Chapters authored
Left Ventricular Noncompaction Cardiomyopathy: From Clinical Features to Animal Modeling
Cardiomyopathy or disease of the heart muscle involves abnormal enlargement and a thickened, stiff, or spongy-like appearance of the myocardium. As a result, the function of the myocardium is weakened and does not sufficiently pump blood throughout the body nor maintain a normal pumping rhythm, leading to heart failure. The main types of cardiomyopathies include dilated hypertrophic, restrictive, arrhythmogenic, and noncompaction cardiomyopathy. Abnormal trabeculations of the myocardium in the left ventricle are classified as left ventricular noncompaction cardiomyopathy (LVNC). Myocardial noncompaction most frequently is observed at the apex of the left ventricle and can be associated with chamber dilation or muscle hypertrophy, systolic or diastolic dysfunction, or both, or various forms of congenital heart disease. Animal models are incredibly important for uncovering the etiology and pathogenesis involved in this disease. This chapter will describe the clinical and pathological features of LVNC in humans and present the animal models that have been used for the study of the genetic basis and pathogenesis of this disease.
Part of the book: Preclinical Animal Modeling in Medicine
A Historical Review of Mechanical Circulatory Support
Meaningful and contemporary data regarding the clinical use of mechanical circulatory support (MCS) is founded on the work conducted in the 1950s when a “heart-lung” machine was incorporated to provide support during surgical interventions. Following this milestone, the need to support artificial circulation in patients with heart failure initiated an investigational and legislative collaboration to implement the mission-oriented Artificial Heart Program in the United States during the 1960s. In the subsequent decades, technological discoveries have integrated a series of mechanical systems employed as therapeutic options for short- and long-term artificial circulation in children and adults with advanced heart failure. Since their clinical application, MCS devices have been employed as a bridge to transplantation in over 4000 patients globally. In recent years, the adverse effects and economic burden of MCS have been counterbalanced by the harmonization of therapeutic protocols, the inclusion of multidisciplinary insight, and the allowance of families and patients to participate in shared decision making to address candidacy. In this chapter, we provide a review of the historical aspects of MCS, a therapeutic option for overcoming complexities encountered in reestablishing adequate hemodynamic states and providing a reasonable quality of life.
Part of the book: Ventricular Assist Devices
Myocardial Remodeling with Ventricular Assist Devices
Most prominent functional abnormalities seen in the failing human heart are impaired contraction and slowed rates of relaxation of cardiac cells in the face of increased neurohormonal activation, sustained inflammation, mechanical and volume overload, and progressive maladaptive remodeling of the myocardium. Mechanical circulatory support devices (MCS) improve cardiac function and outcomes of patients with end-stage heart failure, allowing to bridge to heart transplantation and permitting the removal of MCS device as a bridge to recovery, in some patients with the sufficient recovery of heart function. Numerous reports have demonstrated favorable myocardial recovery and reverse remodeling after prolonged ventricular unloading by MCS. Ventricular unloading by MCS leads to a decreased concentration of peripheral natriuretic peptides in plasma, reduction in cardiac cytokines, kinases, collagens, and proteins involved in hypertrophy, fibrosis, programmed cell death, and necrosis in the heart. This chapter will summarize and review the effects and underlying mechanisms of myocardial remodeling during prolonged MCS in patients with end-stage heart failure. The mechanisms of myocardial recovery are multifactorial and remain to be further explored on cellular, organ, and systems levels.
Part of the book: Ventricular Assist Devices