Anemia in diabetic patients at an internal medicine ward: Clinical correlates and prognostic significance

BackgroundCharacteristics and prognostic significance of anemia in hospitalized diabetic patients are unknown.MethodsWe studied 3145 unselected patients admitted to two Internal Medicine Departments, 872 (27.7%) of whom were diabetic. Forty diabetic patients died during the first hospitalization period. Out of the remaining 832 patients, 334 (40.2%) were anemic and evaluated for survival. In 87 diabetic patients, the cause of anemia was evident on admission, whereas the other 247 had to be further investigated for etiology of anemia.ResultsCompared to non-anemic diabetic patients, the diabetic anemic patients were older (mean age 71.4 vs. 64.4 years, P < .001) and predominantly females (52.4% vs. 44.4%, P < .02). Of the 247 evaluated patients, 38% were deficient in iron, 12% in vitamin B₁₂ and/or folate, 54% had anemia of chronic disease, 47% suffered from heart failure, 39% had renal dysfunction and 22% were complex nursing care patients and/or had diabetic foot. On median follow-up of 19.2 months, mortality rate was higher in anemic compared to non-anemic diabetic patients (17.3% vs. 4%, P < .001), the main cause of death being infection. Male sex (P = .03), albuminuria (P = .01) and heart failure (P = .06) were associated with shorter survival, male sex being the most significant (OR 2.02, 95% CI 1.04 ? 4.00).ConclusionFrequency of anemia was increased in diabetic patients admitted to the Internal Medicine Departments, compared to the studies performed on ambulatory patient populations. Anemia was multifactorial and associated with higher mortality, predominantly from infections. Males with albuminuria and heart failure were at higher risk of death.     

Relationship Between Anemia and Health Care Costs in Heart Failure

BackgroundAnemia is associated with higher morbidity and mortality in patients with heart failure (HF), but its implications for heath care costs are not well described.Methods and ResultsWe analyzed data on 1056 patients with symptomatic HF seen at Duke University between 2002 and 2006. Health care costs were obtained from the hospital cost accounting data system. Adjustments for censoring and covariate imbalance were performed using inverse probability weighted estimators and propensity scores. The prevalence of anemia was 32%. Unadjusted mortality at 3 years was 50.3% in anemic versus 26.5% in non-anemic patients. The adjusted costs per year alive were $22,926 for patients with anemia and $17,189 for those without (P = .04). For those with ejection fraction ≤40% adjusted costs per year alive were $32,914 for anemic versus $18,423 for non-anemic patients (P = .01).ConclusionsAnemia in HF patients was independently associated with greater total costs after accounting for differences in survival, but appeared to be confined primarily to patients with low ejection fraction. These results provide a framework for understanding the economic implications of therapies for anemia in heart failure, and suggest that targeting patients with impaired systolic function has the potential to most favorably affect costs.     

Predictive value of white blood cell subtypes for long-term outcome following myocardial infarction

IntroductionElevation of total white blood cells (WBC) count is associated with higher mortality in patients with acute coronary syndromes. However, it is unknown which specific subset of leukocytes best correlates with increased risk of adverse outcome.Methods and resultsWe prospectively studied the predictive value of WBC subtypes for long-term outcome in 1037 patients with acute myocardial infarction (AMI). Total WBC, neutrophil, monocyte and lymphocyte counts, and high-sensitivity C-reactive protein (CRP) were obtained in each patient. The median duration of follow up was 23 months (range, 6–42 months). Analyzed separately, baseline total WBC (HR 2.2, 95% CI 1.5–3.3; P < 0.0001), neutrophil (HR 2.7, 95% CI 1.8–4.1; P < 0.0001) and monocyte (HR 1.9, 95% CI 1.3–2.8; P = 0.001) counts in the upper quartile, and lymphocyte count in the lower quartile (HR 1.5, 95% CI 1.1–2.3; P = 0.03), were all independent predictors of mortality. Comparing nested models, adding other WBC data failed to improve model based on neutrophil count. In contrast, adding neutrophil count to the models based on total WBC (P = 0.01), on monocyte count (P < 0.0001) or on lymphocyte count (P < 0.0001) improved the prediction of the models. Neutrophil count in the upper quartile (≥9800 μL^?1) remained a strong independent predictor of mortality after adjustment for left ventricular systolic function and for CRP (HR 2.2, 95% CI 1.6–3.0; P < 0.0001).ConclusionOf all WBC subtypes, elevated neutrophil count best correlates with mortality in patients with AMI. Neutrophil count provides additive prognostic information when combined with CRP.     

