Reference hemoglobin (Hb) values for the definition of anemia are still largely based on the 1968 WHO Scientific Group report, which established a cutoff value of <13 g/dL for adult men and <12 g/dL for adult nonpregnant women. Subsequent studies identified different normal values according to race and age. Estimated prevalence of anemia on admission in the setting of an acute coronary syndrome (ACS) is between 10% and 43% of the patients depending upon the specific population under investigation. Furthermore, up to 57% of ACS patients may develop hospital-acquired anemia (HAA). Both anemia on admission and HAA are associated with worse short- and long-term mortality, even if different mechanisms contribute to their prognostic impact. Baseline anemia can usually be traced back to preexisting disease that should be specifically investigated and corrected whenever possible. HAA is associated with clinical characteristics, medical therapy and interventional procedures, all eliciting cardiovascular adaptive response that can potentially worsen myocardial ischemia. The intrinsic fragility of anemic patients may limit aggressive medical and interventional therapy due to an increased risk of bleeding, and could independently contribute to worse outcome. However, primary angioplasty for ST elevation ACS should not be delayed because of preexisting (and often not diagnosed) anemia; delaying revascularization to allow fast-track anemia diagnosis is usually feasible and justified in non-ST-elevation ACS. Besides identification and treatment of the underlying causes of anemia, the only readily available means to reverse anemia is red blood cell transfusion. The adequate transfusion threshold is still being debated, although solid evidence suggests reserving red blood cell transfusions for patients with Hb level <8 g/dL and considering it in selected cases with Hb levels of between 8 and 10 g/dL. No evidence supports the use of iron supplements and erythropoiesis-stimulating agents in the setting of ACS.

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Objective— Aim of this study was to evaluate changes in LCAT (lecithin:cholesterol acyltransferase) concentration and activity in patients with an acute coronary syndrome, to investigate if these changes are related to the compromised capacity of HDL (high-density lipoprotein) to promote endothelial nitric oxide (NO) production, and to assess if rhLCAT (recombinant human LCAT) can rescue the defective vasoprotective HDL function. Approach and Results— Thirty ST-segment–elevation myocardial infarction (STEMI) patients were enrolled, and plasma was collected at hospital admission, 48 and 72 hours thereafter, at hospital discharge, and at 30-day follow-up. Plasma LCAT concentration and activity were measured and related to the capacity of HDL to promote NO production in cultured endothelial cells. In vitro studies were performed in which STEMI patients’ plasma was added with rhLCAT and HDL vasoprotective activity assessed by measuring NO production in endothelial cells. The plasma concentration of the LCAT enzyme significantly decreases during STEMI with a parallel significant reduction in LCAT activity. HDL isolated from STEMI patients progressively lose the capacity to promote NO production by endothelial cells, and the reduction is related to decreased LCAT concentration. In vitro incubation of STEMI patients’ plasma with rhLCAT restores HDL ability to promote endothelial NO production, possibly related to significant modification in HDL phospholipid classes. Conclusions— Impairment of cholesterol esterification may be a major factor in the HDL dysfunction observed during acute coronary syndrome. rhLCAT is able to restore HDL-mediated NO production in vitro, suggesting LCAT as potential therapeutic target for restoring HDL functionality in acute coronary syndrome.

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Early vascular aging is a process characterized by a reduction in arterial elastin with an increase in collagen that has been related to cardiovascular risk factor and can determine an increased arterial stiffness and central blood pressure. It can be measured by several non invasive methods and in different arterial segment. The present paper will focus on functional (local stiffness parameter) and structural (intima media thickness) carotid arteries alterations typically evaluated by ultrasound methods. Methodological, research and clinical issue has been reviewed.