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Knowledge regarding factors that influence deviation of the QRS axis is important when seeking to differentiate between physiological and pathological changes. We hypothesised that, in contrast to those patients with an atrioventricular septal defect and common atrioventricular junction permitting only atrial shunting, those associated with ventricular shunting would show no relationship between the positions of the papillary muscles and the degree of the leftward deviation of the QRS axis.
We compared the positions of endocardial origin of the papillary muscles, and the frontal plane QRS axis, in patients with atrioventricular septal defects and common atrioventricular junction permitting exclusively atrial as opposed to atrial and ventricular shunting.
We analysed 18 patients with atrial and ventricular shunting and 23 patients with exclusively atrial shunting. The correlation coefficient between the ratio of distances of the papillary muscles from the mid-septum and the amount of leftward deviation in the frontal plane QRS axis was 0.1 (p=0.4) in those with ventricular shunting and 0.26 (p=0.01) in those with exclusively atrial shunting.
In contrast to patients with the so-called primum form of atrioventricular septal defect, in whom the locations of the papillary muscles correlate with the degree of QRS axis, such relationships are lacking in patients with defects permitting both atrial and ventricular shunting. It may be, therefore, that the presence of ventricular shunting and/or their younger age causes pressure overload, which negates the leftward QRS forces caused by the abnormally positioned papillary muscles.
Altered levels of coagulation factors are reported in patients with functionally univentricular physiology before and following the second and third stages of reconstructive surgery. The aims of our study were to determine if such abnormalities are also present in newborns with this physiology prior to the first stage of surgical treatment.
Patients and methods
We studied 20 neonates with functionally univentricular physiology admitted to the Children’s Cardiac Centre in Slovakia, using 20 healthy neonates as age-matched controls. Demographic characteristics, and concentration of liver enzymes, serum albumin, and complete blood count, did not differ between the two groups. Concentrations of Factor II, V, VII, VIII, Protein C, Protein S and Antithrombin were compared between the groups, and assessed as variable factors for coagulation.
In those with functionally univentricular physiology, procoagulation Factor II (p < 0.001), VII (p < 0.001), VIII (p < 0.01), anticoagulation Protein C (p < 0.001), Protein S (p < 0.001) and Antitrombin III (p < 0.001) all were present in significantly lower values compared with findings in the control group. D-dimer (p < 0.0001) and Fibrin Degradation Products (p < 0.0001) were present at significantly higher levels, but the concentration of plasminogen was significantly lower (p < 0.0001). The activated partial thromboplastin time (p < 0.012), and the prothrombin time (p < 0.0001), was significantly prolonged in those with functionally univentricular physiology compared with their controls.
The presence of abnormal coagulation factors, markers of thrombolysis in the plasma, and increased risk of bleeding, suggests activation of haemostasis, and consumption of factors responsible for coagulation, in those with functionally univentricular physiology. The question arises whether the reported abnormalities are predictive of the known abnormalities of coagulation occurring during the second and third stages of surgical repair for patients with functionally univentricular hearts.
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