Coronary stenting is associated with an acute increase in plasma myeloperoxidase in stable angina patients but not in patients with acute myocardial infarction

BackgroundMyeloperoxidase (MPO) has emerged as a critical mediator in the physiopathology of atherosclerosis from plaque formation and growth until destabilization and rupture leading to acute coronary syndrome (ACS). Using coronary stenting as a model of plaque injury, we aimed to determine the evolution of systemic MPO levels following coronary stenting in stable angina patients and in patients with acute myocardial infarction (AMI).MethodsPlasma levels of MPO, lactoferrin, interleukin (IL)-6, C-reactive protein and PMN counts were assessed in 13 patients with Non-ST-elevation myocardial infarction (NSTEMI) (Group A) and in 29 patients with stable angina pectoris (Group B), undergoing coronary stenting. Serial blood samples were taken before angioplasty (baseline) and at 1, 6 and 24 h following initial balloon inflation.ResultsFollowing angioplasty, the overall plasma MPO levels significantly increased at 1 h in group B (120.5 ± 79.0 to 166 ± 79.5, p = 0.003) but not in group A (121 ± 63.4 to 124.7 ± 76.9, p = 0.753). In Group B, the increase in MPO levels at 1 h were significantly higher in the presence of complex lesions compared to patients with simple lesions (p = 0.023). Lactoferrin levels showed no change over time except for a significant decrease at 6 h in group B.ConclusionsIn stable angina patients, coronary stenting is associated with an acute and transient increase in plasma MPO levels, but not in lactoferrin levels, with an enhanced response in the presence of complex lesions. In contrast, we observed no changes in plasma MPO and lactoferrin levels following stenting in patients with AMI. Given its pro-inflammatory properties, the potential implication of MPO release on clinical outcome in stable patients undergoing stenting needs further investigation.     

Coronary plaque rupture in patients with myocardial infarction after noncardiac surgery: frequent and dangerous

PurposeThe pathophysiology of acute coronary syndromes (ACS) after noncardiac surgery is not established yet. Thrombosis over a vulnerable plaque or decreased oxygen supply secondary to anemia or hypotension may be involved. The purpose of this study was to investigate the pathophysiology of ACS complicating noncardiac surgery.MethodsClinical and angiographic data were prospectively recorded into a database for 120 consecutive patients that had an ACS after noncardiac surgery (PACS), for 120 patients with spontaneous ACS (SACS), and 240 patients with stable coronary artery disease (CAD). Coronary lesions with obstructions greater than 50% were classified based on two criteria: Ambrose's classification and complex morphology. The presence of Ambrose's type II or complex lesions were compared between the three groups.ResultsWe analyzed 1470 lesions in 480 patients. In PACS group, 45% of patients had Ambrose's type II lesions vs. 56.7% in SACS group and 16.4% in stable CAD group (P < 0.001). Both PACS and SACS patients had more complex lesions than patients in stable CAD group (56.7% vs. 79.2% vs. 31.8%, respectively; P < 0.001). Overall, the independent predictors of plaque rupture were being in the group PACS (P < 0.001, OR 2.86; CI, 1.82–4.52 for complex lesions and P < 0.001, OR 3.43; CI, 2.1–5.6 for Ambrose's type II lesions) or SACS (P < 0.001, OR 8.71; CI, 5.15–14.73 for complex lesions and P < 0.001, OR 5.99; CI, 3.66–9.81 for Ambrose's type II lesions).ConclusionsNearly 50% of patients with perioperative ACS have evidence of coronary plaque rupture, characterizing a type 1 myocardial infarction.     

