Journal of cardiovascular electrophysiology · 2007
Left ventricular conduction delays induced by right ventricular apical pacing: effect of left ventricular dysfunction and bundle branch block.
Сравнительное исследованиеСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Varma Niraj
Аннотация
BACKGROUND: RV apical pacing (RVP) may be deleterious, possibly by simulating LBBB, i.e., prolonging QRS duration (QRSd) and LV activation (LVAT). However, determinants of electrical delays are unknown.
HYPOTHESIS: LV dysfunction (LVEF <or= 40%, HF) and pre-existing conduction system abnormalities may modulate RVP's effects, compared to LBBB.
METHODS: RVP-induced QRSd and LVAT were compared in normal LV to HF, with normal QRS (<120 ms), RBBB, or LBBB. LVAT was estimated by interval from QRS onset to basal inferolateral LV depolarization.
RESULTS: During LBBB and RVP, LVAT/QRSd was >or=85%, i.e., LVAT indicated terminal LV depolarization. In normal LV, LVAT during intrinsic conduction (55 +/- 18 ms) was delayed by RVP (129 +/- 20 ms, n = 58, P < 0.001). RVP's effects were similar to LBBB (P = NS) and unaffected by baseline conduction disease. In HF overall, RVP-induced delays (QRSd 209 +/- 27, LVAT 186 +/- 26 ms, n = 102) were greater than RVP in normal LV (P < 0.001). When baseline conduction system disease was present, RVP's effects were exaggerated (RVP wide QRS [>120 ms]: QRSd 216 +/- 27, LVAT 191 +/- 20 ms, [n = 72] vs RVP normal QRS: QRSd 193 +/- 24, LVAT 169 +/- 24 ms, n = 31, P < 0.001). In patients with LBBB (n = 41), delays during intrinsic conduction (QRSd 163 +/- 29, LVAT 137 +/- 33 ms, n = 41) were enhanced by RVP (QRSd 218 +/- 28, LVAT 191 +/- 22 ms, P < 0.001). RVP's effects were similar in patients with LBBB and RBBB (P = NS).
CONCLUSION: RVP simulated LBBB in normal LV. In HF, RVP induced greater conduction delays than LBBB, enhanced by accompanying conduction disease. These variations may contribute to RVP's mixed clinical effects.
HYPOTHESIS: LV dysfunction (LVEF <or= 40%, HF) and pre-existing conduction system abnormalities may modulate RVP's effects, compared to LBBB.
METHODS: RVP-induced QRSd and LVAT were compared in normal LV to HF, with normal QRS (<120 ms), RBBB, or LBBB. LVAT was estimated by interval from QRS onset to basal inferolateral LV depolarization.
RESULTS: During LBBB and RVP, LVAT/QRSd was >or=85%, i.e., LVAT indicated terminal LV depolarization. In normal LV, LVAT during intrinsic conduction (55 +/- 18 ms) was delayed by RVP (129 +/- 20 ms, n = 58, P < 0.001). RVP's effects were similar to LBBB (P = NS) and unaffected by baseline conduction disease. In HF overall, RVP-induced delays (QRSd 209 +/- 27, LVAT 186 +/- 26 ms, n = 102) were greater than RVP in normal LV (P < 0.001). When baseline conduction system disease was present, RVP's effects were exaggerated (RVP wide QRS [>120 ms]: QRSd 216 +/- 27, LVAT 191 +/- 20 ms, [n = 72] vs RVP normal QRS: QRSd 193 +/- 24, LVAT 169 +/- 24 ms, n = 31, P < 0.001). In patients with LBBB (n = 41), delays during intrinsic conduction (QRSd 163 +/- 29, LVAT 137 +/- 33 ms, n = 41) were enhanced by RVP (QRSd 218 +/- 28, LVAT 191 +/- 22 ms, P < 0.001). RVP's effects were similar in patients with LBBB and RBBB (P = NS).
CONCLUSION: RVP simulated LBBB in normal LV. In HF, RVP induced greater conduction delays than LBBB, enhanced by accompanying conduction disease. These variations may contribute to RVP's mixed clinical effects.