The second in a six-part series that looks at different ‘objects’ in art and how artists explored their subject matter as a stimulus for providing practical early years activities - this month we focus on ‘animals in art’.

AIMS:With improved survival of patients with congenital and inherited heart disease, there is now a younger cohort of patients with an implantable cardioverter defibrillator (ICD) for the prevention and treatment of ventricular dysrrhythmias. Young women with such disorders often wish to embark on pregnancy, but pregnancy outcome data for this group is sparse. We therefore evaluated pregnancy outcome in patients with heart disease and an ICD in situ.METHODS AND RESULTS:A retrospective analysis was performed on all women with an ICD in situ, who had pregnancy care provided by the specialist maternal cardiology service at University College London Hospitals. Data for 19 pregnancies in 14 women were collected. The underlying cardiac diagnoses were congenital heart disease (one), familial hypertrophic cardiomyopathy (eight), familial dilated cardiomyopathy (one), inherited long QT syndrome (one), and idiopathic cardiac arrest (one). Three women had moderate impairment of the left ventricular systolic function (ejection fraction <45%), in the remainder it was normal. Nine ICD implants were for primary prevention of sudden cardiac death (64%) and five for secondary prevention (36%). Of the 19 pregnancies, 18 continued beyond 24 weeks gestation with 18 live births. In eight pregnancies there were medical or device-related complications (42.9%) as follows: arrhythmias (four) (21.1%), heart failure (two) (9.1%), ICD shocks (one) (5.3%), atrial lead fracture (one) (5.3%), and lead-related thrombus (one) (5.3%). There were no inappropriate device shocks or therapies.CONCLUSIONS:Women with heart disease and an ICD implant can have a good outcome during pregnancy but medical and device complications are not uncommon.

Heart disease has been the overall leading cause of maternal death in the UK for the last six years of reporting. It is particularly concerning that half of those who died in the last three-year period had received substandard care. This article aims to provide readers with a broad overview of the haemodynamic changes of pregnancy and an awareness of the issues women with various cardiac conditions face in pregnancy. The early identification of women at risk is important to optimize the chances of a successful pregnancy. Preconception counselling and contraceptive advice should be offered to encourage informed decision-making and planned pregnancies. Follow-up during pregnancy should be tailored to the degree of assessed risk. There is very little evidence on which to base practice. Practitioners are therefore reliant on clinical experience, small case series and expert consensus. Management of women with pre-existing or acquired heart disease should therefore have input from a consultant with an interest in maternal cardiology and an expert multidisciplinary team.

Heart disease has been the overall leading cause of maternal death in the UK for the last 6 years of reporting. It is particularly concerning that half of those who died in the last 3-year period had received substandard care (Cantwell et al. 2011). This article aims to provide readers with a broad overview of the haemodynamic changes of pregnancy and the issues women with various cardiac conditions face in pregnancy. Midwives are at the forefront of antenatal and perinatal care, and in a unique position to facilitate the early identification of high-risk pregnancies. Follow-up during pregnancy should be tailored according to the degree of assessed risk. Management of women with pre-existing or acquired heart disease should therefore have input from a consultant with an interest in maternal cardiology and an expert high-risk multi-professional team.

AIMS:To determine pregnancy outcome and risk factors for adverse events in women with congenital heart disease (CHD) and residual haemodynamic right ventricular (RV) outflow tract (RVOT) lesions.METHODS AND RESULTS:Pregnancy outcome data for women with CHD and residual RVOT lesions have been recorded since 2001. There were 76 pregnancies in 47 women that continued beyond 24 weeks gestation. At conception 20% had RVOT obstruction, 32% had pulmonary regurgitation (PR) and 49% had mixed RVOT obstruction and PR. Moderate-to-severe PR was present in 30 (39%) and RVOT obstruction > or =30 mmHg in 12 (16%) of pregnancies. Seven pregnancies (9%) were complicated by right heart failure (RHF). No arrhythmias were documented. Predictors for RHF were moderate-to-severe PR in combination with at least one additional risk factor (twin pregnancy, branch pulmonary artery stenosis, RV systolic dysfunction, RV hypertrophy). All patients responded to diuretic treatment and had a good pregnancy outcome without foetal complications.CONCLUSION:In patients with CHD and residual RVOT lesions, the outcome of pregnancy is good. Patients with moderate-to-severe PR were at risk for symptomatic RHF only if additional risk factors were present. When treated by a multidisciplinary team, maternal and foetal outcome was good. The general recommendation that pulmonary valve replacement should be undertaken prior to pregnancy in patients with moderate-to-severe PR and RV dilatation needs to be reconsidered.

