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Ann Thorac Surg 1995;59:942-947
© 1995 The Society of Thoracic Surgeons

Effects of Magnesium on Myocardial Function After Coronary Artery Bypass Grafting

Department of Cardiothoracic Surgery, Carmel Medical Center, Haifa, and Soroka Medical Center, Beer-Sheba, Israel

Accepted for publication December 27, 1994.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
The effects of perioperative administration of magnesium sulfate on myocardial function was studied in patients with unstable angina (grade IV) undergoing coronary artery bypass grafting. Myocardial protection consisted of antegrade and retrograde continuous warm blood cardioplegia. Patients were randomly divided into two groups. Group A (50 patients) received intravenous magnesium sulfate (16 mmol) continuously from the time of anesthetic induction to aortic cross-clamping and a second dose (32 mmol) starting after the release of aortic cross-clamp until 24 hours later. Group B (48 patients) did not receive magnesium sulfate and served as control. Left ventricular stroke work index increased in group A from 34 +/- 3 g • m/m² before operation to 42 +/- 3 g • m/m², 45 +/- 2 g • m/m², and 47 +/- 2 g • m/m², 1, 6, and 12 hours after operation, respectively (p < 0.05 versus preoperative), and in group B from 33 +/- 3 g • m/m² before operation to 38 +/- 3 g • m/m², 40 +/- 2 g • m/m², and 41 +/- 2 g • m/m², 1, 6, and 12 hours after operation, respectively (p < 0.05). Left ventricular stroke work index was higher in group A 6 (p = 0.06), 12, and 24 hours (p < 0.05) after operation compared with group B. The incidence of ventricular arrhythmias requiring treatment was significantly higher (p < 0.05) in group B: 14 patients versus 1 patient in group A. Postoperative hypertension was more frequent in group B: 16 patients versus 2 patients in group A (p < 0.05). These results indicate that perioperative administration of magnesium sulfate may contribute to better myocardial recovery and fewer ventricular tachyarrhythmias after operation.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
The goal of cardioplegic solution is to provide adequate myocardial protection during the period of ischemic arrest. The advent of newer cardioprotective techniques, namely antegrade and retrograde cold and warm cardioplegia, generally results in satisfactory operative results [1, 2]. However, preoperative myocardial ischemia and reperfusion injury still contribute to suboptimal operative results despite satisfactory intraoperative myocardial protection. Understanding of intracellular events that occur secondary to ischemia and reperfusion injury stimulated a search for additional methods as an adjunct to cardioplegic solutions, in an attempt to improve myocardial recovery after operation.

Magnesium ion (Mg²⁺) has been shown to be an important cardioprotective ion. Data from experimental studies demonstrated a significant improvement of left ventricular performance after global ischemia when Mg²⁺ was added to the cardioplegic solution [3]. Intravenous magnesium sulfate (MgSO₄) therapy also has been shown to have salutary effects on circulatory function: decrease in systemic vascular resistance and increase in cardiac output [4]. Recent data from the second Leicester Intravenous Magnesium Intervention Trial [5] have shown that patients treated with intravenous MgSO₄ during acute myocardial infarction had a 25% relative reduction in mortality, as well as fewer ventricular arrhythmias. The purpose of this study was to examine the effects of perioperative administration of MgSO₄ on postoperative myocardial function and incidence of ventricular arrhythmias in patients with unstable angina (grade IV) undergoing urgent coronary artery bypass grafting (CABG).

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Ninety-eight consecutive patients with unstable angina (grade IV) undergoing CABG were included in this study. The criteria for unstable angina were the presence of chest pain at rest lasting for more than 15 minutes, associated with transient ST segment changes and with or without hemodynamic instability. Written informed consent was obtained from all patients included in this study.

All preoperative coronary angiograms were reviewed by two cardiologists. A serious lesion was defined as stenosis of 50% or more of the left main trunk and 70% or more for all other major coronary arteries. Patients receiving ß blockers and calcium blockers continued with these medications until the day of operation.

