Left ventricular dysfunction is related to the presence and extent of a septal flash in patients with right ventricular pacing.
Septal flash (SF), a marker of left ventricular (LV) dyssynchrony in the presence of a left bundle branch block (LBBB), has been shown to predict improved ventricular function and outcome when corrected with cardiac resynchronization therapy. We hypothesized that a SF is present in patients receiving right ventricular (RV) pacing and its presence and extent could predict the development of LV dysfunction and remodelling.



Seventy-four consecutive patients receiving conventional RV pacing (>6 months, >85% paced) were studied with two-dimensional (2D) echocardiography. Indications for pacing were sinus-node dysfunction and atrioventricular conduction disorders. The presence of a SF was determined on stepwise advanced 2D echocardiographic views and confirmed using greyscale M-mode. Septal flash excursion was quantified by the amplitude of the early inward motion, measured from QRS onset to maximal inward motion. Fifty-seven (of 74; 77%) patients receiving RV pacing had a detectable SF. Patients with a SF had lower LV ejection fraction (EF) (52 ± 10 vs. 60 ± 4%, P < 0.001) and greater indexed end-systolic volume (33 ± 16 vs. 23 ± 5 mL/m2, P < 0.001). Receiver operating characteristic analysis demonstrated that a SF of 3.5 mm was the optimal cut-off value (area under the curve = 0.95) to identify reduced LV function (EF < 50%) with a sensitivity of 91% and a specificity of 90%.



A SF was present in a majority of patients receiving conventional RV pacing and its magnitude was related to LV dysfunction and adverse remodelling. Given the similarities observed in LBBB and pacemaker-induced dyssynchrony, SF magnitude might be a predictor for the development of LV dysfunction and adverse remodelling in patients receiving conventional RV pacing.
Cardiology Department, Thorax Institute, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.|Department of Cardiology, Oslo University Hospital, Rikshospitalet, and University of Oslo, Oslo, Norway.
Sebastian Imre
SI
Sarvari
Cardiology Department, Thorax Institute, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Marta
M
Sitges
Cardiology Department, Thorax Institute, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Maria
M
Sanz
Cardiology Department, Thorax Institute, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Jose Maria
JM
Tolosana Viu
Department of Cardiology, Oslo University Hospital, Rikshospitalet, and University of Oslo, Oslo, Norway.
Thor
T
Edvardsen
Department of Cardiology, Oslo University Hospital, Rikshospitalet, and University of Oslo, Oslo, Norway.
Thomas Muri
TM
Stokke
Cardiology Department, Thorax Institute, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Lluis
L
Mont
ICREA, Departamento de Información y Comunicación, Universitat Pompeu Fabra, Barcelona, Spain.
Bart
B
Bijnens
D000368:Aged; D000369:Aged, 80 and over; D019540:Area Under Curve; D054537:Atrioventricular Block / Q000150:complications / Q000628:therapy*; D002037:Bundle-Branch Block / Q000150:complications / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D015331:Cohort Studies; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012372:ROC Curve; D012804:Sick Sinus Syndrome / Q000150:complications / Q000628:therapy*; D016896:Treatment Outcome; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology*; D020257:Ventricular Remodeling; D054088:Ventricular Septum / Q000000981:diagnostic imaging / Q000503:physiopathology*