Predictive value of B-type natriuretic peptides in detecting latent left ventricular diastolic dysfunction in β-thalassemia major

Kremastinos, Dimitrios Th.; Hamodraka, E.; Parissis, John; Tsiapras, Dimitrios; Dima, Kleanthi; Maisel, Alan

doi:10.1016/j.ahj.2009.10.025

Cited by 42 publications

(44 citation statements)

References 25 publications

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“…However, the effects of iron chelators on diastolic LV dysfunction have not yet been clarified, and LVEF may still be affected in a small number of cases despite proper chelation therapy. 31,47,48 The efficacy of iron chelators is partly limited by the fact that only a portion of total body iron content is directly chelatable. 13 More specifically, from the 3 forms of stored iron, labile cellular iron is the most accessible to chelation, and hemosiderin is the least accessible one.…”

Section: Kremastinos and Farmakismentioning

confidence: 99%

“…30,31 If the cause of iron overload persists and no proper iron chelation therapy is initiated, the majority of patients with IOC develop LV remodeling that ultimately leads to LV dilatation and reduced LVEF, the so-called dilated phenotype of IOC. 10,32 In a minority of cases (Ͻ10%) characterized by severe iron overload, restrictive LV dysfunction leads, in advanced age, to the development of pulmonary hypertension, right ventricular dilatation, and right-sided heart failure without LV anatomic remodeling and with preserved LVEF, even at the final stages, the so-called restrictive phenotype.…”

Section: Kremastinos and Farmakis Iron Overload Cardiomyopathy 2255mentioning

confidence: 99%

“…10 Indeed, it was shown that amino-terminal pro-B-type natriuretic peptide might be elevated in thalassemia major patients with preserved LVEF before conventional Doppler indices of diastolic function became abnormal 30 or when Doppler and tissue Doppler values were inconclusive. 31 CMR-derived T2* relaxation time is currently the mainstay for the quantitative assessment of cardiac iron deposition. 11 Introduced a decade ago, 33 this modality has revolutionized the clinical management of patients with hemoglobinopathies and other iron overload conditions, because it allows the accurate diagnosis and quantification of myocardial and hepatic iron deposition and hence the tailoring and monitoring of iron chelation therapy.…”

Section: Diagnosis and Screeningmentioning

confidence: 99%

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Iron Overload Cardiomyopathy in Clinical Practice

2011

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Section: Kremastinos and Farmakismentioning

confidence: 99%

Section: Kremastinos and Farmakis Iron Overload Cardiomyopathy 2255mentioning

confidence: 99%

Section: Diagnosis and Screeningmentioning

confidence: 99%

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Iron Overload Cardiomyopathy in Clinical Practice

2011

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“…5) Brain natriuretic peptide (BNP) is known to be a marker for volume and pressure overload 6) and its level increased in documented left ventricular diastolic dysfunction. 7) Periodontitis is a chronic inflammatory disease caused by gram-negative anaerobic bacteria, that results in bone resorption, destruction of the connective tissue, and loss of teeth. 8) Inflammatory cells secrete cytokines and matrix-degrading proteases, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8, prostaglandin E2, and MMPs which play a significant role in periodontal destruction.…”

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confidence: 99%

Periodontal Pathogen Aggregatibacter actinomycetemcomitans Deteriorates Pressure Overload-Induced Myocardial Hypertrophy in Mice

et al. 2012

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SummaryAlthough a relationship between periodontitis and myocardial hypertrophy has been reported, the precise mechanism has not been clarified. The purpose of this study was to investigate the association between periodontal infection and myocardial hypertrophy. Transverse aortic constriction (TAC) was performed. Mice were injected with Aggregatibacter actinomycetemcomitans (A.a.) (0.1 mL of 10 8 CFU/mL) in the infected group and PBS in the control group. Echocardiography, histopathology, and immunohistochemistry were performed. Echocardiography indicated that left ventricular fractional shortening had decreased in the infected group compared to the control group on day 28. Heart to body weight ratio increased in the infected group compared to the control group. Histopathologically, A.a.-infected mice showed markedly enhanced cardiac hypertrophy, fibrosis and arteriosclerosis 4 weeks after TAC operation. Immunohistochemistry revealed that expression of MMP-2 in the interstitial tissue was enhanced in the infected group. These results suggested that the periodontal pathogen caused a deterioration of pressure overload-induced myocardial hypertrophy through MMP activation. (Int Heart J 2012; 53: 324-330)

