Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts › Research Explorer (2023)

Standard

Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts. / Vermeulen, J. T.; McGuire, M. A.; Opthof, T.; Coronel, R.; de Bakker, J. M.; Klöpping, C.; Janse, M. J.

In: Cardiovascular research, Vol. 28, No. 10, 1994, p. 1547-1554.

Research output: Contribution to journalArticleAcademicpeer-review

Harvard

Vermeulen, JT, McGuire, MA, Opthof, T, Coronel, R, de Bakker, JM, Klöpping, C 1994, 'Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts', Cardiovascular research, vol. 28, no. 10, pp. 1547-1554. https://doi.org/10.1093/cvr/28.10.1547

APA

Vermeulen, J. T., McGuire, M. A., Opthof, T., Coronel, R., de Bakker, J. M., Klöpping, C. (1994). Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts. Cardiovascular research, 28(10), 1547-1554. https://doi.org/10.1093/cvr/28.10.1547

Vancouver

Vermeulen JT, McGuire MA, Opthof T, Coronel R, de Bakker JM, Klöpping C et al. Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts. Cardiovascular research. 1994;28(10):1547-1554. https://doi.org/10.1093/cvr/28.10.1547

Author

Vermeulen, J. T. ; McGuire, M. A. ; Opthof, T. ; Coronel, R. ; de Bakker, J. M. ; Klöpping, C. ; Janse, M. J. / Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts. In: Cardiovascular research. 1994 ; Vol. 28, No. 10. pp. 1547-1554.

BibTeX

@article{4f4ecc99f9404159b85824b3e40fc6f2,

title = "Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts",

abstract = "The aim of the study was to assess the occurrence of triggered activity and automaticity in ventricular trabeculae from failing human hearts and normal and failing rabbit hearts during exposure to a normal and altered extracellular environment. Ventricular trabeculae were harvested from failing human hearts (from patients undergoing cardiac transplantation) and from normal and failing rabbit hearts (combined volume and pressure overload). Trabeculae were superfused with normal Tyrode solution followed by a modified Tyrode solution, which mimicked the extracellular milieu in patients with severe heart failure. Modified Tyrode solution contained low potassium (3.0 mM), low magnesium (0.4 mM), and noradrenaline (1 microM). During superfusion with normal Tyrode solution, early afterdepolarisations, delayed afterdepolarisations, and automaticity were not observed in trabeculae from failing hearts. In the modified Tyrode solution, early afterdepolarisations could be induced in 26% of control rabbit and 30% of failing rabbit trabeculae, but never in human trabeculae. During superfusion with the modified solution delayed afterdepolarisations or triggered activity could be induced in 50% of the human failing trabeculae, in 43% of the failing rabbit trabeculae, and in 9% of the normal rabbit trabeculae (p < 0.01); automaticity was observed in 44% of the human trabeculae, and in 7% of the failing rabbit trabeculae, but in none of the control rabbit trabeculae. In failing rabbit myocardium action potential duration was prolonged at cycle lengths > or = 350 ms, but not at shorter cycle lengths. Delayed afterdepolarisations and automaticity, but not early afterdepolarisations, occur more frequently in myocardium from failing hearts, but only during superfusion with a modified Tyrode solution. This emphasises that the extracellular environment is important with respect to arrhythmogenesis in heart failure, apart from the fixed cellular defect due to heart failure per se. Prolongation of the action potential in failing hearts does not occur at physiological and higher heart rates and therefore cannot be regarded as a protective factor in the prevention of reentrant arrhythmias. The rate of triggered and automatic rhythms was slow. Therefore these mechanisms cannot be responsible for clinical ventricular tachycardias or fibrillation, but may serve as triggers for reentrant arrhythmias",

author = "Vermeulen, {J. T.} and McGuire, {M. A.} and T. Opthof and R. Coronel and {de Bakker}, {J. M.} and C. Kl{\"o}pping and Janse, {M. J.}",

year = "1994",

doi = "10.1093/cvr/28.10.1547",

language = "English",

volume = "28",

pages = "1547--1554",

journal = "Cardiovascular research",

issn = "0008-6363",

publisher = "Oxford University Press",

number = "10",

}

RIS

TY - JOUR

T1 - Triggered activity and automaticity in ventricular trabeculae of failing human and rabbit hearts

AU - Vermeulen, J. T.

AU - McGuire, M. A.

AU - Opthof, T.

AU - Coronel, R.

AU - de Bakker, J. M.

AU - Klöpping, C.

AU - Janse, M. J.