Low cardiac output was defined as the requirement of inotropic or intraaortic balloon pump support for longer than 30 minutes to maintain the systolic blood pressure greater than 90 mm Hg and the cardiac index greater than 2.2 L • min^-1 • m^-2.

Atrial and ventricular pacing wires were left in every patient, and atrial, atrioventricular sequential, or ventricular pacing was used only if required. Postoperative hypertension (mean arterial pressure >95 mm Hg) was treated with intravenous nitroprusside.

Twelve-lead electrocardiography was performed before operation and at 6, 12, and 24 hours after operation. Serum levels of creatine kinase and activity of the cardiac-specific isoenzyme of creatine kinase were measured before operation and 1, 6, 12, and 24 hours after operation. A new Q wave, together with an increase in creatine kinase-MB fraction concentration to greater than 5% of total creatine activity, was indicative of perioperative myocardial infarction. All patients underwent electrocardiographic monitoring through the third postoperative day, using the Mennen Horizon 2000 Bedside Arrhythmia Detection System (Mennen Medical Co, Clarence, NY). Postoperative cardiac arrhythmias were defined as (1) premature ventricular contractions of more than 30/hour, (2) ventricular tachycardia of 3 or more premature beats in a row at a rate greater than 100 beats/min, (3) ventricular fibrillation, and (4) supraventricular tachycardia, atrial fibrillation, or flutter at rates greater than 120 beats/min.

Interpretation of the electrocardiogram was done by two cardiologists from our team who were blinded to whether the patients received MgSO₄ and were also blinded to the serum Mg²⁺ level.

Operative Technique
Patients were anesthetized with fentanyl, 40 to 60 µg, and muscular relaxation was achieved with pancuronium, 0.1 mg/kg. The membrane oxygenator was primed with 2 L of lactated Ringer's solution. Cardiopulmonary bypass was established with a single two-stage venous cannula and an ascending aortic cannula. During bypass, the hematocrit was maintained between 20% and 25%, pump flow between 2.0 and 2.5 L • min^-1 • m^-2, and mean arterial pressures between 50 and 60 mm Hg. After application of aortic cross-clamp, all patients received continuous antegrade and retrograde warm blood cardioplegia. The technique of cardioplegia delivery was standardized between the patient groups. Body temperature was allowed to drift to 32°C. Distal anastomoses were performed during a single period of aortic cross-clamping. Proximal vein graft anastomoses were performed with partial aortic occlusion during rewarming. The left internal thoracic artery was used as a bypass conduit to the left anterior descending artery in all patients.

TECHNIQUE OF ADMINISTRATION OF MAGNESIUM SULFATE AND WARM BLOOD CARDIOPLEGIA.
The patients were randomly assigned to receive either MgSO₄ or placebo (20 mL of saline solution) in coded ampules. Fifty patients (group A) received intravenous MgSO₄, 16 mmol continuously with a syringe pump (Graseby 3100; Watford, Herts, UK) during the interval between induction of anesthesia and aortic cross-clamping. After release of the aortic cross-clamp, 32 mmol of MgSO₄ was readministered intravenously for a further 24 hours. Forty-eight patients (group B) who did not receive MgSO₄ acted as controls.

Plasma Mg²⁺ level was measured and determined by atomic absorption spectroscopy [6] at baseline, before aortic cross-clamping, immediately after release of the aortic cross-clamp, and at 4, 8, 12, 16, and 24 hours after operation. Serial measurements of ionized Ca²⁺ and K⁺ concentrations were performed after each serum [Mg²⁺] measurement. Serum ionized Ca²⁺ concentration was maintained at the normal range with supplement of calcium chloride, as required.

