Publications by authors named "Gorica Ristic"

12 Publications

  • Page 1 of 1

H FPEF score predicts atherosclerosis presence in patients with systemic connective tissue disease.

Clin Cardiol 2021 Jul 2;44(7):946-954. Epub 2021 Jun 2.

School of Medicine, University of Belgrade, Belgrade, Serbia.

Background: Cardiovascular diseases are common cause of morbidity and mortality in patients with systemic connective tissue diseases (SCTD) due to accelerated atherosclerosis which couldn't be explained by traditional risk factors (CVDRF).

Hypothesis: We hypothesized that recently developed score predicting probability of heart failure with preserved ejection fraction (H FPEF), as well as a measure of right ventricular-pulmonary vasculature coupling [tricuspid annular plane systolic excursion (TAPSE)/pulmonary artery systolic pressure (PASP) ratio], are predictive of atherosclerosis in SCTD.

Methods: 203 patients (178 females) diagnosed with SCTD underwent standard and stress-echocardiography (SE) with TAPSE/PASP and left ventricular (LV) diastolic filling pressure (E/e') measurements, carotid ultrasound and computed tomographic coronary angiography. Patients who were SE positive for ischemia underwent coronary angiography (34/203). The H FPEF score was calculated according to age, body mass index, presence of atrial fibrillation, ≥2 antihypertensives, E/e' and PASP.

Results: Mean LV ejection fraction was 66.3 ± 7.1%. Atherosclerosis was present in 150/203 patients according to: 1) intima-media thickness>0.9 mm; and 2) Agatstone score > 300 or Syntax score ≥ 1. On binary logistic regression analysis, including CVDRF prevalence, echocardiographic parameters and H FPEF score, only H FPEF score remained significant for the prediction of atherosclerosis presence (χ = 19.3, HR 2.6, CI 1.5-4.3, p < 0.001), and resting TAPSE/PASP for the prediction of a SE positive for ischemia (χ = 10.4, HR 0.01, CI = 0.01-0.22, p = 0.004). On ROC analysis, the optimal threshold value for identifying patients with atherosclerosis was a H FPEF score ≥2 (Sn 60.4%, Sp 69.4%, area 0.67, SE = 0.05, p < 0.001).

Conclusions: H FPEF score and resting TAPSE/PASP demonstrated clinical value for an atherosclerosis diagnosis in patients diagnosed with SCTD.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/clc.23621DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8259163PMC
July 2021

Impact of disease activity on impaired glucose metabolism in patients with rheumatoid arthritis.

Arthritis Res Ther 2021 03 26;23(1):95. Epub 2021 Mar 26.

Department of Rheumatology and Clinical Immunology of the Military Medical Academy and Medical Faculty of the Military Medical Academy, University of Defense in Belgrade, Crnotravska 17, Belgrade, 11000, Serbia.

Objective: To explore glucose metabolism in rheumatoid arthritis (RA) and its association with insulin resistance (IR) risk factors and disease activity indicators, including matrix metalloproteinase-3 (MMP3).

Methods: This single-center study included 127 non-diabetic subjects: 90 RA patients and 37 matched controls. IR-related risk factors, disease activity (DAS28-ESR/CRP), concentrations of inflammation markers, MMP3, glucose, specific insulin, and C-peptide (a marker of β-cell secretion) were determined. Homeostasis Model Assessment was used to establish insulin resistance (HOMA2-IR) and sensitivity (HOMA2-%S). Associations of HOMA2 indices with IR-related risk factors, inflammation markers, and RA activity were tested using multiple regression analyses.

