Epicardial fat, cardiac geometry and cardiac function in patients with non-alcoholic fatty liver disease: association with the severity of liver disease.

BACKGROUND & AIMS: Non-alcoholic fatty liver disease (NAFLD) has been associated with increased cardiovascular risk, including coronary artery disease and cardiac dysfunction. In addition, recent evidence highlighted the possible role of epicardial fat as a new cardiometabolic risk factor. We tested the correlation between epicardial fat, alterations in cardiac geometry and function, and severity of liver damage, in patients with biopsy-proven NAFLD. METHODS: The anthropometric, biochemical and metabolic features were recorded in 147 consecutive biopsy-proven NAFLD cases (Kleiner score). Epicardial fat thickness was measured by echocardiography. RESULTS: Epicardial fat was higher in patients with severe vs. milder fibrosis (8.5 ± 3.0 vs. 7.2 ± 2.3 mm; p=0.006); this association was maintained at multivariate logistic regression analysis (OR 1.22, 95%C.I. 1.01-1.47; p=0.04) after correction for gender, age >50 years, visceral obesity, IFG/diabetes, non-alcoholic steatohepatitis and severe steatosis. Of note, 37.1% of patients with epicardial fat >7 mm (median value) had severe liver fibrosis, compared to 18.3% of the cases with lower epicardial fat (p=0.01). As for echocardiographic indices, after adjusting for cardiometabolic confounders, diastolic posterior-wall thickness (p=0.01), left ventricular mass (p=0.03), relative wall thickness (p=0.02), and left atrial volume (0.04), as well as ejection fraction (p=0.004), lower lateral TDI e' (p=0.009), E/A ratio (0.04) (cardiac geometry alterations and diastolic dysfunction) were linked to severe liver fibrosis. CONCLUSIONS: In patients with NAFLD, a higher epicardial fat thickness is associated with the severity of liver fibrosis, in keeping with a possible pathogenic role of ectopic fat depots in whole body organ damage. In addition, morphological and functional cardiac alterations are more pronounced according to the severity of fibrosis. Further studies are needed to validate our results.

Carotid atherosclerosis and chronic hepatitis C: a prospective study of risk associations.

UNLABELLED: There are contrasting results in studies of cardiovascular risk in patients with genotype 1 chronic hepatitis C (G1 CHC). We evaluated the prevalence of carotid atherosclerosis compared with a control population in order to assess the potential association between atherosclerosis, host and viral factors, and liver histological features. In all, 174 consecutive biopsy-proven G1 CHC patients were evaluated by anthropometric and metabolic measurements and 174 patients attending an outpatient cardiology unit were used as controls. Intima-media thickness (IMT) and carotid plaques, defined as focal thickening of >1.3 mm at the level of common carotid, were evaluated using ultrasonography. All G1 CHC biopsies were scored by one pathologist for staging and grading, and graded for steatosis. Carotid plaques were found in 73 (41.9%) G1 CHC patients compared with 40 (22.9%) control patients (P < 0.001). Similarly, G1 CHC patients had a greater IMT compared with control patients (1.04 ± 0.21 versus 0.90 ± 0.16; P < 0.001). Multivariate logistic regression analysis showed that older age (odds ratio [OR] 1.047, 95% confidence interval [CI]: 1.014-1.082, P = 0.005), and severe hepatic fibrosis (OR 2.177, 95% CI: 1.043-4.542, P = 0.03), were independently linked to the presence of carotid plaques. In patients ≤55 years, 15/67 cases with F0-F2 fibrosis (22.3%) had carotid plaques, compared with 11/21 (52.3%) with F3-F4 fibrosis (P = 0.008). By contrast, in patients >55 years the prevalence of carotid plaques was similar in those with or without severe fibrosis (25/43, 58.1% versus 22/43, 51.1%; P = 0.51). CONCLUSION: Severe hepatic fibrosis is associated with a high risk of early carotid atherosclerosis in G1 CHC patients.

Genistein and endothelial function in postmenopausal women with metabolic syndrome.

