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Correspondence

Myocardial Infarction during Nifedipine Therapy for Preterm Labor

N Engl J Med 1999; 340:154January 14, 1999

Article

To the Editor:

Recent studies have suggested that nifedipine is a safer, more effective treatment for preterm labor than the sympathomimetic agents routinely in use.1,2 On the basis of these promising results, calcium-channel antagonists are increasingly prescribed for tocolysis. On the other hand, a case–control study of hypertensive patients found that patients who were taking calcium-channel antagonists had an increased risk of myocardial infarction,3 and a meta-analysis found a dose-dependent association between the use of nifedipine and the risk of death.4 These data, however, are not necessarily applicable to pregnant women who are being treated for preterm labor. We describe a myocardial infarction in a young pregnant woman during tocolytic therapy with nifedipine.

A healthy 29-year-old woman was admitted during her first pregnancy because of preterm rupture of the membranes and uterine contractions at 29 weeks. The family history was unremarkable; serum lipid levels and the electrocardiographic findings were normal. Tocolytic therapy was started with intravenous ritodrine at a dose of 200 g per minute. Thirty hours later the patient reported chest pain. The blood pressure was 100/60 mm Hg, and the pulse was 82 beats per minute. Electrocardiography was repeated, and the results were still normal. Ritodrine therapy was stopped, and oral treatment with nifedipine (40-mg slow-release tablets three times daily) was started immediately. Four hours later — 45 minutes after the second dose of nifedipine — the woman reported chest pain, with referred pain in the jaw. The blood pressure was 70/50 mm Hg, and the pulse was 124 beats per minute. The electrocardiogram showed a T-wave inversion in lead III. The serum level of creatine kinase was 282 U per liter (normal, <100), with an MB isoenzyme level of 51 U per liter (normal, <15). The patient had an uncomplicated non–Q-wave myocardial infarction. Although tocolytic therapy was stopped, labor did not progress. Eighteen days later a healthy son was delivered by cesarean section. The woman recovered well; four months later, electrocardiography, exercise testing, and echocardiography showed no abnormalities.

The dose of nifedipine used was large but not larger than the doses used in recent studies.2 The short interval between the cessation of ritodrine therapy and the start of nifedipine therapy may have had a role in the development of the hypotension and myocardial infarction. In pregnancy, the intravascular volume increases, peripheral resistance falls, and cardiac output rises in combination with the occurrence of relative anemia and increased oxygen consumption. Sympathomimetic drugs can cause myocardial ischemia in pregnant women by further increasing oxygen consumption, but acute myocardial necrosis is rare.5 It is possible, however, that under these circumstances, nifedipine poses an extra risk by causing hypotension and reflex tachycardia.

S. Guid Oei, M.D., Ph.D.
Saint Joseph Hospital, 5500 MB Veldhoven, the Netherlands

S. Koen Oei, M.D.
Tjongerschans Hospital, 8441 PW Heerenveen, the Netherlands

Hans A.M. Brölmann, M.D., Ph.D.
Saint Joseph Hospital, 5500 MB Veldhoven, the Netherlands

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Citing Articles (28)

Citing Articles

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