All patients received warm blood cardioplegia, which was prepared by mixing 4 parts of oxygenated blood with each part of crystalloid solution containing Mg²⁺, 32 mEq/L (Plegisol; Abbott Laboratories, North Chicago, IL), and was delivered via the Buckeberg-Shiley Plus System (Shiley Inc, Irvine, CA). Cardiac arrest was achieved with an infusion of high-K⁺ cardioplegia (30 mEq/L) delivered into the aortic root for 3 minutes at a flow rate of 300 mL/min and then switched to low K⁺ (8 to 10 mEq/L) cardioplegia, which was delivered retrograde continuously into the coronary sinus with a self-inflating balloon cannula (Research Medical Inc, Midvale, UT) and into each of the constructed distal vein grafts. The flow rate was kept between 100 and 150 mL/min and the pressure in the coronary sinus was maintained at less than 40 mm Hg.

HEMODYNAMIC MEASUREMENTS AND COMPUTATIONS.
A flow-directed thermodilution catheter mounted with a rapid thermistor was introduced through the internal jugular vein of each patient and positioned 3 to 4 cm distally to the pulmonic valve. Using the catheter and computer system (Horizon XL, Mennen Medical Inc, Clarence, NY), hemodynamic data including right atrial pressure, pulmonary capillary wedge pressure, mean arterial pressure, and cardiac output were measured at baseline before administration of MgSO₄ and 1, 6, 12, and 24 hours after termination of cardiopulmonary bypass.

Left ventricular stroke work index (LVSWI) and right ventricular stroke work index (RVSWI) were obtained from thermodilution catheter measurements and calculated using the following formulas:

(1)

(2)

where SVI = stroke volume index, MAP = mean arterial pressure, PCWP = pulmonary capillary wedge pressure, MPAP = mean pulmonary artery pressure, and RAP = right atrial pressure.

Systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were calculated by the following formulas:

(3)

(4)

Statistical Analysis
Hemodynamic data and indices of left and right ventricular function before and after operation were compared using analysis of covariance. Analysis of patients' parameters were compared between the two groups using an unpaired t test and ² test, as required. All statistical analyses were performed with Statistical Analysis Systems programs for the personal computer (SAS Institute, Cary, NC). Continuous variables are listed as the mean +/- standard deviation of the mean. Values of p less than 0.05 were considered significant.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Table 1 shows the preoperative and operative variables of patients in both groups. There were no significant differences between the two groups with regard to sex, age, previous myocardial infarction, use of ß blockers and Ca²⁺ blockers, ejection fraction, left main coronary artery disease, aortic cross-clamping time, and the number of distal anastomoses. Two patients in group A and 1 patient in group B required intraaortic balloon support before operation because of low cardiac output.

There was one operative death in group A due to low cardiac output and multiple organ failure. This patient had diffuse coronary artery disease requiring endarterectomy of both the left anterior descending and right coronary arteries.

None of the patients required intraaortic balloon support after operation. Inotropic support (dopamine >5 µg • kg^-1 • min^-1) because of hemodynamic instability was continued for more than 12 hours in 2 patients (4%) in group A and 9 patients (18%) in group B (p < 0.05).

Table 2 depicts preoperative and postoperative hemodynamic data for both groups. There were no significant differences before operation between the two groups in any of the parameters studied. After operation there was a significant (p < 0.05) decrease in SVR associated with increase in cardiac index in group A. Left ventricular stroke work index significantly increased (p < 0.05) 1, 6, 12, and 24 hours after operation in group A and 6, 12, and 24 hours after operation in group B compared with the preoperative value. In group A, LVSWI was higher at 6 (p = 0.06), 12 (p = 0.05), and 24 hours (p < 0.05) after operation compared with group B. There was no significant difference in mean value of RVSWI and PVR before and after operation and between groups along the course of the study.

None of the patients in this study had a new Q wave or transient ST segment changes after operation. Peak values of creatine kinase-MB after operation were similar in both groups: 24.8 +/- 13 U/L in group A and 29 +/- 14 U/L in group B. There was no case of ventricular fibrillation or ventricular tachycardia in group A after operation, whereas 1 patient in group B had a short run of ventricular tachycardia. Frequent ventricular premature beats (extrasystoles, bigeminy, and couplets) necessitating administration of lidocaine occurred in 12 patients in group B in contrast to 1 patient in group A (p < 0.05). The incidence of postoperative atrial fibrillation was similar: 22 patients in group A and 18 patients in group B. A new conduction abnormality (right or left bundle-branch block) lasting more than 6 hours occurred in 2 patients in this study (1 in each group).

