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Table of Contents
CASE REPORT
Year : 2019  |  Volume : 4  |  Issue : 4  |  Page : 128-130

Spontaneous coronary artery dissection: Two case reports and a brief review


Department of Cardiology, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin, China

Date of Submission17-Feb-2019
Date of Acceptance30-Jul-2019
Date of Web Publication31-Dec-2019

Correspondence Address:
Yong-Le Li
Department of Cardiology, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin 300052
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cp.cp_16_19

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  Abstract 


Spontaneous coronary artery dissection (SCAD) is an unusual, special type of coronary heart disease characterized by various symptoms, such as chest pain, ST-elevation acute coronary syndrome (ACS), ventricular arrhythmia, and sudden cardiac death. Here, we report two different cases who presented with ACS and were found through coronary angiography (CAG) and intravascular ultrasound (IVUS) to have SCAD, but for whom follow-up CAG and IVUS 3 months later showed different outcomes.

Keywords: Acute coronary syndrome, coronary angiography, coronary artery dissection, intravascular ultrasound


How to cite this article:
Song YP, Liu WN, Li YL. Spontaneous coronary artery dissection: Two case reports and a brief review. Cardiol Plus 2019;4:128-30

How to cite this URL:
Song YP, Liu WN, Li YL. Spontaneous coronary artery dissection: Two case reports and a brief review. Cardiol Plus [serial online] 2019 [cited 2020 Jan 26];4:128-30. Available from: http://www.cardiologyplus.org/text.asp?2019/4/4/128/274570




  Introduction Top


Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome (ACS), with diagnosis rates of 0.07%–0.2% in patients referred for coronary angiography (CAG).[1] Female patients account for about 80% of SCAD patients, with peripartum women accounting for approximately one-third of those cases.[2] Here, we present two cases of SCAD to discuss the challenges of diagnosis and management of the disease.


  Case Report Top


Case 1

A 50-year-old female patient was brought into the hospital after 15 h of severe chest pain due to being emotionally excited. The physical examination was routine. She had a history of hypertension and adenomyosis and was in menopause. Electrocardiogram (ECG) showed T-wave inversion in II, III, AVF, and V1–V6. The troponin level was 0.70 ng/mL (normal range: <0.100 ng/ml). She was treated with aspirin, clopidogrel, low-molecular-weight heparin, diltiazem hydrochloride, losartan potassium hydrochlorothiazide, and rosuvastatin. She received an elective CAG that revealed an irregular wall of the proximal segment of the left anterior descending (LAD) artery and 90% stenosis of the distal LAD artery. Other coronary arteries had no significant abnormalities [Figure 1]a. Intravascular ultrasound (IVUS) showed the presence of a hematoma in the distal LAD [Figure 1]c.
Figure 1: (a) Coronary angiographic image showing severe stenosis of the distal left anterior descending artery. (b) The second coronary angiographic image after treatment at the distal left anterior descending showing normal blood flow of the left anterior descending. (c) Intravascular ultrasound showing the intraluminal hematoma in the distal left anterior descending. (d) The final intravascular ultrasound showing no dissection in the distal left anterior descending

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She remained free of chest pain after receiving medical therapy. Three months after discharge, an ECG showed low T-wave levels in the inferior and V1–V6. A subsequent CAG showed that the hematoma in the distal LAD had disappeared completely [Figure 1]b. The IVUS revealed the same outcome as the CAG [Figure 1]d.

Case 2

A 34-year-old female patient was admitted to the hospital for chest pain and dyspnea. She had no other specific diseases. First time, the patient experienced chest pain was because she was angry and had moved heavy boxes at the same time. An ECG showed low T-wave levels in the inferior, V5, and V6 leads. The troponin level was elevated to 0.47 ng/ml. She was treated for ACS. A CAG revealed severe diffuse stenosis of the right coronary arteries (RCAs) [Figure 2]a. The left coronary was normal. The IVUS confirmed the presence of a hematoma extending from the proximal to the distal segment of the RCA [Figure 2]c. The patient remained asymptomatic during her hospitalization and was discharged after 8 days, with continuous medical therapy.
Figure 2: (a) Coronary angiography showing severe diffuse stenosis from proximal to distal of the right coronary artery. (b) A repeated coronary angiography after 3 months showing no dissection, but the middle segment still showed approximately 30% stenosis. (c) Intravascular ultrasound showing the hematoma in the dissection of the right coronary ar teries. (d) Follow-up intravascular ultrasound showing no new dissection in the right coronary arteries, but the hematoma still can be seen in the middle segment