BACKGROUND: Previous data have suggested that genistein could exert beneficial effects on endothelial function and on predictors of cardiovascular risk in healthy postmenopausal women. In a randomized clinical trial, we studied the effects of genistein on endothelial function in postmenopausal women with metabolic syndrome (MS). METHODS: Twenty postmenopausal women with MS, according to modified NCEP-ATP III criteria were randomly assigned to receive placebo or genistein (54 mg/day) for 6 months, along with a Mediterranean-style diet. Postmenopausal women without MS (n = 15), served as controls. The primary goal was the assessment of endothelial function by flow-mediated vasodilation (FMD) of brachial artery; moreover, time-to-peak dilation in the FMD response has been evaluated. Secondary outcomes were fasting glucose, fasting insulin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, visfatin, adiponectin and homocysteine blood levels. Data on adverse events were also recorded. RESULTS: After 6 months of treatment, FMD at 50s and peak FMD significantly increased in genistein recipients compared with placebo. Moreover, genistein significantly decreased the blood levels of total cholesterol, triglycerides, homocysteine and visfatin compared with placebo, while blood adiponectin levels were increased. Genistein recipients neither experienced more side-adverse effects than placebo nor discontinued the study. CONCLUSIONS: Six months of treatment with genistein effectively improves brachial artery flow-mediated vasodilation in postmenopausal women with metabolic syndrome.

Single nucleotide polymorphisms (SNPs) of pro-inflammatory/anti-inflammatory and thrombotic/fibrinolytic genes in patients with acute ischemic stroke in relation to TOAST subtype.

BACKGROUND: The genetic basis of complex diseases like ischemic stroke probably consists of several predisposing risk factors, such as genes involved in inflammation and thrombotic pathways. On this basis the aim of our study was to evaluate the role of SNPs (single nucleotide polymorphisms) of some pro-inflammatory/anti-inflammatory and coagulation/fibrinolytic genes in patients with acute ischemic stroke. METHODS: The study population consisted of 144 consecutive Caucasian adult patients who were hospitalized in the Internal Medicine Department at the University of Palermo between November 2006 and January 2008, and who met inclusion criteria. The cases were patients admitted with a diagnosis of acute ischemic stroke, and age-matched (± 3 years) control subjects: patients admitted to our Internal Medicine Department for any cause other than acute cardiovascular and cerebrovascular events and for routine checkup examinations. Molecular analysis of alleles at the -308 nucleotide (-308G/A) of TNF-α gene, -1082/-819 haplotypes of IL-10 gene, IL-1RN exon 2 VNR polymorphism, alleles at the -174 nucleotide (-174G/C) of IL-6 gene, PAI-1675 5G/4G polymorphism, alleles at the -7351 nucleotide (-7351C/T) of tPA gene was undertaken in both patient groups. RESULTS: We analyzed 96 subjects with acute ischemic stroke and 48 control subjects. We observed a significantly higher frequency of IL-10 1082 AA genotype in stroke patients with a significant risk trend. We also reported a higher frequency in stroke subjects with a significant risk trend of the TPA 7351-CT genotype and of IL-1RN-VNTR 86 bp 2/2 genotype. Moreover, we observed a significant relationship with TOAST subtype only with regard to CC TPA genotype and 1/1 IL-1 VNTR 86 bp and lacunar strokes. CONCLUSIONS: Ischemic stroke is a common multifactor disease, which is affected by a number of genetic mutations and environmental factors. Our findings showing a relationship between pro-inflammatory/anti-inflammatory and thrombotic/fibrinolytic genes SNPs and ischemic stroke may contribute to delineate a possible stroke risk profile in subjects with cerebrovascular risk factors.

Large hiatal hernia at chest radiography in a woman with cardiorespiratory symptoms.

