Cardiogenic Shock due to Tachycardiomyopathy after Heart Transplantation: Successful Treatment with Ivabradine

Zwicker, C.; Becker, Matthias; Lepper, W.; Koch, Keith; Westenfeld, Ralf

doi:10.1159/000318530

Cited by 23 publications

(12 citation statements)

References 10 publications

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“…In this situation, ivabradine might be helpful to control sinus tachycardia. Zwicker et al100 report successful treatment with ivabradine of a heart transplant patient who developed cardiogenic shock due to long-acting tachycardia (sinus tachycardia of 120/min), with further deterioration of cardiac function after administration of the short-acting beta-blocker esmolol under invasive hemodynamic monitoring. Heart rate control by administration of increasing doses of ivabradine supported recovery from cardiogenic shock and led to an improvement in the patient’s clinical condition as well as LV function during follow-up 100…”

Section: Clinical Efficacy Safety and Tolerability Of Ivabradine In Hfmentioning

confidence: 99%

Advances in the management of heart failure: the role of ivabradine

Müller‐Werdan

Stöckl

Werdan

2016

VHRM

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A high resting heart rate (≥70–75 b.p.m.) is a risk factor for patients with heart failure (HF) with reduced ejection fraction (EF), probably in the sense of accelerated atherosclerosis, with an increased morbidity and mortality. Beta-blockers not only reduce heart rate but also have negative inotropic and blood pressure-lowering effects, and therefore, in many patients, they cannot be given in the recommended dose. Ivabradine specifically inhibits the pacemaker current (funny current, If) of the sinoatrial node cells, resulting in therapeutic heart rate lowering without any negative inotropic and blood pressure-lowering effect. According to the European Society of Cardiology guidelines, ivabradine should be considered to reduce the risk of HF hospitalization and cardiovascular death in symptomatic patients with a reduced left ventricular EF ≤35% and sinus rhythm ≥70 b.p.m. despite treatment with an evidence-based dose of beta-blocker or a dose below the recommended dose (recommendation class “IIa” = weight of evidence/opinion is in favor of usefulness/efficacy: “should be considered”; level of evidence “B” = data derived from a single randomized clinical trial or large nonrandomized studies). Using a heart rate cutoff of ≥ 75 b.p.m., as licensed by the European Medicines Agency, treatment with ivabradine 5–7.5 mg b.i.d. reduces cardiovascular mortality by 17%, HF mortality by 39% and HF hospitalization rate by 30%. A high resting heart rate is not only a risk factor in HF with reduced EF but also at least a risk marker in HF with preserved EF, in acute HF and also in special forms of HF. In this review, we discuss the proven role of ivabradine in the validated indication “HF with reduced EF” together with interesting preliminary findings, and the potential role of ivabradine in further, specific forms of HF.

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Section: Clinical Efficacy Safety and Tolerability Of Ivabradine In Hfmentioning

confidence: 99%

Advances in the management of heart failure: the role of ivabradine

Müller‐Werdan

Stöckl

Werdan

2016

VHRM

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“…[1] as well as in transplanted hearts. [9] Some role for genetic predisposition in development of AIC has been found but literature on this is limited. [1] It is anticipated that several other factors might also be playing a role in patient's predisposition to develop AIC, but are not well understood.…”

Section: Causes Of Aicmentioning

confidence: 99%

Arrhythmia-Induced Cardiomyopathy: Prevalent, Under-recognized, Reversible

Dhawan

Gopinathannair

2017

Journal of Atrial Fibrillation

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Arrhythmia-induced cardiomyopathy (AIC) is a clinical condition in which a persistent tachyarrhythmia or frequent ectopy contribute to ventricular dysfunction leading to systolic heart failure. AIC can be partially or completely corrected with adequate treatment of the culprit arrhythmia. Several molecular and cellular alterations by which tachyarrhythmias lead to cardiomyopathy have been identified. AIC can affect children and adults, can be clinically silent in the form of asymptomatic tachycardia with cardiomyopathy, or can present with manifest heart failure. A high index of suspicion for AIC and aggressive treatment of the culprit arrhythmia can result in resolution of heart failure symptoms and improvement in cardiac function. Recurrent arrhythmia, following recovery from the index episode, can hasten the left ventricular dysfunction and result in HF, suggesting persistent adverse remodeling despite recovery of left ventricular function. Several aspects of AIC, such as predisposing factors, early diagnosis, preventive measures to avoid adverse remodeling, and long-term prognosis, remain unclear, and need further research.

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“…78 Biopsy specimens from such patients reveal nonspecific morphological alterations. 75,76,79 Again, the mechanism(s) underlying the development of HF during sustained tachyarrhythmias is/are unclear.…”

Section: Hf In Patients With Tachyarrhythmiamentioning

confidence: 99%

Heart Rate and Heart Failure - Not a Simple Relationship -

Heusch

2011

Circ J

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Cardiogenic Shock due to Tachycardiomyopathy after Heart Transplantation: Successful Treatment with Ivabradine

Cited by 23 publications

References 10 publications

Advances in the management of heart failure: the role of ivabradine

Advances in the management of heart failure: the role of ivabradine

Arrhythmia-Induced Cardiomyopathy: Prevalent, Under-recognized, Reversible

Heart Rate and Heart Failure - Not a Simple Relationship -

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