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At 3-month follow-up, the patient was stable. No obvious abnormalities were found in ECG. A CAG revealed that the RCA was thicker than 3 months prior, and the middle segment still showed approximately 30% stenosis [Figure 2]b. The IVUS indicated that there was no dissection in the proximal and distal segments of the RCA, while the hematoma was still visible in the middle segment [Figure 2]d.


  Discussion Top


SCAD was previously believed to occur in young adults but is now considered to involve subjects aged 18–84 years, with most of the affected individuals being women, such as the present cases.[3] SCAD is probably underdiagnosed in young women (<55 years old) who have symptoms of ACS but have no classical risk factors for cardiovascular disease.[4] The study found that psychiatric conditions are gradually becoming independent risk factors for cardiovascular adverse events.[5] Women are more susceptible to the physiological effects of varying degrees of stress caused by psychiatric conditions compared to men, and these responses may increase coronary shear stress and risk of dissection in patients with SCAD.[6] The role of sex hormones that play in SCAD development is currently unknown and must be studied in the future.[7] The predisposing conditions of SCAD have been reported to include pregnancy, fibromuscular dysplasia, chronic systemic inflammatory diseases, hormonal therapy, connective tissues disorders, and coronary artery spasms, while some possible precipitating factors include extreme emotional stress or intense exercise, sympathomimetic drugs, high-dose hormonal therapy exposure, and intense Valsalva-type activities.[8] The incidence of SCAD in our two patients may have been related to recent emotional agitation and strenuous physical activity in the second case.

Ciraulo and Chesne were the first to diagnose SCAD by a CAG in 1978. This was the first application of imaging techniques in the diagnosis and treatment of this disease, thus making a CAG the gold standard for many years.[9] It is a challenge for doctors to confirm the true lumen and a safe wire placement point, while it is easy to misdiagnose a patient's condition as a result of the inability to distinguishing the narrow lumen caused by atherosclerosis or nonatherosclerosis. Optical coherence tomography or IVUS has been suggested to improve the diagnosis of SCAD. It has been reported that the LAD and its branches are affected in 45%–61% of cases, while the RCA and its branches are involved in 10%–39% of cases and the left main coronary artery is involved in 0%–4% of cases.[3] Our patients were diagnosed by CAG and IVUS. The first middle-aged woman presented distal stenosis of the LAD while the second young woman had severe diffuse stenosis of the RCA.

The treatment of SCAD has varied among conservative medical practices, percutaneous coronary intervention, and coronary artery bypass grafting; it depends on the clinical presentation, outcome of the CAG, and extent of dissection.[10] Conservative medical treatment may be considered when a patient presents clinical and hemodynamic stability and shows limited single-vessel involvement instead of the left main coronary artery being affected. Currently, antiplatelet therapy remains controversial for patients with SCAD. Based on evidence of aspirin in ACS and secondary prevention, aspirin appears to be useful for acute and long-term SCAD management.[11] However, it is still unclear whether clopidogrel is beneficial for patients with SCAD who have not been treated with stents. Considering that SCAD with intimal tears may promote thrombosis, dual antiplatelet therapy (DAPT) may be beneficial. In addition, it can also reduce the thrombus load of the false lumen and then reduce the true lumen compression.[12] Therefore, DAPT is recommended for the majority of patient with SCAD. In our cases, we chose to base the medical treatment on the clinical presentation, the medical history, and the outcome of the CAG. At the outpatient follow-up, the patients were clinically stable, but further CAG and IVUS revealed different outcomes. For the first case, the CAG and IVUS showed that the hematoma disappeared completely; however, the second case indicated that the hematoma was still visible in the middle segment of the RCA. We believe that this may be related to the local anatomy of the RCA or that this may have occurred because insufficient time was given for hematoma absorption in the second case. Recently, it was reported that nine of 272 patients managed conservatively required subsequent in-hospital revascularization.[13] It appears that some patients require revascularization after initial conservative treatment, and a follow-up is necessary.

