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EN
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)
EN
The influence of ischemia on purine nucleotide and their catabolite concentration in human myocardium was investigated during surgery of acquired and congenital heart defects. This was compared with the influence of ischemia on rat heart. Concentrations of adenine and guanine nucleotides and their catabolites were measured in the extracts of heart biopsies taken at the onset of ischemia and at the time of reperfusion. The content of myocardial ATP in human heart decreased from the initial value of 223 ± 1.1 to 14.6 ±1.5 nmol/mg protein and total adenine nucleotide pool decreased from 34.2 ± 1.8 to 27.6 ± 1.5 nmol/mg protein during the operation. Significant increases in myocardial concentrations of purine catabolites were also observed with the most prominent rise in inosine from below 0.5 at the onset of the ischemia to 3.0 ± 0.5 nmol/mg protein at the time of reperfusion. A positive correlation was demonstrated between the concentration of purine catabolites in the heart at the end of ischemia with the decrease of both ATP and the total nucleotide pool. An interesting metabolic specificity of the ischemic human heart appeared to be only a small accumulation of inosine monophospahate (IMP). The increase of IMP in the rat heart after ischemia was several-fold higher.
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