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ABSTRACT: Ischemic heart disease (IHD) is the leading cause of death in women as in men. Several disease mechanisms, however, differ between genders. Women with IHD more frequently than men have normal or non-obstructive epicardial arteries, plaque erosion, spontaneous coronary dissection, microvascular dysfunction, stress cardiomyopathy, and heart rupture after acute infarction. Compared to men, IHD presents 7-10 years later with a heavier burden of cardiovascular risk factors, even after correction for age. The typical woman with IHD is old and frail, with comorbidities such as renal failure. Another vulnerable group comprises those with acute coronary syndromes before the age of 60 in whom hospital mortality is reported to be almost twice that of age-matched men. Such vulnerabilities in women, in apparent contrast with the delayed onset and lesser extent of epicardial atherosclerosis, may be attributable to biases in prevention, presentation, diagnosis and treatment of female IHD, but also to gender-related differences in disease mechanisms.
Giornale italiano di cardiologia (2006) 06/2012; 13(6):396-400.
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ABSTRACT: Excessive body mass among healthy subjects carries an increased risk of subsequent cardiovascular events. Excess weight implies the presence of white, viscero-abdominal fat, that promotes insulin-resistance, is infiltrated by macrophages, and is less differentiated compared to subcutaneous or brown fat. Conversely, among patients with cardiovascular disease, slim patients have a greater risk of recurrent atherothrombotic events than fatter patients ("obesity paradox"). Lean patients with cardiovascular disease, on average, have more comorbidities and haemorrhagic complications than their heavier counteparts, and probably they conceal predisposing factors that are still unknown and therefore difficult to treat.
Recenti progressi in medicina 10/2009; 100(10):447-50.
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Felicita Andreotti,
Luciano Agati,
Elena Conti,
Eleonora Santucci, Teresa Rio,
Federica Tarantino,
Luigi Natale,
Daniele Berardi,
Antonella Mattatelli,
Beatrice Musumeci,
Lorenzo Bonomo,
Massimo Volpe,
Filippo Crea,
Camillo Autore
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ABSTRACT: Erythropoietin (Epo) is a hematopoietic hormone produced mainly by the kidneys in response to hypoxia. Recent acquisitions in the fields of hematology, neurology, cardiology, and experimental medicine show cytoprotective, angiogenetic and antiinflammatory effects of Epo. Exogenous erythroPoietin in Acute Myocardial Infarction: New Outlook aNd Dose Association Study (EPAMINONDAS, EudraCTno. 200500485386) is one of four ongoing randomized controlled trials, each testing the effects of Epo in >or=100 patients with STEMI. EPAMINONDAS is a multicenter, prospective, double-blind, placebo-controlled, dose-finding study assessing intravenous moderate doses of human recombinant Epo (epoietin-alpha, 100 or 200 IU/kg/die) versus placebo, given on the first 3 days, in 102 patients with first ST-segment elevation myocardial infarction. Initial dosing is within 12 h of primary percutaneous coronary revascularization. The primary endpoint is infarct size, quantified by CK-MB time-concentration curve, left ventricular wall motion score index, and pattern of contrast-enhanced magnetic resonance imaging. Secondary endpoints are ischemic recurrences, ventricular remodelling, and safety events, assessed in-hospital and at 12 months' follow-up. The results of current phase II studies will help define the safety/efficacy profile of Epo for patients with STEMI.
Journal of Thrombosis and Thrombolysis 06/2009; 28(4):489-95. · 1.48 Impact Factor
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European Heart Journal 03/2009; 30(7):752-4. · 10.48 Impact Factor
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Atherosclerosis 11/2008; 203(2):353-4. · 3.79 Impact Factor
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ABSTRACT: Erythropoietin (Epo) is synthesized mainly under hypoxic conditions by renal and extrarenal tissues, including liver, spleen, brain, lung, bone marrow, and reproductive organs. Hypoxia abrogates the degradation of hypoxia-inducible factors (HIF)-1 and -2, that can then bind to the hypoxia response element within the Epo gene, activating its transcription. Receptors for Epo are expressed on cells known to synthesize Epo, but also on cardiomyocytes, cardiac fibroblasts, and endothelial, retinal, gastric, prostate and vascular smooth muscle cells. Epo-receptor binding triggers at least three intracellular signalling cascades: (1) janus tyrosine kinase 2 (JAK2)/signal transducer and activator of transcription 5 (STAT5); (2) phosphatidylinositol-3 kinase (PI3K)/Akt, and (3) RAS/mitogen-activated protein kinase (MAPK). Epo also enhances nitric oxide (NO) bioavailability through endothelial NO synthase transcription and activation, and exerts antiapoptotic actions through Bcl-2 and Bcl-XL. NO is a powerful vasodilator, insulin-sensitizer, inhibitor of atherothrombosis and apoptosis, and essential for progenitor mobilization. This article is a concise review of recent advances regarding the molecular and cardiovascular effects of Epo.
Journal of Thrombosis and Thrombolysis 04/2008; 26(3):183-7. · 1.48 Impact Factor