Results: RA patients had significantly increased HOMA2-IR index than controls. In the RA group, multivariate analysis revealed DAS28-ESR, DAS28-CRP, tender joint counts, patient's global assessment, and MMP3 level as significant positive predictors for HOMA2-IR (β = 0.206, P = 0.014; β = 0.192, P = 0.009; β = 0.121, P = 0.005; β = 0.148, P = 0.007; β = 0.075, P = 0.025, respectively), and reciprocal negative for HOMA2-%S index. According to the value of the coefficient of determination (R), DAS28-ESR ≥ 5.1 has the largest proportion of variation in both HOMA2-IR indices. DAS28-ESR ≥ 5.1 and ESR were independent predictors for increased C-peptide concentration (β = 0.090, P = 0.022; β = 0.133, P = 0.022). Despite comparability regarding all IR-related risk factors, patients with DAS28-ESR ≥ 5.1 had higher HOMA2-IR than controls [1.7 (1.2-2.5) vs. 1.2 (0.8-1.4), P = 0.000]. There was no difference between patients with DAS28-ESR < 5.1 and controls [1.3 (0.9-1.9) vs. 1.2 (0.8-1.4), P = 0.375].

Conclusions: RA activity is an independent risk factor for impaired glucose metabolism. DAS28-ESR ≥ 5.1 was the main contributor to this metabolic disturbance, followed by MMP3 concentration, outweighing the impact of classic IR-related risk factors.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s13075-021-02476-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7995801PMC
March 2021

Toxicity and aggregation of the polyglutamine disease protein, ataxin-3 is regulated by its binding to VCP/p97 in Drosophila melanogaster.

Neurobiol Dis 2018 08 26;116:78-92. Epub 2018 Apr 26.

Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI, USA; Department of Neurology, Wayne State University School of Medicine, Detroit, MI, USA. Electronic address:

Among the nine dominantly inherited, age-dependent neurodegenerative diseases caused by abnormal expansion in the polyglutamine (polyQ) repeat of otherwise unrelated proteins is Spinocerebellar Ataxia Type 3 (SCA3). SCA3 is caused by polyQ expansion in the deubiquitinase (DUB), ataxin-3. Molecular sequelae related to SCA3 remain unclear. Here, we sought to understand the role of protein context in SCA3 by focusing on the interaction between this DUB and Valosin-Containing Protein (VCP). VCP is bound directly by ataxin-3 through an arginine-rich area preceding the polyQ repeat. We examined the importance of this interaction in ataxin-3-dependent degeneration in Drosophila melanogaster. Our assays with new isogenic fly lines expressing pathogenic ataxin-3 with an intact or mutated VCP-binding site show that disrupting the ataxin-3-VCP interaction delays the aggregation of the toxic protein in vivo. Importantly, early on flies that express pathogenic ataxin-3 with a mutated VCP-binding site are indistinguishable from flies that do not express any SCA3 protein. Also, reducing levels of VCP through RNA-interference has a similar, protective effect to mutating the VCP-binding site of pathogenic ataxin-3. Based on in vivo pulse-chases, aggregated species of ataxin-3 are highly stable, in a manner independent of VCP-binding. Collectively, our results highlight an important role for the ataxin-3-VCP interaction in SCA3, based on a model that posits a seeding effect from VCP on pathogenic ataxin-3 aggregation and subsequent toxicity.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.nbd.2018.04.013DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7721245PMC
August 2018

Bone scintigraphy can diagnose osteoporotic vertebral compression fractures better than conventional radiography.

Hell J Nucl Med 2017 Sep-Dec;20 Suppl:155

Institute of Nuclear Medicine, Military Medical Academy, Faculty of Medicine of the Military Medical Academy, University of Defense, 11000 Belgrade, Serbia.

Objective: Most difficult and very frequent complications of osteoporosis are vertebral compression fractures (VCF). Bone scintigraphy with Tc-phosphonates enables early detection of vertebral compression fractures in the first 72 hours of occuring. Typical scintigraphic findings is markedly increased radiotracer uptake in the linear pattern, throughout collapsed vertebral body. Bone scintigraphy is usefull in follow-up of vertebral fractures healing, showing reduction of radiotracer uptake in fractured vertebrae. In patients with osteoporosis and suspition of VCF, we detected compression vertebral fracture by bone scintigraphy and compare it with conventional radiography findings.

Patients And Method: Bone scintigraphy was done in 40 patients with osteoporosis and suspition of compression vertebral fractures, 32 women and 8 men, mean age, 71 years. Three hours after iv. injection of 740MBq of Tc-DPD to the patients, a whole body scintigraphy was done. Standard radiographic views AP, lateral, and oblique were done in all patients.