Hiatal hernia (HH) is a frequent entity. Rarely, it may exert a wide spectrum of clinical presentations mimicking acute cardiovascular events such as angina-like chest pain until manifestations of cardiac compression that can include postprandial syncope, exercise intolerance, respiratory function, recurrent acute heart failure, and hemodynamic collapse. A 69-year-old woman presented to the emergency department complaining of fatigue on exertion, cough, and episodes of restrosternal pain with less than 1 hour of duration. Her medical history only included some episodes of bronchitis and no history of hypertension. The 12-lead electrocardiogram demonstrated sinus rhythm with right bundle-branch block. Laboratory tests, including cardiac troponin I, were within normal reference values. Chest radiography showed no significant pulmonary alterations and revealed in mediastinum a huge abnormal shadow overlapping the right heart compatible with a gastric bubble.The gastroscopy confirmed a large HH. A 2-dimensional transthoracic echocardiogram, using all standard and modified apical and parasternal views, revealed an echolucent mass, compatible with HH, compressing the right atrium. Also, it showed an altered left ventricular relaxation and a mild increase of pulmonary artery pressure (35 mm Hg). Spirometry showed a mild obstruction of the small airways, whereas coronary angiography showed normal coronary arteries. We concluded that the patient's symptomatology was related to the compressive effects of the large hiatal ernia, a neglected cause of cardiorespiratory symptoms. The surgical repair of HH was indicated.

Changes in estimating echocardiography pulmonary capillary wedge pressure after hypersaline plus furosemide versus furosemide alone in decompensated heart failure.

BACKGROUND: The aim of the study was to verify the effects of hypertonic saline solution (HSS) plus a high furosemide dose and light restriction of sodium intake compared with a high-dose infusion of furosemide alone on pulmonary capillary wedge pressure (PCWP), as determined by Doppler echocardiography and tissue Doppler imaging in patients suffering from decompensated heart failure. METHODS AND RESULTS: Consecutive patients in New York Heart Association functional class IV, unresponsive to oral high doses of furosemide up to 250-500 mg/d and/or combinations of diuretics, with ejection fraction <40%, serum creatinine <2 mg/dL, blood urea nitrogen ≤60 mg/dL, reduced urinary volume (<500 mL/24 h), and low natriuresis (<60 mEq/24 h) were randomized into 2 groups (double blind). The first group received a furosemide infusion (250 mg) plus HSS (150 mL 3.0% Na) bid and light Na restriction (120 mmol), and the second group received furosemide infusion (250 mg) twice daily, and low Na diet (80 mmol). The fluid intake of both groups was restricted (1 L/d). Body weight, whole-body bioelectrical impedance analysis (BIA), 24-hour urinary volume, and serum and urinary laboratory parameters were measured daily. Estimations of echocardiographic PCWP (Echo-PCWP) were detected on entry, 1 hour after concluding the initial treatment, and 6 days thereafter. A total of 133 patients (47 women and 86 men), aged 65-82 years, met the entry criteria.The HSS group revealed a significant increase in daily diuresis, natriuresis, and serum sodium compared with the furosemide group. Six days after treatment, renal function was significantly improved in the HSS group. Both groups showed a significant reduction in Echo-PCWP, but the HHS group revealed a faster reduction and significant lower values at 6 days compared with the group taking furosemide alone. We observed a positive correlation between values of Echo-PCWP and BNP and an inverse correlation between BIA parameters and Echo-PCWP. CONCLUSIONS: Our data show that the combination of high diuretic dose and HSS infusion plus light restriction in dietary sodium intake determine a more rapid and significant hemodynamic stabilization through the improvement of echo-PCWP, BNP levels, and BIA parameters than the group treated without HSS.

Residual vein thrombosis for assessing duration of anticoagulation after unprovoked deep vein thrombosis of the lower limbs: the extended DACUS study.

The safest duration of anticoagulation after idiopathic deep vein thrombosis (DVT) is unknown. We conducted a prospective study to assess the optimal duration of vitamin K antagonist (VKA) therapy considering the risk of recurrence of thrombosis according to residual vein thrombosis (RVT). Patients with a first unprovoked DVT were evaluated for the presence of RVT after 3 months of VKA administration; those without RVT suspended VKA, while those with RVT continued oral anticoagulation for up to 2 years. Recurrent thrombosis and/or bleeding events were recorded during treatment (RVT group) and 1 year after VKA withdrawal (both groups). Among 409 patients evaluated for unprovoked DVT, 33.2% (136 of 409 patients) did not have RVT and VKA was stopped. The remaining 273 (66.8%) patients with RVT received anticoagulants for an additional 21 months; during this period of treatment, recurrent venous thromboembolism and major bleeding occurred in 4.7% and 1.1% of patients, respectively. After VKA suspension, the rates of recurrent thrombotic events were 1.4% and 10.4% in the no-RVT and RVT groups, respectively (relative risk = 7.4; 95% confidence interval = 4.9-9.9). These results indicate that in patients without RVT, a short period of treatment with a VKA is sufficient; in those with persistent RVT, treatment extended to 2 years substantially reduces, but does not eliminate, the risk of recurrent thrombosis.

