A case of a young, healthy woman with spontaneous coronary artery dissection associated with oral contraceptive use: Long-term residual dissection of the coronary artery

Abstract

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome, typically affecting young, healthy women, particularly during the peripartum period. Oral contraceptive use is also recognized as a risk factor for SCAD. In the present report, we describe a case of a young woman with an anterior wall myocardial infarction caused by SCAD of the left anterior descending artery (LAD). The event was probably associated with the patient's oral contraceptive use. The patient underwent percutaneous coronary intervention, and she did not experience any recurrent chest pain or other cardiac symptoms. Although the coronary angiography revealed good LAD flow and no symptoms after 6 months, cardiac computed tomography and intravascular ultrasound revealed that LAD dissection was still present. We continued to closely follow-up the patient without initiating any additional intervention, and the patient has had no cardiac event for up to 4 years of follow-up.

<Learning objective: We aimed to present a case of spontaneous coronary artery dissection, with a long-term residual dissection. Coronary computed tomography aided the diagnosis of the residual dissection, which was not detected by coronary angiography.>

Introduction

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome and results in fatality, with diagnosis only at autopsy in most early cases of SCAD [1]. The condition typically affects young, healthy women during the peripartum period [2]. Oral contraceptive use is also known as a risk factor for SCAD 2, 3, 4. Several authors have reported cases with acute-stage SCAD but only a few cases in the chronic stage have been reported. We report a case of a young woman taking oral contraceptives who experienced SCAD-induced anterior wall myocardial infarction, and underwent follow-up examinations with various imaging modalities at the chronic stage.

Case report

The patient, a 36-year-old woman, had no significant medical history or history of smoking, but was taking oral contraceptives. Moreover, she did not have any family history of cardiovascular disease. She was admitted to the emergency department with a complaint of acute-onset chest pain during rest. An electrocardiogram revealed ST elevation in leads V2 through V4, with reciprocal ST depression in leads II, III, and aVF. Her blood pressure was 123/68 mmHg, and her pulse rate was 76 beats/min. Cardiac examination did not show any murmurs, rubs, or gallops, and the lungs appeared clear on auscultation. Echocardiography indicated hypokinesis of the apex.

After treatment with 200-mg aspirin and sublingual nitroglycerin, the patient was immediately transferred to the cardiac catheterization laboratory. Coronary angiography (CAG) revealed that the flow in the distal segment of the left anterior descending artery (LAD) was completely obstructed (Fig. 1A), but we could not identify the coronary artery dissection at that time. Therefore, we decided to perform a primary routine coronary intervention. After guidewire crossing, transcatheter thrombectomy was performed, which slightly improved the LAD flow. Intravascular ultrasound (IVUS) did not reveal any atherosclerotic changes, but showed coronary artery dissection from the proximal to the distal segment of the LAD. An intracoronary bare-metal stent (BMS) was successfully implanted in the distal lesion of the LAD. Although the dissection of the proximal to mid-LAD remained, the LAD flow did not worsen after a few minutes of observation. The final angiography demonstrated normal blood flow of the LAD (Fig. 1B). The patient's creatinine kinase level reached a peak of 1220 IU/L. She was treated with oral medications, including aspirin, clopidogrel, carvedilol, pravastatin, and enalapril. In addition, the oral contraceptive treatment was discontinued. The patient had no signs of vasculitis, Marfan syndrome, or coagulation abnormalities. She had no dyslipidemia or impaired glucose tolerance. Therefore, a diagnosis of SCAD was made. Her hospital course was uneventful, and she was discharged home on day 11.

Fig. 1.

(A) Coronary angiographic image showing the obstructed distal left anterior descending artery (LAD). (B) The final angiographic image after stent placement at the distal LAD showing normal blood flow of the LAD.

Following discharge, the patient had no recurrent chest pain or other cardiac symptoms. A cardiac computed tomographic (CT) scan after 6 months showed an abnormal lesion from the ostium of the LAD to the proximal edge of the stent (Fig. 2, Fig. 3). CAG revealed good LAD flow (Fig. 2A). The IVUS confirmed that the residual LAD dissection originated from the ostium of the LAD to the proximal edge of the stent (Fig. 2, Fig. 3). The abnormal lesion of the LAD on the CT scan was in accordance with the residual dissection observed on IVUS (Fig. 3A–C). She remained asymptomatic; in addition, the follow-up CAG revealed good flow, without compression of the true lumen by the residual false lumen. Thereafter, the patient has not experienced any recurrent chest pain or other cardiac symptoms for up to 4 years of follow-up.

Fig. 2.

(A) Coronary angiography did not show any evidence of the coronary dissection. (B) Cardiac computed tomographic (CT) scan of the left anterior descending artery (LAD) performed 6 months after the initial event. (a–f) Intravascular ultrasonography showing the residual dissection from the ostium of the LAD to the proximal edge of the stent in accordance with the previous dissection: a, left main coronary artery; b, the ostium of the LAD; c, the proximal LAD; d, the mid LAD; e, in stent; and f, the distal lesion of the stent.

