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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial hypertrophy is a morphological adaptive response to chronic work overload imposed on the heart. It has been categorized into two distinct basic types: concentric hypertrophy, occurring in response to a sustained pressure overload in which wall thickness increases without chamber enlargement, and eccentric hypertrophy, in response to a chronic volume overload in which chamber volume enlarges without a relative increase in its wall thickness. It should be emphasized, in this context, that these adjectives are somewhat confusing, since the hypertrophy observed is not eccentric in the fashion often seen in the left ventricle of patients with hypertrophic cardiomyopathy. In fact, the hypertrophy is concentric in both instances, but is associated with an increase in chamber volume when described as eccentric, yet occurring with a maintained volume when said to be concentric. In rats made anemic by iron deficiency, the volume overloaded heart achieves an adaptive increase in mass characterized as hypertrophy occurring in the setting of dilated ventricle. This so-called eccentric hypertrophy depends on catecholamines as possible signals for myocardial growth, and progresses with preserved ultrastructure and contractile performance of the cardiac muscle. A gradually imposed volume overload results in a harmonious growth of the heart (it retains a relative normal shape, becoming a magnified normal heart), probably mediated by release of catecholamines into the myocardium. This process resembles the normal cardiac growth in response to the obligatory volume load imposed by an increasing cardiac output (greater metabolic demands) and blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)
Int J Cardiol 1991 May
PMID:Cardiac hypertrophy due to pressure and volume overload: distinctly different biological phenomena? 183 Nov 83

To test the hypothesis that tissue oxygen delivery would be affected by diminished oxygen stores in cyanotic congenital heart disease, serum ferritin, transferrin saturation, hemoglobin, red cell mean corpuscular volume (MCV), red cell 2,3-diphosphoglycerate (DPG), P50, blood gases, oxygen saturations and systemic oxygen transport were measured in 29 hypoxemic infants and children. For the group, aortic saturation was 81 +/- 9%, PaO2 was 50 +/- 12 mm Hg, hemoglobin 16.2 +/- 2.1 gm/dl and systemic oxygen transport 620 +/- 145 ml/min/m2. P50 was increased above normal values (28.8 +/- 2.3 vs 26.6 +/- 1.1 mm Hg, p less than 0.01), and DPG was 2.35 +/- 0.54 mumol/ml, at the upper limits of normal for this assay. Iron deficiency was present in 8. When patients with P50 greater than or equal to 30 mm Hg and P50 less than 30 mm Hg were compared, iron stores were diminished in the high P50 group: [serum ferritin (19 +/- 8 vs 53 +/- 48 ng/ml, p = 0.0006), transferrin saturation (11 +/- 6 vs 23 +/- 11%, p = 0.003) and MCV (79 +/- 8 vs 86 +/- 4 fl, p = 0.05)]. Hemoglobin, aortic oxygen saturation, PaO2 and systemic oxygen transport were similar in both groups. In children with iron sufficiency, 15 of 21 had MCV greater than 90th percentile for age and sex (p less than 0.001 versus expected distribution). Also, MCV greater than 90th percentile for age and sex had a positive predictive value of 0.88 for iron sufficiency. This study demonstrates that diminished iron stores in cyanotic congenital heart disease are associated with a more right-shifted oxyhemoglobin dissociation curve (increased P50).(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1988 Mar 01
PMID:Effect of iron deficiency on tissue oxygen delivery in cyanotic congenital heart disease. 334 85