Results: Radiography findings were positive for vertebral compression fracture in 28 patients (70%), and with bone scintigraphy in 36 patients (90%). In one patient with healed-old vertebral fracture, with positive radiographic finding, scintigraphic finding was negative. Bone scintigraphy incidentally diagnosed bone metastases in 3 patients.

Conclusion: Bone scintigraphy has a very high sensitivity for detection of vertebral compression fractures in osteoporotic patients. Conventional radiography showed a much lower sensitivity and could not differentiate acute from old vertebral compression fractures.
View Article and Find Full Text PDF

Download full-text PDF

Source
June 2019

USP5 Is Dispensable for Monoubiquitin Maintenance in Drosophila.

J Biol Chem 2016 Apr 25;291(17):9161-72. Epub 2016 Feb 25.

From the Departments of Pharmacology and Neurology, Wayne State University School of Medicine, Detroit, Michigan 48201 and

Ubiquitination is a post-translational modification that regulates most cellular pathways and processes, including degradation of proteins by the proteasome. Substrate ubiquitination is controlled at various stages, including through its reversal by deubiquitinases (DUBs). A critical outcome of this process is the recycling of monoubiquitin. One DUB whose function has been proposed to include monoubiquitin recycling is USP5. Here, we investigated whether Drosophila USP5 is important for maintaining monoubiquitin in vivo We found that the fruit fly orthologue of USP5 has catalytic preferences similar to its human counterpart and that this DUB is necessary during fly development. Our biochemical and genetic experiments indicate that reduction of USP5 does not lead to monoubiquitin depletion in developing flies. Also, introduction of exogenous ubiquitin does not suppress developmental lethality caused by loss of endogenous USP5. Our work indicates that a primary physiological role of USP5 is not to recycle monoubiquitin for reutilization, but that it may involve disassembly of conjugated ubiquitin to maintain proteasome function.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1074/jbc.M115.703504DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4861482PMC
April 2016

Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis and Low Cardiovascular Risk: The Role of von Willebrand Factor Activity.

PLoS One 2015 6;10(8):e0130462. Epub 2015 Aug 6.

Department of Rheumatology and Clinical Immunology, Military Medical Academy and Medical Faculty of the Belgrade Defence University, Belgrade, Serbia.

Background: To evaluate association between von Willebrand factor (vWF) activity, inflammation markers, disease activity, and subclinical atherosclerosis in patients with rheumatoid arthritis (RA) and low cardiovascular risk.

Methods: Above mentioned parameters were determined in blood samples of 74 non-diabetic, normotensive, female subjects, with no dyslipidemia(42 patients, 32 matched healthy controls, age 45.3±10.0 vs. 45.2±9.8 years). Intima-media thickness (IMT) was measured bilaterally, at common carotid, bifurcation, and internal carotid arteries. Subclinical atherosclerosis was defined as IMT>IMTmean+2SD in controlsat each carotid level and atherosclerotic plaque as IMT>1.5 mm. Majority of RA patients were on methotrexate (83.3%), none on steroids >10 mg/day or biologic drugs. All findings were analysed in the entire study population and in RA group separately.

Results: RA patients with subclinical atherosclerosis had higher vWF activity than those without (133.5±69.3% vs. 95.3±36.8%, p<0.05). Predictive value of vWF activity for subclinical atherosclerosis was confirmed by logistic regression. vWF activity correlated significantly with erythrocyte sedimentation rate, fibrinogen, modified disease activity scores (mDAS28-ESR, mDAS28-CRP), modified Health Assessment Questionnaire (p<0.01 for all), duration of smoking, number of cigarettes/day, rheumatoid factor concentration (p<0.05 for all), and anti-CCP antibodies (p<0.01). In the entire study population, vWF activity was higher in participants with subclinical atherosclerosis (130±68% vs. 97±38%, p<0.05) or atherosclerotic plaques (123±57% vs. 99±45%, p<0.05) than in those without. Duration of smoking was significantly associated with vWF activity (β 0.026, p = 0.039).