Severe Brochostenosis by Oral Propafenone Immediately After Commencing Treatment.

Propafenone is a membrane-stabilizing agent belonging to a subgroup of the Vaughan Williams class I antidysrhythmic agents, structurally resembling propranolol and characterized by weaker beta-blocking activity. Despite respiratory complications having been reported as examples of side effects, very few reports have been published in the literature.We describe the case of an elderly woman with a history of hypertension and allergy to Parietaria, grass, olive, mites, and with periodic asthmatic manifestations, for whom the administration of oral propafenone for recurrent supraventricular dysrhythmia was associated with the sudden onset of severe bronchostenosis.A 78-year-old woman was frequently admitted to the Emergency Department for a recurrent supraventricular tachycardia, which was treated initially with veramapil and thereafter with ivabradin. During her last visit to the cardiologist, she was prescribed propafenone (150 mg, 3 times a day) in place of ivabradin. After the administration of the second dose on the first day of the therapy, the patient began to complain of the onset of progressively severe dyspnea at rest. In the Emergency Department, respiratory auscultation showed diffuse rhonchi, wheezing, and rales; and arterial pressure was 200/100 mm Hg. Hemogasanalysis revealed hypoxemia, respiratory acidosis with 83% of O2-saturation. Emergency treatment with O2 therapy, methylprednisolone intravenous, furosemide, and then salbutamol was also started; the electrocardiogram only showed sinusal tachycardia. Results of laboratory examinations, including a white cell count and cardiac enzymes, were within the normal range. The patient achieved good respiratory function, after a period of 3 days.This report describes that even a relatively small dose of oral propafenone after commencing treatment can have a severe effect in exacerbating the obstruction of the airways in a susceptible subject. The likely mechanisms are an allergic reaction or a direct bronchospastic effect. Considering the recognized asthmogenicity of propafenone due to beta-blocker activity, we suggest that the cardiologist always refer to the patient's medical history before prescribing this drug, which is capable of producing notable side effects in predisposed individuals, beginning the eventual administration in the hospital setting. The use of bronchial provocation test allows the selection of inclined patients, thus reducing the risk of bronchospasm.

Polypharmacy, length of hospital stay, and in-hospital mortality among elderly patients in internal medicine wards. The REPOSI study.

PURPOSES: We evaluated the prevalence and factors associated with polypharmacy and investigated the role of polypharmacy as a predictor of length of hospital stay and in-hospital mortality. METHODS: Thirty-eight internal medicine wards in Italy participated in the Registro Politerapie SIMI (REPOSI) study during 2008. One thousand three hundred and thirty-two in-patients aged ≥65 years were enrolled. Polypharmacy was defined as the concomitant use of five or more medications. Linear regression analyses were used to evaluate predictors of length of hospital stay and logistic regression models for predictors of in-hospital mortality. Age, sex, Charlson comorbidity index, polypharmacy, and number of in-hospital clinical adverse events (AEs) were used as possible confounders. RESULTS: The prevalence of polypharmacy was 51.9% at hospital admission and 67.0% at discharge. Age, number of drugs at admission, hypertension, ischemic heart disease, heart failure, and chronic obstructive pulmonary disease were independently associated with polypharmacy at discharge. In multivariate analysis, the occurrence of at least one AE while in hospital was the only predictor of prolonged hospitalization (each new AE prolonged hospital stay by 3.57 days, p < 0.0001). Age [odds ratio (OR) 1.04; 95% confidence interval (CI) 1.01-1.08; p = 0.02), comorbidities (OR 1.18; 95% CI 1.12-1.24; p < 0.0001), and AEs (OR 6.80; 95% CI 3.58-12.9; p < 0.0001) were significantly associated with in-hospital mortality. CONCLUSIONS: Although most elderly in-patients receive polypharmacy, in this study, it was not associated with any hospital outcome. However, AEs were strongly correlated with a longer hospital stay and higher mortality risk.