A group of 67 children with cyanotic congenital heart disease (CCHD) were studied, and 35 were given iron treatment according to a regimen that gives iron to patients with a hematocrit (Hct) below 60%. The patients were categorized as iron-deficient and iron-sufficient according to their transferrin saturation and ferritin values. The pretreatment hemoglobin (Hb) and Hct values of the groups were similar. The mean Hct was nearly three times as much as the mean Hb in the iron-sufficient group and more than three times as much as the Hb in the iron-deficient group. Excessive erythrocytosis in the iron-deficient group was impressive. Mean corpuscular volume (MCV) values were below 72.7 fl in all of the iron-deficient patients. After treatment the Hb, Hct, transferrin saturation, and ferritin increased significantly in both groups, with the increments greater in the iron-deficient group. Increments in the erythrocyte (RBC) count were significant in the iron-sufficient group but insignificant in the iron-deficient one. Increments of MCV in the iron-deficient group were significant but insignificant in the iron-sufficient group. Our study demonstrated that prediction of Hb, RBC count, and MCV, measurements of which are easy and inexpensive and require little blood, can suffice for the diagnosis of iron deficiency in patients with CCHD without altering systemic perfusion.
Pediatr Cardiol
PMID:Parameters of iron deficiency in children with cyanotic congenital heart disease. 866 27

A high percentage of cyanotic adults (37%) with cyanotic congenital cardiac disease (CCD) presented with depleted iron stores (13 of 52) or latent iron deficiency (6 of 52), even in a CCD center in which cyanotic patient phlebotomy is mostly avoided. In many of these patients, hypochromia and microcytosis was frequent, whereas hyperchromia and macrocytosis were relatively common.Furthermore, 50% of patients presented with hyperhomocysteinemia, possibly related to folate or B vitamin deficiencies, which may increase red blood cell size and color, explaining the lack of microcytosis and hypochromia in many cyanotic patients with iron deficiency.
Am J Cardiol 2004 Sep 15
PMID:Erythrocyte indexes, iron metabolism, and hyperhomocysteinemia in adults with cyanotic congenital cardiac disease. 1537 2

Anemia and renal dysfunction (RD) are frequent complications seen in chronic heart failure (HF). However, the prevalence and interaction of these co-morbidities in a representative population of outpatients with chronic HF is poorly described. In this study, it was sought to determine the association between RD and anemia in patients with HF enrolled in a community-based HF program. Nine hundred fifty-five patients with HF due to left ventricular systolic dysfunction were investigated for the prevalence of anemia and its cause and followed for a median of 531 days. Anemia was defined as hemoglobin < 12.0 g/dl in women and < 13.0 g/dl in men. RD was defined as a calculated glomerular filtration rate of < 60 ml/min. The prevalence of anemia was 32%. Fifty-three percent of patients with and 27% of those without anemia had > or = 1 test suggesting hematinic deficiency. The prevalence of RD was 54%. Forty-one percent of patients with and 22% of patients without RD had anemia, with similar proportions associated with iron deficiency in the presence or absence of RD. Anemia and RD independently predicted a worse outcome, and this effect was additive. In conclusion, in outpatients with chronic HF, anemia and RD are common and co-exist but confer independent prognostic information. A deficiency of conventional hematinic factors may cause about 1/3 of anemia in this clinical setting.
Am J Cardiol 2006 Aug 01
PMID:Anemia, renal dysfunction, and their interaction in patients with chronic heart failure. 1686 30

Erythrocytosis is an adaptive response to improve oxygen transport in cyanotic congenital heart disease (CCHD). However, at highly increased hematocrit levels patients may experience hyperviscosity symptoms. Iron deficiency in CCHD patients is often overlooked due to elevated hemoglobin concentrations. A 29-year-old male with CCHD was readmitted to our outpatient clinic. Red blood cells (11.65*10(12)/L), hemoglobin (25.7 g/dL), and hematocrit (80%) were extremely elevated. Measurements of iron supply showed a constellation typical for iron deficiency with low ferritin (13.2 microg/L), and high sTfR (20 mg/L). We present a case of extremely high red blood cell counts with concomitant iron deficiency. For appropriate management and to avoid misinterpretation of the iron status, ferritin and sTfR should always accomplish laboratory examination of CCHD patients.
Int J Cardiol 2007 Mar 20
PMID:Iron deficiency in a patient with extreme erythrocytosis due to cyanotic congenital heart disease. 1709 63

