1,721,296 research outputs found

    Nonsteroidal anti-inflammatory drugs and cardiovascular risk: is prostacyclin inhibition the key event?

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    Non steoidal anti-inflammatory drugs induce cardiovascular adverse events, and this appears to be a function of intensity and duration of treatment, irrespectively of their selectivity towards cyclo-oxygenase 2. Deteminants are the degree of inhibiton in prostacyclin synthesis and the residual capacity to synthesize thromboxane in platelets

    Increased oxidative stress in human renovascular hypertension

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    The urinary excretion of 8-iso-prostaglandin (PG) F-2alpha and 11-dehydro-thromboxane (TX) B-2 as indexes of in vivo lipid peroxidation and platelet activation, respectively, in 25 patients with RVD, 25 patients with essential hypertension, and 25 healthy subjects were measured. Plasma renin activity in peripheral and renal veins, angiotensin II in renal veins, cholesterol, glucose, triglycerides, homocysteine, and antioxidant vitamins A, C, and E were also determined.Lipid peroxidation is markedly enhanced in hypertensive patients with RVD and is related to activation of the renin-angiotensin system. Moreover, persistent platelet activation triggered or amplified by bioactive isoprostanes may contribute to the progression of cardiovascular and renal damage in this setting

    Prevalence of hypertension: importance of epidemiologic studies and the need to spot undiagnosed cases

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    The actual prevalence and incidence of hypertension could have been higher and even more impactful on public health. Nonetheless, the work by Cegłowska et al. remains an important epidemiologic study, carefully conducted on nation wide scale. It demonstrates how arterial hypertension is extremely widespread, and highlights the need to improve blood pressure monitoring within a collaborative framework involving patients, general practitioners, and hypertension specialists, aimed at reducing the number of undiagnosed cases and improving patient management and public health. Moreover, since hypertension is becoming more prevalent in the elderly, efforts should be made to tailor health care to particular age groups

    Medication errors: prescribing faults and prescription errors

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    1. Medication errors are common in general practice and in hospitals. Both errors in the act of writing (prescription errors) and prescribing faults due to erroneous medical decisions can result in harm to patients. 2. Any step in the prescribing process can generate errors. Slips, lapses, or mistakes are sources of errors, as in unintended omissions in the transcription of drugs. Faults in dose selection, omitted transcription, and poor handwriting are common. 3. Inadequate knowledge or competence and incomplete information about clinical characteristics and previous treatment of individual patients can result in prescribing faults, including the use of potentially inappropriate medications. 4. An unsafe working environment, complex or undefined procedures, and inadequate communication among health-care personnel, particularly between doctors and nurses, have been identified as important underlying factors that contribute to prescription errors and prescribing faults. 5. Active interventions aimed at reducing prescription errors and prescribing faults are strongly recommended. These should be focused on the education and training of prescribers and the use of on-line aids. The complexity of the prescribing procedure should be reduced by introducing automated systems or uniform prescribing charts, in order to avoid transcription and omission errors. Feedback control systems and immediate review of prescriptions, which can be performed with the assistance of a hospital pharmacist, are also helpful. Audits should be performed periodically

    Inibitori della cicloossigenasi e cardiopatia ischemica

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    trattazione rischio cardiovascoalre associato a uso di FAN

    Could vitamin D supplements be a new therapy for heart failure? Possible pathogenic mechanisms from data of intervention studies

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    Vitamin D deficiency may play a role in the pathogenesis of chronic heart failure (HF), but whether giving patients supplements to raise vitamin D into the normal range improves their survival is not clear. It has been demonstrated that vitamin D deficiency is common in patients with HF, especially the elderly, in obese and in dark skinned people, and that low vitamin D levels are associated with adverse outcome. The epidemiological data have been confirmed by experimental data, which show that knockout mice for the vitamin D receptor developed myocardial hypertrophy and dysfunction. Data from interventional studies are scarce and discordant, and more research is urgently needed to confirm whether add-on supplementation therapy with vitamin D has a role in the management of patients with chronic HF

    Funzione endoteliale e microcircolo nel diabete mellito

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    The role of endothelial dysfunction in the pathogenesis of diabetic microangiopathy is reviewed. Reversible alterations in microcirculation, consisting of increased capillary pressure, blood flow and endothelial permeability, can be detected at an early stage in diabetes mellitus. Irreversible structural modifications of the vascular wall, such as thickening of the basal membrane due to the extracellular accumulation of proteins, take place at later stages. Atherosclerosis further affects microcirculation in diabetes mellitus by decreasing autoregulatory capacity and blood flow reserve. Endothelial dysfunction has been observed to precede the onset of microvascular lesions, as demonstrated by reduction in the vasodilatory response to vasoactive agents and by alterations in the antithrombotic properties of the endothelium. Experimental data available so far suggest that endothelial dysfunction may be directly related to hyperglycemia. Abnormalities in lipoprotein metabolism, generation of glycation end products, and increased oxidative stress may also be responsible for the endothelial dysfunction in diabetes mellitus. Insulin resistance appears to be related to endothelial dysfunction in non-insulin-dependent diabetes mellitus through a reduction in the biological activity of endothelial-derived nitric oxide
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