Summary
Magnesium in coronary artery disease is reviewed with regard to its role in the pathogenesis of arteriosclerosis, coronary spasm, myocardial function, acute myocardial infarction and ventricular arrhythmias. Experimentally, magnesium depletion potentiates and supplementation retards the effect of atherogenic diets. Evidence from human studies is circumstantial. Reactivity of arterial smooth muscle is enchanced by low and suppressed by high magnesium media. Evidence that magnesium depletion may initiate coronary spasm is provided by dog and retrospective human studies.
Although experimental magnesium deficiency disrupts myocardial mitochondria, there are no studies which show that magnesium deficiency will lead to cardiac failure or that replacement will improve cardiac function. It is known that an infarcted or ischaemic myocardium loses magnesium and this may be the basis for ventricular arrhythmias. Coronary occlusion in a previously magnesium-depleted heart will result in a larger area of necrosis and ischaemia. The fall in serum magnesium in acute myocardial infarction is probably due to the formation of soap in fat cells undergoing catecholamine lipolysis.
Ventricular fibrillation in coronary artery disease will respond to parenteral magnesium, even in the presence of normal serum concentrations.
Résumé
Le rôle du magnésium dans la maladie coronarienne est examiné du point de vue de la pathogénie des maladies suivantes: artériosclérose, spasme coronarien, infarctus aigu du myocarde, fonctionnement myocardique, arythmies ventriculaires. Expérimentalement, la déplétion en magnésium potentialise l’effet athérogène de l’alimentation et la supplémentation le retarde. La contractilité du muscle vasculaire lisse est augmentée dans un milieu pauvre en magnésium et diminuée dans un milieu riche. La preuve que le déficit enmagnésium peut être à l’origine de spasme coronarien est fournie par des études chez le Chien et l’analyse rétrospective de données chez l’Homme.
Bien que le déficit expérimental en magnésium provoque un éclatement des mitochondries des cellules myocardiques on ne dispose pas d’études montrant qu’il puisse conduire à une insuffisance myocardique ni que sa correction amène une amélioration de la fonction cardiaque. On sait que les myocardes infarcis ou ischémiés sont le siège d’une perte en magnésium ce qui peut faciliter la survenue d’arythmies. L’occlusion d’une artère coronaire d’un coeur préalablement appauvri en magnésium aura pour conséquence la formation d’une vaste zone de nécrose et d’ischémie. La chute du magnésium sérique au cours de l’infarctus du myocarde est probablement due à une saponification dans les cellules lipidiques qui subissaient une lipolyse adrénergique.
La fibrillation ventriculaire qui survient dans la maladie coronarienne est sensible à l’administration de magnésium par voie parentérale même si sa concentration sérique est normale.
Zusammenfassung
Magnesium bei der Koronararterienerkrankung wird hinsichtlich seiner Bedeutung für die Pathogenese der Arteriosklerose, Koronarspasmen, Myokardfunktion, akuter Herzinfarkt und ventrikulären Arrhythmien betrachtet. Experimentell potenziert ein Magnesiummangel den Effekt einer atherogenen Diät, eine Magnesiumsubstitution verzögert sie. Hinweise aus Humanstudien deuten darauf hin. Die Reaktivität des arteriellen glatten Muskels wird verstärkt durch niedriges und vermindert durch hohes Magnesium. Hinweise für die Auslösung von Koronarspasmen durch Magnesiummangel ergeben sich aus Studien am Hund und retrospektive Erhebungen am Menschen. Obgleich ein experimenteller Magnesiummangel Herzmitochondrien zerstört, gibt es keine Studien, die zeigen, daβ Magnesiummangel zu Herzversagen führt oder daβ der Substitution die Herzfunktion verbessert. Es ist bekannt, daβ ein Infarktherz oder ischämisches Myokard Magnesium verliert, und dies kann die Basis ventrikulärer Arrhythmien sein. Der Koronarverschluβ bei einem vorher Magnesium-verarmten Herzen führt zu einem gröβeren nekrotischen und ischämischen Gebiet. Der Abfall des Serum-Magnesiums beim akuten Herzinfarkt beruht wahrscheinlich auf Verseifungen in den eine Katecholamin-Lypolyse erleidenden Fettzellen.
Kammerflimmern bei Koronararterienerkrankung reagiert, selbst bei Vorliegen normaler Serumkonzentrationen, auf parenterales Magnesium.