Complications of chronic hypoxia, including erythrocytosis, hyperviscosity, abnormalities of hemostasis, cerebral abscesses, stroke, and endocarditis, are among the most common consequences of cyanotic heart disease in adults. The compensatory erythrocytosis of cyanotic heart disease can become pathologic by causing an increase in blood viscosity, thereby decreasing perfusion and resulting in decreased total oxygen delivery and increased risk of venoocclusive/hyperviscosity syndrome. Treatment of hyperviscosity secondary to erythrocytosis in cyanotic heart disease is controversial. Data is limited but suggest that phlebotomy has the potential to increase exercise capacity, reduce the symptoms of hyperviscosity, and reduce the potential risk of vasoocclusive disease in selected patients with polycythemia secondary to cyanotic heart disease. Unfortunately, repeated phlebotomy can quickly lead to iron deficiency, resulting in microcytic erythrocytes that induce higher viscosity than normocytic erythrocytes, which may increase the risk for venoocclusive events. There are limited data on the use of hydroxyurea to suppress erythrocytosis in this patient population. The authors conclude that until newer approaches to decreasing hematocrit without inducing iron deficiency are shown to be safe and efficacious, phlebotomy should only be used for the acute resolution of hyperviscosity symptoms. In addition, the use of hydroxyurea should be limited to patients with recurrent symptoms.
Cardiol Rev
PMID:Blood is thicker than water: the management of hyperviscosity in adults with cyanotic heart disease. 1717 81

Anemia has been recognized as a very common and serious comorbidity in heart failure, with a prevalence ranging from 10 to 79%, depending on diagnostic definition, disease severity and patient characteristics. A clear association of anemia with worse prognosis has been confirmed in multiple heart failure trials. This finding has recently triggered intense scrutiny in order to identify the underlying pathophysiology and the best treatment options. Etiology is multifactorial, with iron deficiency and cytokine activation (anemia of chronic disease) playing the most important roles. Treatment is aimed at not only restoring hemoglobin values back to normal, but also at improving the patient's symptoms, functional capacity and hopefully the outcome. Iron supplementation and erythropoietin-stimulating agents have been used for this purpose, either alone or in combination. In this review, the recent advances in elucidating the mechanisms leading to anemia in the setting of heart failure are presented and the evidence supporting the use of different treatment approaches are discussed.
Future Cardiol 2009 Jan
PMID:Anemia in heart failure: pathophysiologic insights and treatment options. 1937 Dec 5

It is well known that red cell distribution width (RDW) levels are affected by various clinical manifestations such as iron deficiency, thrombocytopenia, and inflammatory diseases. In the present study, the authors investigated to examine the prognostic significance of various plasma biomarkers in patients with known or suspected coronary artery disease. However, they only measured hemoglobin levels. They did not measure other factors including iron, vitamin B12, folate, and platelet count. In this study, because of all these causes, high RDW levels are unavailable as an independent predictor of mortality in patients with acute coronary syndromes.
Int J Cardiol 2010 Nov 19
PMID:Red cell distribution width and acute coronary syndromes. 1914 26

Iron-deficiency anemia is common in patients with heart failure (HF), but the optimum diagnostic tests to detect iron deficiency and the treatment options to replete iron have not been fully characterized. Recent studies in patients with HF indicate that intravenous iron can rapidly replenish iron stores in patients having iron-deficiency anemia, with resultant increased hemoglobin levels and improved functional capacity. Preliminary data from a subgroup analysis also suggest that supplemental intravenous iron therapy can improve functional capacity even in those subjects without anemia. The mechanisms responsible for this observation are not fully characterized, but may be related to beneficial effects of iron supplementation on mitochondrial respiration in skeletal muscle. The long-term safety of using intravenous iron supplementation in HF populations is not known. Iron is a known pro-oxidant factor that can inhibit nitric oxide signaling and irreversibly injury cells. Increased iron stores are associated with vascular endothelial dysfunction and increased risk of coronary heart disease events. Additional clinical trials are needed to more fully characterize the therapeutic potential and safety of intravenous iron in HF patients.
Cardiol Rev
PMID:Treatment of anemia in heart failure: potential risks and benefits of intravenous iron therapy in cardiovascular disease. 2069 72


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