; Manfredini R.; Pala M.; Fabbian F.; Moroni C.; Valente L.; Lopreiato F.; Parente F.; Granata M.; Moia M.; Braham S.; Rossi M.; Pesce M.; Gentile A.; Catozzo V.; Baciarello G.; Cosimati A.; Ageno W.; Rancan E.; Guasti L.; Ciccaglioni A.; Negri S.; Polselli M.; Prisco D.; Marcucci R.; Ferro D.; Perri L.; Saliola M.; DelBen M.; Angelico F.; Baratta F.; Migliacci R.; Porciello G.; Corrao S.; Napoleone L.; Talerico G.; Amoroso D.; Romiti G.F.; Ruscio E.; Toriello F.; Sperduti N.; Todisco T.; DiTanna G.; Sacchetti M.L.; Puddu P.E.; Farcomeni A.; Anzaldi M.; Bazzini C.; Bianchi P.I.; Boari B.; Buonauro A.; Butta C.; Buzzetti E.; Calabria S.; Capeci W.; Caradio F.; Carleo P.; Carrabba M.D.; Castorani L.; Cecchetto L.; Cicco S.; Cimini C.; Colombo B.M.; De Giorgi A.; DeVuono S.; DelCorso L.; Denegri A.; DiGiosia P.; Durante Mangoni E.; Falsetti L.; Forgione A.; Giorgini P.; Grassi D.; Grembiale A.; Hijazi D.; Iamele L.; Lorusso G.; Marchese A.; Marra A.M.; Masala M.; Miceli G.; Montebianco Abenavoli L.; Murgia G.; Naccarato P.; Pattoneri P.; Perego F.; Pesce P.; Piano S.; Pinna M.; Pinto D.; Pretti V.; Pucci G.; Salinaro F.; Salzano A.; Santilli F.; Scarpini F.; Scicali R.; Sirico D.; Suppressa P.; Talia M.; Tassone E.J.; Torres D.; Vazzana N.; Vecchio C.R.; Vidili G.; Vitale F.; Zaccone V.Raparelli, V.; Pastori, D.; Pignataro, S. F.; Vestri, A. R.; Pignatelli, P.; Cangemi, R.; Proietti, M.; Davi, G.; Hiatt, W. R.; Lip, G. Y. H.; Corazza, G. R.; Perticone, F.; Violi, F.; Basili, S.; Alessandri, C.; Serviddio, G.; Palange, P.; Greco, E.; Bruno, G.; Averna, M.; Giammanco, A.; Sposito, P.; Decristofaro, R.; Carulli, L.; Digennaro, L.; Pellegrini, E.; Cominacini, L.; Mozzini, C.; Pasini, A. F.; Sprovieri, M.; Spagnuolo, V.; Cerqua, G.; Cerasola, G.; Mule, G.; Barbagallo, M.; Lo Sciuto, S.; Monteverde, A.; Saitta, A.; Lo Gullo, A.; Malatino, L.; Cilia, C.; Terranova, V.; Pisano, M.; Pinto, A.; Diraimondo, D.; Tuttolomondo, A.; Conigliaro, R.; Signorelli, S.; Depalma, D.; Galderisi, M.; Cudemo, G.; Galletti, F.; Fazio, V.; Deluca, N.; Meccariello, A.; Caputo, D.; Dedonato, M. T.; Iannuzi, A.; Bresciani, A.; Giunta, R.; Utili, R.; Iorio, V.; Adinolfi, L. E.; Sellitto, C.; Iuliano, N.; Bellis, P.; Tirelli, P.; Sacerdoti, D.; Vanni, D.; Iuliano, L.; Ciacciarelli, M.; Pacelli, A.; Palazzuoli, A.; Cacciafesta, M.; Gueli, N.; Lo Iacono, C.; Brusco, S.; Verrusio, W.; Nobili, L.; Tarquinio, N.; Pellegrini, F.; Vincentelli, G. M.; Ravallese, F.; Santini, C.; Letizia, C.; Petramala, L.; Zinnamosca, L.; Minisola, S.; Cilli, M.; Colangelo, L.; Falaschi, P.; Martocchia, A.; Pastore, F.; Bertazzoni, G.; Attalla El Halabieh, E.; Paradiso, M.; Lizzi, E. M.; Timmi, S.; Battisti, P.; Cerci, S.; Ciavolella, M.; Diveroli, C.; Malci, F.; Deciocchis, A.; Abate, D.; Castellino, P.; Zanoli, L.; Fidone, F.; Mannarino, E.; Pasqualini, L.; Oliverio, G.; Pende, A.; Artom, N.; Ricchio, R.; Fimognari, F. L.; Alletto, M.; Messina, S.; Sesti, G.; Arturi, F.; Succurro, E.; Fiorentino, T. V.; Pedace, E.; Scarpino, P. E.; Carullo, G.; Maio, R.; Sciacqua, A.; Frugiuele, P.; Battaglia, G.; Atzori, S.; Delitala, G.; Angelucci, E.; Sestili, S.; Traisci, G.; Defeudis, L.; Dimichele, D