Brain Natriuretic Peptide is Produced Both by Cardiomyocytes and Cells Infiltrating the Heart in Patients with Severe Heart Failure Supported by a Left Ventricular Assist Device

Bruggink, Annette H.; Jonge, Nicolaas de; Oosterhout, Matthijs F.M. van; Wichen, D.F. van; Koning, Erica de; Lahpor, Jaap R.; Kemperman, Hans; Gmelig-Meyling, F.H.J.; Weger, Roel A. de

doi:10.1016/j.healun.2005.09.007

Cited by 76 publications

(59 citation statements)

References 31 publications

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“…This particular distribution has suggested that natriuretic peptides are probably more of an indicator of established cardiac alterations than a factor in their genesis, possibly elicited by ventricular wall stress and, therefore, not unique to Chagas heart disease or specific for T. cruzi infection (Ribeiro et al 2002). This inference is in keeping with the recent observation that brain natriuretic peptide, a cardiac neurohormone, is produced by cardiomyocytes and cells infiltrating the heart tissue of non-chagasic patients with severe heart failure (Bruggink et al 2006). However, increased plasma concentrations of brain-type natriuretic peptide [produced by the ventricles of the heart in response to volume expansion and pressure overload (Maeda et al 1998)] have been found in a number of non-chagasic cardiovascular diseases, including mildly reduced left ventricular diastolic function (Furumoto et al 2006), pressure-load cardiomyopathy (Vanderheyden et al 2004), and others (Cardarelli andLumicao 2003, Witthaut 2004).…”

Section: Natriuretic Peptides and Chagasic Cardiomyopathysupporting

confidence: 73%

Mechanisms of pathogenesis in Chagas disease

Kierszenbaum

2007

Acta Parasitologica

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Chagas disease, caused by the obligate unicellular parasite Trypanosoma cruzi, presents itself in a diverse collection of clinical manifestations, ranging from severe, fatal heart and digestive tract pathologies to unapparent or minor alterations that do not compromise survival. Over the years, a number of mechanisms have been proposed to explain the pathogenesis of chagasic tissue lesions, all of which have faced some criticism or been received with skepticism. This article excludes the autoimmunity hypothesis for Chagas disease because it has been extensively reviewed elsewhere, and summarizes the various alternative hypotheses that have been advanced over the years. For each of these hypotheses, an outline of its main tenets and key findings that support them is presented. This is followed by the results and comments that have challenged them and the caveats that stand on their way to wider acceptance. It is hoped that this writing will draw attention to our shortcomings in understanding the pathogenesis of Chagas disease, which, unfortunately, continues to figure among the most serious health problems of the American continent.

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Section: Natriuretic Peptides and Chagasic Cardiomyopathysupporting

confidence: 73%

Mechanisms of pathogenesis in Chagas disease

Kierszenbaum

2007

Acta Parasitologica

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“…Along the same line of speculation, perhaps what we have seen is related to some degree of cardiomyocyte regeneration reestablishing its capacity to produce BNP, despite the partial clinical improvement. However, we cannot exclude the possibility of other cellular component regeneration contributing to this fact 35 .…”

Section: Bnp (Pg/ml)mentioning

confidence: 90%

Transplante de células da medula óssea na insuficiência cardíaca chagásica: relato da primeira experiência humana

Vilas-Boas¹,

Feitosa²,

Soares³

et al. 2011

Arq. Bras. Cardiol.

