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Background Chronic obstructive pulmonary disease (COPD) is a common respiratory disorder characterized by airflow limitation, persistent respiratory symptoms and chronic lung inflammation. Previous studies reported a robust relationship between COPD and coronary artery disease (CAD). Local and systemic inflammation, known to play a role in atherosclerosis development, has been reported in patients with COPD, and has been proposed as one of the possible pathogenetic factors linking COPD and CAD. However, data on atherosclerotic coronary pattern and coronary inflammation in COPD patients are lacking. Purpose To study the characteristics of atherosclerotic coronary plaques and local inflammation by using optical coherence tomography (OCT) in COPD patients presenting with acute coronary syndromes (ACS). Methods ACS patients undergoing intracoronary OCT imaging of the culprit vessel were retrospectively identified. Coronary plaque characteristics and OCT-defined macrophage infiltration (MØI) were assessed by OCT. ACS patients were divided into 2 groups according to the presence or the absence of an established diagnosis of COPD, and coronary plaque features and MØI both at the culprit plaque site and along the culprit vessel were compared between the two groups. Results Among 146 ACS patients (mean age, 66,1±12,7 years, 109 males), 47 (32,2%) had COPD. Patients with COPD were older, were more frequently on therapy with an angiotensin receptor blocker, had lower hemoglobin, total cholesterol and triglycerides levels, and had higher serum creatinine levels. The prevalence of different mechanisms of ACS were similar between COPD and noCOPD patients (plaque rupture: 57,4% vs. 45,4%, plaque erosion: 23,4% vs. 32,3%, calcified plaque: 19,1% vs. 22,2%, respectively, overall p=0,381). OCT analysis of plaque microstructures showed that COPD patients had significantly higher prevalence of MØI (78,7% vs. 54,4%, p=0,005), thin cap fibroatheroma (TCFA) (48,9% vs. 22,2%, p=0,001), spotty calcium (68,1% vs. 26,3%, p Conclusions In ACS patients undergoing OCT imaging of the culprit vessel, COPD was an independent predictor of local plaque inflammation and plaque vulnerability both at the culprit site and along the culprit vessel. Our results may suggest that a higher inflammatory milieu in COPD patients might enhance local coronary inflammation, promoting CAD development and plaque vulnerability. Funding Acknowledgement Type of funding sources: None.

Background Preclinical predictors of worsening heart failure can be monitored by implanted devices and may support the management of patients with heart failure. However, clinical results of such an approach are controversial. Purpose We aimed to assess if guided heart failure management according to device-based remote monitoring strategies is more effective than standard therapy. Methods A comprehensive literature research for randomized controlled trials (RCTs) comparing a strategy of guided heart failure management versus standard therapy was performed on PubMed, Embase, and CENTRAL databases. Incidence rate ratios (IRRs) and associated 95% confidence intervals (CIs) were calculated using the Poisson regression model with random study effects. The primary outcome was a composite of all-cause death and hospitalizations for heart failure. Secondary endpoints included the individual components of the primary outcome. Results A total of 9216 patients from 14 RCTs were included. The average follow-up duration was of 16 months. Compared with standard therapy, guided heart failure management reduced the risk of the composite of all-cause death and hospitalizations for heart failure (IRR 0.86, 95% CI 0.79–0.94, p Conclusion Device-based remote monitoring systems as a tool to guide the management of patients with heart failure were associated with a valuable reduction in the risks of death, hospitalizations for heart failure, and the composite of both, supporting their routine use in clinical practice. Funding Acknowledgement Type of funding sources: None.

