Presentation of Case
Dr. Rebecca R. Saff (Medicine): A 32-year-old woman, 3 weeks post partum, was seen in the emergency department of this hospital because of substernal chest pain.
The patient had been well until the day of admission when, while she was shopping at 7:25 p.m., pain in the left jaw and substernal area developed suddenly. She drove home and called emergency medical services (EMS). During evaluation by EMS personnel, oxygen was administered; her symptoms resolved after a duration of approximately 20 minutes. She declined further treatment, and the emergency responders departed. Shortly thereafter, the pain recurred, associated with shortness of breath. The patient called EMS again.
On repeat evaluation at 8:34 p.m., the patient rated the pain at 5 (on a scale of 0 to 10, where 10 is the most severe pain) and stated that at its onset, the pain rated a score of 7. The blood pressure was 148/74 mm Hg. An electrocardiogram (ECG) reportedly showed a normal sinus rhythm, with a rate from 90 to 100 beats per minute, and ST-segment elevation of up to 4 mm in leads V3 through V6. Oxygen, acetylsalicylic acid, nitroglycerin, and morphine were administered. The pain resolved while the patient was in the ambulance; a repeat ECG showed ST-segment elevations (1 to 4 mm) in leads V1 through V6; hyperacute T waves in leads V4, V5, and V6; and ST-segment depressions (1 to 1.5 mm) in the inferior leads (Figure 1 in the Supplementary Appendix, available with the full text of this article at NEJM.org). The patient was brought to the emergency department at this hospital 1 hour 25 minutes after the initial onset of symptoms.
The patient did not have diaphoresis, nausea, vomiting, dyspnea, pain or swelling in the legs, or back pain. Three weeks earlier, she had had an uncomplicated, spontaneous vaginal delivery at 39 weeks of gestation. During the first trimester of pregnancy, her systolic blood pressures ranged from 120 to 140 mm Hg, and her diastolic blood pressures from 60 to 80 mm Hg; in the second trimester, 118 to 120 mm Hg systolic and 60 to 82 mm Hg diastolic; and in the third trimester, 104 to 130 mm Hg systolic and 60 to 78 mm Hg diastolic. No antihypertensive medications had been given. The placenta weighed 340 g (less than the 5th percentile in size for gestational age); pathological examination revealed an increased amount of perivillous fibrin. Her child was healthy and was breast-feeding. During her first pregnancy, the patient had hypertension, with onset before 20 weeks of gestation, followed by preeclamptic toxemia that was treated with magnesium sulfate. Between pregnancies, her blood pressure was normal and she took no medications. At the 10-day postpartum visit, she felt well and was ambulating; the blood pressure was 120/80 mm Hg. She lived with her husband and her toddler and newborn and was a physician. She did not smoke, drink alcohol, or use illicit drugs. Her parents had had hypertension and hypercholesterolemia, and a distant cousin had had a stroke at a young age. The patient was taking no medications and had no allergies.
On examination, the temperature was 36.2°C, the blood pressure 143/92 mm Hg in the left arm and 137/81 mm Hg in the right arm, the pulse 83 to 92 beats per minute without ectopy, the respiratory rate 20 breaths per minute, and the oxygen saturation 95% while the patient was breathing ambient air and 100% while she was breathing oxygen (2 liters by nasal cannula). The carotid pulses were 2+ bilaterally, without bruits, and the jugular veins were distended at 6 to 7 cm. The remainder of the examination was normal. ECG revealed a sinus rhythm, 89 beats per minute, with normal intervals; possible left atrial enlargement; incomplete right bundle-branch block; and ST-segment elevation of 1 mm in leads V2 and V3 (Figure 2 in the Supplementary Appendix). Testing for troponin I was negative. The D-dimer level was 1166 ng per milliliter (reference range, <500), and the amylase level was 134 U per liter (reference range, 3 to 100); other tests, including a complete blood count, measurement of electrolyte and glucose levels, and tests of renal and liver function, were normal. A chest radiograph obtained in the emergency department was normal.
While in the emergency department, the patient continued to have episodes of substernal chest pain lasting approximately 5 minutes. Between episodes, the ST-segment changes seen on the ECG resolved completely (Figure 3 in the Supplementary Appendix).
A diagnostic procedure was performed.
Differential Diagnosis
Dr. Marc S. Sabatine: I cared for this patient and am aware of the diagnosis. I would like to ask her to tell us about her symptoms.
The Patient: I was well and was out shopping with my toddler. When I picked him up, I felt transiently ill, possibly nausea, followed by intense pain in my left jaw and by intense, very sharp substernal chest pain, which continued to get worse. I had never experienced anything like this before. I left the store and went home, thinking it would get better. I wasn't thinking about a heart attack.
