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Community-acquired pneumonia (CAP) is complicated by cardiovascular events as myocardial infarction and stroke but the underlying mechanism is still unclear. We hypothesized that endothelial dysfunction may be implicated and that endotoxemia may have a role.Fifty patients with CAP and 50 controls were enrolled. At admission and at discharge, flow-mediated dilation (FMD), serum levels of endotoxins and oxidative stress, as assessed by serum levels of nitrite/nitrate (NOx) and isoprostanes, were studied.At admission, a significant difference between patients with CAP and controls was observed for FMD (2.1±0.3 vs 4.0±0.3%, p0.001), serum endotoxins (157.8±7.6 vs 33.1±4.8pg/ml), serum isoprostanes (341±14 vs 286±10 pM, p=0.009) and NOx (24.3±1.1 vs 29.7±2.2μM). Simple linear correlation analysis showed that serum endotoxins significantly correlated with Pneumonia Severity Index score (Rs=0.386, p=0.006). Compared to baseline, at discharge CAP patients showed a significant increase of FMD and NOx (from 2.1±0.3 to 4.6±0.4%, p0.001 and from 24.3±1.1 to 31.1±1.5μM, p0.001, respectively) and a significant decrease of serum endotoxins and isoprostanes (from 157.8±7.6 to 55.5±2.3pg/ml, p0.001, and from 341±14 to 312±14 pM, p0.001, respectively). Conversely, no changes for FMD, NOx, serum endotoxins and isoprostanes were observed in controls between baseline and discharge. Changes of FMD significantly correlated with changes of serum endotoxins (Rs=-0.315; p=0.001).The study provides the first evidence that CAP is characterized by impaired FMD with a mechanism potentially involving endotoxin production and oxidative stress.

Adults hospitalized for community-acquired pneumonia (CAP) have an increased risk of myocardial infarction. Corticosteroid treatment lowers CAP morbidity and mortality, but it is not known whether it influences in-hospital myocardial infarction.The aim of the present study was to investigate the potential interplay between corticosteroid treatment and in-hospital myocardial infarction in adults with CAP.We retrospectively analyzed adults with CAP referred to the University Hospital Policlinico Umberto I (Rome, Italy), consecutively recruited, and prospectively followed until discharge. The primary outcome was the occurrence of myocardial infarction during hospitalization. We used propensity score-adjusted Cox models to examine the association between corticosteroid use and myocardial infarction.Seven hundred fifty-eight patients (493 males, 265 females; mean ± standard deviation age, 71.7 ± 14.4 yr) were included in the study. Of these, 241 (32%) were treated with systemic corticosteroids (methylprednisolone, betamethasone, or prednisone). During follow-up, 62 (8.2%) had a myocardial infarction during their hospitalization (incidence, 0.72 per 100 person-days; 95% confidence interval [CI], 0.55 to 0.92). Those treated with corticosteroids had a lower incidence of myocardial infarction (0.42 per 100 person-days) than those not treated with corticosteroids (0.89 per 100 person-days; absolute rate difference, -0.48 per 100 person-days; 95% CI, -0.85 to -0.10). In a propensity score-adjusted Cox model, corticosteroid use was associated with a lower incidence of myocardial infarction (hazard ratio, 0.46; 95% CI, 0.24 to 0.88; P = 0.02).We found that in-hospital corticosteroid treatment was associated with a lower incidence of myocardial infarction in adults hospitalized with CAP.

Platelet activation seems to be implicated in the cardiovascular events occurring in patients with community-acquired pneumonia (CAP) but the underlying mechanism is still unclear. Aim of the study was to assess the mechanism involved in platelet activation in CAP patients.Two-hundred-seventy-eight consecutive patients hospitalized for CAP were recruited and followed-up until discharge. Hospitalized patients matched for sex, age and comorbidities but without acute infectious diseases were used as controls.At hospital admission patients disclosed enhanced plasma levels of sP-selectin, a maker of in-vivo platelet activation, serum sNOX2-dp, a marker of NADPH-oxidase activation, serum Lipopolysaccharide (LPS) and serum zonulin, a marker of gut permeability, compared to controls (p 0.001). Baseline sP-selectin was independently associated to serum LPS, sNOX2-sp and Pneumonia Severity Index score (p 0.001). Plasma sP-selectin, serum sNOX2-dp, LPS and zonulin coincidentally decreased at hospital discharge (p 0.001). An in vitro study showed that LPS, at concentration similar to that found in CAP patients, induced sP-selectin release by agonist-activated platelets, a phenomenon that was counteract by treating cells with gp91ds-tat, a specific inhibitor of NOX2.CAP patients display enhanced platelet activation, which is related to LPS-mediated NOX2 activation. Enhanced gut permeability seems be implicated in enhancing circulating levels of LPS.

