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The relationship between calcium and magnesium in pediatric myocardial protection
M Kronon1, K S Bolling, B S Allen
1Division of Cardiothoracic Surgery, University of Illinois at Chicago 60612-7323, USA.
Insights
Magnesium supplementation of cardioplegic solutions is crucial for protecting the neonatal heart during surgery. It prevents detrimental effects of calcium in normocalcemic solutions, ensuring better cardiac function post-procedure.
Area of Science:
- Cardiovascular Research
- Neonatal Cardiology
- Pediatric Cardiac Surgery
Background:
- Calcium has been shown to be detrimental to the neonatal heart under hypoxic conditions.
- Magnesium is known to inhibit calcium transport, but its protective role in cardioplegic solutions is not well-established.
Purpose of the Study:
- To investigate the efficacy of magnesium in preventing calcium-induced damage in neonatal hearts during cardioplegic arrest.
- To compare the effects of hypocalcemic and normocalcemic cardioplegic solutions, with and without magnesium, on myocardial function.
Main Methods:
- Neonatal piglets underwent hypoxic stress followed by cardiopulmonary bypass and cardioplegic arrest.
- Animals received either hypocalcemic or normocalcemic cardioplegic solutions, with or without magnesium supplementation.
- Myocardial function was assessed using pressure-volume loops, and coronary vascular resistance was measured.
Main Results:
- Magnesium did not alter the cardioprotective effects of hypocalcemic solutions.
- Normocalcemic solutions without magnesium significantly impaired post-bypass cardiac function, increasing stiffness and edema.
- Magnesium supplementation of normocalcemic solutions preserved myocardial function and prevented adverse effects.
Conclusions:
- Magnesium does not interfere with the cardioprotective benefits of hypocalcemic cardioplegic solutions.
- Normocalcemic cardioplegic solutions can be harmful to neonatal hearts previously exposed to hypoxic stress.
- Supplementing normocalcemic cardioplegic solutions with magnesium effectively mitigates calcium's deleterious effects, ensuring functional recovery.
Objective:
We previously demonstrated that calcium can be harmful to the hypoxic neonatal heart. Despite the fact that magnesium inhibits membrane transport of calcium, few studies have examined whether magnesium can prevent the deleterious effects of calcium in cardioplegic solutions.
Methods:
Twenty neonatal piglets (5 to 18 days old) underwent 60 minutes of ventilator hypoxia (inspired oxygen fraction 8% to 10%) followed by reoxygenation with the use of cardiopulmonary bypass before cardioplegic arrest to produce a clinically relevant hypoxic "stress" injury. The aorta was then crossclamped for 70 minutes with multidose blood cardioplegia. Ten piglets received a hypocalcemic (0.2 to 0.4 mmol/L) cardioplegic solution without (group 1, n = 5) or with magnesium (10 mEq/L) (group II, n = 5) supplementation. Ten other piglets were protected with a normocalcemic (1.0 to 1.2 mmol/L) cardioplegic solution without (group III, n = 5) or with magnesium (group IV, n = 5). Myocardial function was assessed by means of pressure volume loops and expressed as a percentage of control. Coronary vascular resistance was assessed during each cardioplegic infusion.
Results:
Adding magnesium to a hypocalcemic cardioplegic solution (groups I and II) had no effect: Both groups had complete preservation of postbypass systolic function (end-systolic elastance 101% vs 104%) and preload recruitable stroke work (101% vs 102%), minimal increase in diastolic stiffness (159% vs 153%), and no difference in myocardial tissue edema (78.8% vs 78.9%) or coronary vascular resistance. Conversely, when a normocalcemic cardioplegic solution was administered without magnesium supplementation (group III), the results were markedly poorer than results obtained with magnesium supplementation (group IV). Without magnesium, there was a marked reduction in postbypass systolic function (end-systolic elastance 49% vs 101%; p < 0.05), increased diastolic stiffness (276% vs 162%; p < 0.05), decreased preload recruitable stroke work (53% vs 102%; p < 0.05), increased myocardial tissue edema (80.0% vs 78.9%; p < 0.05), and a rise in coronary vascular resistance (p < 0.05). Magnesium supplementation of the normocalcemic cardioplegic solution, by contrast, resulted in complete functional recovery.
Conclusions:
This study demonstrates that (1) magnesium does not alter the cardioprotective effects of a hypocalcemic cardioplegic solution, (2) a normocalcemic cardioplegic solution is detrimental to neonatal myocardium subjected to a previous hypoxic stress, and (3) magnesium supplementation of normocalcemic cardioplegic solutions prevents the deleterious effects of calcium.