Clinical Symptoms of Mitral Valve Prolapse Are Related to Hypomagnesemia and Attenuated by Magnesium Supplementation

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Abstract

Mitral valve prolapse syndrome (MVP) is a frequent disorder characterized by a number of complaints which lessen the quality of life. The pathogenesis of MVP symptoms has not been fully elucidated. Hyperadrenergic activity and magnesium deficiency have been suggested. This study was designed to verify the concept that heavily symptomatic MVP is accompanied by hypomagnesemia and to elucidate whether magnesium supplementation alleviates the symptoms and influences adrenergic activity. We assessed serum magnesium in 141 subjects with heavily symptomatic primary MVP and in 40 healthy controls. Decreased serum magnesium was found in 60% of patients and in 5% of controls (p <0.0001). Patients with low serum magnesium were subjected to magnesium or placebo supplementation in a double-blind, crossover fashion. Typical symptoms of MVP (n = 13), intensity of anxiety, and daily excretion of catecholamines were determined. After 5 weeks, the mean number of symptoms per patient decreased from 10.4 ± 2.1 to 5.6 ± 2.5 (p <0.0001), and a significant reduction in weakness, chest pain, dyspnea, palpitations, and anxiety was observed. Increased noradrenaline excretion before and after magnesium was seen in 63% and 17% of patients, respectively (p <0.01). Mean daily excretion of noradrenaline and adrenaline was significantly diminished after magnesium. It is concluded that many patients with heavily symptomatic MVP have low serum magnesium, and supplementation of this ion leads to improvement in most symptoms along with a decrease in catecholamine excretion.

This study reveals a high incidence (60%) of hypomagnesemia in 141 patients with symptomatic mitral valve prolapse. After controlled oral magnesium supplementation for 5 weeks in 70 patients, most symptoms were significantly alleviated along with diminution of catecholamine excretion.

Section snippets

Patient Population

The study group consisted of 141 subjects (124 women and 17 men, aged 16 to 57 years, mean ± SD 31 ± 9) with heavily symptomatic MVP who were free of other diseases. They were enrolled in the study from January 1989 to October 1995. During that period, 529 previously nontreated persons had been referred to the outpatient unit of our cardiology department because of suspected MVP. The diagnosis was confirmed by echocardiography in 217 patients. Thirty-two patients with concomitant diseases and

Serum Magnesium and the Incidence of Hypomagnesemia

Serum magnesium in patients with heavily symptomatic MVP and in controls was 0.68 ± 0.11 mmol/L and 0.80 ± 0.05 mmol/L, respectively (p <0.0001) (Fig. 1).

Of 141 heavily symptomatic patients, 84 (60%) had decreased serum magnesium in at least 1 blood sample compared with 2 of 40 controls (5%), p <0.0001. These 84 patients were given magnesium supplementation.

Magnesium Supplementation

Of 84 patients, 14 withdrew in the initial phase of the study because of poor cooperation. Thus, the study was completed by 70 patients (64

Discussion

This study revealed a high incidence of hypomagnesemia in patients with heavily symptomatic MVP. Serum magnesium does not accurately represent intracellular magnesium, because it may change from day to day, and it depends on many factors.[15] However, there is no doubt that when serum magnesium is low, intracellular magnesium is unquestionably low.16, 17 Although the deficit of magnesium in MVP has previously been suspected, little research was done on the subject. Early studies18, 19, 20, 21

Acknowledgements

We thank Jan Tylka, PhD, for his help in the psychological workup. We also thank Maciej Światkowski, MD, and Paweł Maciejewski, MD, for preparation of figures and tables, and Joanna Lis, PhD, for assistance with the statistical analysis.

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