Gender Differences in Health-Related Quality of Life in Patients with Systolic Heart Failure: Results of the VIDA Multicenter Study.

Previous studies have shown that heart failure is associated with worse health-related quality of life (HRQoL). The existence of differences according to gender remains controversial. We studied 1028 consecutive outpatients with heart failure and reduced ejection fraction (HFrEF) from a multicentre cross-sectional descriptive study across Spain that assessed HRQoL using two questionnaires (KCCQ, Kansas City Cardiomyopathy Questionnaire; and EQ-5D, EuroQoL 5 dimensions).

Health-related Quality of Life of Patients With Chronic Systolic Heart Failure in Spain: Results of the VIDA-IC Study.

Introduction And Objectives: Although heart failure negatively affects the health-related quality of life of Spanish patients there is little information on the clinical factors associated with this issue.

Methods: Cross-sectional multicenter study of health-related quality of life. A specific questionnaire (Kansas City Cardiomyopathy Questionnaire) and a generic questionnaire (EuroQoL-5D) were administered to 1037 consecutive outpatients with systolic heart failure.

A real-world perspective on the prevalence and treatment of heart failure with a reduced ejection fraction but no specific or only mild symptoms.

Heart failure (HF) is commonly described according to the severity of symptoms, using the New York Heart Association (NYHA) classification, and the assessment of ventricular function, by measuring the left ventricular ejection fraction (LVEF). It is important to acknowledge, however, that the severity of symptoms does not systematically correlate with the level of ventricular systolic dysfunction. Patients with no or only mild symptoms are still at high risk of HF-related morbidity and mortality.

Coronary heart disease and dyslipidemia: a cross-sectional evaluation of prevalence, current treatment, and clinical control in a large cohort of Spanish high-risk patients: the PRINCEPS study.

The authors assessed a large cohort of patients with coronary heart disease (CHD) or at high risk for developing CHD in terms of lipid profile, lipid-lowering treatment, and attainment of National Cholesterol Education Program (NCEP) target low-density lipoprotein cholesterol (LDL-C) levels. The investigation was a cross-sectional study involving Spanish outpatients treated in primary or secondary care facilities. From a total of 26,598 attending patients, 12,128 with CHD or CHD risk equivalents were recruited by 1875 physicians; 49% had CHD and 69% had multiple risk factors.

Nitric oxide production by neutrophils obtained from patients during acute coronary syndromes: expression of the nitric oxide synthase isoforms.

Objectives: To analyze the differences in the nitric oxide (NO) forming system between neutrophils obtained from patients during unstable angina (UA) and during acute myocardial infarction (AMI).

Background: Neutrophils are involved in the regulation of thrombus formation through the release of active substances such as NO. Acute myocardial infarction is the result of an occlusive thrombus; unstable angina is attributed to intermittent thrombus formation.

[Isolated sensory trigeminal neuropathy caused by a lateral pontine infarct]].

Lesion of cranial nerves due to vascular damage at pontine level generally associates affectation of near nerve tracts. Isolated fifth nerve palsy due to vascular pontine lesions has been scarcely reported. We present a hypertense 57 year old woman who suffered from sudden paresthesias and hypoesthesia on the three divisions of trigeminal nerve without motor involvement and with preservation of corneal and masseter reflexes.

[Absence of pyramidal signs in pyramidal tract postischemic Wallerian degeneration].

Introduction: Wallerian degeneration (WD) is the irreversible axonal and myelin damage after the injury to the proximal portion of the axon or its cell body. The most frequent cause of WD in the central nervous system is ischemic stroke. Various studies have related the presence of pyramidal tract WD with the severity of motor deficit and partial motor improves.

17 Beta-estradiol-stimulated nitric oxide production by neutrophils: effect on platelet activation.

Objective: To evaluate the effect of 17beta-estradiol (E2) on the ability of human neutrophils to produce nitric oxide (NO) and its effects on platelet activation.

Methods: The expression of neuronal nitric oxide synthase (nNOS) protein and the formation of NO by 17beta-E2-incubated neutrophils from men were studied in vitro (ten male volunteers, no medical-surgical antecedents, aged 25-45 years). Platelet aggregometry and changes in cyclic guanosine monophospate (cGMP) levels were used to bioassay the functionality of NO released from neutrophils.

Estrogen stimulates neuronal nitric oxide synthase protein expression in human neutrophils.

Recent studies have postulated the contribution of nitric oxide (NO) released by the endothelium to the beneficial effects of estrogen. Despite a neuronal-type NO synthase (nNOS) described in neutrophils, less is known about the effect of estrogen in these cells. The aim of the present study was to analyze the expression of nNOS protein in human neutrophils under different estrogenic conditions.

NO from smooth muscle cells decreases NOS expression in endothelial cells: role of TNF-alpha.