Sommario
Viene discusso l’uso del magnesio nelle cardiopatia ischemica con particolare attenzione per il suo ruolo nella patogenesi dell’arteriosclerosi, dello spasmo coronarico, delle disfunzioni miocardiche, dell’infarto miocardico acuto e delle aritmie ventricolari. Sperimentalmente la deplezione di magnesio potenzia gli effetti delle diete aterogeniche, mentre la somministrazione di questo sale li ritarda. Sono a disposizione dati particolareggiati ottenuti in studi condotti sull’uomo. La reattivitä della muscolatura liscia arteriosa viene accentuata da soluzioni a bassa concentrazione di magnesio e soppressa da soluzioni ad alta concentrazione. Studi eseguiti nel cane e studi retrospettivi nell’uomo hanno fornito prove che la deplezione di magnesio può innescare lo spasmo coronarico.
Benchè sperimentalmente la carenza di magnesio danneggi i mitocondri del miocardio, non vi è alcuno studio che dimostri come tale condizione possa condurre allo scompenso o che, viceversa, la sua somministrazione migliori la funzione cardiaca. ’E noto che un miocardio ischemico o colpito da infarto si depaupera di magnesio e che ciò può costituire la base per aritmie ventricolari. L’occlusione coronarica in un cuore precedentemente impoverito di magnesio détermina un’area di necrosi e di ischemia di maggiori dimensioni. La riduzione dei livelli plasmatici di magnesio osservata nell’infarto miocardico acuto è probabilmente dovuta alla formazione di saponi nelle cellule adipose ove si verifica una lipolisi catecolamino-dipendente.
La fibrillazione ventricolare che si verifica nella cardiopatia ischemica risponde alla somministrazione parenterale di magnesio anche in presenza di normali concentrazioni plasmatiche.
Resumen
Se revisa el papel del magnesio en la patologia de la arteria coronaria con relación a su papel en la patogenia de arteriosclerosis, espasmo coronario, función miocárdica, infarto agudo de miocardio y arritmias ventriculares. Experimentalmente, la depleciön de magnesio potencia y su suplementación retrasa el efecto de las dietas aterogénicas. Los datos procedentes de estudios sobre humanos son circunstanciales. Los medios con magnesio a baja concentratión acentúan la reactividad de los músculos lisos arteriales, mientras que las concentraciones elevadas la disminuyen. En el perro y en estudios retrospectivos sobre humanos se ha podido comprobar que la depletión de magnesio puede iniciar el espasmo coronario.
Aunque el déficit experimental de magnesio destruye las mitocondrias miocárdicas, no existen estudios que demuestren que el déficit de magnesio dé lugar a insuficiencia cardiaca o que su repositión mejore la función cardiaca. Se sabe que un miocardio infartado o isquémico pierde magnesio, lo que quizás sea le causa de arritmias ventriculares. La oclusión coronaria en un corazón previamente deplecionado de magnesio dará lugar a necrosis e isquemia más extensas. La caida de la concentratión sérica de magnesio en el curso del infarto de miocardio se dette probablemente a la formation de jabones en las células grasas que están experimentando lipólisis inducida por las catecolaminas.
La fibrilación ventricular que puede presentarse en la patologi’a de la arteria coronaria responderá a la administratión parenteral de magnesio, incluso en presencia de concentraciones séricas normales del mismo.
Resumo
O magnésio no quadro das doenças artero-coronárias é analisado no que diz respeito ao seu papel na patogênese da arteroesclerose, dos espasmos coronários, da função do miocárdio, do enfarte agudo do miocárdio e das arritmias ventriculares. Experimentalmente, a depleção de magnésio potencializa e a sua suplementação retarda o efeito das dietas aterogênicas. As provas a partir de estudos com humanos são apenas circunstanciais. A reatividade do mículo liso das artérias é intensificada por uma alta concentração de magnésio e é suprimida por uma baixa. Estudos com cães e estudos retrospectivos com humanos oferecem provas de que a depleção de magnésio pode dar inicio a espasmos coronários.
Embora a deficiência de magnésio em experiências rompa os condriossomos do miocardio, ainda não há estudos mostrando que a deficiência de magnésio conduza a deflciências cardiacas, nem que a sua reposição traga melhoras à função cardiaca. É sabido que um miocárdio enfartado ou isquêmico perde magnésio, e isso pode constituir uma base para arritmias ventriculares. Uma oclusão coronária num coração previamente deficiente de magnésio resultará numa maior área de necrose e em isquemia. A baixa da concentração de magnésio no sero durante o enfarte agudo do miocárdio deve-se provavelmente à formação de sabão nas células gordurosas submetidas à lipólise das catecolaminas.
A fibrilação ventricular ocorrida no quadro de uma doença artero-coronária réagirá à administração parenteral de magnésio, mesmo na presença de concentraçães de magnésio no sero normals.
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Iseri, L.T. Magnesium in Coronary Artery Disease. Drugs 28 (Suppl 1), 151–160 (1984). https://doi.org/10.2165/00003495-198400281-00015
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DOI: https://doi.org/10.2165/00003495-198400281-00015