Dr. Sabatine: Eventually, you were concerned enough to call EMS. What was going through your mind?
The Patient: When I got home, I told my husband to call 911 right away because the pain was so bad. Initially, I thought it might be very severe heartburn. I also considered a pulmonary embolism, because I was post partum. Suddenly, the pain resolved, so I concluded it was not a pulmonary embolism.
Dr. Sabatine: By the time EMS personnel arrived, you were feeling better and you sent them away. They came back a second time and obtained an ECG. Did they show you the ECG?
The Patient: I saw it from about 2 feet away. I could see the changes, and they were shocking to me. At that point, I was happy we were on our way to the hospital.
Dr. Sabatine: The patient's chief symptom, chest pain, is common. Chest pain accounts for approximately 7 million visits per year to an emergency department in the United States.
Causes of Chest Pain
The differential diagnosis of chest pain is well rehearsed and includes cardiovascular, pulmonary, gastrointestinal, and musculoskeletal causes. For a 32-year-old woman, cardiovascular causes would normally be unlikely. However, since the patient was 3 weeks post partum, several potential cardiovascular causes deserve special attention. First, the risk of acute myocardial infarction during pregnancy or the postpartum period is increased by a factor of 3 or 4 as compared with age-matched female control subjects, although the absolute rate remains low at approximately 6 per 100,000 pregnancies.1 Second, pregnancy is considered to be a risk factor for aortic dissection.2 In a 1944 report of an autopsy series, half of the women younger than 40 years of age who had an aortic dissection were pregnant.3 However, rigorous epidemiologic data supporting such an association are lacking.4 Third, the risk of pulmonary embolism during the postpartum period is increased by a factor of 3 or 4 as compared with age-matched female control subjects,5 although the absolute incidence is only 40 per 100,000 pregnancies.
The patient's ECG showed ST-segment elevation in a coronary distribution that, although not pathognomonic, in the context of chest pain strongly suggests acute myocardial infarction. Coronary atherosclerosis is the underlying cause of myocardial infarction in more than 90% of cases. However, in this case, one needs to give serious consideration to events other than rupture of a coronary atherosclerotic plaque as the cause of myocardial infarction (Table 1).
Table 1
Nonatherosclerotic Causes of Myocardial Infarction.
Among postpartum women who present with myocardial infarction and undergo coronary angiography, coronary dissection accounts for approximately 35% of cases, stenosis approximately 30%, thrombus approximately 15%, and spasm less than 5%; normal coronary arteries are found in approximately 10% of cases.6 This categorization is probably imperfect, with unrecognized dissections being classified as stenoses or thrombus and transient spasm being classified as thrombus or normal. Thus, coronary-artery dissection is a likely diagnosis in this case.
Coronary-Artery Dissection
Coronary-artery dissections comprise two main categories: dissections that are secondary to mechanical precipitation, and those that are spontaneous (Table 2). Spontaneous coronary dissection, the most likely diagnosis in this case, is rare14,15; it is noted in approximately 0.2% of coronary angiographies performed16 and in up to 3.5% of coronary angiographies with intravascular ultrasonography performed for acute coronary syndromes.17 The mean age at occurrence is 42 years; nearly three fourths of patients are women, and 30% of the women are peripartum, as was our patient.15
Table 2
Causes of Coronary-Artery Dissection.
Patients with spontaneous coronary dissections can be divided into four subgroups (Table 2). The first group includes patients with preexisting arteritis or an inherited disorder of connective tissue,8–13 in which the integrity of the arterial wall has been compromised by inflammation or defective structural proteins. The second group includes patients with atherosclerosis; almost all these patients are men, with a mean age of 55 years and almost always with involvement of the right coronary artery.18,19 It has been postulated that the rupture of an atherosclerotic plaque creates an intimal disruption that allows a dissection to occur, and that shorter delays to angiography and the availability of newer diagnostic tools such as intravascular ultrasonography have allowed recognition of a ruptured plaque in a greater proportion of patients than had been appreciated previously (up to 80% in one series).17
The third group includes women who are peripartum; three fourths of the cases in this group occur from 1 day to 3 months post partum, with the majority occurring within the first 2 weeks.20 Of the cases of spontaneous coronary-artery dissection that occur during pregnancy, the majority occur in the last 4 weeks. Advancing age and multiparity are risk factors, with the mean age being 33 years and the typical parity 2 or 3. Cases of spontaneous dissection have also been reported under circumstances that involve altered estrogen or progesterone levels, including oral contraceptive use,21,22 menstruation,22–24 and hepatic cirrhosis.25 In contrast to the patients who have underlying atherosclerosis, 87% of peripartum coronary dissections involve the left coronary tree and 40% involve multiple coronary arteries, with one third involving both the left and the right coronary arteries.
