Electrolyte balance in heart failure and the role for magnesium ions

doi:10.1016/0002-9149(92)91357-A

The American Journal of Cardiology

Volume 70, Issue 10, 8 October 1992, Pages 44-49

https://doi.org/10.1016/0002-9149(92)91357-A Get rights and content

Abstract

It is well established that clinically significant changes in a number of electrolytes occur in patients with congestive heart failure (CHF). Magnesium ions are an essential requirement for many enzyme systems, and evidence is rapidly emerging that magnesium deficiency is a major risk factor for survival of CHF patients. In animal experiments, magnesium has been shown to be involved in several steps of the atherosclerotic process and, although in humans the situation is somewhat more complex, magnesium ions play an extremely important role in CHF and various cardiac arrhythmias. A number of drugs commonly used to treat CHF can significantly affect not only cellular magnesium ion homeostasis, but potassium as well. These include mercurial, thiazide, and loop diuretics. It has also been reported that hypomagnesemia is common in digitalis intoxication. In contrast, a number of agents have been shown to have either a magnesium-conserving effect (potassium-sparing diuretics) or not to affect magnesium ion balance (angiotensin-converting enzyme inhibitors). The clinical consequences of magnesium deficiency include the development of various cardiac arrhythmias, all of which respond well to magnesium treatment. Thus, it is more than apparent that magnesium ion homeostasis is of major importance in CHF. Future studies should address the complex role of magnesium ions in electrolyte imbalance, particularly in relation to heart failure.

References (51)

JH Cort et al.
Potassium deficiency in congestive heart failure: three cases with hyponatremia including results of potassium replacement in one case
Lancet
(1954)
E Ryzen et al.
Low blood mononuclear cell magnesium in intensive cardiac care patients
Am Heart J
(1986)
O Storstein et al.
Studies on digitalis XIII. A prospective study of 649 patients on maintenance treatment with digitoxin
Am Heart J
(1977)
RA Reinhart
Clinical correlates of the molecular and cellular actions of magnesium on the cardiovascular system
Am Heart J
(1991)
T Dyckner et al.
Effect of peroral magnesium on plasma and skeletal muscle electrolytes in patients on long-term diuretic therapy
Int J Cardiol
(1988)
LF Iseri et al.
Magnesium: nature's physiologic calcium blocker
Am Heart J
(1984)
SS Gottlieb et al.
Prognostic importance of the serum magnesium concentration in patients with congestive heart failure
J Am Coll Cardiol
(1990)
Y Rayssiguer
Role of magnesium and potassium in the pathogenesis of arteriosclerosis
Magnesium Bull
(1984)
E Löwenhaupt et al.
Basic histologic lesions of magnesium deficiency in rat
Arch Pathol
(1950)
KK Teo et al.
Effects of intravenous magnesium in suspected acute myocardial infarction. Overview of randomid trials
Br Med J
(1991)

AM Thögersen et al.

Magnesium infusion in thrombocytic treated patients with acute myocardial infarctions

PO Wester et al.

Magnesium and hypertension

J Am Coll Nutr

(1987)

PO Wester et al.

Intracellular electrolytes in cardiac failure

Acta Med Scand

(1986)

EJN Camara et al.

Muscle magnesium content and cardiac arrhythmias during treatment of congestive heart failure due to chronic chagasic cardiomyopathy

Braz J Med Biol Res

(1986)

MA Ralston et al.

Magnesium content of serum, circulating mononuclear cells, skeletal muscle, and myocardium in congestive heart failure

Circulation

(1989)

M Brunette et al.

Micropuncture study of magnesium reabsorption in the proximal tubule of the dog

Am J Physiol

(1969)

SG Massry et al.

Effects of NaCl nfusion on urinary Ca⁺⁺ and Mg⁺⁺ during reduction in their filtered load

Am J Physiol

(1967)

HE Abboud et al.

Stimulation of renin by acute selective chloride depletion in the rat

Circ Res

(1979)

J Genest et al.

Factors regulating aldosterone secretion

JJ Mader et al.