PY - 1994

Y1 - 1994

N2 - The aim of the study was to assess the occurrence of triggered activity and automaticity in ventricular trabeculae from failing human hearts and normal and failing rabbit hearts during exposure to a normal and altered extracellular environment. Ventricular trabeculae were harvested from failing human hearts (from patients undergoing cardiac transplantation) and from normal and failing rabbit hearts (combined volume and pressure overload). Trabeculae were superfused with normal Tyrode solution followed by a modified Tyrode solution, which mimicked the extracellular milieu in patients with severe heart failure. Modified Tyrode solution contained low potassium (3.0 mM), low magnesium (0.4 mM), and noradrenaline (1 microM). During superfusion with normal Tyrode solution, early afterdepolarisations, delayed afterdepolarisations, and automaticity were not observed in trabeculae from failing hearts. In the modified Tyrode solution, early afterdepolarisations could be induced in 26% of control rabbit and 30% of failing rabbit trabeculae, but never in human trabeculae. During superfusion with the modified solution delayed afterdepolarisations or triggered activity could be induced in 50% of the human failing trabeculae, in 43% of the failing rabbit trabeculae, and in 9% of the normal rabbit trabeculae (p < 0.01); automaticity was observed in 44% of the human trabeculae, and in 7% of the failing rabbit trabeculae, but in none of the control rabbit trabeculae. In failing rabbit myocardium action potential duration was prolonged at cycle lengths > or = 350 ms, but not at shorter cycle lengths. Delayed afterdepolarisations and automaticity, but not early afterdepolarisations, occur more frequently in myocardium from failing hearts, but only during superfusion with a modified Tyrode solution. This emphasises that the extracellular environment is important with respect to arrhythmogenesis in heart failure, apart from the fixed cellular defect due to heart failure per se. Prolongation of the action potential in failing hearts does not occur at physiological and higher heart rates and therefore cannot be regarded as a protective factor in the prevention of reentrant arrhythmias. The rate of triggered and automatic rhythms was slow. Therefore these mechanisms cannot be responsible for clinical ventricular tachycardias or fibrillation, but may serve as triggers for reentrant arrhythmias

AB - The aim of the study was to assess the occurrence of triggered activity and automaticity in ventricular trabeculae from failing human hearts and normal and failing rabbit hearts during exposure to a normal and altered extracellular environment. Ventricular trabeculae were harvested from failing human hearts (from patients undergoing cardiac transplantation) and from normal and failing rabbit hearts (combined volume and pressure overload). Trabeculae were superfused with normal Tyrode solution followed by a modified Tyrode solution, which mimicked the extracellular milieu in patients with severe heart failure. Modified Tyrode solution contained low potassium (3.0 mM), low magnesium (0.4 mM), and noradrenaline (1 microM). During superfusion with normal Tyrode solution, early afterdepolarisations, delayed afterdepolarisations, and automaticity were not observed in trabeculae from failing hearts. In the modified Tyrode solution, early afterdepolarisations could be induced in 26% of control rabbit and 30% of failing rabbit trabeculae, but never in human trabeculae. During superfusion with the modified solution delayed afterdepolarisations or triggered activity could be induced in 50% of the human failing trabeculae, in 43% of the failing rabbit trabeculae, and in 9% of the normal rabbit trabeculae (p < 0.01); automaticity was observed in 44% of the human trabeculae, and in 7% of the failing rabbit trabeculae, but in none of the control rabbit trabeculae. In failing rabbit myocardium action potential duration was prolonged at cycle lengths > or = 350 ms, but not at shorter cycle lengths. Delayed afterdepolarisations and automaticity, but not early afterdepolarisations, occur more frequently in myocardium from failing hearts, but only during superfusion with a modified Tyrode solution. This emphasises that the extracellular environment is important with respect to arrhythmogenesis in heart failure, apart from the fixed cellular defect due to heart failure per se. Prolongation of the action potential in failing hearts does not occur at physiological and higher heart rates and therefore cannot be regarded as a protective factor in the prevention of reentrant arrhythmias. The rate of triggered and automatic rhythms was slow. Therefore these mechanisms cannot be responsible for clinical ventricular tachycardias or fibrillation, but may serve as triggers for reentrant arrhythmias

U2 - 10.1093/cvr/28.10.1547

DO - 10.1093/cvr/28.10.1547

M3 - Article

C2 - 8001044

VL - 28

SP - 1547

EP - 1554

JO - Cardiovascular research

JF - Cardiovascular research

SN - 0008-6363

IS - 10

ER -

FAQs

What is triggered automaticity? ›

the ability of a cell to depolarize itself, reach threshold potential, and produce a propagated action potential; cells with this capability are called automatic cells.

What causes automaticity of the heart? ›

Automaticity is the property of cardiac cells to generate spontaneous action potentials. Spontaneous activity is the result of diastolic depolarization caused by a net inward current during phase 4 of the action potential, which progressively brings the membrane potential to threshold.

What mechanism causes triggered arrhythmias? ›

While arrhythmias are widely varied in their clinical presentations, they possess shared electrophysiologic properties at the cellular level. The 3 main mechanisms responsible for cardiac arrhythmias are automaticity, triggered activity, and reentry.

What affects cardiac automaticity? ›

Calcium is involved in cardiac automaticity and is required for muscle contraction. Hypocalcemia can therefore result in arrhythmias and reduced myocardial contractility.

Top Articles
Latest Posts
Article information

Author: Tyson Zemlak

Last Updated: 03/17/2023

Views: 6245

Rating: 4.2 / 5 (43 voted)

Reviews: 90% of readers found this page helpful

Author information

Name: Tyson Zemlak

Birthday: 1992-03-17

Address: Apt. 662 96191 Quigley Dam, Kubview, MA 42013

Phone: +441678032891

Job: Community-Services Orchestrator

Hobby: Coffee roasting, Calligraphy, Metalworking, Fashion, Vehicle restoration, Shopping, Photography

Introduction: My name is Tyson Zemlak, I am a excited, light, sparkling, super, open, fair, magnificent person who loves writing and wants to share my knowledge and understanding with you.