The final group is idiopathic spontaneous coronary-artery dissection. The average age is 41 years, and three fourths of the patients are women, almost all of whom are premenopausal and without traditional cardiac risk factors.18,26,27 Some patients are involved in activities that would increase coronary shear stress, including some that would be expected to greatly influence hemodynamics (severe systolic hypertension, cocaine use, snow shoveling, weight lifting)28–32 and others that seem relatively benign (running, aerobics, sneezing).33–35 The onset of chest pain in this patient occurred after she picked up her toddler. One might speculate that the patients involved in the relatively benign activities had an underlying, unappreciated predisposition. More than 80% of idiopathic dissections involve the left coronary tree.
Clinical Presentation and Diagnosis of Spontaneous Coronary-Artery Dissection
The clinical presentation depends on the location and severity of coronary involvement and the resultant severity of the compromise in myocardial blood flow and oxygen supply. The majority of patients present with myocardial infarction with ST-segment elevation, as our patient did, but myocardial infarction without ST-segment elevation, unstable angina, and stable angina have been reported. As with any acute coronary syndrome, patients can present with hemodynamic or arrhythmic complications, including cardiogenic shock and sudden cardiac death, the latter of which may lead to underreporting of the incidence of coronary dissection. Tamponade can develop from adventitial rupture of the dissection.36
Coronary angiography is the diagnostic test of choice. The dissection typically involves the proximal segment of the coronary artery. Angiography may reveal an intimal flap, but if there is no visible flow into the false lumen or if the dissection develops as a consequence of an intramural hematoma, angiography may reveal only a simulated coronary stenosis due to compression of the true lumen.37 Disruption of the vasa vasorum may be a cause of the intramural hemorrhage.30 Intravascular ultrasonography can reveal the dissection in these situations.38 Multidetector-row computed tomographic angiography has also been used to identify and noninvasively track the resolution of a coronary dissection.39
In this case, coronary angiography was performed.
Dr. Marc S. Sabatine's Diagnosis
Postpartum coronary-artery dissection.
Diagnostic Procedure
Dr. Farouc A. Jaffer: I met the patient in the emergency department. We recommended urgent coronary angiography, with the leading considerations of postpartum coronary-artery dissection, coronary arterial vasospasm, and coronary atherosclerosis.
Cardiac catheterization through a femoral artery was performed at approximately 9 p.m., shortly after the patient's arrival at the emergency room. Multiple angiographic projections showed a 35-mm-long segment of severe narrowing (90% stenosis) in the middle of the left anterior descending coronary artery (Figure 1), with a smooth contour that was consistent with intramural hematoma, distal haziness that was consistent with a dissection site, and minimal vascular disease in other coronary arteries that was consistent with the presence of coronary-artery dissection (Video 1, available at NEJM.org). According to the Thrombolysis in Myocardial Infarction (TIMI) criteria for coronary-artery flow, the blood flow in the left anterior descending artery was grade 2 (on a scale of 0 to 3, where 0 is no flow and 3 is normal flow).
Figure 1
Coronary Angiogram on Presentation.
Our diagnosis was postpartum coronary-artery dissection.
Discussion of Management
Dr. Sabatine: Treatment decisions for coronary-artery dissection are largely empirical. As patients typically present with an acute coronary syndrome, treatment with aspirin and heparin is often initiated before the diagnosis is known. In contrast to aortic dissections, for which anticoagulation is avoided to reduce the risk of expansion of the false lumen, for coronary dissections a critical concern is maintaining patency of the true lumen. To that end, short-term use of a glycoprotein IIb/IIIa inhibitor has been reported,40 as has long-term treatment with aspirin and clopidogrel41 and aspirin and enoxaparin42; although the patients did well in these cases, whether the interventions were beneficial remains undetermined.
Fibrinolytic therapy has been used as part of the standard empirical pharmacologic therapy for myocardial infarction with ST-segment elevation. In the case of coronary-artery dissection, the fibrinolytic agent could lyse a thrombus in the true lumen, restoring patency, and could lyse a thrombus in the false lumen, relieving compression of the true lumen, and thus reestablish antegrade flow.43 However, fibrinolysis also runs the risk of precipitating increased flow into the false lumen and propagating the dissection. Clinical deterioration after the use of intravenous fibrinolytic therapy can occur,44 as can an angiographic extension of the dissection after the use of intracoronary fibrinolytic therapy.33 Thus, if coronary dissection is high on the differential diagnosis, empirical fibrinolytic therapy should be avoided if possible.
