AMI Caused by Spontaneous Postpartum Coronary Artery Dissection

Summary

Background: A 34-year-old postpartum woman presented at hospital with chest pain. She had experienced an uneventful delivery of a healthy infant and had no known coronary risk factors. Electrocardiography demonstrated an acute myocardial infarction, which resolved on intravenous glyceryl trinitrate infusion. Coronary angiography revealed diffuse narrowing of the left anterior descending artery and tapering of the left main trunk, but there were no obvious hallmarks of intimal dissection.
Investigations: Electrocardiography, coronary angiography, multidetector CT and intravascular ultrasonography.
Diagnosis: Postpartum coronary artery dissection.
Management: The lesion was stabilized with orally administered amlodipine, aspirin, ticlopidine and pitavastatin, along with intravenous heparin and glyceryl trinitrate. The patient was later discharged on bisoprolol, aspirin, pitavastatin and temocapril.

The Case

A 34-year-old woman gave birth to a healthy male infant following a normal, uneventful vaginal delivery (gravida 1, para 1). One week later, she experienced mild chest pain that subsided after 10 min, but an additional 4 weeks later she developed worse, profuse chest pain. She visited her local physician and was subsequently transferred to a hospital emergency department.

The patient had no coronary risk factors such as hypertension, diabetes or dyslipidemia, had no family history of heart disease, and did not have a history of smoking or oral contraceptive use. Electrocardiography demonstrated the presence of ST-segment elevation in leads I, aVL (both 1 mm) and V1-V3 (all 3 mm), along with reciprocal ST-segment depression in leads II, III and aVF (all 2 mm), suggesting that an acute coronary event had occurred. These changes were completely resolved with intravenous glyceryl trinitrate administration (1 mg bolus). The patient's cardiac enzyme levels were normal, but chest radiography revealed mild lung congestion.

Coronary angiography revealed the presence of a severe diffuse lesion of the left anterior descending artery (LAD) and 40% tapering of the mid-portion of the left main trunk (LMT; Figure 1). Coronary flow in the LAD, however, was nearly Thrombolysis in Myocardial Infarction (TIMI) grade 3, and the diagonal branches had good collateral circulation, although with a severe delay. Severely reduced anteroapical wall motion was noted on left ventriculography.

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Figure 1.

Angiogram of the patient showing a diffuse coronary lesion of the left anterior descending artery and 40% tapering of the left main trunk. Blood flow in the distal half of the left anterior descending artery was delayed, and some distal septal branches were supplied by collateral vessels from the right coronary artery.
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Figure 1.
Angiogram of the patient showing a diffuse coronary lesion of the left anterior descending artery and 40% tapering of the left main trunk. Blood flow in the distal half of the left anterior descending artery was delayed, and some distal septal branches were supplied by collateral vessels from the right coronary artery.

It was unclear whether the lesion was a spiral dissection or a prolonged coronary vasospasm. Emergent coronary angioplasty with a 2.5 mm bare-metal stent was considered but not carried out, as coronary flow in the LAD was not compromised and the chest pain and ST-segment elevation had resolved. Intravascular ultrasonography (IVUS) was also not performed at this point. To stabilize the coronary lesion, glyceryl trinitrate (1 mg/h) and heparin (10,000 U/day) were administered intravenously over the following 10 days, along with orally administered amlodipine (5 mg/day), aspirin (200 mg/day), ticlopidine (200 mg/day) and pitavastatin (4 mg/day).

Subsequent multidetector CT (MDCT) revealed that the coronary lesion had not resolved. Extraluminal lesions were evident throughout the LAD and surrounding the mid-LMT, apparently compressing the true space of the lumen (Figure 2). The CT density throughout the lesion was mostly intermediate, but areas of soft density were noted in the extraluminal lesions.

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Figure 2.

Multidetector CT demonstrated that the coronary lesion had not resolved after 10 days of pharmacological therapy. (A) Multiplanar reconstruction image of the LMT and LAD. Thick extraluminal hematoma (shown by arrows) was noted throughout the left anterior descending artery and left main trunk—most likely contained in the subadventitial space. (B) Cross section of the mid-LMT (corresponding to the black arrow in A), showing compression of the lumen by an extraluminal lesion, further supporting the idea that the lesion was a dissecting hematoma. The CT densities are 107 HU at r1, 172 HU at r2, and 144 HU at r3. (C) Cross section of the mid-LAD (corresponding to the white arrow in A), also demonstrating compression of the lumen. The CT densities are 38 HU at r1 and 64 HU at r2. Both cross sections demonstrate low-density spots in the extraluminal space. Abbreviations: HU, Hounsfield units; LAD, left anterior descending artery; LMT, left main trunk.
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Figure 2.
Multidetector CT demonstrated that the coronary lesion had not resolved after 10 days of pharmacological therapy. (A) Multiplanar reconstruction image of the LMT and LAD. Thick extraluminal hematoma (shown by arrows) was noted throughout the left anterior descending artery and left main trunk—most likely contained in the subadventitial space. (B) Cross section of the mid-LMT (corresponding to the black arrow in A), showing compression of the lumen by an extraluminal lesion, further supporting the idea that the lesion was a dissecting hematoma. The CT densities are 107 HU at r1, 172 HU at r2, and 144 HU at r3. (C) Cross section of the mid-LAD (corresponding to the white arrow in A), also demonstrating compression of the lumen. The CT densities are 38 HU at r1 and 64 HU at r2. Both cross sections demonstrate low-density spots in the extraluminal space. Abbreviations: HU, Hounsfield units; LAD, left anterior descending artery; LMT, left main trunk.

