A comment on terminology in cervical cytology and terminology discussions.
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Female↗
Biomedical subjects
U Baandrup
Publications and source records attributed to U Baandrup.
Prevalence of the parvovirus B19 genome in endomyocardial biopsy specimens.
Although enteroviruses have long been considered the most common cause of inflammatory heart muscle diseases, parvovirus B19 (PVB19) is emerging as a new and important candidate for myocarditis and dilated cardiomyopathy with inflammation (DCMi) and without inflammation (DCM). We investigated left ventricular endomyocardial biopsy specimens from 110 patients with suspected inflammatory heart disease for the presence of PVB19, Coxsackie virus (CVB), and adenovirus (Ad2) genome by polymerase chain reaction. Diagnosis of myocarditis (36 patients), DCM (18 patients), DCMi (13 patients), and perimyocarditis (12 patients) was made by immunohistochemical and histopathological investigation of endomyocardial biopsy specimens. A control group consisting of patients with arterial hypertension was also investigated. Prevalence of the PVB19 genome in endomyocardial biopsy specimens was highest in patients with DCMi (3 of 13) and patients with myocarditis (7 of 36); in patients with DCM and perimyocarditis, prevalence was 3 of 13 and 2 of 12, respectively. In patients with resolved myocarditis, no PVB19 DNA was detected; in patients with no inflammation and controls, prevalence was only 4% and 7%, respectively. CVB-RNA was detected in endomyocardial biopsy specimens from 3 of 37 patients with myocarditis; Ad2-DNA was found in 1 patient with DCM and 1 patient with perimyocarditis. These findings suggest an association of the PVB19 genome in endomyocardial biopsy specimens of adults with the development of DCM, DCMi, and chronic myocarditis more frequently than previously expected. PVB19 should therefore be recognized as a potential cardiotropic pathogen in patients of all ages.
Adult↗
The pulmonary vasculature in a neonatal porcine model with increased pulmonary blood flow and pressure.
INTRODUCTION: Hypertension and hyperperfusion of the pulmonary vascular bed in the setting of congenital cardiac malformations may lead to progressive pulmonary vascular disease. To improve the understanding of the basic mechanisms of this disease, there is a need for clinically relevant animal models which reflect the disease process. MATERIAL AND RESULTS: We randomly allocated 45 newborn pigs, at the age of 48 hrs, to groups in which there was either construction of a 3 mm central aorto-pulmonary shunt, undertaken in 9, or ligation of the left pulmonary artery, achieved in 13. Controls included sham operations in 13, or no operations in 10 pigs. Follow-up was continued for three months. The interventions were compatible with survival in most pigs. The shunts resulted in an acute 85% increase in systolic pulmonary arterial pressure, and a more than twofold increase in pulmonary blood flow. By three months of age, nearly all shunts had closed spontaneously, and haemodynamics were normal. Ligation of the left pulmonary artery resulted in a normal total pulmonary blood flow, despite only the right lung being perfused, and a 33% increase in systolic pulmonary arterial pressure. These haemodynamic changes were maintained throughout the period of study. In both groups, histomorphometry revealed markedly increased muscularity of the intra-acinar pulmonary arteries. Circulating levels of endothelin were normal in the shunted animals, and elevated in those with ligation of the left pulmonary artery. CONCLUSION: In neonatal porcine models of pulmonary vascular disease, created by construction of 3 mm central aorto-pulmonary shunts and ligation of one pulmonary artery, we observed histopathological changes of the pulmonary vasculature similar to early hypertensive pulmonary vascular disease in humans. Elevated circulating levels of endothelin were associated with abnormal haemodynamics rather than abnormal pathology. These findings could be valuable for future studies on the pathogenesis of hypertensive pulmonary vascular disease associated with congenital cardiac malformations.
Animals↗
Sudden death following occlusion of the left coronary artery by a large stalky excrescense.
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Adult↗
Morphological considerations of peri- and myocarditis.
In medicine, and thus in pathology, there are areas/topics of fashion and they shift from time to time. Pericardial diseases are not fashionable. Myocarditis is, and has been for a long time. Due to new ways of retrieving tissue samples from the pericardium the modern diagnostic tools such as immunohistochemistry and molecular pathology can be applied in this context as they have been in myocarditis for a long period. The diagnosis of inflammation rests on many other findings than morphological alterations and it is indeed questionable if inflammation is solely a morphological diagnosis. The methodologies of pathology can be improved and used in a better and more purposeful way even under routine conditions. It is concluded that morphology is still mandatory to make a final diagnosis of peri- and myocarditis.