Background The SARS-CoV-2 pandemic has led to the development of the first mRNA vaccines used in humans. These vaccines are well tolerated, safe, and highly effective; however, post-marketing surveillance is revealing potential rare adverse effects. We report a case of incessant pericarditis following administration of the second dose of mRNA-1273 SARS-CoV-2 vaccine, unresponsive to conventional therapy, and successfully treated with anakinra. Case summary A 30-year-old man presented to the Emergency Department for incessant pericarditis unresponsive to evacuative pericardiocentesis and conventional first-line anti-inflammatory therapy. Given the typical ‘inflammatory phenotype’ clinically characterized by fever, C-reactive protein (CRP) elevation, and leucocytosis, we decided, in agreement with the rheumatologist team, to avoid glucocorticoid and to administer anakinra. A sudden clinical and echocardiographic improvement was observed, with complete resolution of the symptoms and of the pericardial effusion; similarly, CRP values progressively decreased. The patient was discharged at home; no recurrences of pericarditis were described at clinical and instrumental follow-up made 3 months later. Discussion Several cases of pericarditis have been described in patients who received the COVID-19 vaccination, especially with the mRNA vaccine that can induce a non-adaptive immunity response against the viral spike protein, triggering cardiac damage for a molecular mimicry mechanism; however, defined pathogenesis of pericarditis associated with mRNA vaccine is still missing. The clinical scenario described is characterized by the typical ‘inflammatory phenotype’, triggered by a disproportionate and uncontrolled activation of the inflammasome based on an interleukin-1 (IL-1) overproduction. We administered anakinra, an IL-1 blocking drug, with a sharp clinical, echocardiographic and laboratoristic improvement. The complete response observed in this case suggests that vaccine-related pericarditis could be triggered by an auto-inflammatory pathway based on IL-1 overproduction. Further research is, therefore, warranted to determine the mechanisms by which the mRNA vaccine may cause pericarditis in order to choose the most targeted therapy.

SARS-CoV-2 infection is associated with a higher risk of acute right heart failure (RHF) due to primary right ventricle (RV) dilation and systemic inflammatory response, which in turn lead to microvascular and cardiomyocytes dysfunction, local hypoxia and multi-organ failure. In this clinical setting, levosimendan could be a viable therapy thanks to its right-heart tropism and its additional pleiotropic properties.We present the case of a 72 years-old man with positive nasopharyngeal swab for SARS-CoV-2 infection, mild pulmonary involvement and clinical signs of new-onset RHF. We started a 12-hour levosimendan cycle to improve RV performance and reduce cardiac filling pressures.We obtained a net clinical benefit in terms of acute RHF-related signs and symptoms, progressive renal and liver function improvement and concomitant reduction of high-sensitivity C-Reactive Protein and Interleukin-6 (IL-6) levels.Acute RHF during SARS-CoV-2 infection could be related to a convergent widespread systemic inflammatory response. Thanks to its anti-inflammatory and anti-remodeling properties, levosimendan might represent a viable therapy in this clinical setting, contributing to the dampening of the inflammatory response.

Funding Acknowledgements Type of funding sources: None. Background/Introduction Recently, the transcatheter aortic valve replacement (TAVR) has reformed the management of Aortic Stenosis (AS), providing a valid therapeutic alternative to surgical aortic valve replacement (SAVR). Although optimizing the timing of surgery is a crucial aspiration, the introduction of innovative pharmacological therapies able to modify disease evolution might help clinicians to treat patients in a non-invasive way. Several evidences pointed out the role of inflammation, oxidative stress, and pathological remodelling in AS natural history. Purpose The aim of this study is to assess biological pathways modifications after aortic valve replacement, comparing the transcatheter and the surgical approach. Methods We enrolled a total of 35 consecutive patients with severe symptomatic aortic stenosis undergoing aortic valve replacement with transcatheter (n = 19) or surgical (n = 16) approach. Biological samples were collected and stored before (T0) and 72 hours after the procedure (T1). We firstly performed gene expression arrays for a total of 132 genes, on two groups of pooled cDNA from peripheral blood mononuclear cells of TAVR (n = 10) and SAVR (n = 10) patients. Then, taking into account the most relevant result of the arrays, we selected 15 genes for validation. Results Our preliminary data showed several differences in the gene expression levels of the two groups under examination for a large number of molecules, mostly associated with the oxidative balance. More in detail, after procedure, TAVR patients showed higher levels of glutathione peroxidase 1 (GPX1, TAVR p = 0.029; SAVR p = 0.031) and glutathione reductase (GSR, p = 0.029), while SAVR patients showed higher expression of GPX1, catalase (CAT, p = 0.019) and NADPH oxidase 2 (NOX2, p = 0.008), thus confirming an intense post-operative oxidative stress particularly for patients undergoing surgery. Moreover, Caspase 3 (CASP3, p = 0.013), involved in apoptotic pathway and myocyte enhancer factor 2C (MEF2C, p = 0.036), implicated in overload induced hypertrophy genes showed a significantly reduction in their expression after TAVR. Conclusions In our study, we describe different gene expression signatures in patients with an AS diagnosis and their recalibration after AV replacement with two kinds of procedure, TAVR and SAVR. Our data describe for the first time an altered oxidative balance in patient undergoing aortic valve replacement, that is particularly evident for patients undergoing SAVR. A clearer understanding of biological processes taking place in the first hours post AV replacement lays the ground to a more efficient management of post-operative status and, in the incessant research for a tailored therapy, the results of our study add a little piece of information to assist clinicians in selecting the optimal procedure for each patient.

