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Restenosis is a major clinical problem following successful percutaneous transluminal coronary angioplasty. Since magnesium has vasodilator and antithrombotic effects, this study was designed to evaluate its potential to decrease the rate of restenosis. In an open-labelled, randomized controlled study, 148 patients underwent successful coronary angioplasty. Ninety-eight patients were treated with 46—52 mmoll 18–20 h intravenous magnesium sulphate (groups Ml and M2), and 49 of them continued with oral supplements of magnesium hydroxide 600 mg. day−1 (group M2).The other 50 patients served as controls (group C). Coronary angiography was performed before, immediately after and at 6 months follow-up or earlier if clinically indicated. Clinical, laboratory, ergometric and radionuclide evaluations were also carried out. One hundred and thirty-nine patients (94%) with 163 dilated segments completed the study. Intravenous magnesium was well tolerated The cross-sectional area at the site of angioplasty increased by 3.55 ± 201 mm2 in groups Ml and M2 compared with an increase of 2.90 ± 163 mm2 in the control group, (P=003). A trend towards a lower rate of restenosis (>50% reduction in luminal diameter) was noticed in the magnesium groups (28/110, 25%) compared with the control group (20/53, 38%) P=0.10. Oral administration of magnesium was well tolerated, did not have an additive effect on restenosis, but an improved clinical course was noted. It is concluded that intravenous administration of magnesium in patients undergoing coronary angioplasty is feasible and safe and that the beneficial trend of magnesium to prevent acute recoil and late (within 6 months) restenosis is encouraging and should promote further investigation in a larger patient population.

The clinical significance of sustained nonclinical ventricular tachycardia (VT) induced during electrophysiologic studies was studied in 10 amiodarone-treated patients. Nine patients had previous myocardial infarction while 1 patient had right ventricular dysplasia. All patients had only a single morphologic type of VT recorded during the multiple spontaneous episodes of tachycardia. After serial pharmacological electrophysiologic testing, the patients were placed on antiarrhythmic regimens which included amiodarone in all cases. These drugs did not prevent the induction of nonclinical VT in any of the 10 patients and of sustained clinical VT in 7 patients. Nonclinical VT was sustained, requiring cardioversion (7 patients) or rapid ventricular pacing (3 patients) for termination. After a mean follow-up period of 27 +/- 10 months (range 12 to 36 months), 4 patients did not exhibit recurrent VT, 3 patients with inducible clinical VT experienced a recurrent episode of clinical VT after 16, 27 and 49 months, respectively, 2 patients had nonarrhythmia related deaths after 11 and 12 months, and 1 patient died suddenly after 17 months. These results suggest that laboratory induction of sustained nonclinical VT in amiodarone-treated patients does not imply the likelihood of their future spontaneous occurrence and, therefore, their prevention may not be required.

We tested the effect of disopyramide on reperfusion arrhythmias in mongrel dogs. The control group consisted of 27 dogs. Twenty-nine dogs received two intravenous doses of disopyramide (total: 5.3 mg/kg) before and during the occlusion of the left anterior descending coronary artery. The blood levels of disopyramide averaged 3.95 +/- 0.95 micrograms/ml and 5.9 +/- 1.1 micrograms/ml, 2.5 and 9.5 min after the ligation. The incidence of reperfusion arrhythmias was significantly (p less than 0.05) lower in the treated group (7.5%) than in the control group (33.3%). Disopyramide also lowered the incidence of arrhythmias during the occlusion period (14% vs. 52%, p less than 0.01). Both groups showed a correlation between the incidence of arrhythmias during the occlusion period and on reperfusion.