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Ann Thorac Surg 1995;59:502-507
© 1995 The Society of Thoracic Surgeons

Magnesium Sulfate Prophylaxis After Cardiac Operations

Divisions of Cardiac and Thoracic Surgery, Cardiology, and Cardiac Anaesthesia, University of Alberta, Edmonton, Alberta, Canada

Accepted for publication October 27, 1994.

	Abstract

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One hundred patients undergoing elective cardiac operations were randomized into placebo (n = 54) and magnesium (n = 46) groups. The magnesium group received six doses of 2.4 g (19.2 mEq) magnesium sulfate intravenously in the first 24 hours after the cardiac operation. The magnesium group had higher serum magnesium concentrations postoperatively (1.09 ± 0.20 versus 0.75 ± 0.13 mmol/L; p < 0.0001), postoperative day 1 (1.49 ± 0.34 versus 0.70 ± 0.12 mmol/L; p < 0.0001) and postoperative day 2 (0.96 ± 0.19 versus 0.76 ± 0.07 mmol/L; p < 0.0001). Patients in the magnesium group had a lower incidence of ventricular tachyarrythmias (VTs) (17.3% versus 51.9%; p = 0.0006), less need for treatment (6.5% versus 20.3%; p < 0.0001), fewer VT episodes/patient (0.3 ± 0.8 versus 1.39 ± 1.9; p < 0.0001), and a reduction in the severity of VTs as measured by the modified Lown grade (p = 0.0002). No differences were demonstrated with respect to supraventricular tachyarrythmias. The magnesium group had reduced absolute creatine kinase-MB levels (5.3 ± 4.2 versus 28.4 ± 28 IU/L; p = 0.001) as well as creatine kinase-MB fraction (0.01 ± 0.02 versus 0.05 ± 0.04; p = 0.001) on postoperative day 1. Serum magnesium concentrations were lower during VTs than during periods of sinus rhythm (0.75 ± 0.75 versus 1.02 ± 0.35 mmol/L; p < 0.001). Patients with VTs had higher serum creatine kinase-MB levels than those that did not both postoperatively (32.7 ± 26 versus 23.0 ± 14.7 IU/L; p = 0.04) and on postoperative day 1 (29.7 ± 32 versus 10.3 ± 11.7 IU/L; p = 0.019). Magnesium sulfate prophylaxis prevents hypomagnesemia and reduces the incidence and severity of VTs postoperatively, possibly by enhancing myocardial protection.

	Introduction

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Postoperative ventricular tachyarrhythmias (VTs) and supraventricular tachyarrhythmias (SVTs) occur in approximately 30% and 54%, respectively, of patients after open heart operations [1, 2]. Many drugs used as treatment of or prophylaxis against these dysrhythymias are associated with significant complications without a clearly demonstrated benefit [3–13]. Hypomagnesemia has been demonstrated in nearly 70% of patients after cardiopulmonary bypass [14]. Magnesium sulfate administered postoperatively appears to reduce the incidence and severity of VTs and possibly SVTs after cardiac operations [5, 15, 16]. This study was designed to determine whether prophylactic treatment with magnesium sulfate would result in a reduction of SVTs and VTs after elective cardiac operations.

	Material and Methods

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Subjects
One hundred patients who were undergoing elective coronary artery bypass, valve replacement/repair, or a combination of these were enrolled after informed consent was obtained. Exclusion criteria included abnormal renal function, reoperation, emergency operation, evidence of ongoing ischemia (angina, ST changes), the use of medications to control dysrhythmias, and inability to obtain informed consent.

Study Design
The protocol was approved by the Ethics Review Board. All patients underwent operation using moderate hypothermia (28° to 32°C), antegrade blood cardioplegic arrest, and intermittent cardioplegia with a magnesium-free solution. After randomization the magnesium group received 2.4 g (19.2 mEq) of magnesium sulfate in 50 mL of 5% dextrose in water intravenously over 20 minutes at the termination of cardiopulmonary bypass and every 4 hours for a further 5 doses (total, 14.4 g; 115 mEq). The placebo group received 50 mL 5% dextrose in water at the same time points. Patients were followed up for the entire hospital stay.

Potassium (10 to 20 mEq potassium chloride in 50 mL normal saline solution) and calcium (1 g calcium gluconate in 50 mL normal saline solution) were administered as required to maintain the concentrations of potassium at 4.5 mmol/L or greater and ionized calcium at 1.2 mmol/L or greater. Interventions were directed to maintain normal tissue perfusion as indicated by normal urine output, absence of metabolic acidosis, and normal skin temperature and capillary refill. Where Swan-Ganz catheters were employed ``ideal'' target cardiac indices were 2.2 L • min^-1 • m^-2 or greater.