Despite the evidence that cytokines stimulate nitric oxide (NO) production by inducible nitric oxide synthase (iNOS), several reports recently demonstrated that the hypotensive response related to endothelial nitric oxide synthase (eNOS) activity could be inhibited by the same cytokines. The aim of the present work was to analyze whether NO generated by vascular smooth muscle cells (VSMC) could modify eNOS protein expression in endothelial cells. Bovine aortic endothelial cells (BAEC) and bovine VSMC (BVSMC) in coculture were used for the study.

[Recurrent cerebral embolism as the main sign of atrial myxoma].

Atrial myxomas (AM) are the most frequent cardiac tumors. Between 25-45% of the cases present neurologic manifestations, generally owing to cerebral embolic infarcts or intracranial haemorrhages. Cerebral embolism can precede cardiac or constitutional symptoms, but recurrent embolisms as the only disturbance are infrequent.

Aspirin inhibits inducible nitric oxide synthase expression and tumour necrosis factor-alpha release by cultured smooth muscle cells.

Background: Inflammatory related cardiovascular disease, i.e. cardiac allograft rejection, myocarditis, septic shock, are accompanied by cytokine production, which stimulates the expression of inducible nitric oxide (iNOS).

Expression of constitutive and inducible nitric oxide synthases in the vascular wall of young and aging rats.

Two NO synthase (NOS) isoforms have been described in vessels, an endothelial constitutive NOS (eNOS) and an inducible NOS (iNOS). The purpose of the present study was to examine the endothelium-dependent and endothelium-independent hypotensive response in aging rats, analyzing the ability of their vessels to produce NO. The studies were performed in 2 groups of euvolemic, conscious, male Wistar rats: aging rats (n=20, 18 months old) and young rats (n=20, 5 months old).

Nitric oxide reversibly inhibits the epidermal growth factor receptor tyrosine kinase.

Although it has been demonstrated that NO inhibits the proliferation of different cell types, the mechanisms of its anti-mitotic action are not well understood. In this work we have studied the possible interaction of NO with the epidermal growth factor receptor (EGFR), using transfected fibroblasts which overexpress the human EGFR. The NO donors S-nitroso-N-acetylpenicillamine (SNAP), 1,1-diethyl-2-hydroxy-2-nitrosohydrazine (DEA-NO) and N-{4-[1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazino]butyl}propane -1, 3-diamine (DETA-NO) inhibited DNA synthesis of fibroblasts growing in the presence of fetal calf serum, epidermal growth factor (EGF) or EGF plus insulin, as assessed by [methyl-3H]thymidine incorporation.

Role of nitric oxide in autocrine control of growth and apoptosis of endothelial cells.

Nitric oxide (NO) is a growth inhibitor for diverse cellular types. In the present study, we have found that the inhibition of NO production in bovine endothelial cells by an L-arginine competitive antagonist induces DNA replication and promotes the transition from prereplicative to replicative phases of the endothelial cell cycle and an increase in c-myc and c-fos oncogene-encoded protein expression. The inhibition of NO generation had, however, a markedly different outcome depending on the state of confluence of the cells, i.

Phosphorylation of calmodulin by permeabilized fibroblasts overexpressing the human epidermal growth factor receptor.

Detergent-permeabilized EGFR-T17 fibroblasts, which overexpress the human epidermal growth factor (EGF) receptor, phosphorylate both poly-L-(glutamic acid, tyrosine) and exogenous calmodulin in an EGF-stimulated manner. Phosphorylation of calmodulin requires the presence of cationic polypeptides, such as poly-L-(lysine) or histones, which exert a biphasic effect toward calmodulin phosphorylation. Optimum cationic polypeptide/calmodulin molar ratios of 0.

Endothelial cells inhibit NO generation by vascular smooth muscle cells. Role of transforming growth factor-beta.

Endothelial cell (EC)-released agents are active regulators of vascular smooth muscle cell (VSMC) functions. The first aim of the present work was to analyze the effect of ECs on interleukin-1 beta (IL-1 beta)-induced NO production by SMCs. Bovine aortic ECs (BAECs) and BVSMCs in culture were used for the study.

Aspirin-stimulated nitric oxide production by neutrophils after acute myocardial ischemia in rabbits.

Background: In recent studies, it has been hypothesized that the protective anti-ischemic effects of aspirin outweigh the effects of inhibition of platelet thromboxane A2 synthesis. Recently, we have found that the antiaggregating effects of aspirin significantly affect nitric oxide (NO) generation by neutrophils.

Methods And Results: The present study used circulating neutrophils from myocardial ischemic rabbits to assess the effect of aspirin on the circulating neutrophil-derived NO production and, subsequently, on the modulation of platelet activation.