Metabolic syndrome is a predictor for an ECG sign of no-reflow after primary PCI in patients with acute ST-elevation myocardial infarction

Background and aimThe purpose of this study was to evaluate both the predictive value of metabolic syndrome (MS) on no-reflow phenomenon and 30-day clinical outcomes on patients undergoing primary percutaneous coronary intervention (PCI) for acute ST-elevation myocardial infarction (STEMI).Methods and resultsOne hundred and twelve consecutive patients (mean age 57 ± 11 years, 94 male) with acute STEMI treated with primary PCI were analysed prospectively. Sum of ST-segment elevation was obtained immediately before and 60 min after the restoration of TIMI-3 flow. The difference between two measurements was accepted as the amount of ST-segment resolution and was expressed as ∑STR. ∑STR < 50% was accepted as ECG sign of no-reflow phenomenon. Metabolic syndrome was defined based on Adult Treatment Panel-III criteria.The no-reflow was found in 22.3% of the entire group and was significantly higher in patients with MS than those without MS (43.7% vs. 13.7%, p < 0.001). There was no significant difference in no-reflow between patients who had both MS and diabetes mellitus (DM) and patients who had MS but not DM (42.5% vs. 50%, respectively; p > 0.05).ConclusionThe presence of MS may play an important role in the occurrence of no- reflow in STEMI treated with primary PCI.     

Relation between the GRACE score and severity of atherosclerosis in acute coronary syndrome

BackgroundPatients with non-ST-elevation acute coronary syndrome are heterogeneous in terms of clinical presentation and immediate- and long-term risk of death or non-fatal ischemic events. The aim of the present study was to evaluate the relationship between the Global Registry of Acute Coronary Events (GRACE) score and severity of coronary artery disease angiographically evaluated by Gensini score in patients with non-ST-elevation acute coronary syndrome.MethodsA total of 245 patients with non-ST-elevation acute coronary syndrome were enrolled to the study. Based on the GRACE risk score classification system, the patients were divided into low- (n = 97, 39.6%), intermediate- (n = 84, 34.3%), and high- (n = 64, 26.1%) risk groups. All patients underwent coronary angiography within five days after admission.ResultsThe Gensini scores were 26 ± 29 in the low-risk group, 29 ± 19 in the intermediate-risk group, and 38 ± 23 in the high-risk group (p = 0.016). The low-risk group was significantly different from the high-risk group (p = 0.013), and the difference from the intermediate-risk group almost reached significance. Normal, noncritical, one and two, or multivessel disease were identified in 15 (6.1%), 31 (12.7%), 75 (30.6%), and 124 (50.6%) patients, respectively. The prevalence of multivessel disease was 28% in the low-risk group, 30% in the intermediate-risk group, and 42% in the high-risk group. The high-risk group was significantly different from the low-risk group (p < 0.01).ConclusionOur study demonstrates that the GRACE score has significant value for assessing the severity and extent of coronary artery stenosis in patients with non-ST-elevation acute coronary syndrome.     

CagA antigen of Helicobacter pylori and coronary instability: insight from a clinico-pathological study and a meta-analysis of 4241 cases