Spontaneous hypopotassemia, hypomagnesemia, alkalosis and tetany due to hypersecretion of corticosterone-like mineralocorticoid

Am J Med

(1955)

S Wallach

Physiologic and critical interrelations of hormones and magnesium, consideration of thyroid, insulin, corticosteroids, sex steroids and catecholamines

R Vandongen et al.

Adrenergic stimulation of renin secretion in the isolated perfused rat kidney

Circ Res

(1973)

MJ Brown et al.

Hypokalemia from β₂ stimulation by circulating epinephrine

N Engl J Med

(1983)

KF Whyte et al.

Adrenergic control of plasma magnesium in man

Clin Sci

(1987)

GG Belz et al.

Epinephrine infusion decreases magnesium plasma concentration in humans

J Cardiovasc Pharmacol

(1985)

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These in turn, by virtue of renal sodium and fluid retention, produce a rise in extracellular volume, which inhibits tubular magnesium re-absorption and thus exaggerates urinary magnesium loss (Wester, 1992; Douban et al., 1996). Magnesium efflux from the blood compartment into cells may take place under the influence of acidosis or increased catecholamine production, both of which are prevalent in CHF (Wester, 1992; Douban et al., 1996; Kjaer and Hesse, 2001). Hypocalcemia was the predominant electrolyte change associated with HM and presented in 59% (20/31) of patients, following by hypokalemia (51%, 19/32) and hypophosphatemia (42%, 13/31).
Electrolyte abnormalities are frequently observed in elderly long-term care (LTC) patients. Magnesium is a trace mineral, but is the second most abundant intracellular cation and the fourth most abundant cation in the body. This was a cross-sectional study to assess the prevalence of hypomagnesemia (HM) in non-selected elderly LTC patients. A total of 159 patients aged 65 years and older were included in the study. The attributes and variables related to the patients’ hospital course were used to compare the two groups. We used univariate and multivariate analyses to correlate magnesium levels with demographic, clinical factors and laboratory data. HM was found in 36% of the patients, of whom 35% presented with moderate HM (0.8–0.9 μequiv./l) and 18% with severe HM (≤0.7 μequiv./l). Patients with HM had a higher number of comorbid diseases per patient (p = 0.038), low body mass index (BMI) (p = 0.044) and more of them presented with laboratory markers of malnutrition, such as low total cholesterol (TC) and serum albumin (SA) levels. Coexistence with other electrolyte abnormalities was higher among patients with HM than without (p = 0.006), predominantly hypocalcemia and hypokalemia (p = 0.023 and 0.032, respectively). Using regression analysis, independent variables significantly associated with serum magnesium levels were serum albumin, calcium, potassium, urea levels, chronic renal failure (CRF), chronic heart failure (CHF), diabetes mellitus (DM) and diuretic drugs (R² = 0.877). Both early (up to 30 days) and late rate of death were higher in patients with HM. The incidence of HM in LTC elderly patients is high and multifactorial. Understanding the causes of HM, correction of magnesium level, and definitive and effective treatment of the cause leading to HM is important to improve patient prognosis.
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In fact, icMg depletion in HF is more frequent than hypomagnesemia [22,25]. Mg deficiency in HF may result from reduced dietary intake, impaired intestinal Mg absorption and/or exaggerated urinary excretion generated by renin–angiotensin–aldosterone system activation, and/or loop diuretics [17,18]. High catecholamine levels in HF have been reported to increase urinary excretion of Mg [26] and further reduce icMg [27].
Intracellular magnesium (icMg) depletion may coexist with normomagnesemia. Mg deficiency (serum and/or intracellular) and decreased heart rate variability (HRV) are common in heart failure (HF). Since both are predictors of poor prognosis, it was of interest to evaluate the effect of Mg supplementation on HRV in patients with HF.
We investigated the effect of Mg administration on HRV in normomagnesemic patients with systolic HF. HRV, serum Mg and icMg were determined before and after 5-week 300 mg/day Mg citrate treatment in 16 patients (group 1). The control group included 16 Mg-non-treated HF patients (group 2). HRV was determined by a non-linear dynamics analysis, derived from the chaos theory, which calculates HRV–correlation dimension (HRV–CD). After 5 weeks, serum Mg (mmol/l) increased more significantly in group 1 (from 0.78 ± 0.04 to 0.89 ± 0.06, p < 0.001), than in group 2 (from 0.79 ± 0.07 to 0.84 ± 0.06, p = 0.042). IcMg and HRV–CD increased significantly only in group 1 (from 59 ± 7 to 66 ± 9 mmol/g cell protein, p = 0.025, and from 3.47 ± 0.42 to 3.94 ± 0.36, p < 0.001, respectively). In group 2, the differences in the respective parameters were 63 ± 12 to 66 ± 9 mmol/g cell protein (p = 0.7) and 3.59 ± 0.42 to 3.55 ± 0.4 (p = 0.8).
Mg administration to normomagnesemic patients with systolic HF increases serum Mg, icMg and HRV–CD. Increasing of HRV by Mg supplementation may prove beneficial to HF patients.
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Low serum magnesium levels may cause fatal ventricular arrhythmias. However, their long-term effects on mortality and morbidity in chronic heart failure patients are relatively unknown.
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In a propensity-matched population of ambulatory chronic heart failure patients who were balanced in all measured baseline covariates, serum magnesium level 2 mEq/L or less was associated with increased cardiovascular mortality, but had no association with cardiovascular hospitalization.
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Medications, such as loop and thiazide diuretics contribute to urinary magnesium loss. Magnesium deficiency is associated with sodium retention and increased ventricular ectopy [110–112] with associated reduced cardiac contractility and increased peripheral vascular resistance [113,114]. Zinc is a trace mineral that is required for proper function of one of the antioxidant enzyme systems and its deficiency is related to apoptosis of the myocardiocyte [115].
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Electrolyte balance in heart failure and the role for magnesium ions

