Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
WALL MOTION ANALYSIS IN CRT NON-RESPONDERS Dpt. of Cardiology Korff Krause, Hanno Klemm, Kai Jaquet, Florian Hindemith, Karl-Heinz Kuck Asklepios Klinik St. Georg, Cardiology, Hamburg, Germany Introduction: The introduction of cardiac resynchronisation therapy (CRT) in patients with chronic heart failure and left bundle brunch block has improved their outcome. However, there is a rate of non-response in over 30%, particularly in patients with ischemic heart disease. The mechanism of non-response to CRT in chronic ischaemic heart disease patients is not completely understood. Methods and Results: Three months after CRT implantation a modified electromechanical contact mapping system (NOGA, BDS) was performed in 9 patient with ischaemic cardiomyopathy and nonresponse to CRT. Non-response was defined by failure of significant improvement of LVEF (25,5 vs. 27,1%), LVEDV (175,3 vs. 172,6ml), VO2 (11,0 vs.12,0 ml/kg min), 6min walk test (390 vs. 394m), and global strain (6,5 vs. 6,3%). LV Lead positions were: lateral 44%, anterior 33%, and posterior 23%, respectively. The local activation time (LAT) was set by the maximum downslope of the unipolar electrogram. Local wall motion time (LMT) was defined as the time needed for the catheter tip to traverse half of its maximum inward deflection during systole. LAT and LMT were measured relative to the onset of the QRS complex. Electrical activation showed a septal-to-lateral pattern in all patients with a mean endocardial activation time of 91 ± 18 ms. Control subjects (10 patients with ischaemic cardiomyopathy) with narrow QRS complex exhibited 97.5% of all LMTs <290 ± 17 ms, mean 225ms. Viability was defined with unipolar and bipolar voltage amplitude >5 mV and >0.5 mV, respectively. Delayed motion areas (cut-off LMT > 300ms) showed improvement of conduction times after CRT, as shown by ECG, electrical activation analysis and tranverse strain analysis. Mean wall motion time for all segments corrected for differences in electrical activation (LMT-LAT) was still delayed (283± 62ms). 50% of these delayed segments were avital. However, 23% of vital segments exhibited a LMT-LAT>290ms (mean 326ms, representing a delay of electromechanical coupling, intrinsical delay) wheras 27% showed a LMT-LAD <290ms (mean 191ms, electrical delay). Only 20% of these electrically delayed segments were laterally located. Echocardiographic longitudinal strain analysis of all delayed segments (LMT>300ms) could not be improved after CRT (4,5 ±3,2% vs. 4,1±3,4%) compared to regular segments (P = 0.002). Conclusion: CRT non-responders with ischaemic cardiomyopathy show a heterogeneous pattern of electrical and intrinsical delay of wall motion. Both myocardial avitality and delayed electromechanical coupling explain the lack of benefit of ventricular preexcitation in CRT non-responders