Community-acquired pneumonia (CAP) is complicated by cardiac events in the early phase of the disease. Aim of this study was to assess if these intrahospital cardiac complications may account for overall mortality and cardiovascular events occurring during a long-term follow-up. Three hundred one consecutive patients admitted to the University-Hospital, Policlinico Umberto I, with community-acquired pneumonia were prospectively recruited and followed up for a median of 17.4 months. Primary end point was the occurrence of death for any cause, and secondary end point was the occurrence of cardiovascular events (cardiovascular death, nonfatal myocardial infarction [MI], and stroke). During the intrahospital stay, 55 patients (18%) experienced a cardiac complication. Of these, 32 had an MI (29 non-ST-elevation MI and 3 ST-elevation MI) and 30 had a new episode of atrial fibrillation (7 nonmutually exclusive events). During the follow-up, 89 patients died (51% of patients with an intrahospital cardiac complication and 26% of patients without, p0.001) and 73 experienced a cardiovascular event (47% of patients with and 19% of patients without an intrahospital cardiac complication, p0.001). A Cox regression analysis showed that intrahospital cardiac complications, age, and Pneumonia Severity Index were significantly associated with overall mortality, whereas intrahospital cardiac complications, age, hypertension, and diabetes were significantly associated with cardiovascular events during the follow-up. In conclusion, this prospective study shows that intrahospital cardiac complications in the early phase of pneumonia are associated with an enhanced risk of death and cardiovascular events during long-term follow-up.

Background Pneumonia is complicated by high rate of mortality and cardiovascular events (CVEs). The potential benefit of aspirin, which lowers platelet aggregation by inhibition of thromboxane A2 production, is still unclear. The aim of the study was to assess the impact of aspirin on mortality in patients with pneumonia. Methods and Results Consecutive patients admitted to the University‐Hospital Policlinico Umberto I (Rome, Italy) with community‐onset pneumonia were recruited and prospectively followed up until discharge or death. The primary end point was the occurrence of death up to 30 days after admission; the secondary end point was the intrahospital incidence of nonfatal myocardial infarction and ischemic stroke. One thousand and five patients (age, 74.7±15.1 years) were included in the study: 390 were receiving aspirin (100 mg/day) at the time of hospitalization, whereas 615 patients were aspirin free. During the follow‐up, 16.2% of patients died; among these, 19 (4.9%) were aspirin users and 144 (23.4%; P P =0.040). The Cox regression analysis showed that pneumonia severity index ( PSI ), severe sepsis, pleural effusion, and PaO 2 /FiO 2 ratio P =0.029) for total mortality. Conclusions This study shows that chronic aspirin use is associated with lower mortality rate within 30 days after hospital admission in a large cohort of patients with pneumonia.

The brain has a high level of complexity and needs continuous oxygen supply. So it is clear that any pathological condition, or physiological (aging) change, in the cardiovascular system affects functioning of the central nervous system. We evaluated linear aspects of the relationship between the slowness of cortical rhythms, as revealed by the modulation of a graph connectivity parameter, and congestive heart failure (CHF), as a reflection of neurodegenerative processes. Eyes-closed resting electroencephalographic (EEG) data of 10 patients with CHF were recorded by 19 electrodes positioned according the international 10-20 system. Graph theory function (normalized characteristic path length λ) was applied to the undirected and weighted networks obtained by lagged linear coherence evaluated by eLORETA software, therefore getting rid of volumetric propagation influences. The EEG frequency bands of interest were: delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-10.5 Hz), alpha 2 (10.5-13 Hz), beta 1 (13-20 Hz), beta 2 (20-30 Hz), and gamma (30-40 Hz). The analysis between B-type natriuretic peptide (BNP) values and λ showed positive correlation in delta, associated with a negative correlation in alpha 2 band. Namely, the higher the severity of the disease (as revealed by the BNP vales), the higher the λ in delta, and lower in alpha 2 band. Results suggest that delta and alpha λ indices are good markers of the severity of CHF.

Introduction The brain needs continuous oxygen supply even in resting-state. Hypoxia enhances resting-state electroencephalographic (EEG) rhythms in the delta range, and reduces those in the alpha range, with a pattern similar to that observed in Alzheimer's disease (AD). Here we tested whether resting-state cortical EEG rhythms in patients with congestive heart failure (CHF), as a model of acute hypoxia, present frequency similarities with AD patients, comparable by cognitive status revealed by the mini mental state examination (MMSE). Methods Eyes-closed EEG data were recorded in 10 CHF patients, 20 AD patients, and 20 healthy elderly subjects (Nold) as controls. LORETA software estimated cortical EEG generators. Results Compared to Nold, both AD and CHF groups presented higher delta (2–4 Hz) and lower alpha (8–13 Hz) temporal sources. The highest delta and lowest alpha sources were observed in CHF subjects. In these subjects, the global amplitude of delta sources correlated with brain natriuretic peptide (BNP) level in the blood, as a marker of disease severity. Conclusions Resting-state delta and alpha rhythms suggest analogies between the effects of acute hypoxia and AD neurodegeneration on the cortical neurons' synchronization. Significance Acute ischemic hypoxia could affect the mechanisms of cortical neural synchronization generating resting state EEG rhythms, inducing the “slowing” of EEG rhythms typically observed in AD patients.