BackgroundCytotoxin-associated gene-A (CagA) antigen is expressed by some virulent strains of Helicobacter pylori (H. pylori). The role of CagA antigen in coronary instability is unknown. We performed a clinico-pathological study and a meta-analysis in the attempt to shed new light on this complex issue.MethodsIn the clinico-pathological study, 38 patients with unstable angina (UA), 25 patients with stable angina (SA), 21 patients with normal coronary arteries (NCA) and 50 age and sex matched healthy volunteers were enrolled. Serology for CagA was assessed in all patients. Specimens of atherosclerotic plaques were obtained from all patients by directional coronary atherectomy, and prepared for immunohistochemistry using anti-CagA monoclonal antibodies. The meta-analysis includes 9 studies assessing the association between seropositivity to CagA strains and acute coronary events.ResultsThe titre of anti-CagA antibodies was significantly higher in patients with unstable angina (161 ± 90 RU/ml) compared to those with stable angina (83 ± 59 RU/ml p < 0.02), NCA (47.3 ± 29 RU/ml p < 0.01) and healthy controls (73 ± 69 p < 0.02). Anti-CagA antibodies recognized antigens localized inside coronary atherosclerotic plaques in all specimens from both stable and unstable patients. In the meta-analysis, seropositivity to CagA was significantly associated with the occurrence of acute coronary events with an odds ratio (OR) of 1.34 (95% CI, 1.15–1.58, p = 0.0003).ConclusionsTaken together these findings suggest that in a subset of patients with unstable angina, an intense immune response against CagA-positive H. pylori strains might be critical to precipitate coronary instability mediated by antigen mimicry between CagA antigen and a protein contained in coronary atherosclerotic plaques.     

Topical HDL administration reduces vein graft atherosclerosis in apo E deficient mice

ObjectiveUse of autologous vein grafts for surgical revascularisation is limited by vein graft failure. Topical high-density lipoprotein (HDL) administration on the adventitial side of vein grafts was evaluated as a new therapeutic modality to improve vein graft patency and function.MethodsCaval veins of C57BL/6 apo E^?/? mice were grafted to the right carotid arteries of recipient 3 month-old C57BL/6 TIE2-LacZ/apo E^?/? mice. HDL (200 μg/ml; 50 μl) in 20% pluronic F-127 gel was applied on the adventitial side of vein grafts.ResultsTopical HDL application reduced intimal area by 55% (p < 0.001) at day 28 compared to control mice. Blood flow quantified by micro magnetic resonance imaging at day 28 was 2.8-fold (p < 0.0001) higher in grafts of topical HDL treated mice than in control mice. Topical HDL potently reduced intimal inflammation and resulted in enhanced endothelial regeneration as evidenced by a 1.9-fold (p < 0.05) increase in the number of CD31 positive endothelial cells. HDL potently enhanced migration and adhesion of endothelial colony-forming cells (ECFCs) in vitro, and these effects were dependent on signaling via scavenger receptor-BI, extracellular signal-regulated kinases, and NO, and on increased β1 integrin expression. Correspondingly, the number of CD31 β-galactosidase double positive cells, reflecting incorporated circulating progenitor cells, was 3.9-fold (p < 0.01) higher in grafts of HDL treated mice than in control grafts.ConclusionsTopical HDL administration on the adventitial side of vein grafts attenuates vein graft atherosclerosis via increased incorporation of circulating progenitor cells in the endothelium, enhanced endothelial regeneration, and reduced intimal inflammation.     

Endothelin-1 levels predict endothelial progenitor cell mobilization after acute myocardial infarction

IntroductionEndothelin-1 (ET-1), circulating endothelial cells (CEC) and endothelial progenitor cells (EPC) are well-known modulators of endothelial function with important cardiac effects after an acute myocardial infarction. However, the relationship between them has never been assessed.The objective of the present study was to establish the relationship between ET-1, CEC, and EPC concentrations after ST-elevation myocardial infarction (STEMI).MethodsEndothelin-1, CEC, and EPC levels were measured in 61 patients presenting with a first STEMI. Samples were withdrawn acutely 6–24 h and 1 week after admission. Assessments included reperfusion outcomes (angiography), left ventricular ejection fraction (echocardiography), and 30-day mortality.ResultsMean age was 60.6 ± 12.6 years and 45 (74%) were males. Higher ET-1 plasma levels were associated with lower EPC count after 1 week (7.45 ± 2.53 pg/ml if EPCs in the first quartile vs 5.72 ± 1.49 pg/ml if EPCs in the fourth quartile; P = 0.04).In contrast with CEC and EPC count, higher ET-1 concentrations on admission were associated with Killip ≥ 2 (9.92 ± 2.01 pg/ml vs 7.32 ± 2.13 pg/ml; P < 0.001), post-reperfusion thrombolysis in myocardial infarction (TIMI) < 3 (8.65 ± 2.86 pg/ml vs 5.87 ± 1.93 pg/ml; P = 0.002), myocardial blush grade (MBG) < 3 (7.46 ± 2.48 pg/ml vs 5.99 ± 2.01 pg/ml; P = 0.004) and higher 30-day mortality (10.29 ± 2.02 pg/ml vs 6.57 ± 2.20 pg/ml; P = 0.005).ConclusionsIn STEMI patients, high ET-1 levels on admission predict a lower EPC mobilization after 1 week. Endothelin-1 provides better clinical, angiographic and echocardiographic information for prognosis than do CEC and EPC concentrations.     