Patients were continuously monitored for a minimum of 24 hours using bedside monitors (Hewlett-Packard) that are alarm triggered and capable of automated recall. The system is observed constantly by monitor nurses. Electrocardiograms were obtained postoperatively and on the first 2 mornings after the operation. After this period, when there was a question of dysrhythmia either on clinical grounds or by telemetry, a 12-lead electrocardiogram was obtained.

Prophylactic antidysrhythmics were not used. Ventricular tachyarrhythmias were treated if they met the following criteria: greater than 6/min, R on T phenomenon, multifocal, or associated with hypotension. In the absence of these features, couplets, triplets, and nonsustained ventricular tachycardia (less than 30 seconds) were not treated. Treatment consisted of lidocaine, 1 mg/kg, administered over 10 seconds followed by an infusion of up to 4 mg/min. If this was ineffective or if SVTs also occurred, procainamide was added. Cardioversion was performed for any tachyarrythmias that resulted in significant hypotension.

Ventricular tachyarrhythmias were graded according to the modified Lown grade [5, 17] (Table 1). The scoring and designation of the dysrhythmias was performed by blinded cardiac surgeons or cardiologists. Episodes were recorded as the highest grade dysrhythmia that occurred within a 24-hour period, starting with the time cardiopulmonary bypass was terminated. Dysrhythmias that recurred, or continued, into a subsequent 24-hour period were recorded as an additional episode. ST segments were considered to be elevated if they were greater than 3 mm with no evidence of intraventricular conduction abnormality.

If patients had a Swan-Ganz catheter in place cardiac index (CI), left ventricular stroke work index (LVSWI), and stroke volume index (SVI) were calculated at 2 hours and 24 hours after termination of cardiopulmonary bypass. Stroke volume index was calculated according to the following formula: SVI = CI/HR (normal = 40 ± 7 mL/m²), where HR = heart rate. Left ventricular stroke work index was calculated according to the formula: LVSWI = (MAP-PCWP) (SVI) (0.0136) (normal = 43 to 56 g • m/m²), where MAP = mean arterial pressure and PCWP = pulmonary capillary wedge pressure.

Individuals recording data and designating dysrhythmias were not involved in patient management and were blinded to serum magnesium concentrations. Physicians directing therapy were also blinded to all but the initial postoperative serum magnesium results. Magnesium was not given routinely.

Statistical Analysis
Statistical analysis was performed using the SPSS/PC+ software package. Statistical significance was inferred if p was less than 0.05. Discrete variables were analyzed using the ² test. Continuous variables were studied using two-tailed t test. Linear and logistic regression for continuous and discrete variables, respectively, were used to examine effects on dependent variables. Kruskal-Wallace one-way analysis of variance was used to perform rank analysis. Initially, assuming a 30% incidence of VTs and hoping to demonstrate a 50% reduction, we had calculated that a sample size of 154 would be required, using an error of 0.05 and a ß error of 0.1. Review of the literature suggested that significant differences could be identified with a sample size of 100 patients [15, 18], and we decided to perform interim analysis at that point.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Comparison of Groups
There were no significant differences in baseline characteristics between groups save that the magnesium group was significantly older (p = 0.036) (Table 2). There were no differences in postoperative ventilatory or inotropic requirements (Table 3). There were two deaths in the placebo group, one caused by multiple organ failure and the other caused by ventricular fibrillation.

View larger version (21K): [in this window] [in a new window]   Fig 1. . Serum magnesium concentrations in magnesium (top line) and placebo (bottom line) groups at the following time points: 1 = preoperative; 2 = postoperative; 3 = 12 hours after cardiopulmonary bypass; 4 = postoperative day 1; 5 = ostoperative day 2; 6 = ostoperative day 3; 7 = ostoperative day 4.

View larger version (18K): [in this window] [in a new window]   Fig 2. . Classification of arrythmias by modified Lown grade in the first 24 hours after cardiopulmonary bypass. (F = requent; M = ultiformed; N = one; O = ccasional; R = epetitive; S = ustained.)

There was no significant difference noted in the incidence of SVTs, the number of episodes per patient, or the need for treatment.

The magnesium group had a significantly lower incidence of postoperative ST segment elevation. On postoperative day 1 the magnesium group had significantly lower CK-MB levels as well as CK-MB fraction and CK-MB concentrations of 50 IU/L or more (see Table 4).