Biomarkers↗
Monocyte chemoattractant protein 1 (MCP-1) in temporal arteritis and polymyalgia rheumatica.
OBJECTIVE: To examine the localisation of monocyte chemoattractant protein 1 (MCP-1) in the inflamed vessel wall in temporal arteritis (TA) and to measure MCP-1 in plasma both in patients with TA and patients with polymyalgia rheumatica (PMR). METHODS: By immunohistochemical techniques MCP-1 was localised to the vessel wall in patients with TA. In TA, PMR, and healthy controls MCP-1 was quantified by enzyme linked immunosorbent assay (ELISA) in plasma. RESULTS: MCP-1 was localised to the majority of mononuclear cells, some smooth muscle cells, and giant cells in the arterial biopsy specimens from 12 patients with histologically verified TA. In all sections, including the vasa vasorum, the endothelium stained positive. In the intima 73% (range 57-91%), in the media 49% (range 32-67%), and in the adventitia 74% (range of 62-91%) of all cells stained positive. In plasma MCP-1 was significantly raised in untreated TA (n=33) and untreated PMR (n=27) compared with healthy controls (n=12). Untreated TA plasma levels of MCP-1 (mean 391 pg/ml (range 82-778 pg/ml)) were similar to untreated PMR plasma levels (mean 402 pg/ml (range 29-1153 pg/ml)), and no significant difference was found between the two groups of patients. In both patients with TA and patients with PMR no correlation was found between the plasma level of MCP-1 and the erythrocyte sedimentation rate, haemoglobin concentration, and CD4/CD8 ratio. CONCLUSIONS: These results show that MCP-1 plays a part in the disease processes of TA and PMR.
Adult↗
hnRNPs H, H' and F behave differently with respect to posttranslational cleavage and subcellular localization.
hnRNPs H, H' and F belong to a subfamily of the hnRNPs sharing a high degree of sequence identity. Eukaryotic expression and specific C-terminal antibodies were used to demonstrate great variation in the intracellular fate of the proteins. hnRNPs H and H' become posttranslational cleaved into C-terminal 35 kDa proteins (H(C), H'(C)) and possibly into N-terminal 22 kDa proteins. No detectable cleavage was observed for hnRNP F. hnRNP H/H' is almost exclusively localized to the nucleus of many cell types while hnRNP F varies from a predominant nuclear localization in some cells to a predominant cytoplasmic localization in other cells. The different fates may reflect differences in functional roles that so far only have included nuclear functions. The presence of significant quantities of hnRNP F in the cytoplasm of many cells indicates that it also may have a functional role here.
Amino Acid Sequence↗
Alpha-cardiac actin is a novel disease gene in familial hypertrophic cardiomyopathy.
We identified the alpha-cardiac actin gene (ACTC) as a novel disease gene in a pedigree suffering from familial hypertrophic cardiomyopathy (FHC). Linkage analyses excluded all the previously reported FHC loci as possible disease loci in the family studied, with lod scores varying between -2.5 and -6.0. Further linkage analyses of plausible candidate genes highly expressed in the adult human heart identified ACTC as the most likely disease gene, showing a maximal lod score of 3.6. Mutation analysis of ACTC revealed an Ala295Ser mutation in exon 5 close to 2 missense mutations recently described to cause the inherited form of idiopathic dilated cardiomyopathy (IDC). ACTC is the first sarcomeric gene described in which mutations are responsible for 2 different cardiomyopathies. We hypothesize that ACTC mutations affecting sarcomere contraction lead to FHC and that mutations affecting force transmission from the sarcomere to the surrounding syncytium lead to IDC.
Actins↗
Species differences in expression of angiotensin II receptors and angiotensin-converting enzyme in human, canine and rat mitral valve leaflets.
In normal valvular collagen turnover in the rat, angiotensin (Ang) II and angiotensin-converting enzyme (ACE) seem to be involved. In common human and canine valvular diseases, changes in valvular collagen play a pathogenetic role and the valvular renin-angiotensin system is therefore of particular interest in these species. Healthy mitral valve leaflets and adjacent left ventricular myocardium were taken from five rats and five dogs immediately after euthanasia, and from five humans at autopsy. The valvular and myocardial Ang II receptors and ACE were detected and measured by quantitative autoradiography. In rat valves, high levels of Ang II receptors and ACE were found. In human and canine valves, insignificant levels were found. Significant myocardial levels of Ang II receptors and ACE were found only in the rat. The study demonstrated major species differences regarding the level of valvular and myocardial Ang II receptors and ACE in man, dog and rat. The lack of valvular Ang II receptors and ACE in man and dog, suggest that the renin-angiotensin system plays a minor, if any, role in the physiological valvular collagen formation in these two species. The findings in humans, however, need to be confirmed using fresh material.
