SS–15 Is Revascularization Indicated for Every Occluded Spontaneous Coronary Artery Dissection?

Abstract

Introduction and Aim: Spontaneous coronary artery dissection, or SCAD, is an unpredictable and potentially life-threatening condition. It is one of the most common causes of acute coronary syndrome, particularly in young women. SCAD is defined as a tear within the wall of an epicardial coronary artery that occurs in the absence of trauma, coronary intervention, or atherosclerotic plaque rupture. This process leads to the formation of a false lumen, which can partially or completely compress the true lumen and impair coronary blood flow. Patients most commonly present with chest pain, dyspnea, or palpitations. Since ischemic changes may be present on the ECG, the clinical presentation can be difficult to distinguish from acute coronary syndrome caused by atherosclerotic plaque rupture. SCAD mainly affects young and middle-aged women without traditional cardiovascular risk factors. It has been associated with severe physical or emotional stress, migraine, anxiety, depression, fibromuscular dysplasia, hormone replacement therapy, pregnancy, inflammatory conditions, menopause, and genetic variants related to certain connective tissue disorders.

Case Report: A 38-year-old woman with no known chronic medical conditions presented to the emergency department with chest pain. Her initial ECG was consistent with an acute inferior myocardial infarction, and she was immediately transferred to the cardiac catheterization laboratory. Coronary angiography showed a normal left coronary system. In the right coronary artery, a spontaneous coronary artery dissection extending from the ostium to the distal segment was identified, as shown in Figure 1. Since distal coronary flow was preserved, the patient was hemodynamically stable, and her chest pain had improved compared with the initial presentation, no intervention was performed at that time. Instead, close clinical follow-up with serial assessment of symptoms and troponin levels was planned. Medical treatment was initiated, and the patient was admitted to the coronary intensive care unit for continuous monitoring. Transthoracic echocardiography showed a left ventricular ejection fraction of 50 to 55 percent, with mild hypokinesia of the inferolateral wall.On the first day of hospitalization, laboratory tests showed a triglyceride level of 191 milligrams per deciliter, an HDL level of 44 milligrams per deciliter, and a high-sensitivity troponin I level of 1.99 micrograms per liter, with a normal range below 0.1 micrograms per liter. Serial troponin levels were 6.29, 2.13, and 2.20 micrograms per liter. The ST-segment elevations in the inferior leads gradually regressed, and the patient's symptoms improved. The patient remained clinically stable during her intensive care unit follow-up and was subsequently evaluated by the cardiology council. Conservative management was continued, and follow-up coronary angiography was planned for three months later. The patient was discharged with continued medical treatment and bed rest during this period. Three months later, repeat coronary angiography demonstrated complete resolution of the dissection extending from the ostium to the distal segment of the RCA, as shown in Figure 2.

Discussion: The coronary arteries consist of three histological layers: the tunica intima, tunica media, and tunica adventitia. Spontaneous coronary artery dissection occurs when an intramural hematoma develops within the coronary arterial wall. The blood may originate either from injury to the vasa vasorum or from an intimal tear.The intramural hematoma separates the intima from the outer layers of the arterial wall, creating a false lumen. This false lumen compresses the true lumen, reduces coronary blood flow, and may result in acute coronary syndrome.The left anterior descending artery is the most commonly affected vessel.According to reported frequencies, the LAD and its branches are involved in approximately 50 percent of cases, the circumflex artery, ramus intermedius, and obtuse marginal branches in approximately 30 percent, the RCA and its branches in approximately 25 percent, multivessel involvement in approximately 15 percent, and the left main coronary artery in approximately 4 percent.Distal coronary segments are affected more frequently than proximal segments. Patients with SCAD are usually admitted with a suspected diagnosis of acute coronary syndrome.The initial evaluation includes a detailed history and assessment of symptoms, ECG, cardiac biomarkers such as troponin, echocardiography, and coronary angiography.Based on the angiographic appearance, SCAD can be classified into four types.

Type 1 SCAD, or the classic appearance, is characterized by contrast staining of the arterial wall and visualization of a dissection flap, with clearly visible true and false lumens.

Type 2 SCAD, or diffuse stenosis, is the most common type. It usually appears as a long and smooth narrowing, typically extending for more than 30 millimeters. It can be further divided into type 2A, involving the distal segment, and type 2B, extending all the way to the distal end of the vessel.

Type 3 SCAD, or focal stenosis, can closely mimic atherosclerotic disease. These lesions are usually short and focal, and intravascular imaging, such as OCT or IVUS, may be required for diagnosis.

Type 4 SCAD is characterized by complete coronary artery occlusion with absent distal flow.

The clinical presentation of SCAD can range from ST-elevation myocardial infarction and non-ST-elevation acute coronary syndrome to ventricular tachyarrhythmias, congestive heart failure, and sudden cardiac death. The management of SCAD differs from that of conventional ischemic heart disease, and there is still no universally accepted treatment strategy. Most SCAD lesions heal spontaneously within approximately two months. Therefore, medical treatment and conservative management are generally preferred in stable patients. Unlike conventional acute coronary syndrome, percutaneous coronary intervention and coronary artery bypass grafting are not routinely recommended. There are several reasons for this. First, the guidewire may enter the false lumen and occlude the true lumen. Second, balloon angioplasty and stent implantation may extend the dissection or propagate the intramural hematoma, potentially worsening coronary obstruction. Such extension may result in spiral dissection of the distal vessel or retrograde extension into the proximal segments and adjacent branches, including the left main coronary artery. In addition, because SCAD lesions can be very long, long stents may be required. This may increase the risk of in-stent restenosis and stent thrombosis. As the intramural hematoma is gradually resorbed, late stent malapposition may also occur, potentially increasing the risk of late stent thrombosis. Intravascular imaging can help confirm the diagnosis; however, manipulation of the vessel with a guidewire or imaging catheter may itself worsen the dissection. Similarly, during CABG, it may be difficult for the surgeon to determine whether the graft has been placed into the true lumen.

Conclusion: More than 90 percent of patients demonstrate angiographic healing within approximately one month. Therefore, PCI should not routinely be considered as the first-line treatment. In clinically stable patients, conservative management with close monitoring is generally preferred. Our case demonstrates that even in the presence of complete coronary occlusion due to SCAD, spontaneous healing may occur with conservative treatment in selected stable patients.

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