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Quadricuspid pulmonary valve (QPV) is an uncommon congenital defect reported in the general population with a frequency of up to 0.25%. The defect usually does not cause severe clinical complications and its presence frequently remains clinically silent. Moreover, there are several difficulties in visualization of pulmonary valve using basic diagnostic modalities such as echocardiography. Therefore, in the majority of cases, QPV is detected accidentally during cardiac procedures or post mortem. The authors present a case of QPV complicated with aneurysm of the pulmonary trunk, diagnosed with computed tomography in 70-year-old woman. Although the patient had undergone transthoracic echocardiography examinations several times in the past, only computed tomography allowed the detection of the anomalous valve. In addition, the examination confirmed aneurysm of the pulmonary trunk. To the best of our knowledge, this is the first case of QPV diagnosed in vivo with computed tomography. (Folia Morphol 2009; 68, 4: 290–293)
The rate of growth of the pulmonary trunk during gestation has not been sufficiently determined. The present study was performed on 128 spontaneously aborted human foetuses aged 15–34 weeks in order to compile normative data for pulmonary trunk dimensions at various gestational ages. With the use of anatomical dissection, digital-image analysis (the Leica QWin Pro 16 system) and statistical analysis (ANOVA, regression analysis) a range of measurements (length, diameter and volume) was analysed for the pulmonary trunk during gestation. No significant gender differences were found (p > 0.05). Growth curves were generated of the best fit for the plot for each morphometric feature against gestational age. The results obtained show a statistically significant correlation (p < 0.001) between the parameters examined and gestational age. Both the length and diameter of the pulmonary trunk were found to increase in a linear fashion throughout gestation. The length ranged from 3.17 ± 0.36 mm to 13.54 ± 1.39 mm, according to the linear function y = –5.6035 + 0.5705 x ± 0.9171 (r = 0.96). The diameter ranged from 1.51 ± 0.24 mm to 5.30 ± 1.53 mm, according to the linear model y = –1.4813 + 0.2154 x ± 0.7452 (r = 0.86). The pulmonary trunk volume ranged from 5.94 ± 2.21 mm³ to 312.37 ± 154.34 mm³, according to the quadratic function y = 143.2 – 20.961 x + 0.791 x2 ± 63.306 (R² = 0.74). The growth curves generated from my data may be useful as a reference for foetal echocardiographers in the detection of congenital cardiovascular abnormalities.
Micro-anatomical changes in the aorta, pulmonary trunk, and left ventricle of Wistar rats were studied after the administration of streptozotocin. Twenty adult Rattus norvegicus were randomly assigned into two groups (control and diabetic) of ten rats each. Diabetes mellitus was experimentally induced in the diabetic group of rats by daily intra-peritoneal administration of multiple doses of 40 mg/kg streptozotocin dissolved in 0.1 M sodium citrate buffer for five consecutive days. The control group was given the equivalent volume of citrate buffer. The animals were monitored for four weeks after streptozotocin administration. Post sacrifice, the left ventricle, aorta, and pulmonary trunk were excised, weighed, and fixed by immersion in 10% formol saline. The tissues were processed for paraffin embedding, and sections of 6 µm thickness were produced and stained with H & E for general histological observations, and Verhoeff-van Gieson elastic fibre stain to demonstrate elastic fibres in these cardiovascular structures. The data obtained were analyzed with descriptive and inferential statistics. Histopathological and morphometric examinations of the stained sections showed a significant increase in the thickness of the tunica intima of aorta (t = –7.49; df = 9; p < 0.05) and pulmonary trunk (t = –10.81; df = 9; p < 0.05) in diabetic rats (14.59 ± 1.189 μm and 11.307 ± 0.863 mm, respectively) when compared to that of the control group (3.62 ± 0.353 μm and 3.22 ± 0.244 μm, respectively). In addition, the distribution of elastic and collagen fibres was sparse in the hearts of the diabetic group when compared to that of the control group. The findings of this study demonstrated that diabetes mellitus might cause some alterations in the microanatomy of cardiovascular structures. (Folia Morphol 2009; 68, 4: 207–214)
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