Magnesium Deficiency During Lactation as a Precipitant of Ventricular Tachyarrhythmias

Mela, Theofanie; Galvin, Joseph; McGovern, Brian A.

doi:10.1046/j.1460-9592.2002.00231.x

Cited by 4 publications

(3 citation statements)

References 6 publications

(9 reference statements)

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“…All FPVT-mutant channels were phosphorylated to the same degree as RyR2-WT by PKA, as evidenced by immunoblotting using the RyR2-Ser 2809 phospho-epitope antibody. Specificity of PKA phosphorylation and dissociation of calstabin2 was shown in the presence or absence of the PKA inhibitor PKI [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] ( Supplementary Figure, B and C). 12 FPVT-mutant RyR2 channels showed significantly decreased binding affinity of 35 S-labeled calstabin2 ( Figure 2 Unphosphorylated RyR2-WT Ca 2ϩ release channels exhibited low P o (0.2Ϯ0.1%) at 150 nmol/L cytosolic Ca 2ϩ in the presence of 1 mmol/L Mg 2ϩ as expected, because under diastolic conditions, RyR2 channels have to be tightly closed to allow for relaxation of the heart muscle.…”

Section: Ryr2 Missense Mutations Cause a Gain-of-function Defectmentioning

confidence: 99%

Sudden Death in Familial Polymorphic Ventricular Tachycardia Associated With Calcium Release Channel (Ryanodine Receptor) Leak

et al. 2004

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Background-Familial polymorphic ventricular tachycardia (FPVT) is characterized by exercise-induced arrhythmias and sudden cardiac death due to missense mutations in the cardiac ryanodine receptor (RyR2), an intracellular Ca 2ϩ release channel required for excitation-contraction coupling in the heart. Methods and Results-Three RyR2 missense mutations, P2328S, Q4201R, and V4653F, which occur in Finnish families, result in similar mortality rates of Ϸ33% by age 35 years and a threshold heart rate of 130 bpm, above which exercise induces ventricular arrhythmias. Exercise activates the sympathetic nervous system, increasing cardiac performance as part of the fight-or-flight stress response. We simulated the effects of exercise on mutant RyR2 channels using protein kinase A (PKA) phosphorylation. All 3 RyR2 mutations exhibited decreased binding of calstabin2 (FKBP12.6), a subunit that stabilizes the closed state of the channel. After PKA phosphorylation, FPVT-mutant RyR2 channels showed a significant gain-of-function defect consistent with leaky Ca 2ϩ release channels and a significant rightward shift in the half-maximal inhibitory Mg 2ϩ concentration (IC 50 ). Treatment with the experimental drug JTV519 enhanced binding of calstabin2 to RyR2 and normalized channel function. Conclusions-Sympathetic activation during exercise induces ventricular arrhythmias above a threshold heart rate in RyR2 mutation carriers. Simulating the downstream effects of the sympathetic activation by PKA phosphorylation of RyR2 channels containing these FPVT missense mutations produced a consistent gain-of-function defect. RyR2 function and calstabin2 depletion were rescued by JTV519, suggesting stabilization of the RyR2 channel complex may represent a molecular target for the treatment and prevention of exercise-induced arrhythmias and sudden death in these patients.

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Section: Ryr2 Missense Mutations Cause a Gain-of-function Defectmentioning

confidence: 99%

Sudden Death in Familial Polymorphic Ventricular Tachycardia Associated With Calcium Release Channel (Ryanodine Receptor) Leak

et al. 2004

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“…Although lactation has been reported to decrease maternal electrolyte stores [13] and is not advised, our patient's weekly magnesium, sodium and potassium plasma levels were normal during the puerperial period. Therefore, we do not advise abstaining from breastfeeding in early- or mid-stage ARVD, when the patient is not using drugs or when the drugs are safe for breastfeeding.…”

