Myocardial electrical alteration in XXXX preparations with combined chronic rapid pacing and progressive coronary artery occlusion.

@entity296 @entity1165 @entity308 @entity4024 @entity39 @entity235 @entity943 @entity591 @entity3303 @entity1818 @entity25587
Our objective was to create an animal preparation displaying long-term electrical alterations after chronic regional energetic stress without @entity296 . An Ameroid (AM) constrictor was implanted around the left circumflex coronary artery (LCx) 2 wk before chronic rapid ventricular pacing ( @entity25587 ) was initiated at 240 beats/min for 4 wk ( @entity25587 -AM). Comparisons were made with healthy @entity235 and @entity235 with either AM or @entity25587 . Unipolar electrograms were recorded from 191 sites in the LCx territory in open-chest, anesthetized animals during sinus rhythm and while pacing at 120-150 beats/min, with bouts of transient rapid pacing (TRP; 240/min). In @entity25587 -AM and AM, ST segment elevation was identified at central sites and ST @entity308 at peripheral sites, both increasing with TRP. In @entity25587 -AM and @entity25587 , the maximum negative slope of unipolar activation complexes was significantly depressed and activation-recovery intervals prolonged. Areas of inexcitability as well as irregular isocontour patterns displaying localized activation-recovery intervals shortening and gradients >20 ms between neighboring sites were identified in one-third of @entity25587 -AM at slow rate, with increasing incidence and magnitude in response to TRP. In @entity25587 -AM, programmed stimulation-induced marked conduction delay and block as well as polymorphic @entity1165 , which stabilized into @entity591 with the use of @entity3303 or @entity1818 . Whole cell @entity4024 current and channel protein expression were reduced in @entity25587 . Despite complete constrictor closure, small areas of @entity39 were detected in a minority of @entity25587 -AM. Long-term electrical alterations and their exacerbation by TRP contribute to @entity943 formation in collateral-dependent myocardium subjected to chronic tachycardic stress.