Conclusions: We demonstrated association of vWF activity and subclinical atherosclerosis in low-risk RA patients as well as its correlation with inflammation markers, all parameters of disease activity, and seropositivity. Therefore, vWF might be a valuable marker of early atherosclerosis in RA patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0130462PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4527675PMC
May 2016

An optimal ubiquitin-proteasome pathway in the nervous system: the role of deubiquitinating enzymes.

Front Mol Neurosci 2014 19;7:72. Epub 2014 Aug 19.

Department of Pharmacology, Wayne State University School of Medicine Detroit, MI, USA ; Department of Neurology, Wayne State University School of Medicine Detroit, MI, USA.

The Ubiquitin-Proteasome Pathway (UPP), which is critical for normal function in the nervous system and is implicated in various neurological diseases, requires the small modifier protein ubiquitin to accomplish its duty of selectively degrading short-lived, abnormal or misfolded proteins. Over the past decade, a large class of proteases collectively known as deubiquitinating enzymes (DUBs) has increasingly gained attention in all manners related to ubiquitin. By cleaving ubiquitin from another protein, DUBs ensure that the UPP functions properly. DUBs accomplish this task by processing newly translated ubiquitin so that it can be used for conjugation to substrate proteins, by regulating the "where, when, and why" of UPP substrate ubiquitination and subsequent degradation, and by recycling ubiquitin for re-use by the UPP. Because of the reliance of the UPP on DUB activities, it is not surprising that these proteases play important roles in the normal activities of the nervous system and in neurodegenerative diseases. In this review, we summarize recent advances in understanding the functions of DUBs in the nervous system. We focus on their role in the UPP, and make the argument that understanding the UPP from the perspective of DUBs can yield new insight into diseases that result from anomalous intra-cellular processes or inter-cellular networks. Lastly, we discuss the relevance of DUBs as therapeutic options for disorders of the nervous system.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fnmol.2014.00072DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4137239PMC
September 2014

Ubiquitin-binding site 2 of ataxin-3 prevents its proteasomal degradation by interacting with Rad23.

Nat Commun 2014 Aug 21;5:4638. Epub 2014 Aug 21.

1] Department of Pharmacology, Wayne State University School of Medicine, 540 E Canfield, Scott Hall Room 3108, Detroit, Michigan 48201, USA [2] Department of Neurology, Wayne State University School of Medicine, 540 E Canfield, Scott Hall Room 3108, Detroit, Michigan 48201, USA [3] Cancer Biology Program, Wayne State University School of Medicine, 540 E Canfield, Scott Hall Room 3108, Detroit, Michigan 48201, USA.

Polyglutamine repeat expansion in ataxin-3 causes neurodegeneration in the most common dominant ataxia, spinocerebellar ataxia type 3 (SCA3). Since reducing levels of disease proteins improves pathology in animals, we investigated how ataxin-3 is degraded. Here we show that, unlike most proteins, ataxin-3 turnover does not require its ubiquitination, but is regulated by ubiquitin-binding site 2 (UbS2) on its N terminus. Mutating UbS2 decreases ataxin-3 protein levels in cultured mammalian cells and in Drosophila melanogaster by increasing its proteasomal turnover. Ataxin-3 interacts with the proteasome-associated proteins Rad23A/B through UbS2. Knockdown of Rad23 in cultured cells and in Drosophila results in lower levels of ataxin-3 protein. Importantly, reducing Rad23 suppresses ataxin-3-dependent degeneration in flies. We present a mechanism for ubiquitination-independent degradation that is impeded by protein interactions with proteasome-associated factors. We conclude that UbS2 is a potential target through which to enhance ataxin-3 degradation for SCA3 therapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/ncomms5638DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237202PMC
August 2014

Using membrane-targeted green fluorescent protein to monitor neurotoxic protein-dependent degeneration of Drosophila eyes.

J Neurosci Res 2014 Sep 2;92(9):1100-9. Epub 2014 May 2.