Aged↗
Malignant myxoid endobronchial tumour: a report of two cases with a unique histological pattern.
AIMS: To present two cases of malignant endobronchial myxoid tumours with a highly distinctive sarcomatoid pattern not previously described at this site, and discuss their histogenesis in relation to previously documented endobronchial neoplasms. METHODS AND RESULTS: Both tumours presented in young adult females and were purely sarcomatoid with interweaving cords of small uniform, rounded or slightly elongated cells lying within a myxoid stroma. The stroma was alcian blue positive, but sensitive to hyaluronidase in both cases. The tumour cells contained a small volume of periodic acid-Schiff-positive eosinophilic cytoplasm and stained positively for vimentin only, but there also was a prominent background population of CD68-positive dendritic cells. Ultrastructural studies showed that the tumour cells contained an excess of rough endoplasmic reticulum, with some of the cisternae appearing dilated, and scalloping of the cell surfaces, although no intracisternal tubules were identified. CONCLUSIONS: Although the histological pattern was most reminiscent of extraskeletal myxoid chondrosarcoma, the sensitivity of the stroma to pretreatment with hyaluronidase precluded the diagnosis. However, there were similarities with the sarcomatoid component of malignant salivary gland-type mixed tumours of the lung and this tumour possibly represents a variant of a bronchial gland tumour. Despite this uncertainty over origin, this pattern should be recognized as part of the differential diagnosis of myxoid tumours in the lung, as an apparently indolent type of malignant endobronchial neoplasm.
Adult↗
Functional remodelling and left ventricular dysfunction after repeated ischaemic episodes. A chronic experimental porcine model.
This experimental study was set up to investigate left ventricular function and remodelling after repeated ischaemic episodes using magnetic resonance imaging (MRI). A significant reduction in mortality due to coronary heart disease (CHD) has been explained by both a decline in the incidence of acute myocardial infarction (AMI) and an improved post-AMI survival rate, suggesting a change in the natural history of CHD. Experimental intracoronary microembolization can induce different ischaemic patterns and the functional impact of repeated ischaemic episodes different from occlusion of central epicardial arteries can be studied. In this study repeated intracoronary microembolizations were performed in 20 domestic pigs. After 129 d, MRI was performed for assessment of left ventricular volume, mass and wall stress. Six pigs underwent serial MRI at baseline, immediately after embolization and at the end of the observation period. Microembolizations induced acute myocardial infarct expansion and increased left ventricular wall stress preceding chronic remodelling. End systolic and end diastolic volumes increased from 15.1 +/- 2.7 cm3 to 41.3 +/- 11.5 cm 3 (p < 0.002), and from 52.0 +/- 6.7 cm3 to 81.1 +/- 9.2 cm3 (p < 0.0007), respectively. End systolic wall stress increased from and 17.5 +/- 2.7 to 29.7 +/- 6.2 N/m2 (p < 0.001). Left ventricular filling pressures and cardiac index were unchanged. Histological examination revealed a diffuse pattern of perivascular fibrosis covering 12 +/- 3% of the left ventricular wall. This study demonstrates that repeated ischaemic episodes different from confined regional myocardial infarctions induce acute infarct expansion and chronic left ventricular remodelling in pigs. Serial assessment of absolute left ventricular volumes and mass is important during acute/chronic remodelling.
Animals↗
Sudden unexpected cardiac deaths among young Swedish orienteers--morphological changes in hearts and other organs.
During the years 1979-1992 an accumulation of sudden unexpected cardiac deaths (SUD) occurred among young Swedish orienteers. A reevaluation of material saved from 16 autopsies was undertaken. Myocarditis was most frequent. It was found in different stages in the majority of cases, indicating subacute or chronic disease with ongoing reparative processes. There were severe morphological changes in all cases. All but one showed a picture of fibrosis and unspecific hypertrophy and/or degenerative changes in myocytes. The hearts were classified into three groups (A-C), based on the morphological picture of the retrieved heart tissue and the macroscopic description. Group A comprised five cases in which areas with active myocarditis combined with areas of healing or healed myocarditis widely distributed in the left ventricle were the only morphological changes found. Group B comprised four cases demonstrating foci of myocarditis in different stages in the left ventricle and changes resembling those found in arrhythmogenic right ventricular dysplasia (ARVD), including degenerative changes with fibrosis and fatty infiltration located in either ventricle. Group C comprised the remaining seven cases. In none of the cases were coronary artery or valvular anomalies present, nor significant coronary sclerosis or changes outside the heart that could cause SUD.
