[Anti-arrhythmic effects of intravenous magnesium sulfate in paroxysmal supraventricular tachycardia]

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The anti-arrhythmic effects of intravenous magnesium sulfate, on bouts of supraventricular tachycardia (SVT) secondary to reentry phenomenon, are evaluated in twelve patients undergoing an electrophysiological testing, because of paroxysmal SVT, the pathway of which is an intranodal reentry (eight patients) or includes an atrio-ventricular accessory route (orthodromic SVT: four patients). At the completion of the basic testing, a stable SVT is induced and an intravenous bolus of 3 grams of magnesium sulfate is administered in three minutes. The length of the SVT cycle is significantly increased from 349 +/- 71 ms to 394 +/- 70 ms (p 0.001). The injection of magnesium relieves the SVT in less than five minutes in three patients (intranodal reentry: two cases; accessory pathway: one case), or an efficacy of 25 p. cent. No incident is reported following administration of the product; but the functional tolerance may be considered as poor, mainly consisting of flushing sensations of brief duration. This study demonstrates the antiarrhythmic properties of intravenous magnesium sulfate during bouts of SVT; however, its efficacy appears moderate at the dose mentioned.

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... Препараты магния как антиаритмические средства характеризуются сочетанием свойств антиаритмиков I (мембраностабилизирующие) и IV (антагонисты кальция) классов. Принимая участие в процессе деполяризации клетки, магний непосредственно влияет на поддержание ее электрического равновесия, при недостатке магния клетка становится сверхвозбудимой [40][41][42]. ...
... Важным аспектом препаратов магния является их существенно бо`льшая безопасность по сравнению с традиционными антиаритмическими средствами. Это свойство имеет большое значение в лечении нарушений ритма у беременных, для оказания помощи при симпатоадреналовых кризах у пациентов с вегетативной дисфункцией [42,43]. Препараты магния могут применяться в качестве препаратов первой линии у соматически не отягощенных больных при симптоматических аритмиях (например, суправентрикулярной экстрасистолии), ассоциированных с электролитным дисбалансом, а также использоваться в терапии и профилактике аритмий при врожденном и приобретенном синдроме удлиненного интервала QT, дигиталисной интоксикации, остром и хроническом алкогольном поражении сердца, симпатикотонии. ...
... Применение препаратов магния для профилактики и лечения сердечных аритмий Препараты магния давно используются как антиаритмические средства, сочетающие свойства антиаритмиков I (мембраностабилизирующие) и IV классов (естественные антагонисты кальция). Принимая участие в процессе деполяризации клетки, Mg 2+ непосредственно влияет на поддержание её электрического равновесия, при недостатке магния клетка становится сверхвозбудимой [13][14][15]. ...
... Стоит обратить внимание и на еще один аспектпрепараты Mg 2+ существенно безопаснее традиционных антиаритмических средств, и это имеет большое значение в лечении нарушений ритма у беременных пациенток, купировании предсердной экстрасистолии у детей (особенно на фоне дисплазии соединительной ткани), для оказания помощи при симпато-адреналовых кризах у пациентов с вегетативной дисфункцией [15,23]. ...
... В редакционной статье, посвященной данной работе, указывается, что простое следование рекомендациям -назначение АСК пациентам, чей сердечно-сосудистый риск превышает определенные значения, вряд ли может рассматриваться как оптимальное решение [15]. «Для пациентов из группы высокого сердечно-сосудистого риска назначение АСК может принести пользу, и именно здесь есть место для персонализованной медицины. ...
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The results of recent trials on acetylsalicylic acid (ASA) efficacy are presented. Data potentially related to the possibility of ASA indications extension is discussed, in particular that referring to the cancer prevention. This ASA indication should be confirmed in additional studies.
