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Reentry via high-frequency pacing in a mathematical model for human-ventricular cardiac tissue with a localized fibrotic region.

ABSTRACT: Localized heterogeneities, caused by the regional proliferation of fibroblasts, occur in mammalian hearts because of diseases like myocardial infarction. Such fibroblast clumps can become sources of pathological reentrant activities, e.g., spiral or scroll waves of electrical activation in cardiac tissue. The occurrence of reentry in cardiac tissue with heterogeneities, such as fibroblast clumps, can depend on the frequency at which the medium is paced. Therefore, it is important to study the reentry-initiating potential of such fibroblast clumps at different frequencies of pacing. We investigate the arrhythmogenic effects of fibroblast clumps at high- and low-frequency pacing. We find that reentrant waves are induced in the medium more prominently at high-frequency pacing than with low-frequency pacing. We also study the other factors that affect the potential of fibroblast clumps to induce reentry in cardiac tissue. In particular, we show that the ability of a fibroblast clump to induce reentry depends on the size of the clump, the distribution and percentage of fibroblasts in the clump, and the excitability of the medium. We study the process of reentry in two-dimensional and a three-dimensional mathematical models for cardiac tissue.

SUBMITTER: Zimik S

PROVIDER: S-EPMC5681702 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

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Reentry via high-frequency pacing in a mathematical model for human-ventricular cardiac tissue with a localized fibrotic region.

Zimik Soling S Pandit Rahul R

Scientific reports 20171110 1

Localized heterogeneities, caused by the regional proliferation of fibroblasts, occur in mammalian hearts because of diseases like myocardial infarction. Such fibroblast clumps can become sources of pathological reentrant activities, e.g., spiral or scroll waves of electrical activation in cardiac tissue. The occurrence of reentry in cardiac tissue with heterogeneities, such as fibroblast clumps, can depend on the frequency at which the medium is paced. Therefore, it is important to study the re ...[more]

PMID: 29127361

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Project description:AimsThis registry was created to describe the experience of 76 Italian centres with a large cohort of recipients of multipoint pacing (MPP) capable cardiac resynchronization therapy (CRT) devices.Methods and resultsA total of 507 patients in whom these devices had been successfully implanted were enrolled between August 2013 and May 2015. We analysed: (i) current clinical practices for the management of such patients, and (ii) the impact of MPP on heart failure clinical composite response and on the absolute change in ejection fraction (EF) at 6 months. Multipoint pacing was programmed to 'ON' in 46% of patients before discharge. Methods of optimizing MPP programming were most commonly based on either the greatest narrowing of the QRS complex (38%) or the electrical delays between the electrodes (34%). Clinical and echocardiographic follow-up data were evaluated in 232 patients. These patients were divided into two groups according to whether MPP was programmed to 'ON' (n = 94) or 'OFF' (n = 138) at the time of discharge. At 6 months, EF was significantly higher in the MPP group than in the biventricular-pacing group (39.1 ± 9.6 vs. 34.7 ± 7.6%; P < 0.001). Even after adjustments, early MPP activation remained an independent predictor of absolute increase in LVEF of ≥5% (odds ratio 2.5; P = 0.001). At 6 months, an improvement in clinical composite score was recorded in a greater proportion of patients with MPP-ON than in controls (56 vs. 38%; P = 0.009). On comparing optimal MPP and conventional vectors, QRS was also seen to have decreased significantly (P < 0.001).ConclusionThis study provides information that is essential in order to deal with the expected increase in the number of patients receiving MPP devices in the coming years. The results revealed different practices among centres, and establishing the optimal programming that can maximize the benefit of MPP remains a challenging issue. Compared with conventional CRT, MPP improved clinical status and resulted in an additional increase in EF.Clinical trial registrationhttp://www.clinicaltrial.gov/. Unique identifier: NCT02606071.

Project description:BACKGROUND: Quantification of left ventricular (LV) dyssynchrony allows for objective measures of resynchronization therapy (CRT) effectiveness. We tested the hypothesis that site of LV pacing, fusion beats and baseline contractility alter contraction synchrony as quantified by regional and global measures of LV performance. METHODS AND RESULTS: In 8 open-chested pentobarbital-anesthetized canine preparations we compared the effects of right atrial (RA), RA-high right ventricular (RV) free wall, as a model of left bundle branch block contraction pattern, RA-LV apex (LVa), RA-LV free wall (LVfw), and RA-RV-apical LV (CRTa) and RA-RV-free wall LV (CRTfw), as CRT. LV pressure-volume loops recorded using high-fidelity pressure and conductance catheters and echocardiographic angle-corrected color-coded strain imaging of mid-LV short axis views analyzed radial strain from six segments. To control for contractile state esmolol-induced beta blockage was studied, and in 5 dogs to control for RA and ventricular pacing fusion beat artifacts, repeat studies were done following AV node ablation. RA-RV pacing reduced stroke work (SW) (57±18 to 33±13* mmHg·mL,*p<0.05 vs RA pacing), decreased LV end-diastolic volume and induced marked radial dyssynchrony (maximal time difference between peak segmental strain) from 31±15 to 234±60* ms. Changes in radial dyssynchrony correlated significantly with changes in SW (r=-0.53, p<0.01). Dyssynchrony improved with both CRTa and CRTfw (69*±31 and 98*±63 ms, respectively) while SW only improved with CRTa (62±22* and 37±13 mmHg·mL, respectively * p<0.05 vs RV pacing). CRTa also tended to increased LV end-diastolic volume over RA-RV. Esmolol slowed HR from 118±10 to 108±10 beats/min* and tended to decrease contractility (end-systolic elastance (Ees) from 12.1±7.9 to 8.9±3.9 mmHg/ml, p=0.167) but did not alter the degree of RV-pacing induced dyssynchrony. AV ablation had no effect on the observed apical and free wall contraction differences seen during baseline conditions. CONCLUSION: Although both CRTa and CRTfw reduced contraction dyssynchrony, CRTa tended to improve global LV performance more by increasing end-diastolic volume. Thus, CRT may improve global LV performance differently, depending on the LV pacing site.

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Reentry via high-frequency pacing in a mathematical model for human-ventricular cardiac tissue with a localized fibrotic region.

Publications

Reentry via high-frequency pacing in a mathematical model for human-ventricular cardiac tissue with a localized fibrotic region.

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