Clinical symptoms of mitral valve prolapse are related to hypomagnesemia and attenuated by magnesium supplementation.

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.

[Extent of left-ventricular damage after myocardial infarction and the occurrence of mural thrombi]. / Rozleglosc uszkodzenia lewej komory serca po zawale a wystepowanie skrzeplin przysciennych.

The aim of the study was to estimate a detailed relationship between the extent of left ventricular damage after myocardial infarction (MI) and occurrence of mural thrombi examined with two dimensional echocardiography (2Decho). The examinations were undertaken in 47 patients (pts) (age 40-86 years) after transmural anterior MI. 2Decho was performed in all pts according to American Society of Echocardiography from the is day to the 4th month after MI. Heger index was used for the estimation of LV wall motion disturbances. The criterion of mural thrombus was the presence of an additional echo by LV wall visible in at least two echocardiographic views. It was determined that the incidence of mural thrombi is correlated with statistically significant larger LV damage expressed with higher Heger index and higher number of hypo-, a-, and dyskinetic LV segments. The study revealed the relationship between the extent of LV damage after MI, the presence of LV dyskinesia, LV enlargement, ST segment elevation in ecg and the incidence of mural thrombi.

Indomethacin increases abortifacient effect of PGE2 in man.

Results of this study indicate that pretreatment with indomethacin significantly increases the abortifacient effect of an intravenous infusion of PGE2 in patients admitted for abortion as a result of fetal death in utero. Indomethacin pretreatment shortened the duration of PGE2-induced abortion in primigravid and multigravid groups of patients by about 4 and 2 hours respectively. When primigravid and multigravid groups were combined, the dose of PGE2 needed for complete delivery decreases in the indomethacin-treated group by 39.9%.

PIP: Pretreatment with indomethacin (INDO) significantly increased the abortifacient effect of prostaglandin (PG) E2 when administered intravenously to abort pregnancies with fetal death in utero. Of 31 cases trated with PGE2 alone, 24 aborted successfully and 7 were unsuccessful; when INDO was used with PGE2 in 30 fetal-death terminations, 28 cases were successful and 2 were not (P=.081). Duration of delivery was significantly shorter in pretreated (P .05 for multigravidas, and P .001 for primigravidas). In hours, the differences were 4 and 2 for primi- and multigravidas, respectively. Amount of PGE2 needed to induce the 1st uterine contraction, complete cervical dilatation, and deliver the fetus and placenta was smaller in the INDO-pretreated patients than in PGE2 alone patients (P .05 - P . 01). Blood loss was significantly less in the INDO group (P .01). INDO pretreatment did not affect the associated drop in systolic and diastolic pressures which occurs with PGE2 administration.