Coronary angioplasty with a sirolimus-eluting stent was scheduled. Before the patient underwent the procedure, her ticlopidine tolerance was tested over a period of 2 months, with 200 mg administered orally each day. Laboratory data were monitored, including ADP-induced platelet aggregation. At the end of this period, which was uneventful, the patient underwent coronary catheterization. Angiography demonstrated that the severe LAD lesion had dramatically resolved, apart from a mildly stenotic portion of the mid-LAD (Figure 3). Interestingly, there were no signs of the tapering lesion of the LMT that had been evident earlier. Stent implantation was, therefore, aborted.

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Figure 3.

Coronary angiography performed 3 months after the initial myocardial infarction showed complete resolution of the lesion.(A) Right anterior oblique caudal view and (B) straight cranial view. Some focal narrowing of the left anterior descending artery (30%; arrow) was noted distal to the diagonal branch.
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Figure 3.
Coronary angiography performed 3 months after the initial myocardial infarction showed complete resolution of the lesion.(A) Right anterior oblique caudal view and (B) straight cranial view. Some focal narrowing of the left anterior descending artery (30%; arrow) was noted distal to the diagonal branch.

IVUS of the patient demonstrated the presence of subadventitial hematomas in the mid-portions of both the LAD and the LMT (Figure 4). Dissection was noted between the outer media and adventitia in both vessels. No atheromatous plaque was found in the intimal surface of either artery. Left ventriculography showed that wall motion had improved since presentation. Angiography, repeated immediately after IVUS examination, demonstrated coronary artery spasm.

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Figure 4.

Intravascular ultrasonography, performed 3 months after presentation, confirmed the presence of a spiral dissection.A) Cross section of the mid-left anterior descending artery showing an intramural dissection between the outer media and adventitia, spanning from 2 to 7 o'clock. (B) Cross section of the mid-left main trunk demonstrating an intramural dissection between the outermost media and adventitia, spanning from 5 to 8 o'clock. The echo density at the dissected portions is even lower than in the vessel lumen. White dots represent 10 mm intervals.
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Figure 4.
Intravascular ultrasonography, performed 3 months after presentation, confirmed the presence of a spiral dissection.A) Cross section of the mid-left anterior descending artery showing an intramural dissection between the outer media and adventitia, spanning from 2 to 7 o'clock. (B) Cross section of the mid-left main trunk demonstrating an intramural dissection between the outermost media and adventitia, spanning from 5 to 8 o'clock. The echo density at the dissected portions is even lower than in the vessel lumen. White dots represent 10 mm intervals.

The patient was discharged on a daily regimen of aspirin (100 mg), bisoprolol (5 mg), pitavastatin (2 mg) and temocapril (2 mg). Two years later, she remains healthy and continues to take the same medications. She has been advised against further pregnancy because of the high probability of a recurrence of the condition.

Discussion of Diagnosis

Postpartum spontaneous coronary artery dissection (SCAD) is a rare cause of acute myocardial infarction. Survivors of the initial event generally have a good long-term prognosis, and around 70% of cases are diagnosed following the patient's death.[1] The frequency of peripartum or postpartum SCAD is around 1 in 100,000 pregnancies.[1] The case described here is the first encountered at the treating facility in question, out of more than 25,000 coronary procedures performed over the past decade. This center serves a province with a population of 400,000.

Peripartum and postpartum SCADs are usually caused by multiple underlying factors, including sheer mechanical stress on the coronary artery during labor, prolonged coronary artery spasm, the use of a uterine constrictor, and structural changes in the coronary artery medial wall that occur during pregnancy.[1,2,3] SCAD can occur when the coronary media become fragile as a result of defective collagen metabolism, influenced by the hormonal changes associated with pregnancy.[4,5] Another possible mechanism is eosinophilic inflammation, localized to the dissected portion of the coronary adventitia, which is observed in 43% of pathological examinations of patients with SCAD.[6] The inflammation is caused by a protease that is secreted by eosinophils and delivered to the media, which process is postulated to be responsible for further weakening of the vessel walls, leading to hemorrhage from the vasa vasorum of the adventitia. Histological evidence obtained from several autopsy studies indicates that in the majority of postpartum SCAD cases, dissection occurs in the media or in the layer between the outer media and adventitia.[1,2]

The patient described in this report presented with an acute myocardial infarction that resolved on glyceryl trinitrate administration. Angiography subsequently demonstrated that the patient had a diffuse lesion of the LAD, the nature of which was initially unclear. Given the patient's age, medical history, and lack of obvious risk factors, there was a substantial possibility that the lesion was either a spiral dissection or a prolonged coronary vasospasm. MDCT was used to investigate further. The density of the lesion was intermediate (in contrast to a reported case in which acute intramural hematoma had a low CT density,[7] but the possibility of a dissection could not be ruled out.

