Coronary Vasospasm in a Postpartum Woman

ABSTRACT: Acute myocardial infarction during pregnancy or the postpartum period is rare. We report a case of a 40-year-old postpartum woman who developed ST-elevation myocardial infarction due to severe diffuse coronary vasospasm. To our knowledge, this is the first case of angiographically evidenced coronary vasospasm in a postpartum woman, in the absence of vasoconstrictive medications.

Case Report. A 40-year-old G1P1 woman with an uncomplicated term pregnancy presented 2 weeks postpartum with chest pain. The chest pain was sharp, substernal, 6/10 in intensity, radiated to the left arm and spontaneously resolved within 25 minutes and was associated with diaphoresis and shortness of breath. There were no precipitating, exacerbating or alleviating factors. She had never experienced similar pain in the past. Past medical history was significant for gestational diabetes. She did not have a known history of coronary artery disease, dyslipidemia, or thromboembolism. She did not smoke and denied cocaine use. There was no family history of premature coronary artery disease.

On physical examination, vital signs were significant for hypertension with blood pressure of 160/70 mmHg and pulse rate of 72 beats/minute. No jugular venous distension or carotid bruit were appreciated. Cardiac exam was remarkable for a grade 2/6 systolic ejection murmur. Lungs were clear to auscultation bilaterally and no lower extremity edema was noted.

Electrocardiogram (ECG) revealed normal sinus rhythm with a heart rate of 72 beats/minute with no ST-T wave abnormalities. Laboratory evaluation revealed mildly elevated troponin I at 0.06 ng/ml with normal electrolytes and complete blood count. Her lipid profile revealed HDL of 47 and LDL of 107. Radiological evaluation included a computed tomography scan of the lungs which did not reveal pulmonary embolism or lung parenchymal disease. Troponin I repeated 3 hours later increased to and peaked at 0.13 ng/ml. She was orally administered 325 mg of aspirin and 25 mg of metoprolol. Invasive coronary angiogram showed normal coronary arteries with no angiographic evidence of atherosclerotic disease or dissection in the coronaries or thoracic aorta with an ejection fraction (EF) of 60%. The patient was discharged home only to return back in 2 days with recurrent chest pain. This episode was similar to her previous episode, but was of greater intensity. She had taken 3 sublingual nitroglycerin tablets without relief.

ECG now revealed ST elevations in leads II, III and aVF (Figure 1). Given the normal coronaries seen on coronary angiogram performed 2 days prior to this presentation, an etiology of pericarditis was suspected and an emergent echocardiogram was performed. The echocardiogram showed apical hypokinesis and low EF of 50% with no pericardial effusion (Figure 2). Given new regional wall motion abnormalities and ECG changes, an emergent coronary angiogram was performed, which revealed severe diffuse spasms of the posterior descending artery throughout its course across the apex (Figure 3). The patient’s chest pain resolved with 500 mcg of intracoronary nitroglycerin administration. Troponin I peaked at 12.24 ng/ml and was normal on presentation. Urine drug screen was negative for cocaine. Laboratory evaluation for hypercoagulable disorders such as protein C and S deficiency, Factor V Leiden deficiency, and prothrombin 2021A mutation were unremarkable. She was started on intravenous infusion of nitroglycerin and transitioned to oral long-acting nitrates and calcium-channel blockers. An echocardiogram performed 3 days later showed an EF of 60% with no regional wall motion abnormalities. Since then, she has not reported any further cardiac symptoms.

Discussion. Acute myocardial infarction (AMI) is rarely associated with pregnancy and the postpartum period. It is estimated to occur in 6.2/100,000 deliveries.¹ Out of the 208 cases of pregnancy-related AMI reviewed by Roth et al, 78% had undergone coronary angiogram with significant coronary artery stenosis seen in only 42% of the women.^2,3 Dissections and normal coronaries were seen in 22.8% and 20% of the patients, respectively.^2,3 Coronary vasospasm as the cause of AMI was identified in only 3 patients, accounting for only 1.8% of all pregnancy-related AMI patients.^2,3

It is known that coronary vasospasm can be induced by vasoconstrictive agents such as ergonovine, bromocriptine and prostaglandin E2, which are frequently used during pregnancies.^4–7 Most of these cases have a presumed diagnosis of coronary vasospasm as signs of myocardial injury were noted on laboratory evaluation or by imaging in the presence of insignificant coronary artery disease. Short-term complications included heart failure and acute pulmonary edema; however, most of the patients had good long-term outcomes with no recurrence of symptoms. Sung et al reported a case of angiographically documented coronary vasospasm after administration of intravenous prostaglandin that was successfully treated with intracoronary nitroglycerin and had no short- or long-term complications. Iadanza et al reported a case of angiographically documented coronary vasospasm without administration of vasoconstrictive medications during pregnancy.⁸ Our case is unique, as it is the first angiographically documented coronary vasospasm in a postpartum woman without administration of vasoconstrictive medications.

Coronary vasospasm in pregnancy is partly due to increased renin release and angiotensin production from uterine hypoperfusion, which occurs especially when the patient is in the supine position.⁹ Also, endothelial dysfunction¹⁰ or enhanced vascular reactivity to angiotensin II¹¹ and norepinephrine¹² has been considered. In addition, uterine hypoperfusion can occur when ergot derivatives are utilized to control postpartum hemorrhage or post-abortion hemorrhage.^4–7 It is also hypothesized that vasospasm may be the etiology of AMI in patients with normal coronaries or with thrombus formation in the absence of atherosclerotic disease.^13,14 Fukai et al studied 21 patients who developed AMI and did not have significant coronary stenosis; coronary vasospasm was inducible in 16 patients and 11 patients had preinfarction angina at rest.¹³ On the contrary, Betriu et al reported no inducible coronary vasospasm in AMI without significant coronary stenosis.¹⁵ Other etiologies of AMI in pregnant and postpartum woman with normal coronaries include coronary thrombosis with clot lysis due to hypercoagulable state of pregnancy.

Conclusion. Due to difficulty in angiographically diagnosing coronary vasospasm, it can be easily missed. However, it should be strongly considered as the cause of AMI in the absence of significant coronary stenosis. Simply treating with nitrates or calcium-channel blockers can prevent progression to recurrent refractory spasms associated with increased morbidity and even death.

References

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14. Zimmerman FH, Gustafson GM, Kemp HG Jr. Recurrent myocardial infarction associated with cocaine abuse in a young man with normal coronary arteries: Evidence for coronary artery spasm culminating in thrombosis. J Am Coll Cardiol 1987;9:964–968.

15. Betriu A, Pare JC, Sanz GA, et al. Myocardial infarction with normal coronary arteries: A prospective clinical-angiographic study. Am J Cardiol 1981;48:28–32.

From the *Department of Internal Medicine, Saint Joseph Mercy Hospital, Ann Arbor, Michigan and §Michigan Heart, Ypsilanti, Michigan. This abstract was presented at the Society of General Internal Medicine 33rd Annual Meeting, Minneapolis, Minnesota on April 29, 2010 and the American College of Physicians Associates Meeting (Michigan Chapter), Kalamazoo, Michigan on May 15, 2010. The authors report no conflicts of interest regarding the content herein. Manuscript submitted April 13, 2010, provisional acceptance given May 20, 2010, final version accepted June 23, 2010. Address for correspondence: Aditya M Sharma, MD, Internal Medicine Office, Reichert Health Center, 5333 McAuley Dr., Ste. R3009, Ypsilanti MI 48197. E-mail: dradityasharma@yahoo.com