Graduate Program in Cancer Biology, Wayne State University School of Medicine, Detroit, Michigan; Department of Pharmacology, Wayne State University School of Medicine, Detroit, Michigan.

Age-related neurodegeneration has been studied extensively through the use of model organisms, including the genetically versatile Drosophila melanogaster. Various neurotoxic proteins have been expressed in fly eyes to approximate degeneration occurring in humans, and much has been learned from this heterologous system. Although Drosophila expedites scientific research through rapid generational times and relative inexpensiveness, one factor that can hinder analyses is the examination of milder forms of degeneration caused by some toxic proteins in fly eyes. Whereas several disease proteins cause massive degeneration that is easily observed by examining the external structure of the fly eye, others cause mild degeneration that is difficult to observe externally and requires laborious histological preparation to assess and monitor. Here, we describe a sensitive fluorescence-based method to observe, monitor, and quantify mild Drosophila eye degeneration caused by various proteins, including the polyglutamine disease proteins ataxin-3 (spinocerebellar ataxia type 3) and huntingtin (Huntington's disease), mutant α-synuclein (Parkinson's disease), and Aβ42 (Alzheimer's disease). We show that membrane-targeted green fluorescent protein reports degeneration robustly and quantitatively. This simple yet powerful technique, which is amenable to large-scale screens, can help accelerate studies to understand age-related degeneration and to find factors that suppress it for therapeutic purposes.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jnr.23395DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4144675PMC
September 2014

Rheumatoid arthritis is an independent risk factor for increased carotid intima-media thickness: impact of anti-inflammatory treatment.

Rheumatology (Oxford) 2010 Jun 5;49(6):1076-81. Epub 2010 Mar 5.

Department of Rheumatology and Clinical Immunology, Military Medical Academy, Crnotravska 17, 11000 Belgrade, Serbia.

Objectives: To evaluate the extent of subclinical atherosclerosis in patients with RA and low cardiovascular risk by measuring intima-media thickness (IMT) of the carotid arteries and to determine factors associated with increased IMT.

Methods: IMT was measured by ultrasonography in 42 non-diabetic, normotensive, female RA patients and 32 matched healthy controls [age 45.3 (10.0) vs 45.2 (9.8) years] at common carotid arteries (CCAs), carotid bifurcation (BF) and internal carotid arteries (ICAs), bilaterally. Mean and maximal (max) IMTs were calculated from three measurements at each site. Clinical work-up included laboratory analyses, determination of the disease activity and evaluation of treatment.

Results: RA patients had increased IMT (mm) in comparison with controls [CCA(max): 0.764 (0.148) vs 0.703 (0.100); CCA(mean): 0.671 (0.119) vs 0.621 (0.085); BF(max): 1.055 (0.184) vs 0.941 (0.161); BF(mean): 0.889 (0.168) vs 0.804 (0.124); ICA(max): 0.683 (0.108) vs 0.613 (0.093); ICA(mean): 0.577 (0.101) vs 0.535 (0.076)]. Parameters associated with IMT in RA patients were (correlation at x/6 measurement sites): age (6/6), BMI (2/6), smoking (2/6), RF concentration (2/6), sedimentation rate (1/6) and duration of MTX + chloroquine therapy (4/6; inverse correlation). Multivariate regression analysis revealed that RA is an independent risk factor for increased IMT. Factors correlating with IMT in the controls were: age (6/6), BMI (3/6), total cholesterol (5/6), low-density lipoprotein cholesterol (3/6), total/high-density lipoprotein cholesterol (2/6), triglycerides (1/6) and glycaemia (4/6).

Conclusion: Despite a favourable risk profile, our female RA patients had significantly enlarged carotid IMT than controls. RA itself was an independent risk factor for increased IMT. Impact of chronic inflammation on atherosclerosis was confirmed by negative correlation of IMT and duration of anti-inflammatory treatment.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1093/rheumatology/kep456DOI Listing
June 2010

Low bone mineral density and high bone metabolism turnover in premenopausal women with unipolar depression.