In summary, although SCAD is an infrequent cause of ACS, the diagnostic rate is increasing as our understanding of this condition deepens. The recurrence of SCAD is high, and clinicians should be on alert for adverse cardiovascular events as a way to improve the survival rate of SCAD patients. Further efforts are needed to create better guidelines, as well as to identify the exact etiology and the long-term prognosis of this condition.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Acknowledgment

The work was supported by grants from the Technology Research and Development Program of Tianjin (15JCYBJC28000).

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Nishiguchi T, Tanaka A, Ozaki Y, Taruya A, Fukuda S, Taguchi H, et al. Prevalence of spontaneous coronary artery dissection in patients with acute coronary syndrome. Eur Heart J Acute Cardiovasc Care 2016;5:263-70.  Back to cited text no. 1
    
2.
Dhawan R, Singh G, Fesniak H. Spontaneous coronary artery dissection: The clinical spectrum. Angiology 2002;53:89-93.  Back to cited text no. 2
    
3.
Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ, et al. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation 2012;126:579-88.  Back to cited text no. 3
    
4.
Goldberg RJ, McCormick D, Gurwitz JH, Yarzebski J, Lessard D, Gore JM. Age-related trends in short- and long-term survival after acute myocardial infarction: A 20-year population-based perspective (1975-1995). Am J Cardiol 1998;82:1311-7.  Back to cited text no. 4
    
5.
Krantz DS, Whittaker KS, Francis JL, Rutledge T, Johnson BD, Barrow G, et al. Psychotropic medication use and risk of adverse cardiovascular events in women with suspected coronary artery disease: Outcomes from the women's ischemia syndrome evaluation (WISE) study. Heart 2009;95:1901-6.  Back to cited text no. 5
    
6.
Hayes SN, Kim ES, Saw J, Adlam D, Arslanian-Engoren C, Economy KE, et al. Spontaneous coronary artery dissection: Current state of the science: A scientific statement from the American Heart Association. Circulation 2018;137:e523-57.  Back to cited text no. 6
    
7.
Chou AY, Saw J. Basis for sex-specific expression of Takotsubo cardiomyopathy, cardiac syndrome X, and spontaneous coronary artery dissection. Can J Cardiol 2014;30:738-46.  Back to cited text no. 7
    
8.
Saw J, Mancini GB, Humphries KH. Contemporary review on spontaneous coronary artery dissection. J Am Coll Cardiol 2016;68:297-312.  Back to cited text no. 8
    
9.
Ciraulo DA, Chesne RB. Coronary arterial dissection: An unrecognized cause of myocardial infarction, with subsequent coronary arterial patency. Chest 1978;73:677-9.  Back to cited text no. 9
    
10.
Mehta LS, Beckie TM, DeVon HA, Grines CL, Krumholz HM, Johnson MN, et al. Acute myocardial infarction in women: A scientific statement from the American Heart Association. Circulation 2016;133:916-47.  Back to cited text no. 10
    
11.
Antithrombotic Trialists' Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71-86.  Back to cited text no. 11
    
12.
Choi JW, Davidson CJ. Spontaneous multivessel coronary artery dissection in a long-distance runner successfully treated with oral antiplatelet therapy. J Invasive Cardiol 2002;14:675-8.  Back to cited text no. 12
    
13.
Saw J, Humphries K, Aymong E, Sedlak T, Prakash R, Starovoytov A, et al. Spontaneous coronary artery dissection: Clinical outcomes and risk of recurrence. J Am Coll Cardiol 2017;70:1148-58.  Back to cited text no. 13
    


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