Introduction: The diffusion of multidrug-resistant (MDR) bacteria has created the need to identify risk factors for acquiring resistant pathogens in patients living in the community. Objective: To analyze clinical features of patients with community-onset pneumonia due to MDR pathogens, to evaluate performance of existing scoring tools and to develop a bedside risk score for an early identification of these patients in the Emergency Department. Patients and Methods: This was an open, observational, prospective study of consecutive patients with pneumonia, coming from the community, from January 2011 to January 2013. The new score was validated on an external cohort of 929 patients with pneumonia admitted in internal medicine departments participating at a multicenter prospective study in Spain. Results: A total of 900 patients were included in the study. The final logistic regression model consisted of four variables: 1) one risk factor for HCAP, 2) bilateral pulmonary infiltration, 3) the presence of pleural effusion, and 4) the severity of respiratory impairment calculated by use of PaO2/FiO2 ratio. A new risk score, the ARUC score, was developed; compared to Aliberti, Shorr, and Shindo scores, this point score system has a good discrimination performance (AUC 0.76, 95% CI 0.71-0.82) and calibration (Hosmer-Lemeshow, χ2 = 7.64; p = 0.469). The new score outperformed HCAP definition in predicting etiology due to MDR organism. The performance of this bedside score was confirmed in the validation cohort (AUC 0.68, 95% CI 0.60-0.77). Conclusion: Physicians working in ED should adopt simple risk scores, like ARUC score, to select the most appropriate antibiotic regimens. This individualized approach may help clinicians to identify those patients who need an empirical broad-spectrum antibiotic therapy.

A retrospective analysis of white blood cell (WBC) counts and fibrinogen levels was performed on 292 consecutive patients admitted to the emergency department for chest pain likely due to ischaemic heart disease. Aims of the study were to evaluate their utility in discriminating between cardiac and non-cardiac chest pain, and to identify those "chest pain-enzyme negative" patients who are at high risk of developing acute myocardial infarction (AMI). The results obtained showed that WBC (p < 0.0001) and fibrinogen (p < 0.0001) significantly discriminated AMI patients. However, only male gender (p < 0.03), abnormal CK-MB% (p < 0.0001) and neutrophil counts (p < 0.0001) were independently related to AMI. The combined determination of neutrophils and CK-MB% increased the sensitivity from 50% (for CK-MB% alone) to 70% (p < 0.05), with a negative predictive value similar to that observed for CK-MB% alone. These results suggest that determination of neutrophil counts might help to improve the accuracy of AMI diagnosis in emergency patients.

BackgroundTroponins may be elevated in patients with pneumonia, but associations with myocardial infarction (MI) and with platelet activation are still undefined.ObjectivesThe aim of this study was to investigate the relationship between troponin elevation and in vivo markers of platelet activation in the early phase of hospitalization of patients affected by community-acquired pneumonia.MethodsA total of 278 consecutive patients hospitalized for community-acquired pneumonia, who were followed up until discharge, were included. At admission, platelet activation markers such as plasma soluble P-selectin, soluble CD40 ligand, and serum thromboxane B2 (TxB2) were measured. Serum high-sensitivity cardiac troponin T levels and electrocardiograms were obtained every 12 and 24 h, respectively.ResultsAmong 144 patients with elevated high-sensitivity cardiac troponin T, 31 had signs of MI and 113 did not. Baseline plasma levels of soluble P-selectin and soluble CD40 ligand and serum TxB2 were significantly higher in patients who developed signs of MI. Logistic regression analysis showed plasma soluble CD40 ligand (p < 0.001) and soluble P-selectin (p < 0.001), serum TxB2 (p = 0.030), mean platelet volume (p = 0.037), Pneumonia Severity Index score (p = 0.030), and ejection fraction (p = 0.001) to be independent predictors of MI. There were no significant differences in MI rate between the 123 patients (45%) taking aspirin (100 mg/day) and those who were not aspirin treated (12% vs. 10%; p = 0.649). Aspirin-treated patients with MIs had higher serum TxB2 compared with those without MIs (p = 0.005).ConclusionsMI is an early complication of pneumonia and is associated with in vivo platelet activation and serum TxB2 overproduction; aspirin 100 mg/day seems insufficient to inhibit thromboxane biosynthesis. (MACCE in Hospitalized Patients With Community-acquired Pneumonia; NCT01773863)