Cardiac contractility modulation for the treatment of heart failure with reduced ejection fraction
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Cardiac contractility modulation for the treatment of heart failure with reduced ejection fraction Peysh A. Patel 1 & Ramesh Nadarajah 1 & Noman Ali 1 & John Gierula 1 & Klaus K. Witte 1 Accepted: 21 August 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract There has been a progressive evolution in the management of patients with chronic heart failure and reduced ejection fraction (HFrEF), including cardiac resynchronisation therapy (CRT) in those that fulfil pre-defined criteria. However, there exists a significant proportion with refractory symptoms in whom CRT devices are not clinically indicated or ineffective. Cardiac contractility modulation (CCM) is a novel therapy that incorporates administration of non-excitatory electrical impulses to the interventricular septum during the absolute refractory period. Implantation is analogous to a traditional transvenous pacemaker system, but with the use of two right ventricular leads. Mechanistic studies have shown augmentation of left ventricular contractility and beneficial global effects on reverse remodeling, primarily through alterations in calcium handling. This appears to occur without increasing myocardial oxygen consumption. Data from clinical trials have shown translational improvements in functional capacity and quality of life, though long-term outcome data are lacking. This review explores the rationale, evidence base and limitations of this nascent technology. Keywords CHF . CCM . Heart failure . LVSD
Introduction The prevalence of chronic heart failure with reduced ejection fraction (HFrEF) is rising in the twenty-first century, reflective of an ageing population and improvements in the management of comorbidities such as ischaemic heart disease, hypertension and diabetes mellitus [1]. The cohort of patients with HFrEF represents a heterogeneous group in terms of demographics, underlying aetiology and severity. Nonetheless, recent decades have observed a progressive shift in the pharmacological armamentarium available to treat this disorder. Angiotensin-converting enzyme inhibitors (ACE-i), betablockers and mineralocorticoid receptor antagonists (MRA) constitute the mainstay of guideline-based therapy for severe HFrEF and confer symptomatic and prognostic benefit [2]. More recently, sacubitril/valsartan and dapagliflozin have been recommended for use in select cohorts when symptoms are refractory to traditional measures [3, 4]. In terms of device therapy, implantable cardioverter-defibrillators (ICDs) are evidenced to improve survival in those with severe HFrEF who * Peysh A. Patel [email protected] 1
Department of Cardiology, Leeds General Infirmary, Great George Street, Leeds LS1 3EX, UK
are otherwise on optimal medical therapy (OMT) [5]. However, ICDs do not improve symptoms, and the prognostic benefit is less in patients with advanced symptoms. Cardiac resynchronisation therapy (CRT), either with a defibrillator (CRT-D) or without (CRT-P), is evidenced to improve symptoms, reduce hospitalisation and confer survival
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