Sodium thiosulfate not always resolves calciphylaxis: an ambiguous response.

Calciphylaxis is a severe "vascular ossification-calcification," associated with a very high mortality rate that involves arterial wall, venular wall, and nerves resulting in ischemia and necrosis of skin, subcutaneous fat, visceral organs, and skeletal muscles. Sodium thiosulfate has recently been used as a novel treatment option for calciphylaxis because of its dual role as an antioxidant and a chelator. Multiple case reports demonstrated that such therapy has resulted in pain relief and healing of skin ulceration. We report a case of calciphylaxis of large severity that had an ambiguous response to sodium thiosulfate treatment (improvement of symptomatology and skin lesions, improvement of blood parameters, worsening of general conditions, and consciousness until death).

Adiponectin, resistin and IL-6 plasma levels in subjects with diabetic foot and possible correlations with clinical variables and cardiovascular co-morbidity.

INTRODUCTION: It is very suggestive that diabetic foot is characterized by a pronounced inflammatory reaction and the pathogenic significance of this inflammation has received little attention. On this basis the aim of our study was to evaluate plasma levels of adiponectin, resistin and IL-6 in subjects with diabetic foot in comparison with subjects without foot complications. MATERIALS AND METHODS: We recruited 34 subjects with type 2 diabetes mellitus and foot ulceration hospitalized for every condition related to diabetic disease, but not for new vascular events (group A). As controls we recruited 37 patients with type 2 diabetes mellitus without foot ulceration (group B) hospitalized for every condition related to diabetic disease, but not for new vascular events. Adiponectin, Resistin and IL-6 serum levels were evaluated. RESULTS: Subjects of group A showed lower median plasma levels of adiponectin [7.7450 (4.47-12.17) µg/ml vs 8.480 (5.15-12.87) µg/ml], higher median plasma levels of IL-6 [3.21 (1.23-5.34) pg/ml vs 2.73 (1.24-3.97 pg/ml)] and of resistin [3.860 (2.96-6.29 ng/ml) vs 3.690 (2.,37-6.5 ng/ml)]. CONCLUSION: Our study demonstrated that diabetic subjects with diabetic foot showed in comparison with diabetics without diabetic foot higher IL-6 and resistin plasma levels, lower adiponectin plasma levels.

Sudden severe abdominal pain after a single low dose of paracetamol/codein in a cholecystectomized patient: learning from a case report.

We report the case of an elderly patient with diastolic heart failure and renal insufficiency admitted to hospital as he complained of having a history of hypogastric pain and dysuria without fever due to renal lithiasis and urinary infection. Because the pain was persistence, and considering the presence of renal dysfunction, it was administered a single low dose of paracetamol/codein (500/30 mg). After about 1 hour of the administration, he suddenly complained of the onset of a lancinating epigastric pain radiating to the whole abdomen and retrosternum accompanied by nausea. The electrocardiogram (EKG) was negative for myocardial infarction and computed tomography excluded aortic dissection and other causes of acute abdomen. Laboratory tests showed instead liver and pancreatic damage. The symptomatology was relieved 3 hours later of the onset after antispastic treatment with anticholinergics (floroglucine). The likely underlying pathophysiological mechanism is the codein-induced spasm of the sphincter of Oddi combined with dysfunction of the same sphincter and reduced bile storage capacity related to a previous cholecystectomy. When a similar event does not regress, it may lead to more severe conditions such as acute pancreatitis. Since codein is a widely used drug, this report may suggest cholecystectomy as a contraindication during administration for the risk of occurrence of these complications.

Polymyalgia rheumatica and vertebral fractures: a 1-year pilot controlled study.

