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Print ISSN: 2321-6379 Online ISSN: 2321-595X DOI: 10.17354/ijss/2016/343 Origi na l A r tic le Serum Magnesium in Patients with Acute Myocardial Infarction Lakshman Lal1, Hiralal Murmu2 Professor, Department of Biochemistry, Mahatma Gandhi Medical College, Jamshedpur, Jharkhand, 2Professor, Department of Medicine, Mahatma Gandhi Medical College, Jamshedpur, Jharkhand, India 1 Abstract Introduction: Magnesium is also known for its role in the electrical stability and energy balance of cardiomyocytes. Low serum magnesium has been associated with accelerated atherosclerosis. Aim: To estimate the level of serum magnesium in patients with acute myocardial infarction and compare with a normal healthy adult. Materials and Methods: A prospective study was conducted in the Department of Biochemistry at Mahatma Gandhi Memorial Medical College, Jamshedpur. 40 patients with diagnosed case of acute myocardial infarction from Medicine Department were selected for estimation of serum magnesium in Department of Biochemistry. 40 normal healthy adults of both sexes in the age group of 30-79 years were selected for serum magnesium estimation as a control. Result: Serum magnesium concentration in acute myocardial infarction group ranged from 0.42 to 1.56 meq/l with a mean value of 1.01 meq/l and it is statistically significant (P < 0.01). Conclusion: Within first 48 h after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines. Key words: Acute myocardial infection, Arrhythmia, Hypomagnesemia INTRODUCTION Hypomagnesemia is an electrolyte disturbance in which there is low level of magnesium in blood.1 Magnesium is an essential micronutrient for human beings and plays an important role in normal myocardial physiology. It’s a cofactor in more than 300 enzymes system of the body in human cell. Its possible site of action includes vascular smooth muscle, platelets, and myocardial cells.2 Magnesium depletion can induce hyperlipidemia and subsequently atherogenic deposits in coronary arteries leading to atherosclerosis.3 Normal magnesium level fall between 1.7 and 2.2 meq/L. Usually, a serum level <1.7 meq/L is taken as reference. Access this article online www.ijss-sn.com Month of Submission : 04-2016 Month of Peer Review: 05-2016 Month of Acceptance : 05-2016 Month of Publishing : 06-2016 Hypomagnesemia may result from a number of conditions including inadequate intake of magnesium, chronic diarrhea, malabsorption, chronic stress, alcoholism, and medication such as diuretic.4 Magnesium is of major importance in the treatment of arrhythmia and coronary artery disease. Patients with coronary heart disease (CHD) suffer from magnesium deficiency. Oral combination therapy with magnesium and potassium improves endothelial function in these patients and reduce platelet dependent thrombosis. Within the myocardial cell, low magnesium concentration is associated with membrane destabilization, while high magnesium concentration are membrane stabilizing and therefore antiarrhythmic. Magnesium is a potent vasodilator 5,6 and plays an important role in muscle contraction. 7 CHD features among the indications for oral magnesium therapy. It could be shown that magnesium improves exercise duration and general well-being in these patients. Individuals treated with intravenous magnesium postinfarction were at significant lower risk of dying from ischemic heart disease-related complications.8,9 Corresponding Author: Dr. Lakshman Lal, 21 Ashashree Garde, Near RK Mission Ashram, Morabadi, Ranchi, Jharkhand, India. E-mail: [email protected] 167 International Journal of Scientific Study | June 2016 | Vol 4 | Issue 3 Lal and Murmu: Serum Magnesium in Patients with Acute Myocardial Infarction MATERIALS AND METHODS Our study was undertaken in the Department of Biochemistry, Mahatma Gandhi Medical College and Hospital (MGM), Jamshedpur. Ethical approval was taken from Institutional Ethics Committee of MGM. 40 patients with diagnosed case of acute myocardial infarction were selected for estimation of serum magnesium. The control group comprised normal healthy