Myocardial Infarction during Pregnancy: Whose Responsibility?

Jesus G. Mirelis, MD, Jose Antonio Fernandez-Diaz, MD, Javier Goicolea, MD
Jesus G. Mirelis, MD, Jose Antonio Fernandez-Diaz, MD, Javier Goicolea, MD

Case Report. A 37-year-old female in her seventh week of pregnancy presented to the emergency department after the onset of oppressive chest pain which had started 1 hour before. Her 8 previous pregnancies had terminated in abortion. She had no cardiovascular risk except for smoking, nor a history of alcohol or drug abuse. Her father had died of Leriche’s syndrome. A history of untreated peripheral obstructive arteriopathy was reported.
Clinical examination showed obesity. The patient was afebrile. Her blood pressure was 140/100 mmHg with a pulse of 100 beats per minute. Oxygen saturation determined by pulse oximetry was 100%. Nothing abnormal was found in the heart sounds.
Immunologic tests performed prior to admission, which included antiphospholipid antibodies, were negative. Laboratory analyses were normal, except for mild leukocytosis. Electrocardiography showed ST-segment elevation in anterior leads V2–V5, and troponin I levels were elevated. A chest X-ray was not performed because of the patient’s pregnancy.

With the diagnosis of an anterior ST-elevation myocardial infarction (STEMI) the patient was referred for primary angioplasty. Coronary angiography showed normal right and left circumflex coronary arteries. However, total occlusion of the left anterior descending coronary artery after the first septal branch was observed. Catheterization was performed after shielding the patient’s back and abdomen with lead aprons. The occlusion was crossed with a guidewire and balloon predilatation was performed to reestablish patency. Finally, a bare-metal stent was deployed. Final angiography showed satisfactory deployment of the stent and TIMI 3 flow.
Transthoracic echocardiography was performed a few hours later and revealed hypokinesis of the anterior and anterior-septal walls, with an overall ejection fraction estimated at 40%. The right ventricle appeared normal in size and function. No other valvular abnormalities were noted. Chest X-ray was not performed due to the patient’s pregnancy.
Although there were no signs of abortion, a transvaginal ultrasound examination performed the day after the procedure showed that the gestational sac was empty, thereby confirming miscarriage. On the third day, the patient was transferred to another hospital with obstetric facilities where curettage was performed.

Discussion. There are few published statistics concerning acute myocardial infarction (AMI) in pregnant women. The scarce epidemiological studies in the medical literature show that in the United States the incidence of AMI in pregnancy ranges from 2.81 to 6.22 cases per 100,000 deliveries. No figures are available for Europe or other countries. In addition, these studies do not differentiate between AMI with and without ST-segment elevation. Nevertheless, this pathology in this subgroup is a rare event, and neither the management nor the treatment is well established.
A higher incidence of AMI in the last 3 months of pregnancy has been frequently described; this could be due to the fact that during this period there is also a higher occurrence of hypertension and preeclampsia, which are the most important risk factors for AMI in these patients.3 Our case, however, is unusual because the event took place during the first 3 months in the setting of probable atherosclerotic disease and thrombophilia. Although in our case the diagnosis of AMI was clear, the value of troponin I levels is not well established. In fact, fetal levels of troponin I can interfere with the mother’s measurements, and reference values have not been established for pregnant women.4
The physiopathology of acute coronary syndromes (ACS) in pregnant women is quite different from the global population. A study by Roth et al3 reviewed coronary lesions in pregnant patients with ACS. The following results were revealed: 39% of arteries had atherosclerotic lesions, 19% were found to have an intracoronary thrombus without any other lesion, 15% had a coronary dissection, and finally, 27% of the arteries were apparently normal. As can be seen, contrary to the rest of the population, a much higher proportion of normal coronary arteries and intracoronary dissections are the cause of the coronary syndrome. In our patient, several atherosclerotic lesions, in the context of disseminated atherosclerotic disease, were identified in the coronary angiogram. Paradoxical coronary embolism through a patent foramen ovale is an additional potential mechanism of myocardial infarction during pregnancy, although this case shows clear-cut coronary artery disease.
Although guidelines indicate that pregnancy is only a relative contraindication for thrombolysis,5 the high risk of bleeding and the widespread availability of centers where primary angioplasty is performed could make it advisable to treat all cases of STEMI with percutaneous reperfusion. Nevertheless, radiation exposure is highly undesirable in these patients. However, this can be overcome with the use of appropriate radiological protection. In our case, a decision was taken to use lead protection. The patient’s abdomen was covered and, to protect the fetus from excessive radiation, additional protection was also placed between the patient’s back and the table.
Regarding the interventional procedure, it may be more appropriate to use bare-metal stents in these women if we take into account the risk of a prolonged double antiplatelet regime, especially in the early days of pregnancy. In addition, physicians should take great care with the use of glycoprotein IIb/IIIa agents. A bare-metal stent was used in our patient, but glycoprotein IIb/IIIa agents were not administered. Nevertheless, the role of the prothrombophilic state during pregnancy in relation to stent thrombosis has not been established.
Precaution is required in terms of medical treatment after discharge. Angiotensin-converting enzyme inhibitors and statins6 are contraindicated due to their teratogenicity. Apart from these exceptions, all other standard drugs can be prescribed quite safely.7–10 The duration of dual antiplatelet therapy after stent placement when the pregnancy continues and results in labor and delivery is not well established. We recommend the continuation of aspirin and clopidogrel for 4 weeks (for bare-metal stents) unless a complication arises. Our patient received aspirin, clopidogrel, unfractionated sodium heparin and atenolol. The miscarriage, which was probably due to a preexisting thrombophilic disease rather than iatrogenic, was confirmed by obstetric ultrasound.
In conclusion, AMI in pregnancy is a rare event with specific features. High blood pressure is the main risk factor, and there is a higher-than-normal rate of nonatherosclerotic coronary disease. Management of these patients should include the use of bare-metal stents, precaution with the use of antiplatelet therapy, and appropriate protection during radiological procedures.




1. Ladner HE, Danielsen B, Gilbert WM. Acute myocardial infarction in pregnancy and the puerperium: a population-based study. Obstet Gynecol 2005;105:480–484.

2. James AH, Jamison MG, Biswas MS, et al. Acute myocardial infarction in pregnancy: A United States population-based study. Circulation 2006;113:1564–1571.

3. Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. Ann Intern Med 1996; 125: 751– 762.

4. Shade GH Jr, Ross G, Bever FN, et al. Troponin I in the diagnosis of acute myocardial infarction in pregnancy, labor, and post partum. Am J Obstet Gynecol 2002; 187: 1719– 1720.

5. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. J Am Coll Cardiol 2004; 44: E1– E211

6. Henck JW, Craft WR, Black A, et al. Pre- and postnatal toxicity of the HMG-CoA reductase inhibitorator vastatin in rats. Toxicol Sci 1998; 41: 88– 99.

7. Low dose aspirin in pregnancy and early childhood development: Follow up of the collaborative low dose aspirin study in pregnancy. CLASP collaborative group. Br J Obstet Gynaecol 1995; 102: 861– 888.

8. Hauth JC, Goldenberg RL, Parker CR Jr, et al. Low-dose aspirin: Lack of association with an increase in abruptio placentae or perinatal mortality. Obstet Gynecol 1995; 85: 1055– 1058.

9. Rubin PC. Current concepts: beta-blockers in pregnancy. N Engl J Med 1981; 305: 1323– 1326. 10. Butters, L, Kennedy, S, Rubin, PC. Atenolol in essential hypertension during pregnancy. Br Med J 1990; 301: 587– 589.