Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is no univocal clinical cardiovascular pattern associated with magnesium deficiency. Only an acute hypomagnesaemia gives the evidence of a real magnesium deficiency. Arrhythmias corrected by magnesium are associated with potassium deficiency. Magnesium deficiency appears to be one risk factor of arrhythmias and coronary spasms. The influence of intravenous magnesium salts was clearly evaluated on cardiovascular electrophysiology allowing protocols infusion. The major beneficial effect of magnesium on total incidence of arrhythmias appears to have been due to a reduction in supraventricular tachyarrhythmias and especially in "torsade de pointes". Antiarrhythmic mechanisms still remain to be clarified. It is likely that magnesium influences cardiac conduction and refractoriness by affecting calcium dependent processes as if acting as an indirect inactivator of slow inward calcium current, probably secondary to an inward shift of the background potassium mediated current. Recent studies demonstrated beneficial effect of intravenous magnesium treatment in acute myocardial infraction, both as to mortality and to early cardiac insufficiency. Beside antiarrhythmic and vasodilatator effects, magnesium seems to show cardiac cells protective action against ischaemia.
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PMID:[Cardiovascular pathology and magnesium]. 809 45

The oxidation states of intracellular myoglobin and cytochrome oxidase aa3 were monitored by reflectance spectrophotometry in isolated perfused rat hearts subjected to an acutely magnesium deficient environment. After exposure to low extracellular [Mg2+]o (i.e., 0.3 mM) for 30 min, more than 80% of the oxymyoglobin converted to its deoxygenated form. The level of reduced cytochrome oxidase aa3 also increased about 80% in low [Mg2+]o. The deoxymyoglobin was converted further to a species identified as ferrylmyoglobin by its reaction with Na2S to form ferrous sulfmyoglobin which was optically visible. This process, set into motion by acute Mg deficiency, resulted from a direct accessibility of the exogenous peroxide to the cytosolic protein. The results suggest that a pathway leading to cardiac tissue damage, induced by magnesium deficiency, is probably involved in the generation of a ferrylmyoglobin radical which could be prevented by addition of ascorbate, which is known to be a one-electron reductant of this hypervalent form of myoglobin. In further studies, we also investigated whether addition of different concentrations of ascorbic acid (AA) to the perfusate could enhance myocardial function after exposure to low [Mg2+]o perfusion. Four concentrations of AA (0.5, 1, 5, 10 mM) were tested, and the results indicate that they exert their effects in a concentration-dependent manner; 1 mM AA was the most effective dose in improving aortic output in a Mg-deficient heart. Ferrylmyoglobin formation was found to be formed considerably before intracellular release of either creatine phosphokinase or lactic dehydrogenase. These studies may have wide implications as a new mechanism by which low extracellular Mg2+ can induce myocardial injury and subsequent cardiac failure.
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PMID:Ferrylmyoglobin formation induced by acute magnesium deficiency in perfused rat heart causes cardiac failure. 828 Jul 83

1. Controlled trials, of which there are few, do not substantiate claims that diuretics play a role in causing magnesium deficiency. Consequently, the vast majority of patients taking conventional doses of thiazide diuretics (i.e. bendrofluazide 2.5 mg day-1 or equivalent) do not need magnesium supplements. On balance, potassium-sparing diuretics tend to increase serum and intracellular magnesium content; this should not be taken as evidence of prior magnesium deficiency. It remains theoretically possible that large doses of loop diuretics given more than once daily for long periods could induce negative magnesium balance and magnesium deficiency. However, it has been difficult to run appropriately controlled trials in conditions where such therapy is needed (i.e. heart failure) and until more reliable information becomes available no absolute recommendation can be made. 2. Methods for the measurement of intracellular free magnesium levels are now available and are more relevant to the assessment of magnesium deficiency than total intracellular magnesium content; the complex relationship between intracellular free and total magnesium content remains to be defined. Future work involving the effect of diuretics on intracellular free magnesium measurements should make every attempt to avoid the errors of trial design and multiple publication that litter current and past literature.
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PMID:Do diuretics cause magnesium deficiency? 837 6

Electrolyte balance is a critical issue in managing comorbid conditions in both diseased and elderly patients. Patients with hypertension and diabetes need careful regulation of their calcium and magnesium levels, whereas in patients with congestive heart failure, sodium and potassium levels also are critical. Herein we report the outcome of a round table discussion at which issues of renal magnesium clearance, magnesium and arrhythmic risk, ion balance in heart failure, diabetes, ischemic stress, oxidative stress in the cardiomyopathy of magnesium deficiency, roles of magnesium and potassium in bone metabolism and the aging population, and the role of electrolyte balance in hypertension have been discussed. In all these issues the maintaining homeostasis of potassium and magnesium is critical and the various therapies that impact on retaining these ions were discussed. Hallmark studies, i.e., Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial and Studies of Left Ventricular Dysfunction, have provided insight into treatment of patients with cardiovascular and progressive heart failure. These studies and the availability of potassium- and magnesium-sparing diuretics for use in these disorders provide relevant perspectives for treatment.
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PMID:Potassium, magnesium, and electrolyte imbalance and complications in disease management. 1577 33

