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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 6  |  Issue : 4  |  Page : 133-136

Spontaneous coronary artery dissection: A retrospective analysis of 19,676 coronary angiograms


1 Department of Cardiology, Mysore Medical College and Research Institute, Mysore, Karnataka, India
2 Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, Karnataka, India
3 Department of Cardiology, PSG Institute of Medical Sciences and Social Research, Coimbatore, Tamil Nadu, India

Date of Web Publication27-Oct-2017

Correspondence Address:
Dinesha Basavanna
Department of Cardiology, Mysore Medical College and Research Institute, Mysore - 570 001, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JCPC.JCPC_15_17

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  Abstract 

Aim: Spontaneous coronary artery dissection (SCAD) is a rare cause of angina, myocardial infarction (MI), and sudden cardiac death (SCD) and may frequently manifest as acute coronary syndrome (ACS). The diagnosis of SCAD relies on angiographic visualization of a radiolucent intimal flap. Therapeutic options include medical therapy, percutaneous coronary interventions, and bypass surgery. The aim of this study is to analyze the clinical profile, inhospital outcomes, management, and follow-up of patients with angiographic SCAD. Methods: About 19,676 diagnostic coronary angiograms (CAGs) were reviewed retrospectively during a 2-year period; 64 patients had SCAD and were included in the study. Complete medical histories before and during the event as well as treatment regimens were obtained from patients' hospital files. Results: A total of 64 cases of SCAD were considered for the study within an age range of 25–70 years. Fifty-eight patients presented with ACS, two patients presented with unstable angina, one patient presented with rheumatic mitral stenosis in atrial fibrillation, one patient presented with non-ST-elevation myocardial infarction, one patient with dilated cardiomyopathy with left ventricular dysfunction, and one patient with effort. Out of 64 patients, four patients died and the average hospital stay is 3–5 days. Conclusion: SCAD occurs in 0.32% of patients undergoing CAG for evaluation of coronary artery disease. Majority of SCAD occurs in men. The left coronary artery is most commonly affected. The inhospital outcomes are good. Most of the patients with SCAD have good prognosis following optimal medical therapy.

Keywords: Coronary angiogram, coronary artery disease, left coronary artery, spontaneous dissection


How to cite this article:
Basavanna D, Manjunath CN, Panneerselvam A, Ananthakrishna R, Honnayanayak M, Bhat P. Spontaneous coronary artery dissection: A retrospective analysis of 19,676 coronary angiograms. J Clin Prev Cardiol 2017;6:133-6

How to cite this URL:
Basavanna D, Manjunath CN, Panneerselvam A, Ananthakrishna R, Honnayanayak M, Bhat P. Spontaneous coronary artery dissection: A retrospective analysis of 19,676 coronary angiograms. J Clin Prev Cardiol [serial online] 2017 [cited 2019 Mar 24];6:133-6. Available from: http://www.jcpconline.org/text.asp?2017/6/4/133/217390


  Introduction Top


Spontaneous coronary artery dissection (SCAD) is a rare cause of angina, myocardial infarction, and sudden cardiac death. SCAD frequently manifests as acute coronary syndrome (ACS), but the overall prevalence is low. It can be primary (idiopathic) or secondary (traumatic, iatrogenic, as an extension from aortic root dissection).

The exact etiology and pathogenesis remain unclear. Many patients are women in the postpartum or childbearing age groups. Other associations include contraceptive usage and connective tissue disorders, vigorous exercise, vasospasm, fibromuscular dysplasia, Ehlers-Danlos and Marfan's syndrome and polyarteritis nodosa, polycystic kidney disease, and Loeys–Dietz syndrome. Coronary atherosclerosis and peripartum period are the most common pathologies associated with SCAD.

SCAD is thought to be caused by hemorrhagic separation usually occurring in outer third of the tunica media or between media and external elastic lamina. The tear in the intima results in creation of false lumen, the expansion of which causes the distal propagation of the dissection and subsequent compression or occlusion of true lumen. Furthermore, rupture of the vasa vasorum may generate a wall hemorrhage without communication with the lumen. Myocardial infarction (MI) results from the compromise of the true lumen. Cystic medial necrosis is a rare finding in SCAD.

