Inflammatory Markers Are Elevated in Eisenmenger Syndrome

Ramakrishnan, Sivasubramanian; Kukreti, Bharat Bhooshan; Salahuddin, Salman; Pendharkar, Amit; Karthikeyan, Ganesan; Bhargava, Balram; Juneja, Rajnish; Seth, Sandeep; Kothari, Shyam Sunder; Saxena, Anitá; Bahl, Vinay K.

doi:10.1007/s00246-013-0715-3

Cited by 7 publications

(4 citation statements)

References 27 publications

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“…They also found that elevated hs-CRP was associated with older age and shorter 6 min walking distance, but the levels of inflammatory markers were not predictive of clinical events (22). Our study showed that serum hs-CRP levels were significantly elevated in children with severe PAH (p<0.01).…”

Section: Pulmonary Arterial Hypertension (Pah) Iscontrasting

confidence: 49%

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Serum Pentraxin 3 and hs-CRP Levels in Children with Severe Pulmonary Hypertension

Karakurt¹,

Başpınar²,

Çelik³

et al. 2014

Balkan Med J

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Pulmonary arterial hypertension (PAH) is defined as a mean pulmonary arterial pressure of >25 mmHg (1). Although there have been developments in diagnostic tools such as echocardiography and treatment modalities, PAH secondary to undiagnosed or untreated congenital heart diseases, especially left-to-right shunt defects, remains an important cause of pulmonary arterial hypertension in childhood. The pathophysiology of PAH is multifactorial, complex and incompletely understood (2-4). PAH secondary left-to-right shunt defects is related to increased pulmonary blood flow leading to endothelial dysfunction, increased pulmonary vascular resistance, vascular remodelling and luminal obstruction due to in situ thrombosis and neointimal and plexiform lesions (5-7). Some recent studies have shown that inflammation has an important role in the pathophysiology of PAH (8). C-reactive protein (CRP) is a classic short pentraxin that is produced in liver secondary to systemic inflammation. Pentraxin 3 is one of the long pentraxins and is synthesized by local vascular cells, such as smooth muscle cells, endothelium and fibroblasts, as well as innate immune cells at sites of inflammation. Pentraxin 3 plays a key role in the regulation of cell proliferation and angiogenesis (9, 10).Background: Pulmonary arterial hypertension secondary to untreated left-to-right shunt defects leads to increased pulmonary blood flow, endothelial dysfunction, increased pulmonary vascular resistance, vascular remodelling, neointimal and plexiform lesions. Some recent studies have shown that inflammation has an important role in the pathophysiology of pulmonary arterial hypertension. Aims: The aim of this study is to evaluate serum pentraxin 3 and high sensitive (hs)-C reactive protein (hs-CRP) levels in children with severe pulmonary arterial hypertension (PAH) secondary to untreated congenital heart defects and evaluate the role of inflammation in pulmonary hypertension. Study Design: Cross sectional study. Methods: After ethics committee approval and receiving consent from parents, there were 31 children were selected for the study with severe PAH, mostly with a left-to-right shunt, who had been assessed by cardiac catheterisation and were taking specific pulmonary vasodilators. The control group consisted of 39 age and gender matched healthy children. After recording data about all the patients including age, gender, weight, haemodynamic studies and vasodilator testing, a physical examination was done for all subjects. Blood was taken from patients and the control group using peripheral veins to analyse serum Pentraxin 3, N-terminal pro-Brain Natriuretic Peptide (NT-ProBNP) and hs-CRP levels. Serum Pentraxin-3 levels were measured by enzyme linked immunosorbent assay (ELISA) and expressed as ng/mL. Serum hs-CRP levels were measured with an immunonephelometric method and expressed as mg/dL. The serum concentration of NT-proBNP was determined by a chemiluminescent immunumetric assay and expressed as pg/mL. Results: Serum Pentraxin-3 levels were determ...

