Key result
Decreased time-to-peak LV pressure rise during BiV pacing identifies CRT volumetric responders with 0.98 AUC.
Why the study?
To test whether shortening of time-to-peak left ventricular pressure rise (Td) reflects resynchronization and identifies long-term volumetric responders to cardiac resynchronization therapy.
Does shortening of time-to-peak left ventricular pressure rise (Td) predict long-term volumetric response in patients receiving cardiac resynchronization therapy?
Observational (n=45)
No
Does shortening of time-to-peak left ventricular pressure rise (Td) predict long-term volumetric response in patients receiving cardiac resynchronization therapy?
Effect estimate: AUC 0.98 (95% CI 0.93-1)
p-value: p=<0.01
Shortening of a prolonged time-to-peak left ventricular pressure rise (Td) with CRT accurately identifies long-term volumetric responders, offering a potential biomarker for CRT candidate selection.
May support Td shortening to identify CRT responders; leaves open prospective validation before guiding selection.
AIMS: We tested the hypothesis that shortening of time-to-peak left ventricular pressure rise (Td) reflect resynchronization in an animal model and that Td measured in patients will be helpful to identify long-term volumetric responders [end-systolic volume (ESV) decrease >15%] in cardiac resynchronization therapy (CRT). METHODS: Td was analysed in an animal study (n = 12) of left bundle-branch block (LBBB) with extensive instrumentation to detect left ventricular myocardial deformation, electrical activation, and pressures during pacing. The sum of electrical delays from the onset of pacing to four intracardiac electrodes formed a synchronicity index (SI). Pacing was performed at baseline, with LBBB, right and left ventricular pacing and finally with biventricular pacing (BIVP). We then studied Td at baseline and with BIVP in a clinical observational study in 45 patients during the implantation of CRT and followed up for up to 88 months. RESULTS: We found a strong relationship between Td and SI in the animals (R = 0.84, P < 0.01). Td and SI increased from narrow QRS at baseline (Td = 95 ± 2 ms, SI = 141 ± 8 ms) to LBBB (Td = 125 ± 2 ms, SI = 247 ± 9 ms, P < 0.01), and shortened with biventricular pacing (BIVP) (Td = 113 ± 2 ms and SI = 192 ± 7 ms, P < 0.01). Prolongation of Td was associated with more wasted deformation during the preejection period (R = 0.77, P < 0.01). Six patients increased ESV by 2.5 ± 18%, while 37 responders (85%) had a mean ESV decrease of 40 ± 15% after more than 6 months of follow-up. Responders presented with a higher Td at baseline than non-responders (163 ± 26 ms vs. 121 ± 19 ms, P < 0.01). Td decreased to 156 ± 16 ms (P = 0.02) with CRT in responders, while in non-responders, Td increased to 148 ± 21 ms (P < 0.01). A decrease in Td with BIVP to values similar or below what was found at baseline accurately identified responders to therapy (AUC 0.98, P < 0.01). Td at baseline and change in Td from baseline was linear related to the decrease in ESV at follow-up. All-cause mortality was high among six non-responders (n = 4), while no patients died in the responder group during follow-up. CONCLUSIONS: Prolongation of Td is associated with cardiac dyssynchrony and more wasted deformation during the preejection period. Shortening of a prolonged Td with CRT in patients accurately identifies volumetric responders to CRT with incremental value on top of current guidelines and practices. Thus, Td carries the potential to become a biomarker to predict long-term volumetric response in CRT candidates.
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Odland et al. (2021) conducted an observational in Heart failure with left bundle branch block (n=45). Cardiac resynchronization therapy (biventricular pacing) vs. Baseline (intrinsic conduction) was evaluated on Identification of volumetric responders (end-systolic volume decrease >15%) using corrected Td change from baseline (AUC 0.98, 95% CI 0.93-1, p=<0.01). A decrease in time-to-peak left ventricular pressure rise (Td) with biventricular pacing accurately identified volumetric responders to cardiac resynchronization therapy (AUC 0.98).
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