Adolescent↗
[Arrhythmogenic right ventricular cardiomyopathy].
Arrhythmogenic right ventricular dysplasia is a rare cardiomyopathy, but a frequent cause of ventricular tachyarrhythmia and sudden cardiac death among young otherwise healthy individuals. This article contains a review of the current knowledge on epidemiology, diagnosis, symptoms and signs as well as theories on etiology and pathogenesis, prognosis and treatment. The aim is to draw attention to the disease as a cause of syncope, ventricular tachycardia and sudden cardiac death.
Arrhythmogenic Right Ventricular Dysplasia↗
The hemodynamic impact of diffuse myocardial ischemic lesions: an animal experimental model based on intracoronary microembolization.
In ischemic heart disease, left ventricular function is affected by a diffuse and segmental loss of myocardium. The decline in the incidence of myocardial infarction and improved early revascularization in acute transmural ischemia predict a change in the natural history of ischemic heart disease. It is now believed that, minor ischemic episodes, which are known to induce multifocal myocardial degeneration, will predominate in the near future. The objective of the present study was to develop a clinically relevant experimental model for investigation of the pathophysiological significance of diffuse ischemic myocardial lesions. Cardiac performance was gradually depressed by selective intracoronary microembolization in 13 pigs. Left ventricular function was quantitated by ejection fraction (EF), pulmonary pressure, cardiac output, and derivatives of left ventricular pressure. Left ventricular volume was estimated by epicardial echocardiography, using a new, unbiased stereological volume estimator. A chronic substudy was performed in order to characterize the histological changes and to evaluate the feasibility of establishing a chronic preparation of the model. Embolization induced acute left ventricular dysfunction; left ventricular pressure change decreased from 966+/-274 to 637+/-146 mmHg/s, and early diastolic relaxation from 1403+/-515 to 824+/-344 mmHg/s, respectively. Ejection fraction decreased by 45%+/-5% and cardiac output by 29%+/-11%. End-diastolic volume increased significantly, from 66.1+/-13.2 to 77.0+/-19.4 cm3, and end-systolic volume increased from 35.9+/-13.9 to 52.3+/-7.6 cm3. No change in heart rate or left ventricular filling pressure was observed. Diffuse ischemic myocardial injury was identified after a mean follow-up of 40 days. Intracoronary microembolization induces acute left ventricular dysfunction due to microinfarcts. Increased left ventricular end-diastolic volume is the initial compensatory response to the acute impairment of cardiac performance in nontransmural myocardial ischemia. This model is suitable for the evaluation of the hemodynamic changes secondary to acute and chronic diffuse loss of functional myocardium.
Animals↗
Pharmacological characterization of coronary small arteries from pigs with chronic ischaemic myocardial remodelling.
1. The effect of chronic ischaemic myocardial remodelling on small coronary artery reactivity in vitro was studied in a newly developed pig model. 2. Pigs were subjected to selective intracoronary embolizations with microspheres in the left anterior descending artery and circumflex artery causing scattered myocardial fibrosis. After an observation period of 130 days, heart dimensions and ejection fraction were determined with magnetic resonance imaging. Small arteries were isolated from the left ventricle and mounted as ring preparations in a myograph. Control arteries were taken from matched non-embolized pigs. 3. Compared with control pigs, end-systolic and diastolic volumes increased and left ventricular mass nearly doubled in embolized pigs. This indicates substantial myocardial hypertrophy, as the fraction area of fibrosis was only 12%. 4. Coronary small arteries preconstricted with 30 mmol/l KCI showed a normal contractile response to acetylcholine and 5-hydroxytryptamine. Sensitivity of the relaxation to bradykinin was nearly 3-fold increased and also slightly enhanced to isoprenaline in arteries from embolized pigs compared with controls, whereas relaxation to 5-hydroxytryptamine in the presence of ketanserin was similar. After inhibition of nitric oxide synthase with NG-nitro-L-arginine the sensitivity to acetylcholine increased to a similar extent in arteries from embolized pigs and controls. NG-Nitro-L-arginine abolished the relaxing effects of bradykinin and of 5-hydroxytryptamine in the presence of ketanserin. 5. We conclude that both the contractile function of the smooth muscle cells and the endothelial production or action of nitric oxide is preserved or slightly enhanced in coronary small arteries from pigs with chronic myocardial remodelling.