Background/Introduction Acute stress-induced cardiomyopathy, also known as Takotsubo Syndrome (TTS), was originally classified as a benign disease. Nowadays, this assumption has changed, especially in its long-term outcome, due to TTS clinical presentation, that often mirrors the acute myocardial infarction (MI) phenotype. Current knowledge already delineate clinical features distinctive of TTS and MI patients, however, diagnosis requires multiple, expansive, and invasive medical examinations. Moreover, concerning the biological panorama, very slight is known and the lack of a tailored therapy is resented. Therefore, a biological profile for this clinical category could provide easier and less invasive diagnostic tools, leading edge towards novel therapeutic pathways. Purpose The aim of the study is to perform a biological profile of the TTS group compared to the ST Segment Elevation Myocardial Infarction (STEMI) in order to explore the molecular peculiarities attendant the pathophysiologic mechanisms. Methods We performed a gene expression array on two groups of pooled cDNA from peripheral blood mononuclear cells, from TTS (n=11) and STEMI (n=19) patients. We conducted gene expression validations for each enrolled patient through qPCR. Results Our preliminary data displayed several differences in gene expression levels of a grand number of cell adhesion signaling molecule between the two groups. As shown in figure 1, three gene were more expressed in TTS group: Nitric Oxide Synthase 3, also known as endothelial NOS (NOS3; p=0.002), Superoxide dismutase 1 (SOD1; p=0.03) and transferrin receptor (TFRC; p=0.005). Meanwhile, five gene displayed a higher expression in STEMI patients compared to TTS: phospholipase A2 Group 7 (PLA2G7; p=0.04), Galectin 8 (LGALS8; p=0.02), Intercellular Adhesion Molecule 1 (ICAM1; p=0.002), Hyaluronidase 2 (HYAL2; p=0.01) and Hyaluronan Receptor (CD44; p=0.0002). Conclusions The earliest results of this study led us to focus on fewer genes related to endothelial and oxidative stress pathways. TTS is habitually triggered by intense emotional or physical stress. Indeed, our results showed how TTS patients present higher expression of NOS3, SOD1 and TFRC, all components involved in the oxidative stress pathways. In STEMI patients, top expressed genes, such as HYAL2, CD44 and ICAM1, are all associated with extracellular matrix turnover, likely due to the presence of a stenotic plaque and the consequent endothelial derangement. The uncovering of diagnostic biomarkers in TTS might improve the early, non-invasive, stratification of this group of patients, thus facilitating novel and personalized therapeutics design. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): The present study was supported by the Italian National Project Grant PRIN 2017.

Ventricular septal defect (VSD) is an uncommon but frequently fatal complication following acute myocardial infarction. In medically treated patients, mortality rates exceed 90%, while the surgical repair is associated with better outcomes, even though optimal surgical timing is still under debate.We present the case of a 78-years-old man with no previous remarkable cardiological history admitted to our Emergency Department with the diagnosis of anterior ST-elevation myocardial infarction and significant reduction of left ventricular ejection fraction. The emergency coronary angiography showed sub-occlusion of the left anterior descending coronary artery, treated with stent implantation. The post-procedural echocardiography unveiled the presence of an apical VSD with a large left-to-right shunt, significant right ventricular overload and dysfunction. An intra-aortic balloon pump (IABP) was positioned and, after Heart Team evaluation, a delayed surgical approach was planned. As a bridge to the intervention Levosimendan infusion was administered, on top of IABP support, and a significant improvement in bi-ventricular function and pressure profiles was obtained. Cardiac surgery was successfully performed 9 days after the admission without periprocedural complications.This unique case supports the use of Levosimendan as a valid pharmacological strategy for perioperative management of VSD.

