Outcome of resynchronization therapy on superficial and endocardial electrophysiological findings.

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.

Electrocardiographic outcome of resynchronization therapy.

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.

Plasma endothelin-1 levels after stem cell transplantation.

Acute renal failure and veno-occlusive disease of the liver are serious complications following stem cell transplantation (SCT) and contribute to the non-relapse mortality associated with this procedure. Endothelins, a family of vasoconstrictor peptides, may be involved in the pathogenesis of a variety of renal and hepatic diseases, including CsA-associated hypertension and the hepatorenal syndrome. In order to study the relevance of endothelins to SCT-related liver and kidney dysfunction, we determined endothelin-1 (ET-1) levels in plasma samples obtained from 65 patients (38 autologous, 27 allogeneic) 7 days before and 7, 14 and 28 days after SCT. A steady increase in plasma ET-1 was observed after SCT (5.36 pg/ml, 95% CI 4.30-6.43 on day +28 vs 3.82 pg/ml, 95% CI 3.21-4.43 on day -7; P = 0.020). No differences in ET-1 levels existed between autologous and allogeneic SCT recipients at any of the time points studied (P = 0.561). In addition, no significant differences were observed among patients with renal dysfunction vs those without (P = 0.187), nor in patient groups with or without hepatic dysfunction (P = 0.075). In conclusion, even though plasma ET-1 levels showed a steady increase following SCT, no correlation could be found with development of SCT-related kidney or liver dysfunction.