Circulating angiogenic cytokines and stem cells in patients with severe chronic ischemic heart disease — Indicators of myocardial ischemic burden?

BackgroundAngiogenic growth factors and stem cell therapies have demonstrated varying results in patients with chronic coronary artery disease. A reason could be that these mechanisms are already up-regulated due to reduced blood supply to the myocardium. The objective of this study was to examine if plasma concentrations of circulating stem cells and angiogenic cytokines in patients with severe stable chronic coronary artery disease were correlated to the clinical severity of the disease.MethodsFifty-four patients with severe coronary artery disease and reversible ischemia at stress myocardial perfusion scintigraphy were prospectively included. The severity of the disease was quantified by an exercise tolerance test, Canadian Cardiovascular Society angina classification, and Seattle Angina Pectoris Questionnaire. Fifteen persons without coronary artery disease served as control subjects.ResultsPlasma concentration of VEGF-A, FGF-2, SDF-1, and circulating CD34+ and CD34−/CD45− cells were similar in the two groups, but early stem cell markers (CD105, CD73, CD166) and endothelial markers (CD31, CD144, VEGFR2) were significantly different between patients and control subjects (p < 0.005 − 0.001). Diabetic patients had higher concentration of SDF-1 (2528 vs. 2150 pg/ml, p = 0.004). We found significant correlations between both VEGF-A, FGF-2, and CD34+ to disease severity, including degree of reversible ischemia, angina stability score, and exertional dyspnoea.ConclusionsPlasma concentrations of circulating stem cells and angiogenic cytokines have large inter-individual variations, which probably exclude them from being useful as indicators of myocardial ischemic burden.     

Effect of a single high-fat meal on endothelial function in patients with the metabolic syndrome: role of tumor necrosis factor-alpha

Background and aimsA single high-fat meal may induce endothelial activation and dysfunction in both normal subjects and in patients with type 2 diabetes. The aim of this study was to assess the effect of a high-fat meal on endothelial function in patients with the metabolic syndrome.Methods and resultsTwenty-five patients with the metabolic syndrome (ATP III criteria) were matched for sex, age and body mass index with 25 subjects without the metabolic syndrome. All subjects ate under supervision a high fat meal (760 calories) with 59% energy from fat, 12% energy from protein and 29% energy from carbohydrates. Compared with the control group, subjects with the metabolic syndrome had reduced endothelial function, as assessed with the l-arginine test, and higher circulating levels of TNF-α. Following the high-fat meal, both triglyceride and TNF-α levels increased more in subjects with the metabolic syndrome than in subjects without, while endothelial function decreased more in subjects with the metabolic syndrome. There was a significant relation between increases in TNF-α levels and decreases in endothelial function score in subjects with the metabolic syndrome (r = −0.39, P = 0.03).ConclusionTNF-α levels are increased in subjects with the metabolic syndrome; moreover, a high-fat meal produces further increase in its levels associated with endothelial dysfunction.     