.; Fava, A.; Balsano, C.; Deciantis, P.; Desideri, G.; Camerota, A.; Mezzetti, M.; Gresele, P.; Vedovati, C.; Fierro, T.; Puccetti, L.; Bertolotti, M.; Mussi, C.; Boddi, M.; Savino, A.; Contri, S.; Degl'Innocenti, G.; Saller, A.; Fabris, F.; Pesavento, R.; Filippi, L.; Vedovetto, V.; Puato, M.; Treleani, M.; Deluca, E.; Dezaiacomo, F.; Giantin, V.; Semplicini, A.; Minuz, P.; Romano, S.; Fantin, F.; Manica, A.; Stockner, I.; Pattis, P.; Gutmann, B.; Catena, C.; Colussi, G.; Sechi, L. A.; Annoni, G.; Bruni, A. A.; Castagna, A.; Spinelli, D.; Miceli, E.; Padula, D.; Schinco, G.; Spreafico, S.; Secchi, B.; Vanoli, M.; Casella, G.; Pulixi, E. A.; Sansone, L.; Serra, M. G.; Longo, S.; Antonaci, S.; Belfiore, A.; Frualdo, M.; Palasciano, G.; Ricci, L.; Ventrella, F.; Bianco, C.; Santovito, D.; Cipollone, F.; Nicolai, S.; Salvati, F.; Rini, G. B.; Scozzari, F.; Muiesan, M. L.; Salvetti, M.; Bazza, A.; Picardi, A.; Vespasiani-Gentilucci, U.; Devincentis, A.; Cosio, P.; Terzolo, M.; Madaffari, B.; Parasporo, B.; Fenoglio, L.; Bracco, C.; Melchio, R.; Gentili, T.; Salvi, A.; Nitti, C.; Gabrielli, A.; Martino, G. P.; Capucci, A.; Brambatti, M.; Sparagna, A.; Tirotta, D.; Andreozzi, P.; Ettorre, E.; Viscogliosi, G.; Servello, A.; Musumeci, M.; Delfino, M.; Giorgi, A.; Glorioso, N.; Melis, G.; Marras, G.; Matta, M.; Sacco, A.; Stellitano, E.; Scordo, A.; Russo, F.; Caruso, A. A.; Porreca, E.; Tana, M.; Ferri, C.; Cheli, P.; Portincasa, P.; Muscianisi, G.; Giordani, S.; Stanghellini, V.; Sabba, C.; Mancuso, G.; Bartone, M.; Calipari, D.; Arcidiacono, G.; Bellanuova, I.; Ferraro, M.; Marigliano, G.; Cozzolino, D.; Lampitella, A.; Acri, V.; Galasso, D.; Mazzei, F.; Buratti, A.; Galasso, S.; Porta, M.; Brizzi, M. F.; Fattorini, A.; Sampietro, F.; D'Angelo, A.; Manfredini, R.; Pala, M.; Fabbian, F.; Moroni, C.; Valente, L.; Lopreiato, F.; Parente, F.; Granata, M.; Moia, M.; Braham, S.; Rossi, M.; Pesce, M.; Gentile, A.; Catozzo, V.; Baciarello, G.; Cosimati, A.; Ageno, W.; Rancan, E.; Guasti, L.; Ciccaglioni, A.; Negri, S.; Polselli, M.; Prisco, D.; Marcucci, R.; Ferro, D.; Perri, L.; Saliola, M.; Delben, M.; Angelico, F.; Baratta, F.; Migliacci, R.; Porciello, G.; Corrao, S.; Napoleone, L.; Talerico, G.; Amoroso, D.; Romiti, G. F.; Ruscio, E.; Toriello, F.; Sperduti, N.; Todisco, T.; Ditanna, G.; Sacchetti, M. L.; Puddu, P. E.; Farcomeni, A.; Anzaldi, M.; Bazzini, C.; Bianchi, P. I.; Boari, B.; Buonauro, A.; Butta, C.; Buzzetti, E.; Calabria, S.; Capeci, W.; Caradio, F.; Carleo, P.; Carrabba, M. D.; Castorani, L.; Cecchetto, L.; Cicco, S.; Cimini, C.; Colombo, B. M.; De Giorgi, A.; Devuono, S.; Delcorso, L.; Denegri, A.; Digiosia, P.; Durante Mangoni, E.; Falsetti, L.; Forgione, A.; Giorgini, P.; Grassi, D.; Grembiale, A.; Hijazi, D.; Iamele, L.; Lorusso, G.; Marchese, A.; Marra, A. M.; Masala, M.; Miceli, G.; Montebianco Abenavoli, L.; Murgia, G.; Naccarato, P.; Pattoneri, P.; Perego, F.; Pesce, P.; Piano, S.; Pinna, M.; Pinto, D.; Pretti, V.; Pucci, G.; Salinaro, F.; Salzano, A.; Santilli, F.; Scarpini, F.; Scicali, R.; Sirico, D.; Suppressa, P.; Talia, M.; Tassone, E. J.; Torres, D.; Vazzana, N.; Vecchio, C. R.; Vidili, G.; Vitale, F.; Zaccone, V