Fibrosis and Cardiac Arrhythmias

Jong, Sanne de; Veen, Toon A.B. van; Rijen, Harold V.M. van; Bakker, Jacques M.T. de

doi:10.1097/fjc.0b013e318207a35f

Cited by 288 publications

(281 citation statements)

References 71 publications

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“…20 In addition, the changes in the structural organization of the cardiac muscle, and particularly the generation of interstitial fibrosis, lead to serious impairment of impulse propagation and enhance the probability of reentrant rhythms. [21][22][23][24] Interstitial fibrosis, for instance, not only generates cellular sequestration in the ventricular muscle, preventing the impulse propagation reaching the isolated cells, 24 but decreases the transverse conduction velocity, as shown above, facilitating the generation of reentrant rhythms.…”

Section: Discussionmentioning

confidence: 99%

Spironolactone enhances the beneficial effect of aliskiren on cardiac structural and electrical remodeling in TGR(mRen2)27 rats

Mello

2013

J Renin Angiotensin Aldosterone Syst

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Objective: To investigate the influence of simultaneous administration of spironolactone (20 mg/kg per day, intraperitoneal (i.p.)) and aliskiren (50 mg/kg per day, i.p.) for a period of eight weeks on cardiac remodeling in TGR(mRen2)27 rats. Methods: Echocardiographic and electrophysiological and histological methods were used to determine the influence of spironolactone and aliskiren on cardiac remodeling. Results: 1) the beneficial effect of aliskiren on SBP was enhanced by simultaneous administration of spironolactone; 2) echocardiographic studies showed that the left ventricle diameter (LVD), the left ventricle end diastolic volume (LVEDV) and the left ventricle posterior wall thickness (LVPW) were significantly reduced by the combination of both drugs when compared with aliskiren alone; 3) the ejection fraction was also increased; 4) histological studies indicated a greater decline in perivascular and interstitial fibrosis when both drugs were used; 5) the decrease of electrical remodeling of the left ventricle caused by aliskiren was further reduced by simultaneous administration of spironolactone; 6) the cardiac refractoriness increased by aliskiren was further incremented by spironolactone. Spironolactone (20 mg/kg per day) alone increased the ejection fraction and reduced LVD, LVEDV and LVPW but its effect was smaller than that achieved with the combination spironolactone plus aliskiren. Conclusion:The combination of an aldosterone inhibitor with a direct renin inhibitor proved to be of greater benefit for cardiac structural and electrical remodeling in this experimental model of hypertension than aliskiren alone.

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Section: Discussionmentioning

confidence: 99%

Spironolactone enhances the beneficial effect of aliskiren on cardiac structural and electrical remodeling in TGR(mRen2)27 rats

Mello

2013

J Renin Angiotensin Aldosterone Syst

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“…Multiple stressors, such as stretching of atrial myocardium, episodes of AF and other supraventricular arrhythmias, and RAAS activation as well, may favour propagation of AF [14,15]. For instance, molecular and histological effects of high aldosterone activity were evaluated in several studies.…”

Section: Discussionmentioning

confidence: 99%

Ablacja cieśni trójdzielno-żylnej wśród pacjentów z przetrwałym migotaniem przedsionków jako terapia pomostowa celem utrzymania rytmu zatokowego — badanie pilotażowe

Adamowicz

Szponder²,

Sokołowska

et al. 2017

Folia Cardiologica

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“…In accordance with classical literature (32), this difference might provide an explanation for the larger antiarrhythmic action of CPC ϩ GF compared with CPC. Indeed, curing the unfavorable changes in both Cx43-mediated cell coupling and interstitial fibrosis would improve conduction velocity (18,60), offsetting possible reentry pathways through the architectural structure of myocardial tissue. Nevertheless, we found a reduction rather than an increase of CV-l and CV-t in CPC ϩ GF animals vs. CPC, suggesting that other arrhythmogenic substrates/mechanisms were positively influenced by GF adjunct to CPCs, favoring its distinctive antiarrhythmic action.…”