SCAD was first described by Pretty in 1931 in an autopsy study.[1] Currently, the diagnosis of SCAD relies on angiographic visualization of a radiolucent intimal flap. Optical coherence tomography emerged as new technique that provides accurate visualization of the coronary artery with good resolution (15 μm).[2] However, its value in the diagnosis of SCAD remains unsettled. Intravascular ultrasound (IVUS) also provides detailed morphological information. Angiographically, SCAD is graded according to National Heart Lung and Blood Institute (NHLBI) classification system, developed by the Coronary Artery Registry.[3] This system grades SCAD based on angiographic appearance as types A-F. Therapeutic options include medical therapy, percutaneous coronary interventions (PCIs), and bypass surgery. The clinical profile, inhospital outcomes, management, and follow-up of patients have not been studied adequately.


  Methods Top


We retrospectively reviewed medical records and coronary angiograms (CAGs) of patients admitted to our institute from January 2010 to December 2011. Out of 19,676 diagnostic CAGs, 64 patients diagnosed as SCAD were included in the study.

SCAD was identified by a computerized search using the term “dissection” in the angiographic descriptions in the database and the hospital files. All identified cases of SCAD had their CAGs reviewed by an experienced interventional cardiologist to identify the site of entry, the distribution of dissection, and to exclude iatrogenic coronary artery dissection.[4],[5]

Two interventionists reassessed the angiograms in doubtful cases. Complete medical histories before and during the event as well as treatment regimens were obtained from patients' hospital files. Dissections were classified according to the NHLBI classification as follows: Type A dissections represent radiolucent areas within the coronary lumen during contrast injection, with minimal or no persistence of contrast after the dye has cleared. Type B dissections are parallel tracts or double lumen separated by a radiolucent area during contrast injection, with minimal or no persistence after dye clearance. Type C dissections appear angiographically as contrast outside the coronary lumen, with persistence of contrast in the area after clearance of dye from the coronary lumen. Type D dissections represent spiral luminal filling defects, frequently with extensive contrast staining of the vessel. Type E dissections appear as new, persistent filling defects. Type F dissections represent those that lead to total occlusion of the coronary artery, without distal anterograde flow.

Left ventricular (LV) ejection fraction was estimated by echocardiography 1–5 days after the event. Follow-up was conducted through telephonic calls - 6 months to 1 year after hospital discharge.

Statistical analysis

Descriptive statistical analysis has been carried out in the present study. Results on continuous measurements are presented on mean ± standard deviation (minimum − maximum), and results on categorical measurements are presented in number (%). Significance is assessed at 5% level of significance. The following assumptions on data are made: (1) dependent variables should be normally distributed and (2) samples drawn from the population should be random. Cases of the samples should be independent.

Student's t-test (two-tailed, independent) has been used to find the significance of study parameters on continuous scale between two groups' intergroup analysis) on metric parameters. Levene's test for homogeneity of variance has been performed to assess the homogeneity of variance. Chi-square/Fisher's exact test has been used to find the significance of study parameters on categorical scale between two or more groups.


  Results Top


A total of 64 cases of SCAD were identified. The patients comprised 60 (93.8%) males and 4 (6.3%) females with an age range of 25–70 years. Of these, patients aged <40 years constituted 7 (10.9%), 41–50 years - 18 (28.1%), 51–60 years - 30 (46.9%), and 61–70 years - 9 (14.1%) with mean age of 52.45 ± 9.08 years [Table 1].
Table 1: Correlation of clinical variables with incidence of mortality

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Fifty-eight patients presented with ACS, two patients presented with unstable angina, one patient presented with rheumatic mitral stenosis in atrial fibrillation (AF), one patient presented with non-ST-elevation myocardial infarction, one patient with dilated cardiomyopathy with LV dysfunction, and one patient with effort angina.

The incidence of SCAD was 0.32%. Nearly 19 (29.7%) patients had diabetes mellitus, 19 (29.7%) had hypertension, and 32 (50%) patients were smokers. Of the smokers, there was right coronary artery (RCA) involvement in 15 (46.8%), followed by left anterior descending artery (LAD) involvement in 10 (31.3%) and left circumflex artery (LCX) involvement in 7 (21.8%). However, in case of diabetes and hypertension patients, LCX involvement was seen in 7 (36.8%), followed by RCA and LAD in 6 (31.6%).

Atheromatous plaque was seen in 56 (87.5%) patients. Thirty-three (51.6%) patients had ejection fraction of 31%–50%, 15 (23.4%) patients had 51%–60%, and 4 (6.3%) had <30% EF. LV clot was seen in 7 (10.9%) patients and all received anticoagulation.