The use of standard dose low molecular weight heparin (LMWH) to anticoagulate women with mechanical valves in pregnancy is associated with morbidity and mortality. We conducted a prospective audit of the use of adjusted dose high intensity LMWH in 12 pregnancies in 11 women with prosthetic heart valves. LMWH low-dose aspirin was started at therapeutic-dose with monitoring of anti-Xa levels to achieve a target level of 1.0-1.2 IU/mL (0.8-1.2 in the first 3/12 pregnancies). This necessitated a mean increase in the dose of LMWH of 54.4% (SD +/- 33.2) over initial dose. Eleven of 12 pregnancies resulted in live births, with one intrauterine fetal death at 37 weeks. One nonfatal valve thrombosis occurred at 26 weeks gestation associated with subtherapeutic anti-Xa levels. Three patients experienced major bleeding. This regime provides a therapeutic option for women with mechanical heart valves during pregnancy, provided anti-Xa levels are kept within the target range. These patients require close surveillance for bleeding and thrombotic complications within a multidisciplinary setting.

Effective anticoagulation for women with mechanical heart valves during pregnancy remains a major challenge. The use of standard dosage low molecular weight heparin (LMWH) is associated with an unacceptable incidence of morbidity and mortality for this patient group. In this prospective audit of anticoagulation management, we report pregnancy outcome for a cohort of women with mechanical heart valves, who received anticoagulation with a higher dosage LMWH regimen. We audited 12 consecutive pregnancies in 10 women (mean age 27.8 (18–41) years) with mechanical heart valves (mitral 4, aortic 2, aortic and mitral 2, systemic tricuspid AV valve 2). Past obstetric history (on warfarin) included 6 fetal losses: 2 miscarriages <12 weeks and 4 terminations including one therapeutic at 22 weeks gestation because of an intracerebral fetal haemorrhage. In 11/12 pregnancies treated with LMWH, warfarin was discontinued at <6 weeks and in 1/12 at 8 weeks. LMWH (dalteparin 7, enoxaparin 5) +/− low-dose aspirin (4) was then started at full therapeutic dosage (subcutaneous 12 hourly) with regular monitoring to maintain anti-Xa levels at 1.0–1.2U/mL (0.8–1.2 in the first 4/12 pregnancies). This necessitated stepwise increases in LMWH with median doses (12 hourly) pre-delivery 11,750IU for dalteparin and 95mg for enoxaparin, representing a median 47.7% increase over initial dosage. 11/12 pregnancies on LMWH resulted in live births (median BW 2.5 kg (range 1.0–3.7) at median gestation 36 (range 26–38 weeks) with 1 IUFD at 37 weeks. One patient had non-fatal valve-related thrombosis at 26 weeks associated with a sub-therapeutic anti-Xa level (0.64 U/ml). Of note, she had a past history of pulmonary embolism and was heterozygous for the G20210A prothrombin gene mutation. There were no other valve-related thrombotic events. Minor bleeding occurred during 3 pregnancies. There were 5 major bleeding episodes in 4 patients: 3 antepartum (1 with placenta praevia) and 1 post-partum haemorrhage plus 1 abdominal wound haematoma. Our data suggest that in this patient group escalated dose LMWH provides effective anticoagulation. These patients require meticulous anticoagulant monitoring and close surveillance for bleeding and thrombotic complications within a multidisciplinary setting, with urgent intervention when indicated.

In the present study, the complete sequences of the Ig H and L chain variable region genes of twelve RF+ B cell lines from two patients with RA were analyzed. Seven of the RF-producing B cells used VH3 family genes, four used VH4 genes, and one a VH1 gene. All but two of the cell lines expressing VH3 genes utilized different family members; among the VH4-expressing cells, a more restricted pattern was noted. V kappa gene use was restricted to the V kappa I and III families; V lambda gene use was more diverse, involving five different families. Computer comparisons of the expressed VH genes with their presumed germline progenitors indicated significant differences in every instance; eight of the corresponding VL genes also were significantly different. In many cases, assignment of the germline D segment(s) incorporated into the rearranged VH genes was impossible. These differences from the germline gene segments indicated the extensive changes induced by rearrangement, enzymatic activities, and somatic mutation. In hopes of defining a structural reason for the disparate antigen specificities of these cells, the CDR3 amino acid sequences of the multi- vs. the mono-reactive RF-producers were compared. Although CDR3 length was not appreciably different between these two sets of mAb, a greater than two-fold increase in charged amino acids was found in the H chain CDR3 of the multireactive RF. This relationship did not exist for the L chain CDR3. Thus, these sequence data indicate the use of a broad base of Ig V gene segments that have undergone extensive diversification. Based on the localization of R substitutions in the CDR of most of the V genes studied, the diversification appears to be antigen driven and selected. The significance of these findings for the evolution of these B cell clones into isotype-switched producers that are heterogeneous for antigen specificity (mono- vs. multi-reactivity) is discussed.

