Discussion
Formerly assimilated to a classic acute coronary syndrome, the diagnosis of SCAD was based mainly on the presence of an intimal radiolucent flap associated with a contrast in the arterial wall on coronary angiography. Currently, studies on SCAD permit to establish a classification into 3 angiographic types [8]: Type 1 (representing the classic description with intimal flap), type 2 (extensive and diffuse tubular lesions with a plane of dissection not visible which may result in complete coronary occlusion), type 3 (multiple focal tubular lesions due to intramural hematoma mimicking atherosclerosis).
Our patient presented a feature of a double dissection with a type 1 lesion on the distal anterior interventricular artery and a type 2 lesion on the second left marginal. Type 2, sometimes resulting in compression of the vascular lumen due to intramural hematoma without intimal flap, it is the most frequently encountered in the different series representing 67% of cases. Type 1 follow-up with an intimal flap which represents 29% of cases. Type 3 mimicking atherosclerotic lesions is only found in 4% of cases [8]. The descending anterior interventricular artery is usually the most affected during SCAD. However, polyarterial lesions could be found in a range of 20 -25% of cases [9].
Patients with SCAD generally have arterial fragility without atheroma or calcifications which may limit the progression of coronary dissection. This fragility can be acquired during pregnancy, oral contraception, hormone therapy, systemic inflammatory diseases; congenital condition as in fibromuscular dysplasia, Marfan disease, syndrome Ehlers-Danlos, connectivitis, or even idiopathic [10, 11]. In the series by Saw etal assessing the baseline characteristics, predisposing factors and clinical outcomes of 168 patients with a SCAD, the association with a detailed screening of other non-coronary arterial disease had revealed that 72% of these patients also presented with fibromuscular dysplasia [5]. However, our patient did not present clinical elements that could suggest any of the above conditions cited. These changes in the arterial wall are generally not sufficient to explain SCAD. This pathology appears to be multifactorial. An extrinsic trigger appears essential, such as emotional stress, intense physical exercise, or maneuvers such as Valsalva [10, 11]. This is also mentioned in the series by Saw et al . In this study physical or emotional stress was implicated as triggering factors in 56% of cases [5]. Likewise, in our patient we could clearly evoke an emotional and important professional stress. In fact, concomitantly with the occurrence of this case of spontaneous dissection of two coronary arteries, we were living a period of general confinement in France due to the COVID-19 pandemic. Very anxiety-provoking situation both professional and personal for our patient who continue to carry out her professional activities despite the high risk of contracting a particularly fatal viral disease. We therefore think that the strong stress at the same time emotional, physical, and professional would be the triggering factor. The clinical presentation of a SCAD is similar to that of an acute coronary syndrome by rupture atherosclerotic plaque. In more than half of the cases, we note electrocardiographic changes as ST segment elevation associated with elevation of enzymes myocardial (troponin). The rest of the cases will present as acute non-ST elevation coronary syndromes.
Some may also present with short term life-threatening ventricular arrhythmias and others still in cardiac arrest. In our case, we had a typical electrocardiographic presentation of a myocardial infarction with infero-lateral ST segment elevation and an anterior mirror image. Of course, we had an enzymatic movement with elevation of troponins I. In the study done by the Mayo Clinic in the United States of America with the highest number of patients with spontaneous coronary arteries dissection, aimed at determining the prevalence of coronary tortuosity in these patients, it appears that tortuosity of coronary arteries is a risk factor for SCAD and even recurrence [12].
As part of the SCAD, coronary angiography remains the first-line examination and sometimes allows to visualize thrombi in the real channel, but it makes it difficult to visualize hematoma of the artery wall. It also helps to determine the type of lesion. It is therefore systematically recommended an association with intravascular imaging as Optical Coherence Tomography
(OCT) or intravascular ultrasonography (IVUS). The optical coherence tomography has better resolution than intravacular ultrasonography. It allows to confirm the guide’s position in the real channel, detail the site of the wall hematoma and intimal breach; to facilitate an accurate assessment of the size of the artery and optimize stent expansion in the event of underlying angioplasty [13]. However, OCT therefore allows a detailed overview of the arterial anatomy of patients [14]. This technique is limited by its lack of visualizing deep layers of the arterial wall [14]. Compared to intravascular ultrasound, OCT is clearly superior in terms of the location of the initial intimal lesion and in the exploration of the intimo-medial membrane (intimal flap) [14, 15].
The treatment of SCAD could be medical with or without stenting and the prognostic is generally good [13]. Our treatment consists of an antiplatelet drug, a beta-blocker in order to reduce the pressure shearing action on the arterial wall and thus stop intramural bleeding favorizing the repair of intimal breach. The myocardial sequelae were found after one month in our patient probably because of the association of two coronary arteries involvement and the delay of management. Although these sequelae have disappeared after two months with good medical therapy.