individual of both sexes in the age group of 30-79 years. An informed consent was taken. Serum magnesium was estimated with Talmagite Method. RESULTS The above Table 1 shows a significant decline in serum magnesium concentration in the cases of acute myocardial infarction, in comparison to healthy adult (control group). In this study, serum magnesium was estimated in clinically diagnosed case of acute myocardial infarction and healthy adult of both sexes and different age group as the control group. Maximum numbers of patients with myocardial infarction were in the age group 40-69 years. Out of 40 control cases, 25 cases belonged to 40-69 years of age. Serum magnesium concentration in this group ranged from 1.6 to 3.0 meq/L with a mean value of 2.20 meq/L. Out of 40 cases of acute myocardial infarction, 29 cases belonged to 40-69 years of age. 29 were males and 11 were females. A higher incidence of myocardial infarction in male corroborates the fact that incidence of ischemic heart disease is significantly less in premenopausal women. The serum magnesium concentration in acute myocardial infarction group ranged from 0.42 to 1.56 meq/L with a mean value of 1.01 meq/L and found to be statistically significant (P < 0.01). DISCUSSIONS Patients with acute myocardial infarction who have mild hypomagnesemia appear to have two- to three-fold increase in the frequency of ventricular arrhythmia in the first 24 h when compared to those with normal plasma magnesium level.10,11 Uncontrolled studies suggest that Table 1: Comparison of serum magnesium in control group with acute myocardial infarction Serum magnesium (meq/L) Range Mean±SD Standard error of mean (±) Control group Acute myocardial infarction 1.60‑3.00 2.20±2.23 0.35 0.42‑1.56 1.01±0.94 0.14 “P” value for acute myocardial group was <0.01. SD: Standard deviation the administration of intravenous magnesium at this time can reduce the frequency of potentially fatal ventricular arrhythmia.12,13 Magnesium is also known for its role in the electrical stability and energy balance of cardiomyocytes.14 Low serum magnesium has been associated with accelerated atherosclerosis.15 QT prolongation is a well-established risk factor for sudden cardiac disease,16 and serum magnesium was shown to influence the QT interval in a clinical setting.17 The American Heart Association 1992 guidelines for cardiopulmonary resuscitation and emergency cardiac care now include a recommendation that magnesium sulfate be added for the management of torsade de pointes, severe hypomagnesemia, or refractory ventricular fibrillation.18 Torsade de pointes is a unique ventricular tachycardia most commonly precipitated by drugs that prolong QT interval (e.g., Quinidine), electrolyte imbalance (hypokalemia and hypomagnesemia) or a slow heart rate and/or shortening the QT interval. Intravenous magnesium is now regarded as the treatment of choice even when hypomagnesemia is not present. Two large prospective epidemiologic studies have examined the relationship between serum magnesium concentration and the subsequent development of CHD.19 Both suggest that low serum magnesium is a risk factor for CHD. Mild hypomagnesemia is a common electrolyte abnormality,20 particularly in the elderly who have increased magnesium loss due to diuretic therapy or interstitial renal disease. Magnesium regulates several cardiac channels including the calcium channel and outward potassium current through the delayed rectifier.21 Lowering the cytosolic magnesium concentration in magnesium depletion will markedly increase these outward currents, shortening the action potential, and increasing susceptibility to arrhythmia. A relationship has also been found between the plasma magnesium concentration and ventricular arrhythmia occurring in the second or 3rd week after myocardial infarction. In one study, for example, the mean plasma magnesium concentration was 1.83 mg/dl (0.76 mmol/L) in patients with no abnormal rhythm, 1.68 mg/dl (0.7 mmol/L) in those with multifocal ventricular premature complexes and 1.5 mg/dl (0.65 mmol/L) in those with unsustained ventricular tachycardia. 