A large battery of anti-CD23 mAb were compared for their epitope specificities and for their abilities to alter both IgE binding to cell-associated CD23 and IgE production in vitro in response to three sets of stimulants. The nine mAb tested can be divided into four families which define four antigenic epitopes (A-D) of CD23. Of these four families, two bind antigenic sites, (A and D) that appear to lie outside the IgE ligand binding site and two bind sites (B and C) that appear to be located within or close to this site, as determined by the abilities of appropriate mAb to alter IgE binding to CD23. The effects that these mAb had on IgE secretion by normal peripheral blood mononuclear cells (PBMNC) varied depending on the stimulant employed to induce IgE production. Interactions with epitope A, which was found to lie outside the ligand binding site and to be made more accessible by binding of mAb to other epitopes, had different effects on IgE production than interactions with the other epitopes. Indeed, mAb binding to this epitope lead to as much as a 10 fold enhancement in IgE biosynthesis induced by IL-4 alone or by IL-4 + hydrocortisone whereas interactions at the other sites resulted in almost complete inhibition of IgE production. In addition, mAb reactive with epitopes B and C had minimal effects on IgE production induced by IL-4 + anti-CD40 mAb whereas interactions at epitope A consistently enhanced IgE production. Finally, no apparent direct correlation was found between the ability of individual anti-CD23 mAb to alter IgE binding to cell-associated CD23 and their ability to modulate IgE production by PBMNC. These studies suggest that IgE binding to cell-associated CD23 does not have a major role in the de novo synthesis of IgE that involves CD23 interactions. In addition, the different effects that binding to epitope A vs B or C have on IgE synthesis suggest that molecular interactions between distinct portions of the CD23 molecule and other cell surface molecules expressed on the same B cell or adjacent communicating cells may lead to divergent cellular effects on IgE production. Finally these studies imply that only epitope A is involved in the generation of an IgE response through the CD40 pathway.

In an effort to study disease-related autoantibodies in rheumatoid arthritis (RA), rheumatoid factor (RF)-producing B cell lines were developed from the heterogeneous B cell populations infiltrating the synovial tissue of patients with arthritis. Over 125 EBV-transformed B cell cultures were derived from three patients: one with early pre-erosive RA, one with advanced RA, and one with osteoarthritis (OA). IgM, IgG, and IgA RF-producing B cell lines were found in all three series but with several significant differences. In each of the two RA patients, 22% of the Ig-producing cell lines secreted RF compared to 7% in the OA patient. The isotypes of these RF were mostly IgM in the early RA (62%) and the OA patient (60%) as contrasted to predominantly IgA (75%) and, to a lesser extent, IgG (12.5%) in the advanced RA patient. Analyses of the light (L) chain composition of these RF revealed that 82% of the IgM RF used kappa L chains whereas only 31% of the non-IgM RF used kappa chains. Antigen-binding analyses of these RF revealed that all the synovial tissue-derived RF from the advanced RA patient exhibited antigen binding specificities restricted to a narrow range of gamma globulins. In contrast, the synovial RF of the other two patients were either reactive with a broader spectrum of gamma globulins or reactive with a variety of unrelated antigens. In every instance, the gamma globulin-specific RF were of all three major isotypes whereas the polyreactive RF were restricted to the IgM isotype. These data demonstrate that synovial B cells from both RA and OA patients can produce RF and that significant differences can exist among patients in the percentage of RF generated and their H and L chain isotype distribution. The reversal of the kappa:lambda ratio among the IgG and IgA RF and the more restricted antigen-binding specificities of the IgG and IgA vs IgM RF suggest that a non-stochastic, possibly antigen-driven selection process was involved in their generation. The relevance of these differences in RF precursor frequency, H and L chain distribution, and antigen specificity to these two diseases warrants further investigation.

Scandinavian Journal of ImmunologyVolume 31, Issue 1 p. 109-119 Augmentation by Cytochalasin B of Antigen Receptor-Mediated Activation of Normal and Malignant Human B Lymphocytes L. SALTZ, L. SALTZ The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorD. M. KNOWLES, D. M. KNOWLES The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorS. MECHANIC, S. MECHANIC The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorP. PASLEY, P. PASLEY The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorR. BROOKS, R. BROOKS The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorM. WAKAI, M. WAKAI The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorN. CHIORAZZI, Corresponding Author N. CHIORAZZI The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USANicholas Chiorazzi, MD, Division of Rheumatology and Clinical Immunology, Department of Medicine, North Shore University Hospital, 300 Community Drive. Manhasset, New York 11030, USASearch for more papers by this author L. SALTZ, L. SALTZ The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorD. M. KNOWLES, D. M. KNOWLES The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorS. MECHANIC, S. MECHANIC The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorP. PASLEY, P. PASLEY The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorR. BROOKS, R. BROOKS The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorM. WAKAI, M. WAKAI The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USASearch for more papers by this authorN. CHIORAZZI, Corresponding Author N. CHIORAZZI The Laboratory of Immunology, The Rockefeller University New York; The Departments of Medicine, North Shore University Hospital, Manhasset; Cornell University Medical College, New York; and The Department of Pathology, Columbia University College of Physicians and Surgeons, New York, USANicholas Chiorazzi, MD, Division of Rheumatology and Clinical Immunology, Department of Medicine, North Shore University Hospital, 300 Community Drive. Manhasset, New York 11030, USASearch for more papers by this author First published: January 1990 https://doi.org/10.1111/j.1365-3083.1990.tb02749.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Baeker, T.R., Simms, E.R. & Rothstein, T.L. Cytochalasin induces an increase in cytosolic free calcium in murine B lymphocytes. J. Immunol. 138, 2691, 1987. 2 Bigler, R.D., Posnett, D.N. & Chiorazzi, N. 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