Postoperative hypertension requiring treatment with nitroprusside occurred in 14 patients in group B versus 1 patient in group A (p < 0.05).

Baseline value of plasma Mg²⁺ concentration was similar in both groups and significantly higher at all sample times after initiation of MgSO₄ infusion in group A (Table 3). After 36 hours there was no difference in the mean plasma Mg²⁺ concentration between the two groups. Mean values of K⁺ and ionized Ca²⁺ levels were similar in both groups.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment References

The importance of Mg²⁺ as a cardioprotective ion increasingly is becoming recognized. Metaanalysis of several trials has suggested a beneficial role for intravenous MgSO₄ infused 24 hours after acute myocardial infarction [7]. Data from the second Leicester Intravenous Magnesium Intervention Trial [5] showed a 24% relative reduction in mortality and a 25% reduction in the incidence of heart failure related to the reduction of infarct size. Evidence from animal studies demonstrated a rapid increase in free intracellular Mg²⁺ concentration during ischemia [8] due to reduction of adenosine triphosphate formation, which incorporates Mg²⁺. During reperfusion Mg²⁺ is reincorporated into adenosine triphosphate to produce a net decrease in intracellular free Mg²⁺ with reciprocal Ca²⁺ overload.

Brookes and Fry [9] showed that around 24 hours after a cardiac operation the ionized Mg²⁺ is significantly reduced with no change to the total plasma Mg²⁺. The reduction in ionized Mg²⁺ concentration was not associated with a corresponding reduction in ionized Ca²⁺ level. Brookes and Fry hypothesized that the presence of a Mg²⁺-binding ligand of unknown origin in the plasma after a cardiac operation may contribute to hypomagnesemia and cardiac arrhythmias.

Previous experimental studies examined the relationship between Mg²⁺ concentration and myocardial protection during ischemic arrest [3, 10]. These data indicated that modification of Ca²⁺ and Mg²⁺ concentrations in the perfusate and cardioplegic solution of isolated heart models resulted in a better systolic and diastolic myocardial function after normothermic and hypothermic ischemic arrest. Brown and associates [11] showed that increasing Mg²⁺ concentrations in the cardioplegic solution during hypothermic arrest also resulted in a significant increase in adenosine triphosphate level, correlating with a better myocardial functional recovery.

The current use of cardioplegic solutions and the advent of antegrade and retrograde delivery of warm continuous blood cardioplegia, although remaining somewhat controversial [12], has been shown to improve left ventricular performance after CABG [2]. The evolving techniques of myocardial protection reduced the morbidity and mortality of patients undergoing bypass operations, despite a substantial increase in the number of high-risk patients. However, the results are still less than satisfactory, particularly in patients with severe unstable angina or evolving myocardial infarction undergoing urgent or emergency CABG. These hearts have sustained severe normothermic antecedent ischemia during the interval that elapsed from onset of acute ischemia to surgical revascularization. Furthermore, it is conceivable that even an ideal intraoperative myocardial protection could only partially reverse preexisting ischemic damage.

In the myocyte, ischemia and reperfusion injury are associated with excessive Ca²⁺ influx [13]. The increased intracellular Ca²⁺ concentration in proximity to the contractile apparatus leads to persistent activation of actin-myosis cross bridges and disturbed diastolic tone [14]. Furthermore, the presence of high circulating levels of endogenous plasma catecholamines during and after an open heart operation may potentiate any coexisting ischemic damage. Minami and colleagues [15] showed that plasma epinephrine and norepinephrine levels increased 5 minutes after institution of bypass and reached a peak level of ten times the baseline level between the end of bypass and 2 hours after termination of bypass when a nonpulsatile flow was used. Catecholamines enhance transsarcolemmal Ca²⁺ influx and loss of Mg²⁺ from the myocyte magnified by cyclic adenosine monophosphate--mediated ß receptor stimulation [16].