No data exist about the possibility that vertebral fracture in PMR patients could be independent of steroid therapy. For this reason, we aimed to investigate this topic by a case cohort study with a 1-year follow-up for each patient. We selected ten consecutive patients who experienced vertebral fractures (VF-group) during the first month of 1-year follow-up period and without any other significant associated condition. As a control group we studied ten control patients, without vertebral fractures and with a follow-up of 1 year, randomly selected among a larger group of patients affected by polymyalgia rheumatica. The following data were analysed: eritrosedimention rate (ESR), visual analogical scale score (VAS), methyprednisolone daily dosage. Each patient had been monthly evaluated by the aforementioned clinical and laboratoristic parameters during the 1-year follow-up period. The VF-group resulted with a higher and statistically significant median corticosteroid 12-month total dosage [mean 3,480 mg (95%CI 2,805-3,030) vs. 2,760 mg (2,666.25-3,247.5)]. The VF-group had statistically significant higher ESR and VAS AUC when compared to control group (median ESR AUC, 484.75 vs. 288.25; P = 0.0001; median VAS AUC, 70.75 vs. 43.5 P < 0.0001); ESR at the baseline (cut-off >80 mm) showed a specificity of 90% (95%CI 56-100) and sensitivity of 70% (95%CI 35-93). VAS difference from first to second month (cut-off

Outcomes of patients hospitalized with community-acquired, health care-associated, and hospital-acquired pneumonia.

BACKGROUND: Traditionally, pneumonia has been classified as either community- or hospital-acquired. Although only limited data are available, health care-associated pneumonia has been recently proposed as a new category of respiratory infection. "Health care-associated pneumonia" refers to pneumonia in patients who have recently been hospitalized, had hemodialysis, or received intravenous chemotherapy or reside in a nursing home or long-term care facility. OBJECTIVE: To ascertain the epidemiology and outcome of community-acquired, health care-associated, and hospital-acquired pneumonia in adults hospitalized in internal medicine wards. DESIGN: Multicenter, prospective observational study. SETTING: 55 hospitals in Italy comprising 1941 beds. PATIENTS: 362 patients hospitalized with pneumonia during two 1-week surveillance periods. MEASUREMENTS: Cases of radiologically and clinically assessed pneumonia were classified as community-acquired, health care-associated, or hospital-acquired and rates were compared. RESULTS: Of the 362 patients, 61.6% had community-acquired pneumonia, 24.9% had health care-associated pneumonia, and 13.5% had hospital-acquired pneumonia. Patients with health care-associated pneumonia had higher mean Sequential Organ Failure Assessment scores than did those with community-acquired pneumonia (3.0 vs. 2.0), were more frequently malnourished (11.1% vs. 4.5%, and had more frequent bilateral (34.4% vs. 19.7%) and multilobar (27.8% vs. 21.5%) involvement on a chest radiograph. Patients with health care-associated pneumonia also had higher fatality rates (17.8% [CI, 10.6% to 24.9%] vs. 6.7% [CI, 2.9% to 10.5%]) and longer mean hospital stay (18.7 days [CI, 15.9 to 21.5 days] vs. 14.7 days [CI, 13.4 to 15.9 days]). Logistic regression analysis revealed that depression of consciousness (odds ratio [OR], 3.2 [CI, 1.06 to 9.8]), leukopenia (OR, 6.2 [CI, 1.01 to 37.6]), and receipt of empirical antibiotic therapy not recommended by international guidelines (OR, 6.4 [CI, 2.3 to 17.6]) were independently associated with increased intrahospital mortality. LIMITATIONS: The number of patients with health care-associated pneumonia was relatively small. Microbiological investigations were not always homogeneous. The study included only patients with pneumonia that required hospitalization; results may not apply to patients treated as outpatients. CONCLUSION: Health care-associated pneumonia should be considered a distinct subset of pneumonia associated with more severe disease, longer hospital stay, and higher mortality rates. Physicians should differentiate between patients with health care-associated pneumonia and those with community-acquired pneumonia and provide more appropriate initial antibiotic therapy.

Immuno-inflammatory activation in acute cardio-embolic strokes in comparison with other subtypes of ischaemic stroke.