22 13 patients with complex arrhythmia and hypomagnesemia received IV magnesium over 24 h, a normal rhythm was restored in ten. Low serum magnesium has been implicated in cardiovascular mortality, but results are conflicting. Total body magnesium International Journal of Scientific Study | June 2016 | Vol 4 | Issue 3 168 Lal and Murmu: Serum Magnesium in Patients with Acute Myocardial Infarction depends on dietary intake and recent studies showed that vast majority of elderly do not consume the average dietary requirement for magnesium.23 The prevalence of magnesium in the general population is estimated at 2%,24 but it may be as high as 53% in specific highrisk group such as patients with chronic heart failure.25 Although hypomagnesemia may have acute and chronic complications, serum magnesium is still measured relatively in frequently.26 In recent study, low serum magnesium has been associated with inflammation27 and disturbance in the regulation of vascular tone and endothelial function.28,29 These mechanisms are thought to contribute to the development and progression of atherosclerosis, potentially worsening CHD.30 CONCLUSION Magnesium influences endothelial function, inflammation, blood pressure, and diabetes.31 With the first 48 hrs after heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines. REFERENCES 1. Taylor EJ. Hypomagnesemia at Dorland’s Medical Dictionary. Philadelphia, PA: Saunders; 2011. 2. Altura BM, Altura BT, Carella A, Turlapaty PD. Hypomagnesemia and vasoconstriction: Possible relationship to etiology of sudden death ischemic heart disease and hypertensive vascular diseases. Artery 1981;9:212-31. 3. Altura BM, Zhang A, Altura BT. Magnesium hypertensive vascular disease, atherogenesis, subcellar compatmentation of Ca2+ and Mg2+ and vascular contractility. Minor Electrolyte Meab 1993;19:323-36. 4. Romani AM. Magnesium in Health & Disease. Ch. 3. New York: Springer; 2013. p. 49-79. 5. Askar AO, Mustafa SJ. Role of magnesium in the treatment of cardiac arrhythmias. Magnesium 2000;2:17-25. 6. Rasmussen HS, Larsen OG, Meier K, Larsen J. Hemodynamic effects of intravenously administered magnesium on patients with ischemic heart disease. Clin Cardiol 1988;11:824-8. 7. 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Ann Noninvasive Electrocardiol 2006;11:163-9. 18. Grillo JA, Gonzalez ER. Changes in the pharmacotherapy of CPR. Heart Lung 1993;22:548-53. 19. Liao F, Folsom AR, Brancati FL. Is low magnesium concentration a risk factor for coronary heart disease? The Atherosclerosis Risk in Communities (ARIC) Study. Am Heart J 1998;136:480-90. 20. Schimatschek HF, Rempis R. Prevalence of hypomagnesemia in an unselected German population of 16,000 individuals. Magnes Res 2001;14:283-90. 21. Agus ZS, Morad M. Modulation of cardiac ion channels by magnesium. Annu Rev Physiol 1991;53:299-307. 22. Ceremuzynski L, Van Hao N. Ventricular arrhythmias late after myocardial infarction are related to hypomagnesemia and magnesium loss: Preliminary trial of corrective therapy. Clin Cardiol 1993;16:493-6. 23. Del Gobbo LC, Imamura F, Wu JH, de Oliveira Otto MC, Chiuve SE, Mozaffarian D. 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Low magnesium promotes endothelial cell dysfunction: Implications for atherosclerosis, inflammation and thrombosis. Biochim Biophys Acta 2004;1689:13-21. 29. Bernardini D, Nasulewic A, Mazur A, Maier JA. Magnesium and microvascular endothelial cells: A role in inflammation and angiogenesis. Front Biosci 2005;10:1177-82. 30. Amighi J, Sabeti S, Schlager O, Mlekusch W, Exner M, Lalouschek W, et al. Low serum magnesium predicts neurological events in patients with advanced atherosclerosis. Stroke 2004;35:22-7. 31. Song Y, Manson JE, Cook NR, Albert CM, Buring JE, Liu S. Dietary magnesium intake and risk of cardiovascular disease among women. Am J Cardiol 2005;96:1135-41. How to cite this article: Lal L, Murmu H. Serum Magnesium in Patients with Acute Myocardial Infarction. Int J Sci Stud 2016;4(3):167-169. Source of Support: Nil, Conflict of Interest: None declared. 169 International Journal of Scientific Study | June 2016 | Vol 4 | Issue 3