Anemia and Cardiovascular Disease

作者: Antonis S. Manolis , Spyridon Koulouris , Kostas Triantafyllou , Dimitris Sakellariou , Sokratis Pastromas

DOI: 10.1002/9781444319583.CH20

关键词:

摘要: Anemia is a well-recognized risk factor in vari-ety of medical conditions, including cardiovasculardisease (CVD), where close link between anemiaand the development CVD being increasinglyappreciated over recent years.Classically, chronic anemia has been associ-ated with high-output heart failure (HF) espe-cially when hemoglobin (Hgb) levels are ≤8mg/dL[1]. This type HF characterized by (i) re-duced afterload due to decreased systemic vascularresistance and reduced blood viscosity (due de-crease erythrocyte number hematocrit); (ii)increased preload an increase venous re-turn; (iii) increased left ventricular (LV) systolicperformance both andin sympathetic activity [2, 3]. Mechanisms induc-ing arterial dilatation include hypoxic vasodila-tion hypoxia-generated metabolites; (ii)flow-mediated vasodilation bloodflow, effect mediated endothelial cells andendothelium-derived nitric oxide (NO) [4]. Beyondvasodilation, vascular bed torecruitment new vessels formation collat-erals arteriovenous shunts seems play ad-ditional minor role [5]. Ensuing pathophysiologicchanges tissue hypoxia, volume overloadwith its attendant LV hypertrophy, dilation,may ultimately lead circulatory decompensationespecially presence associated pathologicalconditions, such as hypertension, diabetes mellitus(DM), uremia (Figure 20.1) [6–12].In patients end-stage renal disease (ESRD),a significant correlation andmass severity duration in-dependently from age, DM, hypertension hasbeen repeatedly demonstrated [13, 14]. But evenin milder forms impairment,a decrease Hgb level better predictor ofLV hypertrophy (LVH) than systolic pressure[15–19]. holds true for general populationas well, was shown Framingham Heartstudy [16], Atherosclerosis Risk Com-munities (ARIC) study [20]. In ARIC study,which investigated 14,410 individuals without CVDat baseline, defined 13 g/dL inmen 12 women independentlyassociated 1.4 times higher myocardialinfarction (MI), coronary angioplasty (PCI), coro-nary artery bypass surgery (CABG) or definite death entire cohort during mean fol-low up approximately 6 years [20].Beyond potentially causative de-velopment subjects withoutcardiovascular factors re-nal insufficiency, also aggravatethe prognosis those who already suffer car-diovascular complications. Patients

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