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Troponin I in the diagnosis of acute myocardial infarction in pregnancy, labor, and post partum
Troponin I in the diagnosis of acute myocardial infarction in pregnancy, labor, and post partum George H. Shade, Jr, MD,a Gary Ross, DO,b Frank N. Bever, MD,c Zi Uddin, PhD,c Lingareddy Devireddy, MD,d and Julius M. Gardin, MDe Detroit and Warren, Mich Cardiac troponin I has become the marker of choice for the diagnosis of acute myocardial infarction. There are specific characteristics of this test that makes it desirable for the diagnosis of acute myocardial infarction in pregnancy, labor, and post partum. (Am J Obstet Gynecol 2002;187:1719-20.)
Key words: Acute myocardial infarction, pregnancy, cardiac troponin I
The diagnosis of acute, evolving, or recent myocardial infarction (AMI) in view of recent published criteria1 has been greatly facilitated by the use of cardiac-specific troponin I (cTnI). cTnI has also emerged as a marker of choice of cardiac injury in pregnant woman for three reasons: (1) cTnI is never increased above the upper limit of normal value in healthy pregnant woman, 30 minutes, 12 hours, and 24 hours after delivery, (2) cTnI is not affected by obstetric anesthesia (epidermal or spinal), prolonged labor, or operative delivery, and (3) uterine contractions and cell breakdown that normally occur during labor and delivery are responsible for the significant increase in other cardiac markers (myoglobin, creatine kinase, creatine kinase isoenzyme MB) because of their presence in uterus and placenta but have no effect on cTnI. Case report This case involved a 18 year-old woman, gravida 2, para 1, in labor at 39 weeks of gestation. After augmentation with oxytocin, the placenta was spontaneously delivered. The patient had supraventricular tachycardia (SVT) immediately post partum and was treated with adenosine (Adenocard), which converted the heart rhythm to sinus rhythm. The patient’s blood pressure was maintained with no evidence of any hypotension, and she was placed on heparin, β-blockers, and aspirin.
From the Departments of Obstetrics and Gynecology,a Clinical Resource Management,b and Pathology,c St John Detroit Riverview Hospital, the Department of Cardiology, St John Macomb Hospital,d and the Cardiology Division, St John Hospital and Medical Center.e Received for publication April 16, 2002; accepted May 15, 2002. Reprint requests: George H. Shade, Jr, MD, FACOG, FACPE, Department of Obstetrics and Gynecology, St John Detroit Riverview Hospital, 7733 E Jefferson Ave, Detroit, MI 48214-2598. E-mail: [email protected] © 2002, Mosby, Inc. All rights reserved. 0002-9378/2002 $35.00 + 0 6/1/126648 doi:10.1067/mob.2002.126648
There had been no complaints before delivery or during delivery of chest discomfort, but when tachycardia developed, the patient had an unusual sensation in the chest. There was no history of heart disease. The electrocardiogram (ECG) after conversion from SVT was completely normal. Repeat ECGs did not demonstrate any sign of myocardial infarction. On the third postpartum day, the patient had a nuclear isotope myocardial perfusion scan with wall motion analysis and ejection fraction calculations. The patient’s ejection fraction was estimated at 61% and there was mild to moderate reduced activity in the anterior wall during both phases of the study with use of thallium at rest and tetrofosmin (Myoview) given during peak exercise. The echocardiogram noted normal valvular structure, no pericardial effusion, a mildly dilated left ventricle, normal systolic left ventricular function, paradoxical septal motion at the base, and no atrial or ventricular septal defects. The first cTnI result (10 hours after delivery) was 11.6 ng/mL (diagnostic criteria for AMI >4.5 ng/mL), and the subsequent four results (up to 32 hours after delivery) exhibited a classic pattern of cTnI in AMI.1 Comment In view of the nondiagnostic ECGs in about 50% of AMI cases and the commonality of the classic symptoms of myocardial necrosis (chest pain, diaphoresis, and shortness of breath) with the normal physiologic changes of pregnancy and the symptoms resulting from β-sympathomimetic therapy for tocolysis or intravenous magnesium sulfate therapy for eclampsia prophylaxis, the diagnosis of AMI in pregnancy is often difficult. However, this task was simplified by the high sensitivity and specificity of cTnI at lower levels, adherence to the cTnI assay protocol (timed specimens), and the observation of its rapid rise and gradual fall1 after AMI as is exemplified by the case presented here. We believe that this is the first 1719
1720 Shade et al
case in the literature where cTnI was exclusively used for the diagnosis of AMI that occurred immediately after the delivery of a baby. Two other cases are known in the literature where cTnI was also used as a cardiac marker for the diagnosis of AMI; however, in both of these cases (case a, AMI at 23 weeks of gestation with normal delivery at 38 weeks’ gestation; case b, AMI after cesarean delivery) the ECG was positive for AMI.2 Among the various complications of pregnancy, the frequency of diagnosed myocardial infarction is relatively low (perhaps 1 in 10,000); however, this occurrence may increase statistically in view of childbearing at an older age and other identifiable risk factors (eg, cigarette smoking, hyperlipoproteinemia, oral contraceptive use,
December 2002 Am J Obstet Gynecol
thrombophilia, thyroid disease, collagen tissue disorder, employment-associated stress, and the use of advanced technology for the diagnosis of AMI). We propose that, under appropriate clinical conditions, cTnI is the marker of choice in the diagnosis of AMI during pregnancy, labor, and post partum. REFERENCES
1. Alpert JS, Thygesenk K, Antman E, Bassand JP, et al. Myocardial infarction redefined—a consensus document of the Joint Euoropean Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. J Am Coll Cardiol 2000;36:959-69. 2. Krahenmann F, Hucha A, Atar D. Troponin I measurement in the diagnosis of myocardial injury during pregnancy and delivery: two cases. Am J Obstet Gynecol 2000;183:1308-10.