Magnesium ion has been proposed as a native physiologic Ca²⁺ blocker, although the exact cardioprotective mechanism remains unclear. Data from animal studies suggest that Mg²⁺ has a direct Ca²⁺ antagonistic effect on the cell membrane of vascular smooth muscle. Within the muscle cell Mg²⁺ blocks the influx of Ca²⁺ through the slow channels [17], inhibits release of Ca²⁺ from the sarcoplasmic reticulum in response to sudden influx of extracellular Ca²⁺, which normally stimulates its release [18], and competes with Ca²⁺ over nonspecific binding sites on troponin-C and myosin, thus affecting the ability of Ca²⁺ to develop maximal tension at any given Ca²⁺ concentration. It also activates the Ca²⁺ adenosine triphosphatase of the sarcoplasmic reticulum, which, by removing Ca²⁺ from the cytosol, decreases diastolic tone [19]. The direct competitive antagonism of Mg²⁺ with Ca²⁺ at the cell membrane of vascular smooth muscle may explain the relaxation of resistance vessels and the significant increase in coronary perfusion. In a comparative study, Kimura and associates [20] found that Mg²⁺ inhibits the periodic as well as the tonic contraction of isolated human coronary arteries better than diltiazem and nitroglycerin.

The present study clearly demonstrated the advantageous use of Mg²⁺ as a myoprotective ion. Postischemic systolic indices of contractility were significantly higher in group A. Magnesium-induced left ventricular afterload reduction, which occurred without a significant increase in heart rate, also may contribute to the improved cardiac function. We are aware of the limits of using load-dependent indices of myocardial contractility, as preload and afterload may, in fact, influence contractility under certain circumstances. Alternatively, load-insensitive indices of contractility are used widely in clinical and experimental studies. However, the slope of the end-systolic pressure--volume relationship is dependent on absolute ventricular size, making comparison of subjects with differences in ventricular size uncertain. Although infusion of Mg²⁺ produces effects similar to hyperkalemia, including decreased atrioventricular conduction, decreased intraventricular conduction, and suppression of sinus node function [21], there was no need for external pacing in these patients. In similar studies, Ca²⁺ antagonists [22, 23] have been shown to provide potent antiischemic and antiarrhythmic protection in patients undergoing CABG. However, Mg²⁺ favorably compares with these medications as also being a cofactor of the Mg²⁺-dependent adenosine triphosphatase enzyme, which provides energy for myocardial contraction and allows the Na⁺-K⁺ membrane pumps to maintain intracellular hemostasis. Harris and associates [24] showed that administration of Mg²⁺ immediately after aortic cross-clamping significantly reduced the incidence of ventricular arrhythmias. England and co-workers [25] also showed that Mg²⁺ administration increased the stroke volume and decreased the frequency of postoperative ventricular dysrhythmias. The difference between these studies is in respect to the use of Mg²⁺-containing cardioplegic solution as opposed to the use of Mg²⁺-free cardioplegic solution and infusion of Mg²⁺ only after operation, as opposed to perioperative administration of Mg²⁺.

In summary, intravenous Mg²⁺ infusion in patients with myocardial ischemia undergoing urgent CABG has shown beneficial antiischemic and antiarrhythmic properties. Further study is required to investigate the mechanism of Mg²⁺ action.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Address reprint requests to Dr Caspi, Department of Cardiothoracic Surgery, Soroka Medical Center, Beer-Sheba, PO Box 151, Israel 84101.

	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): Joseph Caspi Ehud Rudis Ilan Bar Tammah Safadi Milton Saute Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Caspi, J. Articles by Saute, M. Search for Related Content PubMed PubMed Citation Articles by Caspi, J. Articles by Saute, M.