Funding Acknowledgements Type of funding sources: None. Background High-flow nasal cannulae oxygen therapy (HFNCOT) represents a better tolerated alternative to non-invasive pressure support ventilation (NIPSV) for acute cardiogenic pulmonary edema (ACPE) treatment. However, there are still few data on the effect of HFNCOT on cardiac function and hemodynamic. Purpose To assess and compare the effects of NIPSV and HFNCOT in ACPE setting on right ventricular (RV) systolic function and on indices of cardiac filling and output, as measured by echocardiography. Methods This is a cross-over controlled study, enrolling 15 consecutive patients admitted to our Cardiovascular Intensive Care Unit for ACPE and hypoxaemic, normo/hypocapnic acute respiratory failure, with P/F ratio < 200. Each patient received NIPSV, followed by HFNCOT. Full echocardiographic assessment and blood gas analysis (BGA) were performed 40 minutes from onset of each ventilation modality, respectively before NIPSV to HFNCOT switch and before HFNCOT interruption. In particular, RV function parameters, together with RV and atrial strain, were prospectively collected. Results In spite of not significant changes in BGA, RV function was significantly improved under HFNCOT, as compared to NIPSV, as assessed by the following parameters: tricuspid annular plane excursion (TAPSE) (P = 0.001), RV S’ wave (P = 0.007), RV fractional area change (RVFAC) (P = 0.006). Strain analysis confirmed the significant improvement in RV function, with free wall global longitudinal strain (GLS) and free wall and septum GLS significantly higher under HFNCOT, as compared to NIPSV (-21% vs -18% P Conclusions NIPSV significantly affect RV function making more complex the management of patients presenting with ACPE. In this setting, HFNCOT represents a valuable alternative, providing similar respiratory outcomes while preserving good right ventricle performance.

Background Coronary microvascular obstruction (MVO) is a noxious condition frequently occurring in patients with ST-elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI). However, multiple mechanisms are involved in the pathogenesis of MVO and not yet fully understood. Recent studies suggested that perilipin 2 (PLIN2) may play an important role in lipid metabolism of macrophages resident in atherosclerotic plaques along with a role in enhancing oxidative stress. Purpose To study the association between PLIN2 and MVO in STEMI patients undergoing primary PCI. We also assessed the role of PLIN2 to predict future major cardiovascular events (MACEs). Methods STEMI patients undergoing primary PCI were enrolled. PLIN2 was dosed within 24 hours from admission in peripheral blood monocytes. MVO was assessed using TIMI flow grade and myocardial blush grade on coronary angiogram after PCI, and patients were stratified accordingly (MVO or noMVO). Major adverse cardiac events (defined as a composite of cardiac death, non-fatal myocardial infarction, re-admission for heart failure and target vessel revascularization) were assessed at clinical follow-up. Results Among 100 STEMI patients (mean age, 65.2±12.0 years, 81 males), 33 (33.0%) had MVO. Patients with MVO were older, had higher troponin I peak, C-reactive protein and lower left ventricular ejection fraction on admission. Patients with MVO had significantly higher levels of PLIN2 (1.03±0.28 vs. 0.90±0.16, p=0.019) compared to noMVO patients. Age [OR (95% CI) per year, 1.045 (1.005–1.087), p=0.026] and PLIN2 [OR (95% CI) per unit, 16.606 (2.027–136.030), p=0.009] were associated with MVO at univariate logistic regression analysis. However, only PLIN2 levels [OR (95% CI) per unit, 12.325 (1.446–105.039), p=0.033] were independently associated with MVO at multivariate analysis. Follow up data were available for 76 patients (76%). After a mean follow up of 182.2±126.6 days, 13 MACEs occurred. Patients with MVO had more MACEs [9 (37.5%) vs. 4 (7.7%), p Conclusions In STEMI patients undergoing primary PCI, PLIN2 was independently associated with MVO. PLIN2 was an independent predictor of MACEs at clinical follow-up. These findings suggest that PLIN2 may represent a promising therapeutic target, opening the avenue towards novel therapeutic approaches for MVO. Funding Acknowledgement Type of funding source: None

