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Postpartum acute myocardial infarction Gregorio S. Santos, MD, and Ara Sadaniantz, MD Providence, Rhode Island We report a postpartum acute myocardial infarction that occurred during the first week after cesarean section delivery. We also calculated the rate of postpartum myocardial infarction as related to all women with myocardial infarctions seen in our hospital. (Am J Obstet Gynecol 1997;177:1553-5.) Key words: Myocardial infarction, pregnancy Fewer than 100 cases of postpartum myocardial infarc- tion have been reported in the literature, 1 but the disorder has been associated with significant morbidity and mortality for both mother and neonate. With the current trend in the United States for childbearing later in life, the incidence of myocardial infarction after pregnancy is likely to increase. We report an acute myocardial infarction that occurred during the first week after cesarean section delivery and we calculate the rate of peripartum myocardial infarction. Case report A 43-year-old multigravid woman's pregnancy was complicated by gestational hypertension and diabetes. She had smoked for 15 years and her family history was significant for premature coronary artery disease. She was delivered of a single healthy baby by an uneventful cesarean section. Six days later she was admitted with complaints of dyspnea and intermittent chest pain of 2 days' duration. Blood pressure was 130/78 mm Hg and pulse was 130 beats/min. $2 and an $3 gallop were heard. There were no murmurs or rubs. Electrocardiog- raphy showed normal sinus rhythm, with 2 to 3 mm ST segment elevation and Qwaves in leads V2 to V5 (Fig. 1). The creatine kinase peak was 1474 IU with positive creatine phosphokinase MB isoenzyme. Arterial blood gas on room air showed pH 7.51, Pco 2 22 mm Hg, and Po 2 50 man Hg. The chest x-ray film showed increased vascular markings consistent with pulmonary edema. The left ventricular systolic function was moderately decreased with anterolateral and apical hypokinesis and an apical thrombus. Because of her young age and the complication of the myocardial infarction with pulmo- nary edema, the patient underwent coronary angiogra- phy. The left anterior descending artery was 100% ste- nosed and the left circumflex had a 50% lesion (Fig. 2); the right coronary artery had a 20% to 30% lesion. Angioplasty of the left anterior descending artery was From the Divisio~ of Cardiology, Miriam Hospital, Brown University School of Medicine, Received for publieation January 27, 1997; revised February 11, 1997; acceptedApril 28, 1997. Reprint requests:A~zzSadaniantz, MD, Division of Cardiology, Miriam Hospital, 164 Summit Ave., Providence, RI 02906. Copyright © 1997 by Mosby-Year Book, Inc. 0002-9378/97 $5.00 + 0 6/1/82914 attempted but was unsuccessful. The patient was dis- charged home in satisfactory condition on a medical regimen of furosemide 20 mg orally daily, captopril 37.5 nag orally three times a day, metoprolol 12.5 mg orally twice daily, warfarin 5 mg orally daily, and aspirin 325 mg orally daily. Methods and results Information was entered into a database from May 1991 to June 1996 for each patient admitted to the coronary care unit of The Miriam Hospital. The number of patients with acute myocardial infarction (chest pain for >20 minutes with typical ST segment elevations) was 405, of whom 157 were women. This case is the first that was seen in our institution with peripartum myocardial infarction. Therefore the ratio of postpartum myocardial infarction compared with all women with acute myocar- dial infarction in our hospital from May 1991 to June 1996 was 1:157. Assuming childbearing age as up to 50 years, there were only 10 women of childbearing age seen for acute myocardial infarction. Therefore 1 of 10 (10 %) cases of acute myocardial infarction was related to peripartum causes among women aged <50 years. Comment The precipitating factors of acute myocardial infarc- tion during the postpartum period are unclear. Physio- logic events during pregnancy, intra partum, and post partum, such as hormonal and neurohormonal changes, increases intravascular volume and oxygen demand, which may make atherosclerotic plaque more likely to rupture. During labor cardiac output, blood pressure, and heart rate increase. With each uterine contraction 300 to 500 ml of uterine blood enters the maternal circulatory system. These changes, as well as blood loss of up to 500 ml during vaginal delivery or up to 1000 ml during cesarean section, can increase myocardial oxygen demand.i, 2 Coronary artery disease is the leading cause of death in the western world. It is rare in young women, but the incidence increases with age. In the United States the rate of first births among women -->40 years old has 1553

Postpartum acute myocardial infarction

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Postpartum acute myocardial infarction

Gregorio S. Santos, MD, and Ara Sadaniantz, MD

Providence, Rhode Island

We report a postpartum acute myocardial infarction that occurred during the first week after cesarean section delivery. We also calculated the rate of postpartum myocardial infarction as related to all women with myocardial infarctions seen in our hospital. (Am J Obstet Gynecol 1997;177:1553-5.)

Key words: Myocardial infarction, pregnancy

Fewer than 100 cases of postpartum myocardial infarc-

tion have been reported in the literature, 1 but the

disorder has been associated with significant morbidity

and mortality for both mother and neonate. With the

current trend in the United States for childbearing later

in life, the incidence of myocardial infarction after

pregnancy is likely to increase. We report an acute

myocardial infarction that occurred during the first week

after cesarean section delivery and we calculate the rate

of peripartum myocardial infarction.