The initial presentation and subsequent course for each patient experiencing a tachyarrhythmia was reviewed. In the placebo group, 20 patients presented initially with modified Lown grade occasional or frequent VTs. Of these 2 progressed to nonsustained ventricular tachycardia without hypotension and resolved spontaneously. Eight patients presented with higher grade VTs, 4 of whom had short runs of ventricular tachycardia, with 2 requiring lidocaine. Multifocal premature ventricular contractions developed after coronary artery bypass grafting in 1 patient and progressed to ventricular fibrillation despite lidocaine and procainamide treatment; this patient could not be resuscitated.

In the magnesium group, 4 patients presented with modified Lown grade occasional or frequent VTs, none of which were associated with hypotension. Four patients presented with higher grade VTs, 1 with a five-beat burst of ventricular tachycardia that did not result in hypotension and resolved spontaneously.

Tachyarrhythmias
Subgroup analysis, considering dysrhythmias rather than randomization into placebo or magnesium groups, was performed. Magnesium concentrations were significantly lower during episodes of VTs compared with normal sinus rhythm (0.75 ± 0.75 versus 1.02 ± 0.35 mmol/L; p < 0.001). There were no significant differences noted preoperatively or intraoperatively between patients who experienced VTs and those who did not with respect to cross-clamp time, cardiopulmonary bypass time, number of grafts, valve operation, age, sex, preoperative history of VTs or SVTs, Canadian Cardiovascular Society score, or New York Heart Association score. Patients who experienced VTs had significantly lower preoperative ejection fraction (0.43 ± 0.11 versus 0.50 ± 0.12; p = 0.007) and demonstrated prolonged length of stay (9.8 ± 13.8 versus 5.9 ± 1.7 days; p = 0.028), elevated postoperative CK-MB level (32.7 ± 14.7 versus 23.0 ± 14.7 IU/L; p = 0.041) and elevated CK-MB levels on postoperative day 1 (29.7 ± 32 versus 10.3 ± 11.7 IU/L; p = 0.019). Regression analysis studying the effects of being in placebo or magnesium group, preoperative history of arrhythmias or palpitations, valve operation, number of grafts, age, ejection fraction, CK-MB level and CK-MB fraction, cross-clamp time, and cardiopulmonary bypass time revealed that the only factor correlating with absence of VTs was being in the magnesium group (p < 0.001).

Twenty-five patients experienced at least one episode of SVT (atrial flutter, 1; junctional tachycardia, 1; atrial fibrillation, 23). Supraventricular tachyarrhythmias resolved spontaneously in 3 cases. Medical therapy resulted in conversion to sinus rhythym in 15 patients (6 with digoxin, 6 with sotalol, 3 with sotolol after failure with digoxin). Seven patients were discharged in atrial fibrillation. None of these patients experienced hypotension.

Serum magnesium concentrations during episodes of SVTs (0.92 ± 0.33 mmol/L) did not differ from those during normal sinus rhythm (p = 0.193). Patients who experienced SVTs had a significantly increased length of stay as opposed to those who did not (11.2 ± 16.7 versus 6.0 ± 1.9 days; p = 0.001). Multivariate analysis studying the same factors as with VTs revealed that only elevated postoperative CK-MB level and CK-MB fraction correlated with SVTs (p < 0.05). There was no correlation with the preoperative use of beta blockers, digoxin, or calcium-channel blockers and subsequent development of SVTs.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
The provision of 2.4 g of magnesium sulfate every 4 hours for a total dose of 14.4 g in the first 24 hours resulted in a significant reduction in the incidence and severity of VTs during the entire hospitalization, as well as the need for treatment. Magnesium prophylaxis did not influence the incidence of SVTs. There was a marked reduction in CK-MB levels on postoperative day 1 and in ST changes immediately postoperatively that suggests a possible benefit in terms of myocardial protection. Subgroup analysis, comparing patients with VTs to those without, also suggested a relationship between ischemia and VTs, as well as hypomagnesemia and VTs.

Hypomagnesemia is common and persistent after cardiac operations [14, 16]. A number of factors have been implicated, including increased urinary loss; the use of acid citrate dextrose prime; hemodilution; hormonal changes, including elevated epinephrine levels, associated with the stress response; diabetes mellitus; and the preoperative use of digoxin, beta blockers, or diuretics [14–16]. Postoperative hypomagnesemia has been implicated in the need for prolonged ventilation and in the development of SVTs [14]. In the setting of myocardial infarction, hypomagnesemia is associated with an increased incidence and severity of dysrhythmias [18, 19]. In our study, the placebo group had significantly lower serum magnesium concentrations for the first 2 postoperative days; however, hypomagnesemia did not correlate with an increased incidence of ventilator dependance or with an increased incidence of SVTs. There was a correlation with postoperative hypomagnesemia and postoperative VTs.