Antiischemic therapy with beta-blockers and nitrates is frequently initiated, with the latter potentially also helping reduce the risk of superimposed vasospasm. For that reason, calcium-channel blockers are sometimes used in addition to or instead of beta-blockers.
Reperfusion therapy is mandated if the patient has ongoing symptoms of myocardial ischemia, compromised coronary flow, or inducible ischemia on stress testing. Percutaneous coronary intervention with stenting has become the treatment of choice,45 although it carries additional risk in patients with coronary-artery dissection, particularly involving passage of the guidewire down the false lumen and extension of the dissection.46 In cases in which an intimal tear is visualized, a stent can be placed at the entry site and, without further inflow, the false lumen can become obliterated over time.47 In the absence of an intimal tear, stenting of the entire length of the dissection has been performed to prevent expansion of the intramural hematoma.48 Intravascular ultrasonography can be used to guide the intervention by confirming true and false lumina and to confirm sealing of the dissection, adequate compression of the intramural hematoma, or both.38
Coronary-artery bypass grafting (CABG) is typically reserved for patients with persistent ischemia in whom the location or extent of disease precludes percutaneous coronary intervention.
Dr. Eric S. Rosenberg (Pathology): Dr. Jaffer, can you tell us how you managed the patient's condition?
Dr. Jaffer: Our therapeutic options consisted of supportive management with medical therapy with or without an intraaortic balloon pump, percutaneous coronary intervention (PCI), and CABG surgery. The patient was pain free and the ST-segment elevation had resolved. Since coronary dissections may heal without mechanical intervention, and in view of the risk of entering the false lumen during PCI, we elected supportive therapy.
An intraaortic balloon pump was placed to augment coronary arterial blood flow in the left anterior descending artery. In addition, we administered an anticoagulant agent (heparin) and an antiplatelet agent (aspirin), as well as beta-blockers and statins, based on American College of Cardiology–American Heart Association guidelines for acute coronary syndrome. I favored initiation of statins because of the likely presence of intramural hematoma in the coronary vessel wall. As shown by preclinical and autopsy investigations, red cells in the arterial wall may stimulate atherogenesis by means of the deposition of free cholesterol, inducing macrophage infiltration.49 We did not administer glycoprotein IIb/IIIa antagonists, since we were concerned that if the dissection worsened, the patient could need emergency cardiac surgery. Cardiac biomarkers later indicated the presence of a small myocardial infarction. Cardiac ultrasonography showed an ejection fraction of 75%, without wall-motion abnormalities. An angiotensin-converting–enzyme inhibitor was initiated, but hypotension developed and it was discontinued.
After 48 hours, a second coronary angiogram (Video 2, available at NEJM.org) showed improved blood flow (TIMI grade 3), a shorter segment of stenosis of the left anterior descending artery (approximately 25 mm), and resolution of the distal dissection flap. These findings indicated favorable healing of the coronary-artery dissection. The intraaortic balloon pump was discontinued. Since surgery was unlikely to be required, clopidogrel was administered according to ACS guidelines. In addition, we elected to initiate warfarin to provide maximal anticoagulation on an outpatient basis, with the goal of averting thrombosis of the left anterior descending artery. The patient recovered well and was discharged on hospital day 8, taking warfarin, clopidogrel, atenolol, simvastatin, and aspirin. We planned to discontinue clopidogrel after 1 year and recommended aspirin indefinitely.
Dr. Sabatine: I would like to ask Dr. Staats and Dr. Stone to discuss the pathological features of the placenta and of the heart in this and other cases.
Pathological Discussion
Dr. Paul N. Staats: The placenta was small for the gestational age, with a fresh weight of 340 g after removal of the fetal membranes and umbilical cord, as compared with a mean of 540 g and a 10th percentile of 430 g for a gestational age of 39 weeks.50 It was otherwise grossly normal. Histologic examination revealed a slightly greater deposition of perivillous fibrin (Figure 2A) than normal and rare foci of accelerated branching of villi near the maternal floor, characterized by small terminal villi with sclerosis, increased numbers of prominent syncytial knots, and fewer intermediate-size villi than normal, with a concomitant increase in the amount of intervillous space (Figure 2B). Although a similar pattern is frequently seen beneath the fetal surface of normal placentas, the presence of this pattern near the maternal floor suggests placental ischemia.51,52 Pregnancy-induced hypertension and preeclampsia are believed to be caused by abnormal conversion of maternal vasculature during implantation. The resulting poor perfusion and ischemia cause the placental findings.53 Placental ischemia due to maternal hypertension is generally seen with chronic or poorly controlled hypertension and preterm pre-eclampsia.52 The most common finding is a small placenta (less than the 10th percentile by weight), as seen in this case. Placental infarcts are more common and more extensive in cases of maternal hypertension than in women with normal placentas. Rather than the pyramid-shaped infarcts involving the basal plate (maternal floor) that are often seen at term because of senescence, the infarcts associated with maternal hypertension are often smaller, intraparenchymal, and rounded, suggesting watershed ischemia.52 We did not see such infarcts in this case. Decidual vasculopathy is the most characteristic finding in placentas with clinically significant maternal hypertension, but it is seen only infrequently and was not present in this case.51,52 The accelerated branching of villi seen in this case is apparent in placental ischemia from any cause and is thought to be an adaptive response to the ischemia.51
Figure 2
Placental Histology.