Section: Discussionmentioning

confidence: 58%

Management of a rare case of arrhythmogenic right ventricular dysplasia in pregnancy: a case report

et al. 2011

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IntroductionArrhythmogenic right ventricular dysplasia is a heritable disease of the heart muscle characterized by fibrofatty degeneration of cardiomyocytes. Patients present with ventricular arrhythmias or congestive heart failure, and sometimes sudden cardiac death occurs. Prenatal diagnosis has become possible with the detection of mutations, but, to the best of our knowledge, no case of prenatal diagnosis has been reported previously. There is little information about the management of arrhythmogenic right ventricular dysplasia in pregnancy, and the preferred mode of delivery is not certain; therefore, we present the case of a patient with arrhythmogenic right ventricular dysplasia and discuss the prenatal diagnosis, patient management and prognosis in pregnancy.Case presentationA 26-year-old Caucasian woman who presented to our hospital with heart palpitations was diagnosed with arrhythmogenic right ventricular dysplasia, and, after three years of follow up with anti-arrhythmic drugs, she wanted to conceive. During pregnancy, she ceased taking her medication. She tolerated pregnancy very well but her cardiac symptoms recurred after her 30th week of pregnancy. She delivered a baby via cesarean section under general anesthesia in her 38th week of pregnancy. She was discharged without any medications and continued lactation for six months.ConclusionPatients with mild to moderate arrhythmogenic right ventricular dysplasia tolerate pregnancy and breastfeeding very well, but patients with end-stage arrhythmogenic right ventricular dysplasia should be discouraged from conception.

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“…In postpartum period, analgesia is so important because pain can promote sympathic stimulation which can result in severe arrhythmia [ 8 ]. Breastfeeding can cause loss of electrolytes especially magnesium which may promote arrhythmias [ 23 ]. For our patient breastfeeding was proscribed not only for this reason but also because of the crossing of anti-arrhythmic drugs in breast milk.…”

Section: Discussionmentioning

confidence: 99%

Management of a rare case of arrhythmogenic right ventricular dysplasia in pregnancy: a case report

Jarraya¹,

Smaoui²,

Kolsi³

2014

Pan Afr Med J

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Arrhythmogenic right ventricular dysplasia is a rare but not exceptional inherited cardiomyopathy characterized by fibrofatty replacement of the myocardium of the right ventricular which could lead to serious arrhythmia and sudden death. Only a few cases of pregnancies with ARVD have been reported. The aim of this case presentation is to describe the clinical characteristics and anesthetics specificities in management of this disease in pregnancy and in delivery. We report the case of a young woman aged 28 years old with a past history of ARVD treated by medical treatment with radiofrequency ablation. This patient was pregnant and it was scheduled for cesarean section delivery. Preoperative evaluation showed a well tolerated pregnancy inspite of the severity of the ARVD. It was a severe form of ARVD because of RV dilation, the spread of the disease to LV and the history of ventricular tachycardia during an attempted of ablation by radio frequency. The treatment received by the patient was kept until the day of surgery. The act took place under general anesthesia. The postoperative period was uneventful and morphine titration was used for pain relief. The patient exits the hospital 3 days after delivery and breastfeeding was forbidden. We should pay attention on this disease witch is not yet well known and witch is highly risky in the peri-partum period. Even if pregnancy may be tolerated in moderate forms of ARVD, conception and delivery sould be discouraged especially in severe forms.

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Magnesium Deficiency During Lactation as a Precipitant of Ventricular Tachyarrhythmias

Cited by 4 publications

References 6 publications

Sudden Death in Familial Polymorphic Ventricular Tachycardia Associated With Calcium Release Channel (Ryanodine Receptor) Leak

Sudden Death in Familial Polymorphic Ventricular Tachycardia Associated With Calcium Release Channel (Ryanodine Receptor) Leak

Management of a rare case of arrhythmogenic right ventricular dysplasia in pregnancy: a case report

Management of a rare case of arrhythmogenic right ventricular dysplasia in pregnancy: a case report

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