Background PLATO study showed that Ticagrelor (Ti) significantly reduced the rate of death from vascular causes, myocardial infarction or stroke without a significant increase of major bleeding vs Clopidogrel (Cl). Previous studies demonstrated the stronger direct anti-platelet effect of Ti versus Cl. Few data exist about the indirect anti-platelet properties and pleiotropic effects, eventually involved in the positive effect of Ti on acute coronary syndrome (ACS) outcome. Aim As Ti has multiple pleiotropic effects, we sought to assess whether the different outcome of Ti versus Cl in NSTE-ACS patients could be explained, at least in part, by different modulation of circulating microRNA (miRNA). The primary endpoint was to characterize the effect of the two different P2Y12 inhibitors on miRNA expression. Secondary endpoint was to correlate miRNA profile to clinical outcome. Methods Thirty-one patients with a diagnosis of NSTE-ACS were enrolled in this study. Patients were randomized for Ti or Cl assumption before undergoing PCI. Clinical characteristics were homologues between Ti and Cl groups. Blood samples were drawn at different time point (T0, T1 and T2) to test miRNA modulation and stability (T0, at baseline; T1, three hours after drug administration; T2, twenty-four hours after coronarography). Plasma RNA was extracted and pooled for microarray PCR based panel of ninety miRNA analysis. MiRNA expression was normalized on the global mean of each patient. Levels of circulating miRNAs were compared using statistical tests, assuming significance at P Results A panel of seven circulating miRNAs associated with atherosclerosis, thrombosis and inflammation were selected for validation (miR-652-3p; miR-26-5p; miR-25-3p; miR-let7c; miR-155-5p; miR-222-3p; miR-223-3p). Microarray analysis showed an opposite modulation of most miRNAs at T0, T1 and T2 in patients with Cl or Ti treatment. In particular, Cl group showed an upregulation of most miRNAs, while Ti administration caused their down-regulation. Of the seven miRNA selected for validation, miR-652-3p, expression at T1 showed a significantly modulation in patients in Cl treatment compared to Ti (T1 Cl 2,637±1,092, T1 Ti 0,660±0,171; p=0.03). MiRNA-652-3p has a validated pro-atherogenic role. On five-years follow, an higher rate (40%) of cardiovascular events (new ACS, recurrent ischemia and stent thrombosis) was reported in the Cl group compare to Ti. Indeed, no one death or bleeding occurred. Conclusion This data suggest that Ti has a protective role down-regulating pro-atherogenic and pro-thrombotic miRNAs (miR-652-3p, miR-let7c, miR-223-3p, miR-155-5p) and promoting the expression of anti-atherogenic miRNAs (miR-25-3p) when compared to Cl. This may contribute to explain the positive effect on clinical outcome of Ti. Although the small number of patients, this pilot study gives another evidence about the multiple positive pleiotropic effect of Ti. Figure 1. miRNA 652-3p expression Funding Acknowledgement Type of funding source: None

Background The imbalance between protective and harmful bacteria in the microbial communities leads to a non-physiological condition, known as “dysbiosis”. In the last decade, several studies have suggested that gut microbiota can contribute to the development and progression of various disease including cardiovascular disease through metabolism-mediated pathways. The production and the release of bacterial metabolites, including Trimethylamine N-oxide (TMAO), can affect host health acting to distant organs. Purpose The aim of the present study was to explore the gut microbiota and the levels of TMAO in patients with stable angina (SA) and acute coronary syndrome (ACS) with or without elevation of the ST segment, respectively STEMI and NSTEMI, and in control subjects. Methods Feces were obtained from ACS (n=31) and SA (n=23) patients and controls (n=24). Genomic DNA was isolated using the QIamp DNA Stool Mini Kit. Samples were subjected to 16S rRNA gene V3–V4 region sequencing by an Illumina MiSeq TM platform. A combination of software packages QIIME and VSEARCH was used to generate a biological observation matrix (BIOM) at different taxonomic levels (from phylum to genus). The BIOM was analysed using the Web-based program MicrobiomeAnalyst. β-diversity between groups was obtained by weighted UniFrac distance metric analysis. Serum TMAO levels were measured with a UPLC-MS/MS mass spectrometry in SA and ACS patients. Results β-diversity analysis showed a different bacterial composition in SA and ACS patients and controls ([PERMANOVA] F-value: 1.9706; R-squared: 0.050567; p-value Conclusion These results, taken together, suggest that gut microbiota and its derived metabolites might play an essential role in the progression of atherosclerosis and in coronary plaque instability. Funding Acknowledgement Type of funding source: Other. Main funding source(s): Linea D1 Università Cattolica del Sacro Cuore

The aim of the study was to evaluate the influence of cleanliness of cattle slaughtered on hide and carcass contamination as indicated by aerobic colony count (ACC) and Enterobacteriaceae count (EC). Cattle in two slaughterhouses were visually inspected and assigned to a category from 1 (very clean) to 5 (very dirty) based on cleanliness. Fifteen animals for each category were randomly selected in each slaugterhouse and the hides and carcasses sampled and analyzed for ACC, EC. Results showed that the increasing dirt of the cattle was associated with higher ACC and EC on the hides and with higher ACC on carcasses in both slaughterhouse. In one slaughterhouse a correlation between hide cleanliness and EC was shown. The different characteristics of the slaughterhouses may influence the transfer of bacteria from hide to carcass. The study supports the conclusion that the pre-slaughter visual evaluation of animal cleanliness and application of corrective actions can be an effective aid to reduce carcass contamination in both slaughterhouses.