The final pathological diagnosis in this case was a small, mature placenta (340 g) with mildly increased perivillous fibrin deposition and focal accelerated villous branching. Although the findings are nonspecific, they are consistent with placental ischemia due to maternal hypertension.
Dr. Nancy Lee Harris (Pathology): Dr. Sabatine, do you think that hypertension during pregnancy contributed to this dissection?
Dr. Sabatine: Hypertension is a risk factor for peripartum myocardial infarction due to atherosclerosis. Acute, severe systolic hypertension has been associated with coronary-artery dissection. Gestational hypertension has not been noted to be particularly frequent among cases of peripartum coronary-artery dissection.
Dr. Rosenberg: Dr. Stone, can you tell us about the pathology of coronary-artery dissection?
Dr. James R. Stone: The pathology of spontaneous coronary-artery dissection has largely been deduced from autopsy cases, although a few explanted hearts from patients undergoing cardiac transplantation have been studied (Figure 3A).26,54 The dissection typically occurs in the outer portion of the medial layer, resulting in an intramural hematoma that compresses the true lumen. The cause is not well understood. Most often an intimal tear is not present in pathologic specimens.26,55 In some cases, an adventitial or periadventitial inflammatory infiltrate, most often containing predominantly eosinophils, has been reported,55 but this is most likely a response to and not the cause of the dissection. Severe medial degeneration typical of connective tissue disorders and true necrotizing vasculitis are typically not present. In patients who survive the initial spontaneous coronary-artery dissection, the dissection channel will organize, in some cases resulting in a coronary artery with a double lumen (Figure 3B).
Figure 3
Pathologic Features of Spontaneous Coronary-Artery Dissection in Another Patient.
Prognosis of Coronary-Artery Dissection
Dr. Sabatine: Angiographic resolution of the dissection typically occurs after several months,18 but some dissections progress,56 and pseudoaneurysms can form at the site of the dissection.57 Several cases have been reported of coronary dissections developing at separate sites several months after the index presentation.58 Some data suggest a mortality rate of 5 to 10% in the acute phase16,18,19,27 and a rate approaching 0% among peripartum patients who survive the acute phase and subsequently undergo angiography.20
Dr. Jaffer: The patient did well, without angina, dyspnea, or evidence of congestive heart failure. We initially deferred her enrollment into cardiac rehabilitation because of concern that exercise could increase coronary wall stress and extend her dissection. We suggested a moderate level of activity. A follow-up coronary angiogram obtained 3 months after her initial presentation, after the discontinuation of warfarin, showed nearly complete resolution of the dissection, minimal irregularities in the left anterior descending artery at the site of the dissection, and normal left ventricular function (Video 3, available at NEJM.org). She subsequently completed a cardiac rehabilitation program. I would like to invite the patient to tell us how she is doing now.
The Patient: I have gone back to work and regular activity without any problems. I feel great.
Dr. Rosenberg: Would you recommend that the patient avoid a future pregnancy?
Dr. Jaffer: Recurrences of coronary-artery dissection have been documented in the literature. For future pregnancies, we would request consultation with the maternal–fetal medicine division for additional guidance.
Anatomical Diagnosis
Postpartum coronary-artery dissection.
Dr. Staats is now affiliated with the Department of Pathology, University of Maryland School of Medicine, Baltimore.
Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.
This case was presented at the Medical Case Conference, June 12, 2009.
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From the Division of Cardiovascular Medicine, Brigham and Women's Hospital (M.S.S.); the Division of Cardiology, Department of Medicine (M.S.S., F.A.J.), and the Department of Pathology (P.N.S., J.R.S.), Massachusetts General Hospital; and the Departments of Medicine (M.S.S., F.A.J.) and Pathology (P.N.S., J.R.S.), Harvard Medical School — all in Boston.
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