Differential expression of Toll-like receptor 4 and human monocyte subsets in acute myocardial infarction

ObjectiveTo investigate the involvement of Toll-like receptor 4 (TLR4) expression on two monocyte subsets in the pathologic processes related to acute coronary syndrome. How monocytes, which have recently been shown to comprise two distinct subsets, mediate the process of coronary plaque rupture remains to be fully elucidated. Recent studies have shown that TLR4 is involved in monocyte activation of patients with accelerated forms of atherosclerosis.MethodsWe enrolled 65 patients with acute myocardial infarction (AMI, n = 22), unstable angina pectoris (UAP, n = 16), and stable angina pectoris (SAP, n = 27) who underwent coronary angiography and 15 healthy controls. The expression of TLR4 on two monocyte subsets (CD14⁺CD16^? and CD14⁺CD16⁺) was measured by flow cytometry.ResultsIn patients with AMI, TLR4 was more expressed on circulating CD14⁺CD16⁺ monocytes than on CD14⁺CD16^? monocytes (p < 0.001). The expression levels of TLR4 on CD14⁺CD16⁺ monocytes were significantly elevated in patients with AMI compared with other 3 groups. TLR4 expression levels on CD14⁺CD16⁺ monocytes were significantly elevated at the culprit site compared with the systemic level (p = 0.044). The up-regulation of TLR4 on admission was remarkably decreased 12 days after AMI (p < 0.001). In addition, plasma levels of tumor necrosis factor-α were positively correlated with TLR4 expression levels on monocytes in patients with AMI (r = 0.47, p = 0.027).ConclusionTLR overexpression on CD14⁺CD16⁺ monocytes in AMI, as demonstrated both in the circulation and at the coronary culprit site, might be associated with the pathogenesis of AMI.     

Long-term cardiac rehabilitation and exercise training programs improve metabolic parameters in metabolic syndrome patients with and without coronary heart disease

Background and aimsThe effectiveness of long-term cardiac rehabilitation and exercise training programs on metabolic parameters was evaluated in metabolic syndrome subjects with and without coronary heart disease (CHD).Methods and resultsFifty-nine CHD and 81 non-coronary patients with metabolic syndrome (59 ± 8 vs 56 ± 9 years) were identified retrospectively at entry into identical cardiac rehabilitation and exercise-training programs. Metabolic syndrome was defined using modified Adult Treatment Panel III criteria. Exercise training occurred approximately twice per week. Metabolic and exercise testing data were collected at baseline and after 12 months during the course of the program. Mean duration of cardiac rehabilitation and exercise training programs was over one year in both coronary and non-coronary patients (366 ± 111 vs 414 ± 102 days for CHD and non-coronary CHD cohorts respectively, p < 0.01). Significant improvements in bodyweight, body mass index, blood lipids, triglyceride/HDL ratio and exercise tolerance were noted in both cohorts. At the end of follow-up, 31% of CHD and 20% of non-CHD subjects no longer possessed diagnostic criteria for metabolic syndrome (p < 0.0001 and p < 0.001 respectively).ConclusionsA long-term cardiac rehabilitation program reduces metabolic syndrome prevalence in CHD patients and results in a similar improvement in risk factor control for metabolic syndrome patients without CHD.     

CRP and CD14 polymorphisms correlate with coronary plaque volume in patients with coronary artery disease--IVUS substudy of the ENCORE trials

BackgroundSeveral proinflammatory single-nucleotide polymorphisms (SNPs) have been linked to the progression of atherosclerosis and coronary artery disease (CAD). Plaque size and its destabilization by inflammatory processes are major determinants of ischemia and acute coronary syndromes. Intravascular ultrasound (IVUS) allows for quantification of plaque size in vivo. We therefore investigated the relation of plaque size with mutations of proinflammatory genes in patients with CAD.MethodsIn 196 patients with stable CAD enrolled in the ENCORE trials coronary plaque and vessel volume was assessed by IVUS. 173 patients were successfully genotyped for polymorphisms of proinflammatory genes CD14 C(?260)T and CRP C(+1444)T using the single-nucleotide polymorphism polymerase chain reaction (SNP PCR) approach.ResultsBaseline characteristics were comparable for all genotype groups. Higher ratios of plaque volume/vessel volume were observed in patients with the CRP 1444TT (n = 11) and CD14 260TT (n = 33) genotypes (p = 0.016 and p = 0.026, respectively).ConclusionIn patients with stable coronary artery disease the CRP 1444TT and CD14 260TT variants are associated with larger coronary plaque volume independently of concomitant cardiovascular risk factors.     