Proposta di FSO (Food Safety Objective) per V. parahaemolyticus in molluschi bivalvi

Patients with ischaemic heart disease and low ejection fraction (EF) are at increased risk of sudden death. MADIT (Multicenter Automated Defibrillator Implantation Trial) II has shown that implantable cardioverter-defibrillators (ICDs) reduce the risk of death by 31% at two years in patients with previous myocardial infarction and EF < 30%.1 The absolute risk reduction over an average follow up of 20 months, however, was only 5.6%. In addition, the high prevalence of patients who have had a myocardial infarction with EF ⩽ 30% makes the cost of this strategy high. This has led to an ongoing search for reliable markers of future episodes of life-threatening ventricular tachycardia (VT) or ventricular fibrillation (VF) to identify a higher-risk subgroup in which ICD therapy can be more beneficial and cost effective. The difficulty in predicting major ventricular arrhythmias probably reflects a limited understanding of their complex mechanisms. This is particularly true for patients who have had a myocardial infarction and with LV dysfunction, in whom myocardial ischaemia may trigger major ventricular arrhythmias. C reactive protein (CRP) concentration has been shown to be raised both in subjects studied …

Inflammatory mechanisms play a pivotal role in the atherosclerotic process. At the base of atherogenesis there are complex interactions between macrophages, T lymphocytes and smooth muscle cells. A growing body of experimental evidences suggest that inflammation is involved in the pathogenesis of acute coronary syndromes (ACS) and influences their clinical evolution. In fact, in patients with ACS, coronary atherosclerotic plaques are characterized by an abundant inflammatory infiltrate. Moreover, in these patients systemic signs of inflammatory reaction can be observed: activated circulating inflammatory cells (neutrophil, monocytes and lymphocytes) and increased concentrations of pro-inflammatory cytokines, such as interleukin (IL)-1 and 6, and of acute phase reactants, in particular C-reactive protein (CRP). Recent data demonstrate that CRP is a strong independent predictor of adverse cardiac events and death in patients with ACS, but also in patients with stable ischemic heart disease and in apparently healthy men and women. Furthermore, CRP is an important prognostic index, for early and late outcome, in patients undergoing percutaneous coronary interventions, and may be useful in choosing the therapeutic management of the patient. Although the causes of inflammation in patients with ACS are not yet clear, this new line of research may open the way to a different clinical approach for these patients.

Inflammation has recently been shown to be an important pathogenetic component of atherosclerosis in general and of acute coronary syndromes in particular. Not only activated inflammatory cells have been found in the plaques, but, more interestingly, also activated circulating inflammatory cells as well as elevated levels of systemic markers of inflammation have been described. Among these, C-reactive protein is of clinical value, as its levels are associated with the outcome. Inflammation is important also in triggering the mechanisms of restenosis and CRP has been recently described as a useful pre-procedure marker of risk of restenosis. The cause of inflammation, what triggers the shift from an indolent disease to the acute coronary syndromes and the more appropriate therapies are still a matter of debate.

Inflammation and possibly chronic infections are associated with acute coronary syndromes; however, the mechanisms responsible for this association are not yet fully elucidated. The aim of this study was to assess whether the hyperreactivity of the inflammatory system, that we have shown in unstable patients with persistently elevated C-reactive protein and with recurrence of symptoms, was associated with chronic infection.In 20 unstable angina patients seropositivity and antibody levels vs Cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae were measured and correlated with the interleukin-6 production in vivo in 1 ml of whole blood stimulated with 0.1 microgram lipopolysaccharide for 4 hours.No positive correlation was found between antibody titer and interleukin-6 levels. No correlation was also found between seropositivity to Cytomegalovirus, Helicobacter pylori or Chlamydia pneumoniae and interleukin-6 levels.Our study suggests that seropositivity for infective agents, including Chlamydia pneumoniae, does not affect the monocyte response to lipopolysaccharide and thus cannot account for the enhanced interleukin-6 production observed in unstable angina patients with raised levels of C-reactive protein and worse prognosis, and suggests the predominant role of the individual response to different stimuli.