Section: Impact Of Cpc and Cpc ϩ Gf Administration On Basic Cardiac Ementioning

confidence: 99%

Antiarrhythmic effect of growth factor-supplemented cardiac progenitor cells in chronic infarcted heart

Savi

Bocchi

Rossi

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Kit pos cardiac progenitor cells (CPCs) represent a successful approach in healing the infarcted heart and rescuing its mechanical function, but electrophysiological consequences are uncertain. CPC mobilization promoted by hepatocyte growth factor (HGF) and IGF-1 improved electrogenesis in myocardial infarction (MI). We hypothesized that locally delivered CPCs supplemented with HGF ϩ IGF-1 (GFs) can concur in ameliorating electrical stability of the regenerated heart. Adult male Wistar rats (139 rats) with 4-wk-old MI or sham conditions were randomized to receive intramyocardial injection of GFs, CPCs, CPCs ϩ GFs, or vehicle (V). Enhanced green fluorescent protein-tagged CPCs were used for cell tracking. Vulnerability to stress-induced arrhythmia was assessed by telemetry-ECG. Basic cardiac electrophysiological properties were examined by epicardial multiple-lead recording. Hemodynamic function was measured invasively. Hearts were subjected to anatomical, morphometric, immunohistochemical, and molecular biology analyses. Compared with V and at variance with individual CPCs, CPCs ϩ GFs approximately halved arrhythmias in all animals, restoring cardiac anisotropy toward sham values. GFs alone reduced arrhythmias by less than CPCs ϩ GFs, prolonging ventricular refractoriness without affecting conduction velocity. Concomitantly, CPCs ϩ GFs reactivated the expression levels of Connexin-43 and Connexin-40 as well as channel proteins of key depolarizing and repolarizing ion currents differently than sole GFs. Mechanical function and anatomical remodeling were equally improved by all regenerative treatments, thus exhibiting a divergent behavior relative to electrical aspects. Conclusively, we provided evidence of distinctive antiarrhythmic action of locally injected GF-supplemented CPCs, likely attributable to retrieval of Connexin-43, Connexin-40, and Cav1.2 expression, favoring intercellular coupling and spread of excitation in mended heart. cardiac progenitor cells; growth factors and cytokines; myocardial infarction; arrhythmia; cardiac gap junction connexins NEW & NOTEWORTHY Repair of infarcted heart by local injection of c-kit pos cardiac progenitors supplemented with hepatocyte growth factor and IGF-1 has distinctive antiarrhythmic effects involving recovery of Connexin-43, Connexin-40, and Ca v1.2 expression levels differently than progenitors or cytokines alone. This new insight into the impact of regenerative therapies on cardiac electrogenesis has clinical relevance.HEART FAILURE (HF) very often proceeds as a consequence of myocardial infarction (MI) (59) and continues to be a major health problem (49). Over the past 15 yr, cell therapy has emerged as a new strategy aimed at revitalizing dead myocardium, thus circumventing the unfavorable outcome of degenerative heart diseases, including the vicious circle of MI/HF (67). However, results obtained so far in clinical trials with a large sample size using cells of different origin, mainly skeletal myoblasts (44) and bone marrow cells (78), have been contradictor...

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Fibrosis and Cardiac Arrhythmias

Cited by 288 publications

References 71 publications

Spironolactone enhances the beneficial effect of aliskiren on cardiac structural and electrical remodeling in TGR(mRen2)27 rats

Spironolactone enhances the beneficial effect of aliskiren on cardiac structural and electrical remodeling in TGR(mRen2)27 rats

Ablacja cieśni trójdzielno-żylnej wśród pacjentów z przetrwałym migotaniem przedsionków jako terapia pomostowa celem utrzymania rytmu zatokowego — badanie pilotażowe

Antiarrhythmic effect of growth factor-supplemented cardiac progenitor cells in chronic infarcted heart

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