Acetylcholine↗
Myocardial structure as a determinant of pre- and postoperative ventricular function and long-term prognosis after valve replacement for aortic stenosis.
BACKGROUND: Long-term results after aortic value replacement for aortic stenosis can be correlated to a cardiac-related pre-operative risk profile. This predictability indicates that there is a common basis in subtle or overt structural abnormalities of left ventricular myocardium. METHODS AND RESULTS: Forty-nine patients aged 24-82 (mean 61) years, with aortic stenosis had a full wall thickness transmural biopsy of the left ventricular antero-lateral free wall during aortic valve replacement. Echocardiography and radionuclide ventriculography were performed prior to, and 18 months (n = 41) after, the operation. Postoperative follow-up to a maximum of 7.7 years was 100% complete. Pre-operatively, all patients had an increase in both the left ventricular mass index (202 +/- 67 g.m-2) and the muscle cell diameter (41 +/- 8 microns); other morphological data included a muscle cell nucleus volume of 752 +/- 192 microns3, a muscle cell mass index of 163 +/- 54.m-2, and a fibrous tissue mass index of 39 +/- 16 g.m-2. Patients with a pre-operative episode of clinical left ventricular failure (n = 19) had significantly greater morphological variables than those without. Pre-operative ejection fraction and other measures of systolic function correlated inversely with the morphological data, except for the fibrous tissue mass index; diastolic function indices correlated inversely with all the morphological variables. At the 18-month re-study, the same general picture was noted, but with an underlying strengthening, especially of the muscle cell mass index. Overall, the mass index dropped to 152 +/- 51 g.m-2 (P < 0.0001), but in 17% of the patients it became normal; the mass index at 18 months was directly correlated to morphological variables. A high muscle cell nucleus volume was identified as an independent predictor of early and late mortality. CONCLUSIONS: Abnormalities of the hypertrophied left ventricular muscle cell and the degree of muscle hypertrophy are, to some degree, underlying determinants of pre-operative symptomatology, pre- and postoperative ventricular function, and early and late mortality after valve replacement for aortic stenosis. Incomplete hypertrophy impaired results, was related to pre-operative myocardial structural abnormalities.
Adult↗
Parvovirus B19 infection associated with myocarditis following adult cardiac transplantation.
A 56-year-old woman underwent an uneventful cardiac transplantation due to dilated cardiomyopathy. One week later the patient developed clinical and histological signs of myocarditis. We report for the first time a case of myocarditis in an adult heart transplant recipient, possibly induced by parvovirus B19, as evidenced by the finding of specific IgM in serum and specific DNA in the myocardial cells. Furthermore, this is the first time parvovirus B19 DNA has been observed in the myocardium of an adult. In conclusion, parvovirus B19 should be recognized as a potential pathogen causing myocarditis in heart transplant recipients. In order to establish a definite and rapid diagnosis, a search for specific IgM should be supplemented with PCR investigations of serum and myocardial biopsies when available.
Antibodies, Viral↗
Gentacoll hampers epithelialisation and neovascularisation in excisional wounds in hairless mice.
Our aim was to analyse the effect of Gentacoll on the rate of epithelialisation and neovascularisation in wound healing. Standardised circular full thickness dermal wounds 2.25 mm in diameter were created on the dorsum of each ear on 24 hairless homozygous mice (n = 48). The cartilaginous layer was left intact. The wounds were treated in a randomised blinded fashion with bovine collagen implants with gentamicin (Gentacoll) (n = 17); bovine collagen implants without gentamicin (n = 15); and Silicone film (n = 16). Epithelialisation and neovascularisation were measured directly by intravital video-microscopy and computerised planimetry immediately after the wounds had been made and every third day until the wounds closed. Only five of the wounds treated with Gentacoll (n = 17) epithelialised completely; and their mean (SEM) epithelialisation time was 22.8 (1.6) days, significantly longer than controls without gentamicin (n = 15) for which the corresponding figures were 14.5 (0.6) days. In nine wounds treated with Gentacoll the ear cartilage in the wound bed perforated and two wounds developed severe inflammation, which was followed by self-mutilation. Neovascularisation was incomplete in all of the wounds in the Gentacoll group, whereas it was completed by 25.3 (0.7) days in the control group treated with implants without gentamicin. In the silicone treated group (n = 16), epithelialisation was completed by 12.7 (0.7) days and neovascularisation by 25.1 (0.5) days. None of wounds treated with collagen or silicone alone showed reactions similar to the Gentacoll-treated ears. Gentacoll hampers epithelialisation and neovascularisation, and might damage exposed cartilage.
Animals↗