A rare case of narrow QRS tachycardia with "hidden" concealed left-sided accessory pathway.

A 54-year-old-woman with narrow QRS tachycardia (heart rate, 210 beats per minute) was admitted to the authors' hospital. Tachycardia terminated after administration of adenosine. The 12-lead electrocardiogram after conversion to sinus rhythm was unremarkable. During electrophysiological study, tachycardia could be easily induced by programmed atrial stimulation without jump phenomenon. The cycle length was 260 ms. During tachycardia, the atrial activation sequence in the coronary sinus (CS) was distal-to-proximal. However, during decremental ventricular pacing, retrograde conduction showed exclusively proximal-to-distal activation in the CS. What is the underlying mechanism?

Blood vessel reactivity on noradrenaline, vasopressin, and prostaglandin F2 alpha, resp., in the isolated perfused hind legs of rats with edemas or adjuvant arthritis.

In the isolated perfused hind legs of rats with enemas induced by carrageenin, dextran or Freund's adjuvant in both paws, resting perfusion pressure was slightly increased whereas the vasopressor action of noradrenaline, lysine-vasopressin and prostaglandin F2 alpha, was decreased. Admixture of indomethacin (3 micrograms.ml-1) to the perfusion fluid led to a decrease of resting perfusion pressure whereas its influence on EAmax of noradrenaline was only weak under these conditions. Concomitantly, the contents of prostaglandin E-like substances in the perfusate decreased. Prostaglandin F2 alpha exhibits only weak vasopressor activity in isolated perfused hind legs of rats with carrageenin edema. Altogether, the effect of indomethacin on resting perfusion pressure as well as on EA and EAmax, resp., of agonists is difficulty to explain by its effect on arachidonic acid cascade. The pD2-value of noradrenaline (4.68 - 4.87) and lysine-vasopressin (6.02 - 6.04) was apparently not changed, at least not decreased, in the acute phase of inflammation indicating no impairment of receptor affinity of noradrenaline and vasopressin in inflammation. Blood vessel reaction is apparently influenced in inflammation mechanically by the increased tissue pressure as well as by molecular mechanisms consisting in the presence of inflammatory mediators and/or particularly in a reduced intrinsic sensitivity of the blood vessel muscle itself.