Central Sympathetic Activation and Arrhythmogenesis during Acute Myocardial Infarction: Modulating Effects of Endothelin-B Receptors

Kolettis, Theofilos M.; Kontonika, Marianthi; Barka, Eleonora; Daskalopoulos, Evangelos P.; Baltogiannis, Giannis; Tourmousoglou, Christos; Papalois, Apostolos; Kyriakides, Zenon S.

doi:10.3389/fcvm.2015.00006

Cited by 13 publications

(15 citation statements)

References 52 publications

(77 reference statements)

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“…The mechanisms underlying arrhythmogenesis during evolving MI are more complex. We have presented evidence supporting a role of central sympathetic activation [11] , but the similar conduction delay seen in our untreated and clonidine-treated wild-type rats refutes major effects on conduction; alternative mechanisms such as repolarization dispersion appear to be more likely [12] .…”

Section: Discussionsupporting

confidence: 64%

Local conduction during acute myocardial infarction in rats: Interplay between central sympathetic activation and endothelin

Kolettis

Kontonika

Rocca

et al. 2016

Journal of Arrhythmia

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We investigated the effects of autonomic dysfunction and endothelin on local conduction and arrhythmogenesis during myocardial infarction. We recorded ventricular tachyarrhythmias, monophasic action potentials, and activation sequences in wild-type and ETB-deficient rats displaying high endothelin levels. Central sympathetic inputs were examined after clonidine administration. Clonidine mitigated early and delayed arrhythmogenesis in ETB-deficient and wild-type rats, respectively. The right ventricular activation delay increased in clonidine-treated ETB-deficient rats and slightly decreased in wild-type rats. The left ventricular voltage rise decreased in all groups, whereas the activation delay increased mainly in clonidine-treated ETB-deficient rats. Central sympathetic activation and endothelin modulate ischemia-induced arrhythmogenesis. Ischemia alters excitability, whereas endothelin impairs local conduction, an action partly counterbalanced by central sympathetic activity.

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Section: Discussionsupporting

confidence: 64%

Local conduction during acute myocardial infarction in rats: Interplay between central sympathetic activation and endothelin

Kolettis

Kontonika

Rocca

et al. 2016

Journal of Arrhythmia

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“…It is not known why BB protect only on the short-term. During acute MI, the sympathetic nervous system is activated 13 and plasma catecholamines are elevated 14 , which increases the risk of arrhythmogenesis 15 . It is believed that BB counteract those deleterious pathophysiological effects, decrease the myocardial oxygen demand and reduce the infarct size 8 ; hence decreasing the risk of short-term mortality post-MI.…”

Section: Discussionmentioning

confidence: 99%

Beta-blockers and Short-Term Cardiovascular Outcomes In Patients Hospitalized For Acute Coronary Syndrome and a Left Ventricular Ejection Fraction ≥40%

Khalil

Zubaid

Mekhaimar

et al. 2020

Sci Rep

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Beta-blockers (BB) have been traditionally associated with improvement in cardiovascular disease outcomes in patients with ischemic cardiomyopathy. Whether they're still efficacious in the postreperfusion era is currently debated in the light of recent controversial reports. In-hospital, 6-month and 12-month mortality were studied in the GULF-COAST, a prospective multicenter cohort of acute coronary syndrome (ACS), in relation to BB use: prior to admission, 24-hour post-admission and on discharge in patients with a left ventricular ejection fraction (LVef) ≥ 40%. On admission, 50.9% of the cohort participants had a LVef ≥ 40%, of whom 1203 (55.4%) were on BB whilst 905 (44.6%) were not. Mean age was 60 (13) years old and 66% were males. Prior BB use or its administration in 24 hours decreased in-hospital mortality (OR = 0.25, 95% CI [0.09-0.67]; OR = 0.16, 95% CI [0.08-0.35]; respectively). BB on discharge lowered 1-month mortality (OR = 0.28, 95% CI [0.11-0.72]), but had a neutral effect on mortality, reinfarction and stroke at 6 and 12 months. Results were unchanged after multivariable adjustments and further sensitivity analysis. In this retrospective cohort of ACS, BB improved in-hospital and 1-month mortality in patients with a LVEF ≥ 40% but had a neutral effect on longer-term outcome.Several trials conducted in the late 1970's and 1980's, such as ISIS-1 (First International Study of Infarct Survival) 1 and BHAT (Beta-Blocker Heart Attack Trial) 2 , showed that beta blockers (BB) decrease mortality after myocardial infarction (MI). An earlier meta-analysis of studies in which MI patients were treated with BB reported a 25 percent reduction in one-year mortality 3 .The treatment of ischemic cardiomyopathy has been revolutionized during the past 2 decades with the introduction of new treatment regimens such as dual anti-platelets, statins and most importantly reperfusion therapy. Progressively, the long-term protective role of BB in MI, once vital, is being questioned. A large metanalysis that included over 100 000 MI patients showed that BB reduce mortality in the pre-reperfusion era but failed to report any long-term survival benefit of BB in trials performed in the post-reperfusion era 4 .There is still convincing evidence that BB use is beneficial on the short-term outcome. A 2013 meta-analysis of randomized trials concluded that early BB therapy in ACS patients reduces in-hospital mortality, re-infarction and arrhythmias 5 . Nevertheless, it is not known how long BB treatment beneficial post-ACS is. In this paper, we report that previous BB therapy and/or BB treatment up to 24 hours after admission is associated with improved in-hospital outcome. However, BB therapy on discharge was associated only with decreased 1-month mortality, with no effect on mortality at 6 and 12 months. measures and baseline patients' characteristics were compared between the two groups: BB versus no BB using the χ 2 test (or Fisher's exact test when expected cell counts fell below 5) for categorical variables and the student's ...

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“…Likewise, a study from our group[19] examined the incidence of VTs post-ligation in rats pretreated with clonidine, a centrally acting inhibitor of sympathetic preganglionic-neurons; treated rats displayed a lower incidence of VTs occurring during the delayed phase post-MI, but early phase arrhythmogenesis was unaffected[19]. …”

Section: Analysis Of Recent Experimental Studiesmentioning

confidence: 99%

Autonomic function and ventricular tachyarrhythmias during acute myocardial infarction

Kolettis

2018

WJEM

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Most cases of sudden cardiac death are attributed to sustained ventricular tachyarrhythmias (VTs), triggered by acute coronary occlusion. Autonomic dysfunction, an important arrhythmogenic mechanism in this setting, is being actively investigated, aiming at the advent of preventive strategies. Recent experimental studies have shown vagal withdrawal after anterior myocardial infarction, coinciding with high incidence of VTs, followed by more gradual sympathetic activation coinciding with a second arrhythmia peak. This article summarizes recent knowledge on this intriguing topic, generating hypotheses that can be investigated in future experimental and clinical studies.

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Central Sympathetic Activation and Arrhythmogenesis during Acute Myocardial Infarction: Modulating Effects of Endothelin-B Receptors

Cited by 13 publications

References 52 publications

Local conduction during acute myocardial infarction in rats: Interplay between central sympathetic activation and endothelin

Local conduction during acute myocardial infarction in rats: Interplay between central sympathetic activation and endothelin

Beta-blockers and Short-Term Cardiovascular Outcomes In Patients Hospitalized For Acute Coronary Syndrome and a Left Ventricular Ejection Fraction ≥40%

Autonomic function and ventricular tachyarrhythmias during acute myocardial infarction

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