The heart normally is an efficient physiological pump whose muscular compartment is composed of a syncytium of cardiomyocytes nourished by a coronary vasculature and housed within a scaffolding of structural proteins. The contractile properties of cardiomyocytes are governed by the direct interplay between Ca²⁺ and contractile proteins, actin and myosin, and their intracellular handling of Ca²⁺. Likewise, extracellular Ca²⁺ handling, or Ca²⁺ homoeostasis, can indirectly influence cardiomyocyte contractility. Herein, we briefly examine Ca²⁺ dyshomoeostasis and heart failure.

CALCIUM DYSHOMOEOSTASIS

Plasma Ca²⁺ concentrations are highly regulated and maintained within a narrow range. If disturbed, a series of controlling factors and feedback mechanisms are called into play. Overall Ca²⁺ homoeostasis relates to its dietary intake; absorption and excretion from gut and kidneys; bone storage; and the modifying influence of such calcitropic hormones as calcitriol (activated vitamin D) and parathyroid hormone (PTH).

In utero, the availability of Ca²⁺ for fetal growth and development, including the bony skeleton, depends on maternal factors such as: (a) dietary Ca²⁺ intake, which may be reduced, particularly in vegans or in some women with lactose intolerance, who avoid dairy products; (b) urinary and fecal Ca²⁺ losses; (c) Ca²⁺ bone stores that may be mobilised if Ca²⁺ availability is compromised; and (d) vitamin D status, as assessed by serum 25-hydroxyvitamin D (25-(OH)D) levels. 25-(OH)D levels are chiefly dependent on supplementation and sunlight exposure that may be limited by culturally imposed dress code, skin pigmentation, where melanin is a natural sunscreen that mandates longer exposure to the UVB component of sunlight to generate vitamin D, senescent skin less able to produce vitamin D, obesity where adipocytes sequester it, the altitude, latitude and locale (urban vs rural) of …