Prevalence of anemia among elderly patients in an emergency room setting

PurposeAnemia is highly prevalent in geriatric patients and associated with increased morbidity, functional and cognitive decline. German prevalence data are rare and no treatment guidelines exist for the elderly. Anemia often remains unconsidered in this population. This study evaluates prevalence of anemia among geriatric patients in an emergency room (ER) setting and the performed diagnostic and therapeutic steps.SubjectsData of 1045 elderly patients > 70 years admitted to the ER at our university hospital between January and August 2010 were retrospectively analyzed (384 female and 474 male in-patients, 92 female and 95 male out-patients). Anemia definition: hemoglobin < 12 g/dL (female) and < 13 g/dL (male). Diagnostic and therapeutic steps, medication and hemoglobin (hb) characteristics at transfer from ER to other departments were evaluated.ResultsAmong in-patients anemia was found in 54.2%, among out-patients in 36.4% (P < 0.001). Hb was significantly lower in anemic in-patient men (P = 0.007) compared to anemic out-patient men. No such difference was found among women. Anemic patients’ age did not influence the hb level. There were department specific differences in hb level as well as diagnostics and therapy of anemia. Only 12% of all evaluable anemic in-patients received a non-drug anemia treatment, mostly consisting of transfusions.Discussion/ConclusionMore than 50% of all elderly patients suffered from anemia; less than one fifth received either anti-anemic medication or non-drug treatment; insufficiency of medical care in this study group can be assumed; close intersdisciplinary cooperation with geriatrician in ER is necessary with development of diagnostic and therapeutic guidelines for anemic elderly.     

Anemia as a risk factor for low bone mineral density in postmenopausal Turkish women

BackgroundWe investigated the association of bone mineral density (BMD) by detected dual-energy X-ray absorptiometric (DXA) method and hemoglobin (Hb) levels in a large sample.MethodsThe current study enrolled 371 postmenopausal women (82 anemic patients), who were screened for osteopenia or osteoporosis by DXA. Patients with osteopenia or osteoporosis (T score < ? 1.0 SD) were grouped as having low bone mass (LBM).ResultsAnemic patients were older and had significantly higher duration of menopause. When compared with subjects with normal Hb, anemic patients had significant lower femur t score, femur BMD, femur Z score, spinal t score, spinal BMD and spinal Z score (p < 0.001). Additionally, the ratio of subjects with LBM in the femur and spine were significantly high in anemic patients (p < 0.002, p < 0.002, respectively). There were significant correlations between Hb values and femur t score, femur BMD, spine t score, and spine BMD values of the study population in bivariate correlation analysis (r = 0.150, p = 0.004, r = 0.148, p = 0.004, r = 0.160, p = 0.002, r = 0.164, p = 0.001, respectively). Furthermore, presence of anemia was found to be an independent predictor of LBM for spine [OR: 2.483 (95% CI: 1.309–4.712), p < 0.005] in logistic regression analysis. Additionally, number of anemic patients was significantly high in low femur and spine BMD groups (56 vs. 26; p = 0.01, 66 vs. 16; p = 0.002, respectively).ConclusionWe have found that the presence of anemia was as an independent predictor of LBM for spine after adjusting for body mass index and other confounders in postmenopausal Turkish women.     

