BACKGROUND: We investigated the relationship between wavefront curvature and slowing of conduction both within and outside the diastolic pathway of circuits causing ventricular tachycardia (VT) in the infarcted human heart. METHODS AND RESULTS: Propagation was determined around the reentrant circuits of 11 VT (cycle length, 348+/-75 ms) in 8 patients undergoing high-resolution noncontact mapping. The diastolic pathway had a mean wavefront velocity of 0.82+/-0.49 m/s and occupied 68+/-7% of VT cycle length. Significant changes (>5 degrees/mm) in trajectory of propagation occurred in 8 diastolic pathway segments (10.1+/-3 degrees/mm) in which wavefront propagation slowed to 0.41+/-0.11 m/s compared with the segments immediately preceding (0.91+/-0.16 m/s, P< 0.05) and following (1.07+/-0.33, P<0.05) the change in trajectory. At the turning points of entry (9.3+/-3.9 degrees/mm) and exit (9.0+/-4.8 degrees/mm) of the diastolic pathway propagation, velocity slowed at entry from 1.23+/-0.4 to 0.6+/-0.26 ms (P<0.001) and was more rapid at exit turning points (0.8+/-0.25 m/s) (P<0.05). There was an inverse relationship between wavefront curvature and velocity, both within and outside the diastolic pathway (r=0.46, P=0.0001), and VT cycle length correlated with total curvature multiplied by length of the diastolic pathway (P< 0.01). CONCLUSIONS: Slowing of propagation in circuits causing VT in the infarcted human heart occurs over regions of wavefront turning, with an inverse relationship between wavefront curvature and velocity, both within and outside the diastolic pathway. Conduction is slower at entry than exit turning points of the diastolic pathway but is slowest during turns within the diastolic pathway.
BACKGROUND: We investigated the relationship between wavefront curvature and slowing of conduction both within and outside the diastolic pathway of circuits causing ventricular tachycardia (VT) in the infarctedhuman heart. METHODS AND RESULTS: Propagation was determined around the reentrant circuits of 11 VT (cycle length, 348+/-75 ms) in 8 patients undergoing high-resolution noncontact mapping. The diastolic pathway had a mean wavefront velocity of 0.82+/-0.49 m/s and occupied 68+/-7% of VT cycle length. Significant changes (>5 degrees/mm) in trajectory of propagation occurred in 8 diastolic pathway segments (10.1+/-3 degrees/mm) in which wavefront propagation slowed to 0.41+/-0.11 m/s compared with the segments immediately preceding (0.91+/-0.16 m/s, P< 0.05) and following (1.07+/-0.33, P<0.05) the change in trajectory. At the turning points of entry (9.3+/-3.9 degrees/mm) and exit (9.0+/-4.8 degrees/mm) of the diastolic pathway propagation, velocity slowed at entry from 1.23+/-0.4 to 0.6+/-0.26 ms (P<0.001) and was more rapid at exit turning points (0.8+/-0.25 m/s) (P<0.05). There was an inverse relationship between wavefront curvature and velocity, both within and outside the diastolic pathway (r=0.46, P=0.0001), and VT cycle length correlated with total curvature multiplied by length of the diastolic pathway (P< 0.01). CONCLUSIONS: Slowing of propagation in circuits causing VT in the infarctedhuman heart occurs over regions of wavefront turning, with an inverse relationship between wavefront curvature and velocity, both within and outside the diastolic pathway. Conduction is slower at entry than exit turning points of the diastolic pathway but is slowest during turns within the diastolic pathway.
Authors: David E Gutstein; Stephan B Danik; Steve Lewitton; David France; Fangyu Liu; Franklin L Chen; Jie Zhang; Newsha Ghodsi; Gregory E Morley; Glenn I Fishman Journal: Am J Physiol Heart Circ Physiol Date: 2005-05-13 Impact factor: 4.733