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Section: Pulmonary Arterial Hypertension (Pah) Iscontrasting

confidence: 49%

“…Ramakrishnan et al (22) showed that interferon-ɣ and hs-CRP levels are significantly elevated in Eisenmenger syndrome. They also found that elevated hs-CRP was associated with older age and shorter 6 min walking distance, but the levels of inflammatory markers were not predictive of clinical events (22).…”

Section: Pulmonary Arterial Hypertension (Pah) Ismentioning

confidence: 99%

Serum Pentraxin 3 and hs-CRP Levels in Children with Severe Pulmonary Hypertension

Karakurt¹,

Başpınar²,

Çelik³

et al. 2014

Balkan Med J

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“…Reversal of flow through a septal defect in Eisenmenger syndrome is associated with a systemic proinflammatory response, with increased C-reactive protein (CRP) and Interferon (IFN)-γ levels ( 125 ). Elevation of hsCRP is considered an independent predictor of cardiovascular morbidity and all-cause mortality in patients with CHD ( 126 ).…”

Section: Aging Mechanisms In Congenital Heart Diseasementioning

confidence: 99%

Accelerated Cardiac Aging in Patients With Congenital Heart Disease

Iacobazzi

Alvino

Caputo

et al. 2022

Front. Cardiovasc. Med.

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An increasing number of patients with congenital heart disease (CHD) survive into adulthood but develop long-term complications including heart failure (HF). Cellular senescence, classically defined as stable cell cycle arrest, is implicated in biological processes such as embryogenesis, wound healing, and aging. Senescent cells have a complex senescence-associated secretory phenotype (SASP), involving a range of pro-inflammatory factors with important paracrine and autocrine effects on cell and tissue biology. While senescence has been mainly considered as a cause of diseases in the adulthood, it may be also implicated in some of the poor outcomes seen in patients with complex CHD. We propose that patients with CHD suffer from multiple repeated stress from an early stage of the life, which wear out homeostatic mechanisms and cause premature cardiac aging, with this term referring to the time-related irreversible deterioration of the organ physiological functions and integrity. In this review article, we gathered evidence from the literature indicating that growing up with CHD leads to abnormal inflammatory response, loss of proteostasis, and precocious age in cardiac cells. Novel research on this topic may inspire new therapies preventing HF in adult CHD patients.

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“…In some untreated septal defects or left to right shunts, the pressures in the right heart can become greater than that of the left heart, leading to the reversal of flow, known as Eisenmenger syndrome. This also creates a systemic pro-inflammatory response, with increased C-reactive protein (CRP) and Interferon (IFN)-γ levels ( 29 ). Furthermore, in children with coarctation of the aorta, increased inflammatory and apoptotic mediators, including Interleukin (IL)-6, IL-10, TNF-α, and soluble Fas (sFas), may contribute to vascular disease as these children age ( 30 ).…”

Section: Clinical Immunologic Implications Of Chdsmentioning

confidence: 99%

Congenital Heart Disease: An Immunological Perspective

Singampalli

Jui

Shani

et al. 2021

Front. Cardiovasc. Med.

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Congenital heart disease (CHD) poses a significant global health and economic burden—despite advances in treating CHD reducing the mortality risk, globally CHD accounts for approximately 300,000 deaths yearly. Children with CHD experience both acute and chronic cardiac complications, and though treatment options have improved, some remain extremely invasive. A challenge in addressing these morbidity and mortality risks is that little is known regarding the cause of many CHDs and current evidence suggests a multifactorial etiology. Some studies implicate an immune contribution to CHD development; however, the role of the immune system is not well-understood. Defining the role of the immune and inflammatory responses in CHD therefore holds promise in elucidating mechanisms underlying these disorders and improving upon current diagnostic and treatment options. In this review, we address the current knowledge coinciding CHDs with immune and inflammatory associations, emphasizing conditions where this understanding would provide clinical benefit, and challenges in studying these mechanisms.

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Inflammatory Markers Are Elevated in Eisenmenger Syndrome

Cited by 7 publications

References 27 publications

Serum Pentraxin 3 and hs-CRP Levels in Children with Severe Pulmonary Hypertension

Serum Pentraxin 3 and hs-CRP Levels in Children with Severe Pulmonary Hypertension

Accelerated Cardiac Aging in Patients With Congenital Heart Disease

Congenital Heart Disease: An Immunological Perspective

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