Abstract
Background: Chronic heart failure (CHF) is characterized by sustained activation of neurohormonal and cytokine systems leading to a series of end-organ changes within the myocardium referred to as left ventricular remodeling. Renin-Angiotensin system activation leading to secondary hyperaldosteronism is accompanied by ionized hypocalcemia with secondary hyperparathyroidism which causes dyshomeostasis of extra and intracellular calcium leading to cardiomyocyte necrosis. Objectives: To study the levels of serum calcium in patients of heart failure and its association with severity and duration of chronic heart failure. Methods: The study was conducted on 50 patients with CHF after taking informed consent. All patients met inclusion and exclusion criteria and underwent blood sampling, urine examination and other relevant investigations. Serum calcium levels were correlated with the severity and duration of CHF statistically. Results: Among the patients studied, 96% with ejection fraction (EF)≤ 35%, 87.5% with EF between 35-40% and 44.4% with EF ≥ 40% had low serum calcium values ≤9 mg/dl (p-value <0.001). All patients with duration of heart failure ≥ 2 years and 70.4% patients with duration of heart failure 1-2 years had low serum calcium levels ≤ 9 mg/dl (p value =0.001). Conclusion: There is a significant positive correlation of serum calcium levels with severity of heart failure as measured by EF and significant negative correlation with duration of CHF and NYHA functional grades. The degree of hypocalcemia correlates with severity of cardiomyocyte injury and extent of the neurohormonal response, and accordingly the corresponding risk of adverse cardiovascular events.
Highlights
Chronic heart failure (CHF) is a progressive disorder that is initiated after an index event which either damages the heart muscle, with a resultant loss of functioning cardiac myocytes, or disrupts the ability of the myocardium to generate force, thereby preventing the heart from contracting normally [1]
These include plasma-ionized hypocalcemia and hypomagnesemia that account for secondary hyperparathyroidism (SHPT) and elevated plasma parathyroid hormone (PTH) levels, together with hypovitaminosis D that further compromises calcium (Ca2+) balance, hypozincemia, and hyposelenemia [4,5,6,7,8]
PTHmediated intracellular Ca2+ overloading is coupled to an induction of oxidative stress in cardiomyocytes and their mitochondria that triggers the downhill final common cell death pathway leading to cardiomyocyte necrosis and subsequent replacement fibrosis
Summary
Chronic heart failure (CHF) is a progressive disorder that is initiated after an index event which either damages the heart muscle, with a resultant loss of functioning cardiac myocytes, or disrupts the ability of the myocardium to generate force, thereby preventing the heart from contracting normally [1]. Persistent neurohormonal activation involving the RAS and sympathetic nervous system occurs with protracted CHF causing a dyshomeostasis of divalent cations These include plasma-ionized hypocalcemia and hypomagnesemia that account for secondary hyperparathyroidism (SHPT) and elevated plasma parathyroid hormone (PTH) levels, together with hypovitaminosis D that further compromises calcium (Ca2+) balance, hypozincemia, and hyposelenemia [4,5,6,7,8]. The calcium-sensing receptor of the parathyroid glands, in turn, responds to hypocalcemia with increased secretion of parathyroid hormone (PTH) [11,12,13,14,15,16] In cardiomyocytes, these calcitropic hormones, simultaneously promote L-type Ca2+ channel activity leading to increased cytosolic free Ca2+ and, in turn, mitochondrial Ca2+ overloading with organellar-based oxidative stress. Renin-Angiotensin system activation leading to secondary hyperaldosteronism is accompanied by ionized hypocalcemia with secondary hyperparathyroidism which causes dyshomeostasis of extra and intracellular calcium leading to cardiomyocyte necrosis
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