The characteristics of the LAD lesion became clearer when IVUS was performed 3 months after the patient's initial presentation; subadventitial hematoma was apparent, with no atheromatous plaque. These observations, coupled with the complete resolution of the extramural diffuse lesion throughout the LAD over the intervening period, indicated that the lesion seen earlier on MDCT was composed of a spiral dissection and extraluminal hematoma, situated between the adventitia and the outer third of the media. The intermediate CT density of the lesion could be a sign that the dissection was progressing relatively slowly, which might also account, in part, for its benign course. It should be acknowledged, however, that the time delay means that these findings are not necessarily representative of the initial condition, and that the dissection might have sealed during this time.

It is unclear exactly where the primary dissection occurred in this patient. The fact that no hallmarks of intimal dissection were evident on the first angiogram, and the presence of subadventitial hematoma as noted on IVUS, suggest that there was a primary subadventitial and medial dissection, rather than an intimal dissection that extended to the medial and subadventitial space.

There are more than 60 cases of postpartum SCAD in the literature and, in most cases, SCAD was proved on angiography to be an intimal flap or a spiral dissection.[1] In hindsight, the diagnosis in the present case could have been made earlier, on the basis of the initial angiogram. An experienced angiographer might have recognized the lesion as a spiral dissection rather than a diffuse atheromatous lesion. IVUS could have helped to clarify the nature of the lesion at this point, but instead further invasive procedures were initially withheld owing to the diffuse morphology of the lesion, the preservation of coronary flow, the resolution of ST-segment elevation, and the patient's young age and lack of obvious coronary risk factors. When IVUS was later performed, coronary spasm was noted on angiography immediately afterwards, suggesting that had IVUS been carried out at the time of the initial angiogram, it could have triggered an intractable coronary vasospasm and resulted in serious coronary flow compromise.

Six cases of SCAD without angiographically proven dissection have been reported in the literature, although these are not related to the postpartum period.[8,9] There is one reported postpartum case of LMT focal tapering, which was proved to be intramural hematoma on IVUS.[10] The complex characteristics of the lesion in the present case underscore the importance of performing IVUS as promptly as possible. Mild, focal coronary lesions are generally suitable for immediate IVUS examination,[10] but caution should be exercised with diffuse tortuous lesions, such as that seen in the present case. The performance of invasive procedures in patients with this type of lesion carries a high chance of complications and could lead to unavoidable multiple stenting or repeated in-stent restenosis.

Treatment and Management

There are an increasing number of reports of spontaneous healing of SCAD, and medical therapy is generally advocated for nonischemic cases in which coronary blood flow is uncompromised.[11,12,13] It is difficult, however, to predict short-term outcomes such as reinfarction or destabilization of the coronary lesion in individual cases.[11]

In the present case, revascularization of the LAD was initially planned, but the patient's condition stabilized and her coronary blood flow was uncompromised, so the procedure was postponed until a drug-eluting stent could be implanted. The lesion resolved over time, however, most likely because the lack of intimal tearing ensured that less pressure was placed on the lumen by the intramural hematoma. Furthermore, the coronary spasm could have been alleviated by the medications taken over the intervening period.

Immunosuppressants (including cyclophosphamide and prednisone) were administered in a case of angiographically documented postpartum SCAD in conjunction with periadventitial eosinophilic inflammation.[13] The coronary lesion was successfully resolved in this case, but it is unclear whether immunosuppression is always necessary given that other case reports of peripartum SCAD have documented spontaneous resolution without these medications. Pitavastatin, which was prescribed in the present case, has anti-inflammatory properties, which could have contributed to the successful resolution of the lesion.[14]

Conclusions

This case highlights the need to raise awareness of postpartum SCAD, so that an accurate diagnosis can be made promptly in the future, particularly when risk factors for coronary artery disease are absent. Great caution is needed when interpreting the results of angiography, as the findings can influence the decision-making process from the beginning. IVUS and MDCT can assist with a diagnosis, although the benefits of invasive intracoronary procedures must be balanced carefully against the risks of exacerbating coexisting coronary vasospasm, which could potentially cause further dissection.


Source : http://www.medscape.com/viewarticle/567057