In order to evaluate whether different clinical presentations of unstable angina are associated with a different degree or pattern of activation of the hemostatic, fibrinolytic and inflammatory systems, we measured plasma levels of thrombin-antithrombin III, plasmin-alpha2- antiplasmin complexes and C-reactive protein, as markers of activation of coagulation, fibrinolysis and inflammation respectively, in two groups of patients: 7 patients with de novo unstable angina (Group 1) and 7 patients with destabilizing unstable angina (Group 2). Blood samples were taken on admission for measuring levels of C-reactive protein and during ischemic episodes at the onset of ECG changes and pain (0 min) and after 5, 15 and 60 min in order to assess the peak values of thrombin-antithrombin III and plasmin-alpha2-antiplasmin during the episode. Thrombin-antithrombin III levels in Group 1 were 1.8 microgram/l (0.3-4.15) at 0 min and increased to 17 micrograms/l (2.8-60) after 5 to 15 min (p = 0.013); conversely thrombin-antithrombin III levels in Group 2 were 2.15 microgram/l (1.4-3.8) at 0 min and raised to 4 micrograms/l (2-43) after 5 to 15 min (NS). No significant differences in both groups were observed in plasmin-alpha2-antiplasmin levels (Group 1:650 micrograms/l, ranged 492-956, at 0 min vs 670 microgram/l, range 415-977, at peak; Group 2: 480 micrograms/l, range 274-955, at 0 min vs 502 micrograms/l, range 304-1027, at peak; NS). Inversely, C-reactive protein levels on admission were 4 mg/dl (range 2-27) in Group 1, and 1 mg/dl (range 0.6-4) in Group 2 (p = 0.006). In conclusion, patients with de novo unstable angina have significantly enhanced thrombin (but not plasmin) production during spontaneous ischemic episodes than patients with destabilizing unstable angina. Furthermore, patients with de novo unstable angina have enhanced acute phase responses than patients with destabilizing unstable angina. Our data suggest that different pathogenetic mechanisms may be responsible for acute ischemic episodes in unstable angina and may explain different response to antithrombotic therapy in unstable angina patients.

Activated mast cells are present in human coronary atheromas, as well as in the adventitia of patients with variant angina, and may play an important role in plaque rupture and coronary vasomotion. To assess whether or not activation of mast cells is a primary event, we measured serum levels of tryptase, a specific marker of mast cell activation, in 8 patients with unstable angina during a spontaneous ischemic episode (Group 1) and in 5 patients with variant angina (Group 2) during ergonovine-induced coronary spasm. Blood samples were collected as soon as possible after the onset of pain and ECG changes (0 min), and after 5, 15 and 60 min. Tryptase levels in Group 1 were 0.13 U/l (range 0.017-0.44) at the onset of pain and significantly raised to 0.75 U/l (range 0.05-2.49) at 5 min, decreasing to 0.076 U/l (range 0.018-0.16) at 15 min and to 0.085 U/l (range 0.01-0.25) at 60 min (p = 0.035). Conversely, tryptase levels in Group 2 were 0.09 U/l (range 0.07-0.13) at 0 min, 0.11 U/l (range 0.07-0.22) at 5 min, 0.10 U/l (range 0.07-0.18) at 15 min, 0.11 U/l (range 0.07-0.17) at 60 min (NS). In conclusion, tryptase levels raise during spontaneous ischemic episodes in unstable angina, but not after ergonovine-provoked ischemia in variant angina, suggesting that a primary, yet unknown stimulus, may activate mast cells during some ischemic episodes in unstable angina.

Until a few years ago coronary atherosclerosis was thought to be a slowly progressive disease eventually leading to total coronary occlusion and myocardial infarction. Recent angiographic studies have shown, instead, that mild or moderate coronary stenoses have the highest risk of causing acute coronary syndromes when complicated by thrombus formation which, in turn, appears to be due to a complex interaction between the atherosclerotic background and acute ischemic stimuli. The tendency of the atherosclerotic background to develop thrombosis may be different in different patients, as indicated by the observation that the risk factor profile of patients who present with chronic coronary syndromes is different from that of patients who present with acute syndromes. The acute ischemic stimuli so far identified are: a sudden local thrombogenic stimulus; a transient systemic increase in systemic pro-coagulant activity; a transient increase in proximal and/or distal coronary tone. The recent observation of inflammatory cells activation, including T-lymphocytes, in patients with acute ischemic syndromes raises the intriguing possibility that a specific antigenic stimulus may play an important pathogenetic role.