Magnesium (Mg), a cofactor in numerous enzymatic reactions, is often ignored by clinicians, as the symptomatology of Mg depletion is not specific and usually associated with that of the cause of the depletion. Futhermore, the plasma Mg concentration (0.8 to 1.1 mmol · L−1) is only equivalent to one percent of the total body content. A Mg deficit may exist while plasma Mg concentration is normal. Therefore other techniques for Mg assessment, such as the repletion test, as well as red blood cell and lymphocyte concentrations have been used. A renewed interest for Mg occurred as numerous studies have shown the therapeutic efficiency of Mg and as the mechanisms of its haemodynamic effects have been recognized. Mg regulates Na-K-ATPase activity, K channels activity and, most of all, it is a natural calcium channel blocking agent. These properties explain its important place in electrophysiology of myocardial cells and the effects on the tension of smooth muscles, resulting in a vasodilation and a bronchodilation respectively. The antagonistic effect of Mg on calcium decreases the presynaptic release of acetylcholine at the neuromuscular junction and the release of epinephrine at the peripheral sympathic nerves and the adrenals. Mg potentiates the effect of non-depolarizing muscle relaxants.A Mg deficiency occurs often in ICU patients, in alcoholics and during use of diuretics. Simultaneous administration of Mg is often required for treatment of potassium deficiency. Mg has an anti-arrhythmic effect towards digoxin-mediated dysrhythmias and torsades de pointes, and can be efficient in other arrhythmias. Systematic use of Mg seems to decrease mortality of acute myocardial infarction and is justified during cardiac surgery, often associated with hypomagnesemia, because of vasodilation of coronary arteries and in order to prevent occurrence of arrhythmias. Mg, because of its calcium channel blocking properties and as it lowers the release of epinephrine, is indicated for surgery of pheochromocytoma. In eclamptic and pre-eclamptic patients, the use of Mg is valuable, but not as an anti-epileptic agent. Other clinical uses of Mg have been proposed, but they are either anecdotal or of uncertain efficiency.
Magnesium plays an important role as a cofactor in many of the body's critical functions. Levels of magnesium are controlled by the kidneys and gastrointestinal tract. Magnesium deficiency is found in about 40% of critically ill patients and may complicate many diseases. Manifestations of magnesium deficiency include alteration in calcium and potassium homeostasis along with cardiac, neuromuscular and neuropsychiatric disorders. Its treatment consists of parenteral administration of magnesium and depends on the clinical setting. Hypermagnesemia is often iatrogenic. The first symptom is a diminution of deep tendon reflexes, then paralysis of voluntary muscles may produce quadriplegia or apnea. Peritoneal dialysis or hemodialysis may be required. Magnesium treatment is a viable therapeutic option when other antiarrhythmic agents fail to suppress numerous types of arrhythmias. Magnesium administration is a very effective and safe treatment for « torsade de pointesand for preeclampsia-eclampsia. Some results suggest that magnesium is a useful adjunct to the central nervous system depressants traditionally used in the treatment of severe tetanus induced autonomic dysfunction and in patients with moderate to severe asthma who show little improvement with β-agonists.
This paper reviews the pharmacological effects on the cardiovascular system which occur when serum magnesium concentration is raised above the physiological range (0.7-0.95 mM), and considers how the clinical course of acute myocardial infarction might be modified in consequence
To examine the effect of doubling serum magnesium concentration on the incidence of arrhythmias in patients with suspected acute myocardial infarction. Randomised double blind clinical trial. Coronary care unit of a teaching hospital. Clinical data were collected on 2316 randomised patients with suspected acute myocardial infarction. Holter monitoring was performed in a subgroup of 70 patients and analysed in 48 patients in whom acute myocardial infarction was confirmed. By random allocation, patients received either an intravenous loading dose of 8 mmol magnesium sulphate over five minutes plus 65 mmol over the next 24 hours, or equal volumes of saline. (a) Clinically documented arrhythmias; (b) use of antiarrhythmic treatments, cardioversion, and insertion of a pacemaker; (c) incidence of all abnormal rhythms during Holter monitoring. In the main trial the incidence of rhythm disturbance while in the coronary care unit (expressed as the odds ratio (OR) for magnesium: placebo and its 95% confidence interval) was not significantly different between treatment groups for ventricular fibrillation (OR 0.74; 0.46 to 1.20), ventricular tachycardia (OR 0.87; 0.63 to 1.20), supraventricular tachycardia (OR 0.69; 0.38 to 1.26), atrial fibrillation (OR 0.92; 0.69 to 1.23), or heart block of any degree (OR 1.17; 0.83 to 1.65). Sinus bradycardia was significantly more common in the magnesium group (OR 1.38; 1.03 to 1.85; p = 0.02). These findings were corroborated by the use of treatments for rhythm disturbance and the data from Holter monitoring. The regimen of intravenous magnesium sulphate used here had no significant effect on arrhythmia in acute myocardial infarction. The reduction in mortality that has been shown with this form of treatment is not attributable to suppression of life threatening rhythm disturbances.
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