The present study proposed procedure for predicting an optimal left and right ventricular pacing interval delay (V-V interval). In 16 patients (heart failure, left bundle branch block, biventricular pacing) two methods (A and B) identifying optimal V-V interval were tested. Method A: predicted optimal V-V interval A (POVV-A) = electromechanical delay of the segment paced by left ventricle lead minus electromechanical delay of the segment paced by right ventricle lead. Method B: predicted optimal V-V interval B (POVV-B) = difference in the onset of aortic and pulmonary flows. Both methods were validated using echocardiography and right-sided heart catheterization. Cardiac output during POVV-A (4.6 l.min-1 ) was significantly better than that during POVV-A minus 20 ms (4.3 l.min-1, p<0.01) and POVV-A plus 20 ms (4.3 l.min-1 , p<0.01), and than that during POVV-B (4.4 l.min-1, p<0.05). LV dP/dt during POVV-A (818 mm Hg.s-1 ) exceeded that during POVV-A plus 20 ms (717 mm Hg.s-1 , p<0.05) and POVV-A minus 20 ms (681 mm Hg.s-1, p<0.05), and that during POVV-B (727 mm Hg.s-1 , p<0.01). The time difference in onsets of myocardial deformation of left ventricle segment paced by the left ventricle and right ventricle lead allows identifying the optimal V-V interval and improves left ventricle performance., M. Novák, J. Lipoldová, J. Meluzín, J. Krejčí, P. Hude, V. Feitová, L. Dušek, P. Kamarýt, J. Vítovec., and Obsahuje bibliografii a bibliografické odkazy
Cardiac resynchronization therapy (CRT) has proven efficacious in reducing or even eliminating cardiac dyssynchrony and thus improving heart failure symptoms. However, quantification of mechanical dyssynchrony is still difficult and identification of CRT candidates is currently based just on the morphology and width of the QRS complex. As standard 12-lead ECG brings only limited information about the pattern of ventricular activation, we aimed to study changes produced by different pacing modes on the body surface potential maps (BSPM). Total of 12 CRT recipients with symptomatic heart failure (NYHA II-IV), sinus rhythm and QRS width ≥120 ms and 12 healthy controls were studied. Mapping system Biosemi (123 unipolar electrodes) was used for BSPM acquisition. Maximum QRS duration, longest and shortest activation times (ATmax and ATmin) and dispersion of QT interval (QTd) were measured and/or calculated during spontaneous rhythm, single-site right- and left-ventricular pacing and biventricular pacing with ECHO-optimized AV delay. Moreover we studied the impact of CRT on the locations of the early and late activated regions of the heart. The average values during the spontaneous rhythm in the group of patients with dyssynchrony (QRS 140.5±10.6 ms, ATmax 128.1±10.1 ms, ATmin 31.8±6.7 ms and QTd 104.3±24.7 ms) significantly
differed from those measured in the control group (QRS 93.0±10.0 ms, ATmax 79.1±3.2 ms, ATmin 24.4±1.6 ms and QTd 43.6±10.7 ms). Right ventricular pacing (RVP) improved significantly only ATmax [111.2±10.6 ms (p<0.05)] but no other measured parameters. Left ventricular pacing (LVP) succeeded in improvement of all parameters [QRS 105.1±8.0 ms (p<0.01), ATmax 103.7±7.1 ms (p<0.01), ATmin 20.2±3.7 ms (p<0.01) and QTd 52.0±9.4 ms (p<0.01)]. Biventricular pacing (BVP) showed also a beneficial effect in all parameters [QRS 121.3±8.9 ms (p<0.05), ATmax 114.3±8.2 ms (p<0.05), ATmin 22.0±4.1 ms (p<0.01) and QTd 49.8±10.0 ms (p<0.01)]. Our results proved beneficial outcome of LVP and BVP in evaluated parameters (what seems to be important particularly in the case of activation times) and revealed a complete return of activation
times to normal distribution when using these CRT modalities.
Cardiac resynchronization therapy (CRT) has proven efficacious
in the treatment of patients with heart failure and
dyssynchronous activation. Currently, we select suitable CRT
candidates based on the QRS complex duration (QRSd) and
morphology with left bundle branch block being the optimal
substrate for resynchronization. To improve CRT response rates,
recommendations emphasize attention to electrical parameters
both before implant and after it. Therefore, we decided to study
activation times before and after CRT on the body surface
potential maps (BSPM) and to compare thus obtained results with
data from electroanatomical mapping using the CARTO system.
Total of 21 CRT recipients with symptomatic heart failure (NYHA
II-IV), sinus rhythm, and QRSd ≥150 ms and 7 healthy controls
were studied. The maximum QRSd and the longest and shortest
activation times (ATmax and ATmin) were set in the BSPM maps
and their locations on the chest were compared with CARTO
derived time interval and site of the latest (LATmax) and earliest
(LATmin) ventricular activation. In CRT patients, all these
parameters were measured during both spontaneous rhythm and
biventricular pacing (BVP) and compared with the findings during
the spontaneous sinus rhythm in the healthy controls. QRSd was
169.7±12.1 ms during spontaneous rhythm in the CRT group and
104.3±10.2 ms after CRT (p<0.01). In the control group the
QRSd was significantly shorter: 95.1±5.6 ms (p<0.01). There
was a good correlation between LATmin(CARTO) and
ATmin(BSPM). Both LATmin and ATmin were shorter in the
control group (LATmin(CARTO) 24.8±7.1 ms and ATmin(BSPM)
29.6±11.3 ms, NS) than in CRT group (LATmin(CARTO) was
48.1±6.8 ms and ATmin(BSPM) 51.6±10.1 ms, NS). BVP
produced shortening compared to the spontaneous rhythm of
CRT recipients (LATmin(CARTO) 31.6±5.3 ms and ATmin(BSPM)
35.2±12.6 ms; p<0.01 spontaneous rhythm versus BVP). ATmax
exhibited greater differences between both methods with higher
values in BSPM: in the control group LATmax(CARTO) was
72.0±4.1 ms and ATmax (BSPM) 92.5±9.4 ms (p<0.01), in the
CRT candidates LATmax(CARTO) reached only 106.1±6.8 ms
whereas ATmax(BSPM) 146.0±12.1 ms (p<0.05), and BVP paced
rhythm in CRT group produced improvement with
LATmax(CARTO) 92.2±7.1 ms and ATmax(BSPM) 130.9±11.0 ms
(p<0.01 before and during BVP). With regard to the propagation
of ATmin and ATmax on the body surface, earliest activation
projected most often frontally in all 3 groups, whereas projection
of ATmax on the body surface was more variable. Our results
suggest that compared to invasive electroanatomical mapping
BSPM reflects well time of the earliest activation, however
provides longer time-intervals for sites of late activation.
Projection of both early and late activated regions of the heart on
the body surface is more variable than expected, very likely due
to changed LV geometry and interposed tissues between the
heart and superficial ECG electrode.