Few studies have examined the relationship between inflammatory biomarker blood levels, cardioembolic stroke subtype and neurological deficit. So the aim of our study is to evaluate plasma levels of immuno-inflammatory variables in patients with cardio-embolic acute ischaemic stroke compared to other diagnostic subtypes and to evaluate the relationship between immuno-inflammatory variables, acute neurological deficit and brain infarct volume. One hundred twenty patients with acute ischaemic stroke and 123 controls without a diagnosis of acute ischaemic stroke were evaluated. The type of acute ischaemic stroke was classified according to the TOAST classification. We evaluated plasma levels of IL-1beta, TNF-alpha, IL-6 and IL-10, E-selectin, P-selectin, sICAM-1,sVCAM-1, vWF, TPA and PAI-1. Patients with ischaemic stroke classified as cardio-embolic (CEI) showed, compared to other subtypes, significantly higher median plasma levels of TNF-alpha , IL-6 and IL-1beta. Furthermore stroke patients classified as lacunar showed, compared to other subtypes, significantly lower median plasma levels of TNF-alpha, IL-6 and IL-1beta. Multiple linear regression showed a significant association between the Scandinavian Stroke Scale (SSS) score at admission and diagnostic subtype, infarct volume of cardio-embolic strokes and some inflammatory variables. Our findings confirm that cardio-embolic strokes have a worse clinical presentation and produce larger and more disabling strokes than other ischaemic stroke subtypes reporting a possible explanation of higher immuno-inflammatory activation of the acute phase.

Long-term effects of dietary sodium intake on cytokines and neurohormonal activation in patients with recently compensated congestive heart failure.

BACKGROUND: A growing body of evidence suggests that the fluid accumulation plays a key role in the pathophysiology of heart failure (HF) and that the inflammatory and neurohormonal activation contribute strongly to the progression of this disorder. METHODS AND RESULTS: The study evaluated the long-term effects of 2 different sodium diets on cytokines neurohormones, body hydration and clinical outcome in compensated HF outpatients (New York Heart Association Class II). A total of 173 patients (105 males, mean age 72.5+/-7) recently hospitalized for worsening advanced HF and discharged in normal hydration and in clinical compensation were randomized in 2 groups (double blind). In Group 1, 86 patients received a moderate restriction in sodium (120mmol to 2.8g/day) plus oral furosemide (125 to 250mg bid); in Group 2, 87 patients: received a low-sodium diet (80mmol to 1.8g/day) plus oral furosemide (125 to 250mg bid). Both groups were followed for 12 months and the treatment was associated with a drink intake of 1000mL daily. Neurohormonal (brain natriuretic peptide, aldosterone, plasma rennin activity) and cytokines values (tumor necrosis factor-alpha, interleukin-6) were significantly reduced with a significant increase of the anti-inflammatory cytokine interleukin-10 at 12 months in normal, P < .0001) than low-sodium group. The low-sodium diet showed a significant activation of neurohormones and cytokines and worsening the body hydration, whereas moderate sodium restriction maintained dry weigh and improved outcome in the long term. CONCLUSIONS: Our results appear to suggest a surprising efficacy of a new strategy to improve the chronic diuretic response by increasing Na intake and limiting fluid intake. This counterintuitive approach underlines the need for a better understanding of factors that regulate sodium and water handling in chronic congestive HF. A larger sample of patients and further studies are required to evaluate whether this is due to the high dose of diuretic used or the low-sodium diet.

Immuno-inflammatory predictors of stroke at follow-up in patients with chronic non-valvular atrial fibrillation (NVAF).

The aim of the present study was to determine the rates of stroke in patients with chronic NVAF (non-valvular atrial fibrillation), evaluating the relationship between plasma levels of inflammatory variables at admission and the occurrence of stroke during a 3-year follow-up. A total of 373 consecutive patients with chronic NVAF were enrolled. Blood samples were drawn within 72 h of admission, and we evaluated plasma levels of IL (interleukin)-1beta, TNF-alpha (tumour necrosis factor-alpha), IL-6, IL-10, E-selectin, P-selectin, ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular cell adhesion molecule-1) and vWF (von Willebrand Factor). Subsequent patient events (stroke at follow-up) were monitored over a 3 year period. By multivariate analysis, only age, hypertension and high levels of IL-6, TNF-alpha and vWF remained significant predictors of a higher risk of experiencing ischaemic stroke at follow-up. Moreover, plasma values of TNF-alpha, IL-6 and vWF had a significant area under the ROC (receiver operating characteristic) curve. In conclusion, baseline plasma levels of TNF-alpha, IL-6 and vWF are predictors of new-onset ischaemic stroke at follow-up in patients with chronic NVAF.