Regulatory T cells and IL-10 levels are reduced in patients with vulnerable coronary plaques

BackgroundDespite having a similar large extent of atherosclerotic coronary affliction, some patients suffer of recurrent cardiac events, whereas others remain asymptomatic.HypothesisWe hypothesized the existence of a systemic “signature” that could distinguish “vulnerable” patients with preexisting coronary atherosclerosis from those having similar risk factors and atheromatous burden, but no history of clinically evident plaque rupture/erosion.MethodsTwenty three patients who had at least two prior myocardial infarctions (“vulnerable group”) were matched in respect to their background and coronary atherosclerosis extent with twenty one patients without a history of previous myocardial infarction who underwent routine coronary angiography before valvular surgery. We studied a panel of cytokines, antibodies and hormones including IL-6, IL-10, IL-12, antibodies to β2 glycoprotein I (β2GPI), antibodies to oxidized-LDL, adiponectin and resistin, along with levels of circulating EPCs and Tregs.ResultsA significantly higher level of Treg cells was present in the control (73.4% ± 4) than in the “vulnerable patient” group (62.2% ± 10.7), p < 0.001. IL-10 level was also significantly higher in the control than in the vulnerable patients (2.6 ± 1.2 pg/ml versus 0.9 ± 0.1 pg/ml respectively, p = 0.03). There was no significant difference in the circulating levels of the other cytokines, hormones or EPCs between the two groups.ConclusionRegulatory T cells and serum IL-10 may discriminate “vulnerable” versus stable patients and may have a protective role against plaque rupture in patients with coronary atherosclerosis.     

Anemia-prevalence and risk factors in pregnancy

BackgroundTo assess the prevalence of decreased iron stores and anemia in pregnant women. To determine whether the risk factors: socio-demographic background, age, BMI, and parity are associated with abnormal hemoglobin concentrations and/or abnormal iron status.MethodsA longitudinal study was carried out at the Department of Obstetrics, University Hospital of Zurich to establish the risk factors and prevalence of the decreased iron stores and anemia in early pregnancy. In order to determine the hematological parameters and ferritin levels, venous blood samples of 470 singleton pregnancies between 16 and 20 pregnancy weeks were collected. According to hemoglobin and iron status, the patients were divided into four groups: patients with iron deficiency anemia, patients with decreased iron stores, patients with anemia for other reasons and normal patients. The determinants socio-demographic background, age, BMI and parity were explored using multiple logistic regression analysis.ResultsThe prevalence of decreased iron stores (ferritin < 20 μg/l) was observed in 31.8% of subjects (149/470) and anemia (Hb < 110 g/l) in 18.5% (87/470). The prevalence of iron deficiency anemia was higher among women coming from former Yugoslavia and developing countries (p = 0.004 and p = 0.012). In patients coming from developing countries, a significant increase of anemia for other reasons was observed (p = 0.027) and in patients older than 30 years, a significant increase of decreased iron stores (p = 0.018).ConclusionsIn our study population with low parity, the prevalence of abnormal hemoglobin and abnormal iron status was 50.2% (236/470), and socio-demographic background was the most important risk factor of anemia.     

Effect of statin therapy on coronary fibrous-cap thickness in patients with acute coronary syndrome: assessment by optical coherence tomography study

BackgroundThe thickness of coronary fibrous caps is a major determinant of vulnerable plaques. Several clinical trials have suggested that statin therapy could stabilize vulnerable plaques. Recently, optical coherence tomography (OCT) has been proposed as an effective histology-resolution imaging modality for assessing such micro-structural changes.MethodsForty AMI patients with hyperlipidemia were enrolled and underwent percutaneous coronary intervention (PCI). They were divided into two groups; statin treatment group (n = 23) or control group (n = 17). Serial OCT analyses were performed at baseline and 9-month follow-up for a non-PCI lipid-rich plaque lesion.ResultsThe LDL-cholesterol level in the statin group was significantly lower than that in the control group at follow-up. Although the fibrous-cap thickness was significantly increased in both the statin treatment group (151 ± 110 to 280 ± 120 μm, p < 0.01) and the control group (153 ± 116 to 179 ± 124 μm, p < 0.01) during follow-up period, the degree of increase was significantly greater in the statin treatment group than in the control group (188 ± 64% vs. 117 ± 39%, p < 0.01). Furthermore, when the patients in the statin treatment group were divided into two subgroups (fibrous-cap thickness ConclusionThe lipid-lowering therapy with statin for 9 months after the onset of acute myocardial infarction significantly increased the fibrous-cap thickness in patients with hyperlipidemia.