Twelve (18.8%) patients were lysed with injection streptokinase (SK), no mortality recorded up to 5 days after injection SK. Out of 64 patients, four patients died (three males, one female).

Fifty-five (85.9%) patients had single-vessel involvement, 7 (10.9%) patients had double-vessel involvement, and two (3.1%) patients had triple-vessel involvement.

LAD was involved in 34 (45.3%) patients, RCA in 28 (37.3%), LCX in 7 (9.3%), and posterior descending artery (PDA) involvement in 1 (1.3%) patient noted. Average length of the dissection was <10 mm noted in 20 (26.7%) patients, 16–20 mm noted in 16 (21.3%), 21–25 mm in 5 (6.7%), and >25 mm noted in 12 (16.0%) patients.

Thrombus was seen in 13 (20%) patients, and collaterals were seen in 56 (87.5%) patients.

Average hospital stay is 3–5 days. Dual antiplatelet therapy was prescribed in 63 (98.4%) patients, statins in 64 (100%), beta-blockers in 51 (79.7%), angiotensin-converting-enzyme (ACE) inhibitors in 52 (81.3%) patients.


  Discussion Top


Our study represents one of the largest case series of SCAD in the literature. Diagnosis and management of SCAD is very challenging. However, an accurate and early diagnosis remains of paramount importance. In this retrospective study, 64 patients were identified. The included patients were characterized by a relatively older age group in both the male and female group. Only four patients had a follow-up period of 6 months to 1 year.

The typical appearance of dissection including an obvious false lumen and delayed clearance of contrast material confirmed the diagnosis of SCAD. The incidence in our study is 0.32% (total number is 19,676 patients). This incidence is lower than previously reported rates of 0.1%–1.1% of CAGs.[4]

The acute prognosis of SCAD has been reported to be unfavorable with mortality rates of 10%–30% and with many cases diagnosed through postmortem.[6],[7] In this study, all patients survived the immediate postinfarction period, and we observed four deaths. The first being a postmenopausal female with ACS-inferior wall MI, not lysed, with dissection of proximal-mid LAD and significant mid-distal right carotid artery (RCA) stenosis died after 6 month with sudden cardiac death (SCD). Two of the patients had both diabetes and hypertension and presented with acute coronary syndrome - inferior wall myocardial infarction with dissection of RCA > 25 mm, not lysed. Another patient presented with ACS-IWMI with proximal LCX dissection of >16 mm with proximal LAD and proximal RCA stenosis. In this group, undoubtedly sudden acute deterioration was because of extension of the dissection or the development of dissection elsewhere in the coronary tree. The fourth patient was a known case of diabetes and hypertension, and smoker, had SCAD at mid, distal, and up to bifurcation of RCA and stenosis of proximal LAD and LCX, and died after 5 months. He was on adequate medical management.

Our study showed a significance of SCAD length and stenosis of other vessels which significantly contribute to mortality in spite of taking adequate medication. In support of this, one of the patients, a 50-year-old male, presented with rheumatic heart disease with mitral stenosis with AF, smoker had SCAD of three vessels (RCA - proximal, PLV - distal, and RV branch - distal) with adequate medications, has been surviving for 2.5 years.

In one study, 2.5% of the patients were treated with PCI or surgery.[7] Some authors recommend PCI if left main coronary artery (LMCA) is not involved and dissection is limited to single vessel. PCI is the preferred modality of treatment in pregnancy also. Coronary artery bypass grafting (CABG) is preferred in LMCA dissection, multiple vessel dissection, and occlusion of true lumen preventing passage of guide wire.[8],[9]

In our study, one of the patients, a 60-year-old male, known diabetic underwent CABG after 1 month because of recurrent chest pain in spite of adequate medications. He had SCAD of proximal PDA branch and significant stenosis of proximal RCA - 80%, mid-LAD - 100%. The study does not explain the background of the encountered favorable SCAD prognosis. However, we suggest that a well-functioning prehospital diagnosis and adequate medication is part of the explanation.

The study confirms that SCAD usually but not always affects younger females. We found significant gender differences in age, presence of atherosclerotic coronary artery disease (CAD), smoking, statin treatment, or hypertension. It is, however, likely that a larger study cohort could reveal differences between males and females.[10],[11],[12]

Overall, in females, SCAD had preponderance of occurring in the left-sided coronary arteries. In our study, out of four female patients, three had SCAD of LAD whereas one patient had SCAD of RCA. In males, generally, there is predilection for RCA SCAD as compared to left coronary artery preponderance in females as described earlier. However, this was not seen in our study. We found that LAD was the most commonly involved artery in men also. In our study, 34 patients (45.3%) had SCAD of LAD, 28 (37.3%) had SCAD of RCA, 7 (9.3%) had SCAD of LCX, and 1 (1.3%) had SCAD of PDA.