Abstract

Lancet

Am Heart J

Am Heart J

Am Heart J

Int J Cardiol

Am Heart J

J Am Coll Cardiol

Role of magnesium and potassium in the pathogenesis of arteriosclerosis

Magnesium Bull

Basic histologic lesions of magnesium deficiency in rat

Arch Pathol

Effects of intravenous magnesium in suspected acute myocardial infarction. Overview of randomid trials

Br Med J

Magnesium infusion in thrombocytic treated patients with acute myocardial infarctions

Magnesium and hypertension

J Am Coll Nutr

Intracellular electrolytes in cardiac failure

Acta Med Scand

Muscle magnesium content and cardiac arrhythmias during treatment of congestive heart failure due to chronic chagasic cardiomyopathy

Braz J Med Biol Res

Magnesium content of serum, circulating mononuclear cells, skeletal muscle, and myocardium in congestive heart failure

Circulation

Micropuncture study of magnesium reabsorption in the proximal tubule of the dog

Am J Physiol

Effects of NaCl nfusion on urinary Ca++ and Mg++ during reduction in their filtered load

Am J Physiol

Stimulation of renin by acute selective chloride depletion in the rat

Circ Res

Factors regulating aldosterone secretion

Spontaneous hypopotassemia, hypomagnesemia, alkalosis and tetany due to hypersecretion of corticosterone-like mineralocorticoid

Am J Med

Physiologic and critical interrelations of hormones and magnesium, consideration of thyroid, insulin, corticosteroids, sex steroids and catecholamines

Adrenergic stimulation of renin secretion in the isolated perfused rat kidney

Circ Res

Hypokalemia from β2 stimulation by circulating epinephrine

N Engl J Med

Adrenergic control of plasma magnesium in man

Clin Sci

Epinephrine infusion decreases magnesium plasma concentration in humans

J Cardiovasc Pharmacol

Effects of NaCl nfusion on urinary Ca⁺⁺ and Mg⁺⁺ during reduction in their filtered load

Hypokalemia from β₂ stimulation by circulating epinephrine