Left Ventricular Restoration Devices | SpringerLink

4 downloads 6512 Views 4MB Size Report
Feb 27, 2014 - Left Ventricular Restoration Devices. Authors; Authors and affiliations. Guilherme H. OliveiraEmail author; Sadeer G. Al-Kindi; Hiram G. Bezerra ...
J. of Cardiovasc. Trans. Res. (2014) 7:282–291 DOI 10.1007/s12265-014-9552-x

Left Ventricular Restoration Devices Guilherme H. Oliveira & Sadeer G. Al-Kindi & Hiram G. Bezerra & Marco A. Costa

Received: 4 February 2014 / Accepted: 14 February 2014 / Published online: 27 February 2014 # Springer Science+Business Media New York 2014

Abstract Left ventricular (LV) remodeling results in continuous cardiac chamber enlargement and contractile dysfunction, perpetuating the syndrome of heart failure. With current exhaustion of the neurohormonal medical paradigm, surgical and device-based therapies have been increasingly investigated as a way to restore LV chamber architecture and function. Left ventricular restoration has been attempted with surgical procedures, such as partial left ventriculectomy, surgical ventricular restoration with or without revascularization, and devices, such as the Acorn CorCap, the Paracor HeartNet, and the Myocor Myosplint. Whereas all these techniques require surgical access, with or without cardiopulmonary bypass, a newer ventricular partitioning device (VPD) called Parachute, can be delivered percutaneously through the aortic valve. Designed to achieve LV restoration from within the ventricle, this VPD partitions the LV by isolating aneurysmal from normal myocardium thereby diminishing the functioning cavity. This review aims to critically appraise the above methods, with particular attention to device-based therapies. Keywords Heart failure . Left ventricular remodeling . Ventricular partitioning device . Ventricular restoration

Introduction The nonappearance of new pharmacological therapies of proven benefit for heart failure (HF) patients in almost two decades [1] has boosted development of novel device and Associate Editor Craig Stolen oversaw the review of this article G. H. Oliveira (*) : S. G. Al-Kindi : H. G. Bezerra : M. A. Costa Department of Medicine, Division of Cardiovascular Medicine, Harrington Heart and Vascular Institute, University Hospitals Case Medical Center, Case Western Reserve University School of Medicine, Cleveland, OH, USA e-mail: [email protected]

surgical treatments for these patients. At present, in addition to neurohormonal blockade, developed in the latter part of the last millennium, selected patients with advanced HF are offered devices such as implantable cardiac defibrillators (ICD), cardiac resynchronization therapy (CRT), left ventricular assist devices (LVAD), as well as surgical therapies, including orthotopic heart transplantation (OHT). Furthermore, HF incidence continues to rise in the United States and 825,000 new cases were diagnosed in 2013 [2]. The last report from the NHLBI indicates that 5.1 million Americans over the age of 20 have HF, projected to increase by 46 % to over 8 million by 2030. Indeed, one in nine deaths in this country is attributable to HF, highlighting the fact that despite all medical and surgical advances, 50 % of patients diagnosed with HF will die within 5 years [2]. The process by which HF progresses and leads to death is called ventricular remodeling: an alteration in ventricular architectural phenotype characterized histologically by myocyte hypertrophy, apoptosis, and interstitial fibrosis [3]. It begins with an inciting insult, such as myocardial infarction, that produces initial fibrotic repair of the necrotic area, resulting in scar formation and subsequent wall thinning [4]. Despite muscle loss, cardiac output is maintained at the cost of a larger stroke volume, which leads to ever increasing end-diastolic pressures and wall stress. Left unchecked, a vicious cycle is established causing increased chamber size and sphericity of the LV with decreased contractile function [5]. This process has been shown to perpetuate itself inexorably, independent of the initial inciting cause [6]. Consequently, most interventions for HF, whether device-based or medical, have focused on arresting or reversing ventricular remodeling. Ventricular restoration is the general term used to describe methods to attempt reverse remodeling of the LV by reducing ventricular cavity, normalizing ventricular architecture, and reducing wall stress. It has been attempted both surgically and with devices, by either resection, compression, or isolation of nonfunctional myocardium. Herein, we will critically

J. of Cardiovasc. Trans. Res. (2014) 7:282–291

appraise the different ventricular restoration strategies, reviewing their applicability, method of implantation, and outcomes, with a specific focus on device-based therapies.

Historical Overview of LV Restoration

283

rehospitalizations for cardiac causes (58 % CABG+SVR vs. 59 % CABG) [16]. The results of the STICH trial were received with skepticism by both the surgical and medical HF community, and further scrutiny of the trial’s design, execution, and reporting have solidified the feeling that its conclusions should neither be widely applied nor lead to an immediate change in practice [17, 18].

Surgical Approaches Device-Based Approaches In the mid 1990s, Brazilian surgeon Randas Batista aroused the world’s attention by reporting a pioneering procedure to reduce ventricular size and wall stress in end-stage patients with dilated cardiomyopathy and EF