The administration of magnesium sulfate has been shown to reduce dysrythmias both after myocardial infarction and in the first 24 hours after a cardiac operation. Possible mechanisms include magnesium's ability to alter cellular transmembrane potential and thus reduce conduction velocity [20], its role as a cofactor for Na-K adenosine triphosphatase in maintaining cellular potassium levels, and its ability to stabilize calcium fluxes [14–16, 18]. Abraham and associates [18] showed that administration of 2.4 g of magnesium sulfate after acute myocardial infarction reduced the severity and incidence of VTs for approximately 4 hours. The administration of 2 g of magnesium sulfate after a cardiac operation resulted in the prevention of hypomagnesemia and a significant reduction in the incidence of VTs, but not SVTs, in the first 24 hours [15]. Magnesium sulfate administered as a constant infusion for 4 days after coronary artery revascularization resulted in a decrease in the number of episodes of atrial fibrillation, although there were no differences in the number of patients who experienced SVTs or in the incidence of VTs [16]. This may reflect differences in protection of the atria and atrial septum [21].

The precise clinical significance of postoperative VTs is not clear, and although it does appear that high-grade VTs may be associated with increased morbidity [5], the risks associated with routine prophylaxis with antidysrhythmic agents does not seem to be justified by any clinical benefit [3], and VTs may simply be a sign of ischemia [1]. To a large extent, the nature of the monitering system influences evaluations. Holter systems detect more dysrythmias than bedside moniters, although the clinical significance of the ``missed'' rhythm disturbances is debatable [1, 4, 6, 10, 12, 13, 16]. This study did demonstrate the safety and efficacy of magnesium prophylaxis.

Because at the cellular level magnesium is a calcium antagonist, it has been suggested that the administration of magnesium sulfate therapy may result in decreased contractility [5, 22, 23]. However, magnesium prophylaxis has been associated with enhanced myocardial performance [15, 24]. Magnesium, possibly through its calcium-channel blockade effect or its role as a cofactor for oxidative phosphorylation and restoration of adenosine triphosphate, may reduce reperfusion injury and result in enhanced myocardial protection [14, 15, 25–27]. In addition cellular magnesium plays an important critical role in muscle relaxation through its action on troponin subunits and inhibition of actomyosin adenosine triphosphatase [28]. The second Leicester Intravenous Magnesium Intervention Trial [29] demonstrated enhanced myocardial protection when magnesium sulfate was administered both before thrombolytic therapy and subsequently as an infusion over 24 hours. It has been suggested that VTs may reflect perioperative ischemia [1]. It may be that magnesium sulfate reduces VTs in part through its ability to enhance myocardial protection. Future studies should evaluate the possible benefit of administrating magnesium sulfate before bypass.

Limitations of the Current Study
Total serum magnesium concentration may not reflect intracellular magnesium homeostasis as well as ultrafilterable magnesium levels [15]. Creatine kinase-MB concentrations may lack the precision of cardiac-specific proteins, such as cardiac troponin I [30]. Measuring CK-MB and aspartate transaminase levels at 2, 4, 8, 16, and 48 hours after release of the cross-clamp would have provided a more accurate measure of ischemia [21]. This study analyzed dysrhythmias detected by two vastly different methods. Bedside monitering was used in the first 24 hours after cardiopulmonary bypass, and essentially clinical events were followed up subsequently. Continuous monitoring of cardiac activity during the entire hospitalization would have been more sensitive and precise, but significant differences were noted between the two groups in both monitoring periods.

Conclusions
Magnesium prophylaxis was associated with a reduction in the incidence, severity, and need for treatment of VTs after cardiac operations, without associated cardiac or respiratory depression. Magnesium sulfate prophylaxis appears to have some ability to enhance myocardial protection after ischemic arrest, and this may play some role in its ability to reduce VTs.

	Footnotes

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Address reprint requests to Dr Karmy-Jones, Department of Surgery, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202-2689.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Riyad Karmy-Jones Arvind Koshal Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Karmy-Jones, R. Articles by Koshal, A. Search for Related Content PubMed PubMed Citation Articles by Karmy-Jones, R. Articles by Koshal, A.