Our study strongly suggests involvement of RCA followed by LAD and LCX in smokers and involvement of LCX followed by RCA and LAD in case of diabetes and hypertension patients.

In our study, majority of the patients were male (60 in number) patients. Out of four female patients, two females were postmenopausal and two were perimenopausal age group; this is not in accordance with the previously reported studies where SCAD has shown to be seen more in young females,[11] during pregnancy and in the early puerperium. However, due to the limitations of the data, no observations were made as regards to pregnancy, early puerperium, and the risk of SCAD. Hormonal changes and hemodynamic stress related to pregnancy and labor contribute during the postinfarction period to SCAD.

In our study, 120 patients had been lysed with injection SK, all patients survived postinfarction period, and they were asymptomatic with adequate medical management. No glycoprotein IIb/IIIa inhibitors were used in any of the patients. Thrombolytic therapy is relatively contraindicated in SCAD due to the potential risk of worsening of dissection.[6]

In this study, all patients were treated conservatively with aspirin, clopidogrel, beta-blockers, atorvastatin, ACE inhibitors, and nitrates; all were asymptomatic with adequate medications during follow-up without angina. This is in contrast to iatrogenic dissections after drug-eluting stent deployment, which has a poor outcome when left untreated.[13]

Revascularization in patients with SCAD should be, therefore, limited to cases with ongoing ischemia, and the treatment targeted only to flow limiting dissections. Overall the treatment options for SCAD is not well defined, but options have increased significantly. These include medical therapy, PCI, and coronary bypass. However, it is not possible to define an optimal treatment because no single option is superior to the others.[8],[14],[15]

Study limitation

Some limitations of the present study should also be acknowledged. First, there are inherent limitations involved with a retrospective analysis of a case series at a single institution. Second, there were only four females in our study population. Not all patients admitted with CAD underwent angiogram, so possible cases of dissection could have been missed. Furthermore, angiographic diagnosis of dissection has several limitations and the lack of imaging modality like IVUS is a major limitation of this study.[16]


  Conclusion Top


SCAD occurs in 0.32% of patients undergoing CAGs for evaluation of CAD. Majority of SCAD occurs in men.[6] The left coronary artery is most commonly affected followed by RCA and LCX. The inhospital outcomes are good. Most of the patients with SCAD have good prognosis following optimal medical therapy. A small subset requires intervention for management of recurrent angina.

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Pretty HC. Dissecting aneurysm of coronary artery in a woman aged 42. Br Med J 1931;1:667.  Back to cited text no. 1
    
2.
Alfonso F, Paulo M, Gonzalo N, Dutary J, Jimenez-Quevedo P, Lennie V, et al. Diagnosis of spontaneous coronary artery dissection by optical coherence tomography. J Am Coll Cardiol 2012;59:1073-9.  Back to cited text no. 2
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Mortensen KH, Thuesen L, Kristensen IB, Christiansen EH. Spontaneous coronary artery dissection: A Western Denmark Heart Registry study. Catheter Cardiovasc Interv 2009;74:710-7.  Back to cited text no. 4
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Arrigo C, Bochicchio M, Pezzotti S, Amato M, Carminati L, Crocco G, et al. Spontaneous coronary artery dissection in a young woman without risk factors. J Emerg Med 2013;44:e165-8.  Back to cited text no. 10
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Cheng CI, Wu CJ, Hsieh YK, Chen YH, Chen CJ, Chen SM, et al. Percutaneous coronary intervention for iatrogenic left main coronary artery dissection. Int J Cardiol 2008;126:177-82.  Back to cited text no. 14
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Klutstein MW, Tzivoni D, Bitran D, Mendzelevski B, Ilan M, Almagor Y. Treatment of spontaneous coronary artery dissection: Report of three cases. Cathet Cardiovasc Diagn 1997;40:372-6.  Back to cited text no. 15
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Ito H, Taylor L, Bowman M, Fry ET, Hermiller JB, Van Tassel JW. Presentation and therapy of spontaneous coronary artery dissection and comparisons of postpartum versus nonpostpartum cases. Am J Cardiol 2011;107:1590-6.  Back to cited text no. 16
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