Bone 2008 Mar 4;42(3):582-90. Epub 2007 Dec 4.

Clinic of Rheumatology, Military Medical Academy, Crnotravska 17, Belgrade, Serbia.

Introduction And Hypothesis: The majority of studies reporting decreased bone mineral density (BMD) in patients with unipolar depression neglected sex and age differences and menopause as the most important risk factor for osteoporosis. We presumed that physically healthy premenopausal women with unipolar depression have decreased BMD and altered bone cell metabolism.

Methods: BMD at lumbar spine and femoral neck by dual X-ray absorptiometry, bone alkaline phosphatase sera activity, 5b-tartarate resistant acid phosphatase sera activity and urine N-terminal telopeptide were measured in 73 premenopausal women with unipolar depression and compared with 47 healthy, age- and osteoporosis risk factors-matched premenopausal women. The duration and severity of depression, hormonal status (cortisol, prolactin, parathormone, oestradiol), antidepressive treatment, and physical activity through whole and modified QUALEFFO-41 questionnaire were evaluated. The results were statistically elaborated by the chi-square test, Student's t-test for independent samples, one-way analysis of variance - ANOVA, one-sample Kolmogorov-Smirnov test. Correlations were assessed by means of Pearson's coefficient.

Results: Patients with unipolar depression had significantly lower BMD, the decrease of which correlated only with the duration of depression. High bone metabolism turnover was found with a predomination of osteoresorption which, but not osteosynthesis, correlated with the severity of depression, estimated through Hamilton depression scores. Despite higher but not significant levels of cortisol in women with unipolar depression, the BMD decrease and high bone turnover seem not to be the consequence of hormonal changes or medical treatment. The significant correlations between physical activity and osteoresorption markers were found indicating possible underlying mechanism.

Conclusions: Premenopausal women with unipolar depression have significantly lower BMD because of stimulated bone cell metabolism with predomination of osteoresorption process, mostly due to decreased physical activity in depression. These women should be investigated for osteoporosis and the multidisciplinary team approach is advocated.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bone.2007.11.010DOI Listing
March 2008

Pericardial disease in pregnancy.

Herz 2003 May;28(3):209-15

University Institute for Cardiovascular Disease, Clinical Center of Serbia, Belgrade, Serbia and Montenegro.

Background: There is no evidence that pregnancy affects susceptibility to pericardial disease. However, when such a condition occurs, its proper diagnosis and management may be crucial for the outcome of the pregnancy.

Incidence And Diagnosis: Hydropericardium is the most frequent form of pericardial involvement in pregnancy. It is typically a small, clinically silent pericardial effusion present in the third trimester in approximately 40% of healthy pregnant women. Small amounts of fetal pericardial fluid (< 2 mm in echocardiography, in diastole) can be detected after 20 weeks of gestation. Larger effusions should raise clinical concern for hydrops fetalis, Rh disease, hypoalbuminemia, and infectious or autoimmune disorder. Wide varieties of etiologic forms of pericardial diseases occur sporadically in pregnant women. Significant symptoms, electrocardiographic changes, or physiologic impairment warrant hospitalization.

Treatment: Most pericardial disorders are managed during pregnancy as in nonpregnant patients (i.e., nonsteroidal antiinflammatory drugs for acute, antibiotics and drainage for purulent pericarditis, and corticosteroids for systemic autoimmune disorders). However, colchicine is contraindicated in pregnancy, and pericardiocentesis should be performed only for very large effusions causing clinical signs of cardiac tamponade or if presence of suppurative, tuberculous or neoplastic pericardial effusion is suspected. Echocardiographic guidance of pericardiocentesis is preferred to fluoroscopic guidance in order to avoid fetal X-ray exposure. Pericardiectomy should be reserved for significant pericardial constriction and resistant bacterial infections. Delivery of normal infants in term after pericardiocentesis or pericardiectomy is expected, whenever natural history of causative disease allows. Pericardiectomy itself is not a contraindication for subsequent successful pregnancies.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00059-003-2470-3DOI Listing
May 2003
-->