1. Genetic Pathogenesis of Hypertrophic and Dilated Cardiomyopathy
Amanda C. Garfinkel, BA, Jonathan G. Seidman, PhD, Christine E. Seidman, MD 
Heart Failure Clinics 
Volume 14, Issue 2, Pages (April 2018)
DOI: /j.hfc
Copyright © 2018 The Authors Terms and Conditions

2. Fig. 1
The sarcomere. Cardiac sarcomeres are composed of highly organized thick and thin myofilaments that produce bands that are visible by microscopy (top image). One sarcomere encompasses the region between 2 Z bands, where titin and thin filaments are anchored and interact with other Z-disc proteins. The I band denotes the region lacking thick filament motor proteins that reside in the A band. The M band is an overlap region that interconnects thick filament proteins within each sarcomere. Each titin molecule spans from the Z disc to the M band, encompassing one-half of a sarcomere. The thick filament fulfills motor and regulatory functions through proteins much as cardiac β-myosin heavy chain (MYH7) and myosin binding protein C (MYBPC3). The thin filament system contains actin as well as the troponin-tropomyosin calcium-regulatory apparatus that enables and regulates actomyosin interactions. Titin(TTN) plays multiple roles in sarcomere function, stability, and regulation.
Heart Failure Clinics  , DOI: ( /j.hfc )
Copyright © 2018 The Authors Terms and Conditions

3. Fig. 2
A schematic of sarcomere conformations and associated energy consumption throughout the cardiac cycle. A pair of myosin molecules is depicted, with each head denoted as blocked (BH) or free (FH). During contraction, both the BH and the FH are available for actomyosin interactions and ATP hydrolysis. During relaxation, myosins assume 2 dynamic and asymmetric conformations through the myosin IHM. In disordered relaxation (DRX), one myosin head is bound onto the thick filament backbone and is unavailable for actomyosin interactions. Energy consumption is at an intermediate level during DRX. In SRX, both myosin heads are docked onto the thick filament and energy conservation is maximized because both myosin ATPase domains are inhibited.
Heart Failure Clinics  , DOI: ( /j.hfc )
Copyright © 2018 The Authors Terms and Conditions