The aim of this study was to provide a further contribution to the study on the alterations of left ventricular diastolic function induced by dialysis, using simple indexes of diastolic function obtained with Doppler. The study is conduced in 15 patients with renal failure aged between 22 and 51 years old by means of echocardiography M-2D a pulsed Doppler analysis of the left ventricular refilling flow, evaluated before and after dialysis. By the results is risen up that the dLA has had a significant reduction (p = 0.032), the dSLV have undergone a reduction that is not being significant, while the dDLV has had a significant reduction (p = 0.029), shortening fraction is improved even if in a not significant manner. Also the Doppler indexes has had a behaviour homogeneous in the group of studied patients. Early ventricular refilling is reduced, as showed by the reduction of E, consequence of the reduction preload, while the diastolic late refilling has showed a little increment, expressed by the increase af the peak A. The variations of these indexes, even if not statistically significant, express an alteration of pattern diastolic Doppler caused by both the reduction of preload and the alteration of ventricular relaxation. Besides this alteration, to our notice, is not to consider expression of myocardial compromise in this group studied patients. It would be however useful enlargement of the study to greater number of patients with follow-up for better comprehension of this cardiopathy and makes a more individual treatment of these patients.

During the last few years, quite a number of studies have been done, or are still in course, on disinfection of urban liquid wastes by means of ionizing radiations. The experience gained by SANDIA pilot plant of irradiation on dried sewage sludge, together with the recently presented conceptual design of another plant handling granular solids, characterized by high efficiency and simple running, have shown the possibility of extending this process to the treatment of urban solid wastes. As a matter of fact, the problems connected to the pathogenic aspects of sludge handling are often similar to those met during the disposal of urban solid wastes. This is even more so in the case of their reuse in agriculture and zootechny. The present paper introduces the results of an analysis carried out in order to evaluate the economical advantage of inserting irradiation treatment in some process scheme for management of urban solid wastes. Taking as an example a comprehensive pattern of urban solid wastes management which has been analysed and estimated economically in previous works, we first evaluated the extra capital and operational costs due to the irradiation and then analysed economical justification, taking into account the increasing commercial value of the by-products.

Superoxide dismutase (SOD) activity and reduced glutathione (GSH) content in erythrocytes (RBC) of uremic patients on chronic dialysis were determined. Specific SOD activity and GSH content were found lower in RBC from uremic patients before hemodialysis compared to normal RBC; after hemodialysis, the specific activity of SOD and GSH content were significantly increased.

It has been suggested that performance in an industrial inspection task can be improved by rapidly alternating images of the item to be inspected and a perfect item onto the visual field of the inspector. Such a blink inspection system was evaluated for a complex item (a printed circuit board which could contain three flaws) and a simple item (a blank field which could contain one flaw) using eight student subjects for each of five inspection conditions. Three groups, one using blink inspection and two control groups, inspected circuit boards; two groups (one blink and one control) inspected blank fields. Search time was improved by blink inspection for the circuit boards and with different defects showing different degrees of improvement. Only one type of defect showed both reduced search times and reduced errors. For blank fields, performance was worse under blink inspection. Subjects showed a consistent tendency to terminate their search for defects in a logical manner, with stopping time related to search difficulty. Measures of heart rate mean and variability were taken as a pilot study to measure task stress. There was little evidence from the heart rate measures that the task was stressful.

C-reactive protein (CRP), the prototypic acute phase reactant and a sensitive marker of inflammation, consistently predicts new coronary events, including myocardial infarction and death, in patients with ischemic heart disease. The data are very consistent with regard to the long-term outcome, but in many studies are also significant for in-hospital events. The predictive value of CRP is, in the majority of the studies, independent of and additive to that of the troponins. Moreover recent data suggest that CRP may be a reliable marker of the risk of restenosis after percutaneous coronary interventions and that its levels can be modulated by statins. Taken together, all these data suggest that CRP, probably with different cut-offs, should be used as a marker of risk and as a guide to therapy in patients hospitalized for acute coronary syndromes and in outpatients suffering from ischemic heart disease.