Hypomagnesemia continues to cause difficult clinical problems, such as significant cardiac arrhythmias where intravenous magnesium therapy can be lifesaving. Nutritional deficiency of magnesium may present with some subtle symptoms such as leg cramps and occasional palpitation. We have investigated dietary-induced magnesium deficiency in rodent models to assess the pathobiology associated with prolonged hypomagnesemia. We found that neuronal sources of the neuropeptide, substance P (SP), contributed to very early prooxidant/proinflammatory changes during Mg deficiency. This neurogenic inflammation is systemic in nature, affecting blood cells, cardiovascular, intestinal, and other tissues, leading to impaired cardiac contractility similar to that seen in patients with heart failure. We have used drugs that block the release of SP from neurons and SP-receptor blockers to prevent some of these pathobiological changes; whereas, blocking SP catabolism enhances inflammation. Our findings emphasize the essential role of this cation in preventing cardiomyopathic changes and intestinal inflammation in a well-studied animal model, and also implicate the need for more appreciation of the potential clinical relevance of optimal magnesium nutrition and therapy.
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PMID:The role of magnesium deficiency in cardiovascular and intestinal inflammation. 2097 97

The combination of a magnesium deficiency, heart failure and anxiety-depressive disorders are accompanied by the imposition of symptoms, differential diagnosis difficulties and requires special attention in treating elderly and senile patients. The study of 74 patients with chronic heart failure of 60 to 95 years in urban medical district revealed that the majority of people had depressive disorders, disturbances of electrical stability of the heart in the form of increasing the duration of the QT interval and magnesium deficiency. Frequency and severity of the latter increase with age, increase of a functional class of heart failure, worsening the severity of anxiety-depressive syndrome and prolongation QT.
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PMID:[Magnesium deficiency and anxiety-depressive syndrome in elderly patients with chronic heart failure]. 2328 18

The paper considers the consequences and causes of magnesium deficiency in patients with cardiovascular diseases. The features of magnesium metabolism in atherosclerosis, hypertension, and heart failure are described. Prospects of magnesium therapy in cardiology practice are discussed.
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PMID:[Magnesium deficiency in cardiology]. 2580 50

Introduction: The objective of this study was to review the current status of drug-induced hypomagnesemia and its adverse effects on cardiovascular disease (CVD) and hypertension. Since magnesium is a potent vasodilator, which modulates vasomotor tone, peripheral blood flow, and hypertension, its deficiency could have significant cardiovascular and blood pressure (BP) effects.Areas covered: Studies have shown that several factors can contribute to magnesium deficiency including age, diet, disease, and certain drugs such as diuretics and proton-pump inhibitors (PPIs). For an updated perspective of drug-induced hypomagnesemia, a Medline search of the English language literature was conducted between 2010 and 2019 using the terms diuretics, proton-pump inhibitors, hypomagnesemia, cardiovascular disease, hypertension, and 35 pertinent papers were retrieved.Expert opinion: The data showed that magnesium deficiency is difficult to occur since it is plentiful in green leafy vegetables, cereals, nuts, and the drinking water. However, magnesium deficiency can occur with the use of diuretics for the treatment of hypertension and heart failure, or the use of PPIs for the treatment of gastroesophageal reflux disease. Therefore, magnesium deficiency should be detected and treated to prevent the aggravation of hypertension and the onset of CVD and serious cardiac arrhythmias including torsades de points.
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PMID:Adverse cardiovascular and blood pressure effects of drug-induced hypomagnesemia. 3179 77

Robust clinical data indicate that inhibitors of the sodium/glucose cotransporter 2 (SGLT2) dramatically improve clinical outcomes in diabetes, especially heart failure and progression of kidney disease. Factors that may contribute to these findings include: 1) improved glycemic control, 2) diuresis and reduced extracellular fluid volume, 3) reduced serum uric acid levels, 3) direct myocardial effects, 4) reduction in proteinuria and preservation of kidney function, and 5) correction of diabetic magnesium deficiency. Understanding the mechanisms by which SGLT2 inhibitors improve cardiovascular outcomes has the potential to improve clinical management not only of diabetes, but also of other cardiovascular disorders such as heart failure and chronic kidney disease.
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PMID:Evolving understanding of cardiovascular protection by SGLT2 inhibitors: focus on renal protection, myocardial effects, uric acid, and magnesium balance. 3268 81


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