Case report

A 43-year-old multigravid woman's pregnancy was complicated by gestational hypertension and diabetes. She had smoked for 15 years and her family history was significant for premature coronary artery disease. She was delivered of a single healthy baby by an uneventful cesarean section. Six days later she was admitted with complaints of dyspnea and intermittent chest pain of 2 days' duration. Blood pressure was 130/78 mm Hg and pulse was 130 beats/min. $2 and an $3 gallop were heard. There were no murmurs or rubs. Electrocardiog- raphy showed normal sinus rhythm, with 2 to 3 mm ST segment elevation and Qwaves in leads V2 to V5 (Fig. 1). The creatine kinase peak was 1474 IU with positive creatine phosphokinase MB isoenzyme. Arterial blood gas on room air showed pH 7.51, Pco 2 22 mm Hg, and Po 2 50 man Hg. The chest x-ray film showed increased vascular markings consistent with pulmonary edema. The left ventricular systolic function was moderately decreased with anterolateral and apical hypokinesis and an apical thrombus. Because of her young age and the complication of the myocardial infarction with pulmo- nary edema, the patient underwent coronary angiogra- phy. The left anterior descending artery was 100% ste- nosed and the left circumflex had a 50% lesion (Fig. 2); the right coronary artery had a 20% to 30% lesion. Angioplasty of the left anterior descending artery was

From the Divisio~ of Cardiology, Miriam Hospital, Brown University School of Medicine, Received for publieation January 27, 1997; revised February 11, 1997; accepted April 28, 1997. Reprint requests: A~zz Sadaniantz, MD, Division of Cardiology, Miriam Hospital, 164 Summit Ave., Providence, RI 02906. Copyright © 1997 by Mosby-Year Book, Inc. 0002-9378/97 $5.00 + 0 6/1/82914

attempted but was unsuccessful. The patient was dis- charged home in satisfactory condition on a medical regimen of furosemide 20 mg orally daily, captopril 37.5 nag orally three times a day, metoprolol 12.5 mg orally twice daily, warfarin 5 mg orally daily, and aspirin 325 mg orally daily.

Methods and results

Information was entered into a database from May

1991 to June 1996 for each patient admitted to the coronary care unit of The Miriam Hospital. The number

of patients with acute myocardial infarction (chest pain

for >20 minutes with typical ST segment elevations) was

405, of whom 157 were women. This case is the first that

was seen in our institution with peripartum myocardial

infarction. Therefore the ratio of postpartum myocardial

infarction compared with all women with acute myocar-

dial infarction in our hospital from May 1991 to June

1996 was 1:157. Assuming childbearing age as up to 50 years, there were only 10 women of childbearing age

seen for acute myocardial infarction. Therefore 1 of 10

(10 %) cases of acute myocardial infarction was related to

peripartum causes among women aged <50 years.

Comment

The precipitating factors of acute myocardial infarc-

tion during the postpartum period are unclear. Physio-

logic events during pregnancy, intra partum, and post

partum, such as hormonal and neurohormonal changes,

increases intravascular volume and oxygen demand,

which may make atherosclerotic plaque more likely to

rupture. During labor cardiac output, blood pressure,

and heart rate increase. With each uterine contraction 300 to 500 ml of uterine blood enters the maternal

circulatory system. These changes, as well as blood loss of up to 500 ml during vaginal delivery or up to 1000 ml during cesarean section, can increase myocardial oxygen demand.i, 2

Coronary artery disease is the leading cause of death in the western world. It is rare in young women, but the

incidence increases with age. In the United States the rate of first births among women -->40 years old has

1553

1554 Santos and Sadaniantz December 1997 .aan J Obstet Gynecol

rq J

Fig. 2. Coronary angiography of left corona~ Tar te t T system is shown. Lef~ anterior descending coronas' / artery is completely occluded soon after its origin (arrow). Left main and circumflex arteries have no significant narrowings.

Volume 177, Number 6 Santos and Sadaniantz 1555 Am J Obstet Gynecol

doubled between 1976 to 1986. This tendency toward

advanced childbearing age may be associated with in- creased myocardial infarction during gestation and the

peripartum period. Labor may precipitate myocardial

ischemia or infarction in women with preexisting coro-

nary artery disease. Our data are unique in that we included all patients

with acute ST segment elevation myocardial infarction

who have been seen at our hospital to calculate the rate

of peripartum myocardial infarction. We choose this

population because ST segment elevation myocardial

infarction differs in its pathogenesis, treatment, and

outcome from the other types of myocardial infarctions.

Because of the tendency toward advanced childbear-

ing age, the risk of myocardial infarction related to pregnancy may be increased. The potential benefit of

prepregnancy screening for coronary artery disease, par-

ticularly in those women with risk factors for premature

atherosclerosis, need to be studied.

REFERENCES

1. Sheikh AU, Harper MA. Myocardial infarction during preg- nancy: management and outcome of two pregnancies. Am J Obstet Gynecol 1993;169:279-84.

2. Samra D, Samra Y, Hertz M, Maier M. Acute myocardial infarction in pregnancy and puerperium. Cardiology 1989; 76:455-60.