[...] the increase platelet adhesiveness found in persistent Cpn infections and MS could increase the possibility of restenosis following attempted venoplasty and, therefore, the authors do not recommend interventional procedures to treat IJV obstructions in these patients.
Η αρχική του υπόθεση εργασίας είναι πως τα παρασιτικά βακτήρια Chlamydophila pneumoniae εμπλέκονται στην παθογένεση της σκλήρυνσης, προκαλώντας μολυσματικές αγγειίτιδες, και κατά συνέπεια στενώσεις, στις εξωκρανιακές φλέβες, κυρίως τις σφαγίτιδες και τις σπονδυλικές. Η παρούσα υπόθεση δε δέχεται τον ισχυρισμό του Zamboni πως οι στενώσεις είναι αποτέλεσμα εμβρυολογικής ανωμαλίας.
This theory postulates that infective Cpn organisms are transmitted through peri-hilar lymph nodes within infected blood monocytes to the thoracic duct and right lymphatic duct. From these lymphatic conduits, the monocytes can transmit the Cpn EBs to the venous endothelium firstly through communications of the thoracic duct with the azygos vein in the chest, then finally at the respective confluences of the internal jugular, vertebral and subclavian veins bilaterally (Figure 8(a) and (b)). Once blood borne, the Cpn can also ‘metastasize’ to distant vascular sites whilst harbouring within the infected blood monocytes.
The main finding of this study is that obstructed venous blood flow in the major extracranial veins of the neck in subjects with MS can be improved by a
prolonged CAP specifically designed to treat persistent Cpn infection. Moreover, this effect was significant in those subjects that tested positive with Cpn serology.
There was a lesser, non-significant effect seen in those who had negative serology to Cpn. The improved blood flow in the affected veins was consistently associated with corresponding reduction in collateral flow in the unaffected side in those subjects with unilateral disease. In addition, there was an increase in global arterial flow [...]