Key words: Acute myocardial infarction, pregnancy, cardiac troponin I
The diagnosis of acute, evolving, or recent myocardial infarction (AMI) in view of recent published criteria1 has been greatly facilitated by the use of cardiac-specific troponin I (cTnI). cTnI has also emerged as a marker of choice of cardiac injury in pregnant woman for three reasons: (1) cTnI is never increased above the upper limit of normal value in healthy pregnant woman, 30 minutes, 12 hours, and 24 hours after delivery, (2) cTnI is not affected by obstetric anesthesia (epidermal or spinal), prolonged labor, or operative delivery, and (3) uterine contractions and cell breakdown that normally occur during labor and delivery are responsible for the significant increase in other cardiac markers (myoglobin, creatine kinase, creatine kinase isoenzyme MB) because of their presence in uterus and placenta but have no effect on cTnI. Case report This case involved a 18 year-old woman, gravida 2, para 1, in labor at 39 weeks of gestation. After augmentation with oxytocin, the placenta was spontaneously delivered. The patient had supraventricular tachycardia (SVT) immediately post partum and was treated with adenosine (Adenocard), which converted the heart rhythm to sinus rhythm. The patient’s blood pressure was maintained with no evidence of any hypotension, and she was placed on heparin, β-blockers, and aspirin.
From the Departments of Obstetrics and Gynecology,a Clinical Resource Management,b and Pathology,c St John Detroit Riverview Hospital, the Department of Cardiology, St John Macomb Hospital,d and the Cardiology Division, St John Hospital and Medical Center.e Received for publication April 16, 2002; accepted May 15, 2002. Reprint requests: George H. Shade, Jr, MD, FACOG, FACPE, Department of Obstetrics and Gynecology, St John Detroit Riverview Hospital, 7733 E Jefferson Ave, Detroit, MI 48214-2598. E-mail: [email protected] © 2002, Mosby, Inc. All rights reserved. 0002-9378/2002 $35.00 + 0 6/1/126648 doi:10.1067/mob.2002.126648
There had been no complaints before delivery or during delivery of chest discomfort, but when tachycardia developed, the patient had an unusual sensation in the chest. There was no history of heart disease. The electrocardiogram (ECG) after conversion from SVT was completely normal. Repeat ECGs did not demonstrate any sign of myocardial infarction. On the third postpartum day, the patient had a nuclear isotope myocardial perfusion scan with wall motion analysis and ejection fraction calculations. The patient’s ejection fraction was estimated at 61% and there was mild to moderate reduced activity in the anterior wall during both phases of the study with use of thallium at rest and tetrofosmin (Myoview) given during peak exercise. The echocardiogram noted normal valvular structure, no pericardial effusion, a mildly dilated left ventricle, normal systolic left ventricular function, paradoxical septal motion at the base, and no atrial or ventricular septal defects. The first cTnI result (10 hours after delivery) was 11.6 ng/mL (diagnostic criteria for AMI >4.5 ng/mL), and the subsequent four results (up to 32 hours after delivery) exhibited a classic pattern of cTnI in AMI.1 Comment In view of the nondiagnostic ECGs in about 50% of AMI cases and the commonality of the classic symptoms of myocardial necrosis (chest pain, diaphoresis, and shortness of breath) with the normal physiologic changes of pregnancy and the symptoms resulting from β-sympathomimetic therapy for tocolysis or intravenous magnesium sulfate therapy for eclampsia prophylaxis, the diagnosis of AMI in pregnancy is often difficult. However, this task was simplified by the high sensitivity and specificity of cTnI at lower levels, adherence to the cTnI assay protocol (timed specimens), and the observation of its rapid rise and gradual fall1 after AMI as is exemplified by the case presented here. We believe that this is the first 1719
1720 Shade et al
case in the literature where cTnI was exclusively used for the diagnosis of AMI that occurred immediately after the delivery of a baby. Two other cases are known in the literature where cTnI was also used as a cardiac marker for the diagnosis of AMI; however, in both of these cases (case a, AMI at 23 weeks of gestation with normal delivery at 38 weeks’ gestation; case b, AMI after cesarean delivery) the ECG was positive for AMI.2 Among the various complications of pregnancy, the frequency of diagnosed myocardial infarction is relatively low (perhaps 1 in 10,000); however, this occurrence may increase statistically in view of childbearing at an older age and other identifiable risk factors (eg, cigarette smoking, hyperlipoproteinemia, oral contraceptive use,
December 2002 Am J Obstet Gynecol
thrombophilia, thyroid disease, collagen tissue disorder, employment-associated stress, and the use of advanced technology for the diagnosis of AMI). We propose that, under appropriate clinical conditions, cTnI is the marker of choice in the diagnosis of AMI during pregnancy, labor, and post partum. REFERENCES
1. Alpert JS, Thygesenk K, Antman E, Bassand JP, et al. Myocardial infarction redefined—a consensus document of the Joint Euoropean Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. J Am Coll Cardiol 2000;36:959-69. 2. Krahenmann F, Hucha A, Atar D. Troponin I measurement in the diagnosis of myocardial injury during pregnancy and delivery: two cases. Am J Obstet Gynecol 2000;183:1308-10.