In adapting to disease and loss of tissue, the heart shows great phenotypic plasticity that
involves changes to its structure, composition and electrophysiology. Together with parallel …

Ca 2+ is a central player in the excitation-contraction coupling of cardiac myocytes, the
process that enables the heart to contract and relax. Mishandling of Ca 2+ is a central cause …

Ca2+ in cardiac myocytes regulates contractility and relaxation, and Ca2+ and Na+
regulation are linked via Na+/Ca2+ exchange (NCX). Heart failure (HF) is accompanied by …

In myocytes from failing hearts, Ca2+ delivery into and removal from the cells is altered in a
way that ultimately produces smaller intracellular Ca2+ transients. Ca2+ plays a …

Cardiac myocyte excitation—contraction coupling is complex. There are many systems
involved that interact to form varied, but well‐tuned, effects that are essential to contractile …

Key points During compensated hypertrophy in vivo fractional shortening (FS) remains
constant until heart failure (HF) develops, when FS decreases from 70% to 39 …

Myocytes from the failing myocardium exhibit depressed and prolonged intracellular Ca2+
concentration ([Ca2+] i) transients that are, in part, responsible for contractile dysfunction …

Ventricular arrhythmias and contractile dysfunction are the main causes of death in human
heart failure (HF). In a rabbit HF model reproducing these same aspects of human HF, we …

Ca 2+ is a major intracellular messenger and nature has evolved multiple mechanisms to
regulate free intracellular (Ca 2+) i level in situ. The Ca 2+ signal inducing contraction in …

For many years, the treatment of heart failure has focused, successfully, on the
neurohumoral pathways, but recently more attention has again been given to the heart itself …