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“…N-terminal pro-B-type natriuretic peptide (NT-proBNP) and B-type natriuretic peptide (BNP) are significantly increased in documented LV diastolic dysfunction, whereas NT-proBNP appears to have better predictive value in detecting latent LV diastolic dysfunction. 92 However, one study showed poor correlation of BNP against low myocardial T2*, which predicts future HF. 50 One possible explanation for this finding is cardiac endocrinopathy and reduced BNP secretion caused by iron toxicity.…”

Section: Basic Testsmentioning

confidence: 99%

Cardiovascular Function and Treatment in β-Thalassemia Major

Pennell¹,

Udelson²,

Arai³

et al. 2013

Circulation

331

172

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This aim of this statement is to report an expert consensus on the diagnosis and treatment of cardiac dysfunction in β-thalassemia major (TM). This consensus statement does not cover other hemoglobinopathies, including thalassemia intermedia and sickle cell anemia, in which a different spectrum of cardiovascular complications is typical. There are considerable uncertainties in this field, with a few randomized controlled trials relating to treatment of chronic myocardial siderosis but none relating to treatment of acute heart failure. The principles of diagnosis and treatment of cardiac iron loading in TM are directly relevant to other iron-overload conditions, including in particular Diamond-Blackfan anemia, sideroblastic anemia, and hereditary hemochromatosis. Heart failure is the most common cause of death in TM and primarily results from cardiac iron accumulation. The diagnosis of ventricular dysfunction in TM patients differs from that in nonanemic patients because of the cardiovascular adaptation to chronic anemia in non–cardiac-loaded TM patients, which includes resting tachycardia, low blood pressure, enlarged end-diastolic volume, high ejection fraction, and high cardiac output. Chronic anemia also leads to background symptomatology such as dyspnea, which can mask the clinical diagnosis of cardiac dysfunction. Central to early identification of cardiac iron overload in TM is the estimation of cardiac iron by cardiac T2* magnetic resonance. Cardiac T2* <10 ms is the most important predictor of development of heart failure. Serum ferritin and liver iron concentration are not adequate surrogates for cardiac iron measurement. Assessment of cardiac function by noninvasive techniques can also be valuable clinically, but serial measurements to establish trends are usually required because interpretation of single absolute values is complicated by the abnormal cardiovascular hemodynamics in TM and measurement imprecision. Acute decompensated heart failure is a medical emergency and requires urgent consultation with a center with expertise in its management. The first principle of management of acute heart failure is control of cardiac toxicity related to free iron by urgent commencement of a continuous, uninterrupted infusion of high-dose intravenous deferoxamine, augmented by oral deferiprone. Considerable care is required to not exacerbate cardiovascular problems from overuse of diuretics or inotropes because of the unusual loading conditions in TM. The current knowledge on the efficacy of removal of cardiac iron by the 3 commercially available iron chelators is summarized for cardiac iron overload without overt cardiac dysfunction. Evidence from well-conducted randomized controlled trials shows superior efficacy of deferiprone versus deferoxamine, the superiority of combined deferiprone with deferoxamine versus deferoxamine alone, and the equivalence of deferasirox versus deferoxamine.

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Predictive value of B-type natriuretic peptides in detecting latent left ventricular diastolic dysfunction in β-thalassemia major

Cited by 42 publications

References 25 publications

Iron Overload Cardiomyopathy in Clinical Practice

Iron Overload Cardiomyopathy in Clinical Practice

Periodontal Pathogen Aggregatibacter actinomycetemcomitans Deteriorates Pressure Overload-Induced Myocardial Hypertrophy in Mice

Cardiovascular Function and Treatment in β-Thalassemia Major

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