Fig. 3.

(A) Cross-sectional view of the mid left ascending coronary artery on intravascular ultrasonography. (B) Computed tomography (CT) scan of the same area. (C) Color mapping of the CT scan.

Discussion

SCAD is a rare cause of ischemic heart disease, and occurs without any evident causes such as trauma or extension of aortic dissection. The clinical presentation spectrum can range from unstable angina and acute myocardial infarction to sudden death. The underlying mechanism of SCAD is not entirely known. Most of the patients are young women with no conventional risk factors for coronary artery disease, and this condition commonly occurs during late pregnancy and the postpartum period [2]. In such cases, SCAD may develop not only due to the shear stress present during labor but also possibly due to changes in the media by increasing hormone levels. High progesterone levels are probably implicated in the changes in connective tissue that occur during pregnancy [5]. In addition, female hormones contribute to fluid retention and reduction of peripheral resistance, resulting in increased cardiac output, and thus facilitating the development of SCAD [3]. Our patient was neither pregnant nor in the postpartum period, but was taking oral contraceptives. Several authors have reported cases of SCAD that were induced by oral contraceptive use 3, 4. Tweet et al. [2] reported that 13% of women who experienced SCAD used oral contraceptives. The pathogenic mechanisms of SCAD related to oral contraceptive use, in which hormones are taken exogenously, may be similar to those implicated during the peripartum period [3].

DeMaio et al. reported in 1989 that most patients with SCAD had a poor prognosis with high mortality rates [1]. The prognosis is found to be better in later years [6]. Early diagnosis and an aggressive approach could improve the prognosis of patients with SCAD 5, 6. The optimal management of SCAD has not been well defined. The decision depends on the clinical presentation, hemodynamic state, site and extent of the dissection, and number of vessels involved. In the present case, because the patient showed typical chest pain and an electrocardiographic change, we decided to perform CAG and IVUS, through which the diagnosis of SCAD could be immediately made. Although the dissection extended from the ostium to the distal portion of the LAD, LAD flow was preserved, except at the distal segment where the coronary flow was completely obstructed by the false lumen. An early recanalization of the distal LAD by intracoronary stenting for the obstructive lesion and the preservation of the LAD flow improved the patient's prognosis with relatively mild myocardial infarction. Thus, stent implantation should be mainly considered as the primary therapeutic approach for treating SCAD. However, regarding stent selection, the risk and benefit of a drug-eluting stent (DES) versus BMS has not yet been established. In the present case, we selected BMS, instead of DES, even in the small distal LAD vessel, considering the potential risk of bleeding from the uterus upon receiving long-term double antiplatelet therapy, because the patient had taken oral contraceptives for hypermenorrhea on admission. In fact, we subsequently noted that she had a uterus myoma that caused the hypermenorrhea, leading to severe anemia. It was essential that she had to discontinue the use of oral contraceptives even if this led to exacerbation of the hypermenorrhea. Moreover, a relatively low incidence of restenosis may be expected in such cases based on the non-atherosclerotic pathogenesis of SCAD and the absence of any conventional pro-atherosclerotic risk factor in the patient. In addition, we did not identify any significant restenosis on the follow-up examination. Thus, we have an idea that the use of DES should be avoided in young women with SCAD, if possible, considering the balance between its risk and benefit. The data of the multicenter prospective registries for SCAD, such as the DISCOVERY trial [7], will facilitate the development of an appropriate therapeutic strategy.

Only a few SCAD cases have been followed-up by imaging modalities at the chronic stages. Some of the cases of SCAD that were followed-up by CAG showed complete resolution of the dissection 3, 4. Koh et al. reported a case of SCAD that was treated with conservative therapy. The patient showed complete healing of the previous dissection after 6 months, which was observed on CAG, IVUS, and coronary CT [8]. Our patient underwent coronary CT scanning after 6 months; the findings indicated an abnormal lesion from the ostium of the LAD to the proximal edge of the stent. Therefore, we performed a repeat CAG; however, the findings did not reveal the persistence of the dissection, but IVUS showed a residual dissection, which was in accordance with the abnormal findings on the CT scan. Several authors have reported the use of coronary CT imaging in cases of coronary dissection, wherein it was possible to distinguish a false lumen from a true lumen 9, 10. Although we examined the patient using 64-multi-detector row spiral CT in the present case, the findings could not confirm the presence of the residual dissection. We retrospectively analyzed the cross-sectional coronary CT imaging finding, and noted that there was the lesion which had a lower CT value than the coronary lumen in the eccentrically enlarged vessel wall (Fig. 3B). Color mapping using the CT value provided clarity (Fig. 3C), and the findings were in accordance with the residual dissection observed on IVUS imaging (Fig. 3A). We believe that the residual dissection may have been thrombosed, due to which the dissection could not be detected on CAG and the false lumen could not be clearly identified on CT imaging.

In cases such as the present one, where the residual dissection cannot be confirmed on CAG, careful analysis of a coronary CT scan may aid the diagnosis of residual dissection.