Defective excitation-contraction coupling in heart failure may result from altered density or function of proteins relevant for calcium homeostasis.
Heart failure (HF) has reached epidemic proportions in the United States and is one of the most important challenges to public health. Severe congestive HF is associated with substantial morbidity and mortality. HF afflicts approximately 5 million patients and contributes to 3 million hospitalizations and 300,000 deaths yearly. Late-stage HF has a poor prognosis, and therapeutic options are limited. Defective excitation–contraction (EC) coupling in HF may result from altered density or function of proteins relevant for Ca2+ homeostasis.
Hadri et al. (Wed,) conducted a review in Heart failure. Defective excitation-contraction coupling in heart failure may result from altered density or function of proteins relevant for calcium homeostasis.