One-year renal and cardiac effects of bisoprolol versus losartan in recently diagnosed hypertensive patients: a randomized, double-blind study.

BACKGROUND AND OBJECTIVES: Hypertension is a significant cause of chronic renal injury and its effective treatment is capable of reducing the rate of renal failure. beta-Adrenoceptor antagonists (beta-blockers) have been reported to induce a deterioration in renal function, while several data have indicated a renoprotective effect of treatment with the angiotensin II type 1 receptor antagonist losartan. Previous studies of the interaction between the selective beta(1)-blocker bisoprolol and kidney function were performed only for short- and medium-term periods. The aim of this study was to compare the antihypertensive efficacy and renal and cardiac haemodynamic effects of bisoprolol with those of losartan over a 1-year time period in patients with essential hypertension. METHODS: Seventy-two patients (40 males) with recently diagnosed uncomplicated (European Society of Hypertension [ESH] criteria stage 1-2) hypertension (mean +/- SD age 52 +/- 12 years) were enrolled in the study. After a run-in period of 14 days on placebo, the patients were randomized in a double-blind, prospective study to receive either bisoprolol 5 mg or losartan 50 mg, administered once daily for 1 year. At recruitment and 12 months after treatment, cardiac output and renal haemodynamics and function were evaluated by echocardiography and radionuclide studies, respectively. RESULTS: There were no significant differences in baseline clinical data, including glomerular filtration rate and blood pressure, between the two treatment groups. At 1 year, blood pressure had decreased significantly (p < 0.001) with both treatments, and heart rate was reduced only in the group taking bisoprolol. The long-term effects on renal haemodynamics and cardiac function were similar with both drugs, the only change being a significant reduction in the filtration fraction for each group. CONCLUSIONS: These data suggest that both bisoprolol and losartan are effective agents for the treatment of patients with recently diagnosed ESH stage 1-2 hypertension. Over a 1-year period, both agents maintained good renal and cardiac performance and haemodynamics.

The usefulness of bioelectrical impedance analysis in differentiating dyspnea due to decompensated heart failure.

BACKGROUND: Acute dyspnea poses a diagnostic challenge for physicians, and the current methods in differentiating cardiac from non-cardiac causes have been limited to date. Recently, the brain natriuretic peptide (BNP) rapid test has been validated in the emergency room. Nevertheless, the early accumulation of fluid in the interstitial space in the body and in the lungs, which characterizes patients with ADHF, is well estimated by BIA. We investigate whether bioelectrical impedance analysis (BIA) can serve as a noninvasive diagnostic tool in the differential diagnosis of acute decompensated heart failure (ADHF) in the emergency department (ED). METHODS AND RESULTS: A total of 292 patients presenting with acute dyspnea to the ED were evaluated by using a conventional diagnostic strategy and rapid BNP measures. Segmental (Seg) and whole-body (WB) BIA resistance (Rz) and reactance (Xc) on entry were immediately detected. After hospital discharge, an expert team classified enrolled patients into ADHF and non-ADHF. A total of 58.9% of patients had ADHF, whereas 41.1% were non-ADHF. ADHF patients showed significantly (P < .001) higher BNP values (591.8 +/- 501 versus 69.5 +/- 42 pg/mL), a significant (P < .001) reduction of Seg (35.5 + 8.2 versus 66.4 + 10.5) and WB (402.3 + 55.5 versus 513.2 + 41.8) Rz (Ohm), and a significant correlation (P < .0001) between BNP and Seg (r = -0,62) and WB (r = -0.63) bioelectrical Rz was also identified. Multiple regression analysis revealed that whole body and segmental BIA were strong predictors of ADHF alone or in combination with BNP. CONCLUSIONS: Our data suggest that Seg and WB BIA are a useful, simple, rapid, and noninvasive diagnostic adjunct in the early diagnosis of dyspnea from ADHF.