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“…1,2 In addition, pressure and volume unloading of the left ventricle (LV) by LVAD can reverse left ventricular dilatation and leads to regression of left ventricular hypertrophy and neurohormonal changes. [3][4][5][6] The understanding of this process, referred to as 'reverse remodeling,' 7 is important for a better insight into both myocardial events during LVAD support and the processes leading to heart failure. Additionally, several institutions described the possibility of LVAD explantation without the need for HTx (weaning).…”

mentioning

confidence: 99%

“…5,6 Since reverse remodeling not only involves the cardiomyocytes but also the extracellular matrix (ECM), we have focused on the changes in ECM before and after LVAD support. The ECM, which consists of the fibrillar collagens, type I and III collagen, and comprises a basement membrane (BM) surrounding cardiomyocytes, forms a continuum between different cell types within the myocardium and provides a structural supporting network to maintain myocardial geometry.…”

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confidence: 99%

Type IV collagen degradation in the myocardial basement membrane after unloading of the failing heart by a left ventricular assist device

Bruggink

Oosterhout

Jonge

et al. 2007

Laboratory Investigation

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After left ventricular assist device (LVAD) support in patients with end-stage cardiomyopathy, cardiomyocytes decrease in size. We hypothesized that during this process, known as reverse remodeling, the basement membrane (BM), which is closely connected to, and forms the interface between the cardiomyocytes and the extracellular matrix, will be severely affected. Therefore, the changes in the myocardial BM in patients with end-stage heart failure before and after LVAD support were studied. The role of MMP-2 in this process was also investigated. Transmission electron microscopy showed that the BM thickness decreased post-LVAD compared to pre-LVAD. Immunohistochemistry indicated a reduced immunoreactivity for type IV collagen in the BM after LVAD support. Quantitative PCR showed a similar mRNA expression for type IV collagen pre-and post-LVAD. MMP-2 mRNA almost doubled post-LVAD (Po0.01). In addition, active MMP-2 protein as identified by gelatin zymography and confirmed by Western blot analysis was detected after LVAD support and in controls, but not before LVAD support. Active MMP was localized in the BM of the cardiomyocyte, as detected by type IV collagen in situ zymography. Furthermore, in situ hybridization/immunohistochemical double staining showed that MMP-2 mRNA was expressed in cardiomyocytes, macrophages, T-cells and endothelial cells. Taken together, these findings show reduced type IV collagen content in the BM of cardiomyocytes after LVAD support. This reduction is at least in part the result of increased MMP-2 activity and not due to reduced synthesis of type IV collagen. Left ventricular assist devices (LVADs) are commonly used in patients with heart failure as a bridge to heart transplantation (HTx). In most cases, LVAD support extends the patient's lifespan and improves the quality of life. 1,2 In addition, pressure and volume unloading of the left ventricle (LV) by LVAD can reverse left ventricular dilatation and leads to regression of left ventricular hypertrophy and neurohormonal changes. [3][4][5][6] The understanding of this process, referred to as 'reverse remodeling,' 7 is important for a better insight into both myocardial events during LVAD support and the processes leading to heart failure. Additionally, several institutions described the possibility of LVAD explantation without the need for HTx (weaning). 4,[8][9][10][11] This requires a profound knowledge of the process of reverse remodeling.In previous studies with cardiac unloading, we demonstrated partial recovery of the contractile myofilaments in the cardiomyocytes 12 and decreased natriuretic peptide levels both in the plasma of the patients and in the heart. 5,6 Since reverse remodeling not only involves the cardiomyocytes but also the extracellular matrix (ECM), we have focused on the changes in ECM before and after LVAD support. The ECM, which consists of the fibrillar collagens, type I and III collagen, and comprises a basement membrane (BM) surrounding cardiomyocytes, forms a continuum between different cell types within t...

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Brain Natriuretic Peptide is Produced Both by Cardiomyocytes and Cells Infiltrating the Heart in Patients with Severe Heart Failure Supported by a Left Ventricular Assist Device

Cited by 76 publications

References 31 publications

Mechanisms of pathogenesis in Chagas disease

Mechanisms of pathogenesis in Chagas disease

Transplante de células da medula óssea na insuficiência cardíaca chagásica: relato da primeira experiência humana

Type IV collagen degradation in the myocardial basement membrane after unloading of the failing heart by a left ventricular assist device

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