Cardiac Resynchronization Therapy May Be Antiarrhythmic Particularly in Responders

Saini, Aditya; Kannabhiran, Munish Kumar; Reddy, Pratap; Gopinathannair, Rakesh; Olshansky, Brian; Dominic, Paari

doi:10.1016/j.jacep.2015.10.007

Cited by 15 publications

(8 citation statements)

References 37 publications

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“…A recent meta-analysis indicated that this intervention may significantly reduce the risk of ventricular arrhythmias when compared with patients receiving ICDs. Interestingly the same study also showed that patients who were not-responsive to CRT may have had a significantly higher risk of ventricular arrhythmias ( Saini et al, 2016 ). Furthermore, it was also shown that CRT was able to efficiently reduce subcellular heterogeneity of structure and function of RyRs and T-tubules in a canine model of HF, potentially due to the restoration of ventricular synchrony ( Li et al, 2015 ).…”

Section: Therapeutic Interventionsmentioning

confidence: 95%

Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium

Johnson

Antoons

2018

Front. Physiol.

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Heart failure (HF) is associated with elevated sympathetic tone and mechanical load. Both systems activate signaling transduction pathways that increase cardiac output, but eventually become part of the disease process itself leading to further worsening of cardiac function. These alterations can adversely contribute to electrical instability, at least in part due to the modulation of Ca2+ handling at the level of the single cardiac myocyte. The major aim of this review is to provide a definitive overview of the links and cross talk between β-adrenergic stimulation, mechanical load, and arrhythmogenesis in the setting of HF. We will initially review the role of Ca2+ in the induction of both early and delayed afterdepolarizations, the role that β-adrenergic stimulation plays in the initiation of these and how the propensity for these may be altered in HF. We will then go onto reviewing the current data with regards to the link between mechanical load and afterdepolarizations, the associated mechano-sensitivity of the ryanodine receptor and other stretch activated channels that may be associated with HF-associated arrhythmias. Furthermore, we will discuss how alterations in local Ca2+ microdomains during the remodeling process associated the HF may contribute to the increased disposition for β-adrenergic or stretch induced arrhythmogenic triggers. Finally, the potential mechanisms linking β-adrenergic stimulation and mechanical stretch will be clarified, with the aim of finding common modalities of arrhythmogenesis that could be targeted by novel therapeutic agents in the setting of HF.

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Section: Therapeutic Interventionsmentioning

confidence: 95%

Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium

Johnson

Antoons

2018

Front. Physiol.

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“…Up to now there is insufficient clinical data from randomized clinical trials to prove superiority of a combined CRT and ICD implantation (CRT-D) over CRT pacemakers (CRT-P) [1, 4]. Besides improvement of LVEF there is evidence for anti-arrhythmic effects following CRT implantation [5]. A recent meta-analysis of more than 12,000 patients demonstrated a reduction in the risk of all-cause mortality for CRT-D, which was more pronounced in patients suffering from ischemic cardiomyopathy (ICM) compared to non-ischemic dilated cardiomyopathy (DCM) [4].…”

Section: Introductionmentioning

confidence: 99%

Increased mortality and ICD therapies in ischemic versus non-ischemic dilated cardiomyopathy patients with cardiac resynchronization having survived until first device replacement

Beiert

Straesser

Malotki

et al. 2019

aoms

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Introduction Cardiac resynchronization therapy combined with an implantable cardioverter defibrillator (CRT-D) is widely applied in heart failure patients. Sufficient data on arrhythmia and defibrillator therapies during long-term follow-up of more than 4 years are lacking and data on mortality are conflicting. We aimed to characterize the occurrence of ventricular arrhythmia, respective defibrillator therapies and mortality for several years following CRT-D implantation or upgrade. Material and methods Eighty-eight patients with ischemic (ICM) or non-ischemic dilated cardiomyopathy (DCM) and at least one CRT-D replacement were included in this study and analyzed for incidence of non-sustained ventricular tachycardia (NSVT), defibrillator shocks, anti-tachycardia pacing (ATP) and mortality. Results ICM was the underlying disease in 59%, DCM in 41% of patients. During a mean follow-up of 76.4 ±24.8 months the incidence of appropriate defibrillator therapies (shock or ATP) was 46.6% and was elevated in ICM compared to DCM patients (57.7% vs. 30.6%, respectively; p = 0.017). Kaplan-Meier analysis revealed significantly higher ICD therapy-free survival rates in DCM patients ( p = 0.031). Left ventricular ejection fraction, NSVT per year and ICM (vs. DCM) were independent predictors of device intervention. The ICM patients showed increased mortality compared to DCM patients, with cumulative all-cause mortality at 9 years of follow-up of 45.4% and 10.6%, respectively. Chronic renal failure, peripheral artery disease and chronic obstructive pulmonary disease were independent predictors of mortality. Conclusions The clinical course of patients with ICM and DCM treated with CRT-D differs significantly during long-term follow-up, with increased mortality and incidence of ICD therapies in ICM patients.

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“…Third, QRS duration was not compared between the CeP and CoP groups in a parallel fashion, as the QRS duration was intrinsic in the CeP group while only paced QRS duration was collected in the CoP group, and instead we could only evaluate changes of QRS duration in separate groups. Fourth, previous studies demonstrated reverse remodeling after CRT was associated with reduced risk of ventricular arrhythmia episodes as well as mitral regurgitation; thus it would be worth evaluating the effect of pacing cessation on these parameters, whereas we did not collect and analyze the data. Lastly, we used a comprehensive definition of super‐response after CRT, and thus our results should be interpreted with caution and not be extrapolated to other possible super‐responder populations.…”

Section: Discussionmentioning

confidence: 99%

Cessation of pacing in super‐responders of cardiac resynchronization therapy: A randomized controlled trial

Liang

Wang

Zhang

et al. 2018

Cardiovasc electrophysiol

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Cardiac Resynchronization Therapy May Be Antiarrhythmic Particularly in Responders

Abstract: CRT may significantly reduce risk of VA compared with ICDs in patients who meet criteria for CRT. CRT responders have significant reduction in VA compared with nonresponders. CRT nonresponse might significantly increase risk of VA.

Cited by 15 publications

References 37 publications

Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium

Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium

Increased mortality and ICD therapies in ischemic versus non-ischemic dilated cardiomyopathy patients with cardiac resynchronization having survived until first device replacement

Cessation of pacing in super‐responders of cardiac resynchronization therapy: A randomized controlled trial

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