Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome and sudden cardiac death. The first case of SCAD was reported by Pretty [1] in 1931, while the first angiographic diagnosis was not made until 1978 [2]. SCAD occurs mostly in female patients during the peripartum period, but it can also occur in patients with atherosclerosis or in patients without any of these features [3,4]. Its incidence, etiology, and pathogenesis remain unclear. The clinical presentation of SCAD depends on the extent and flow-limiting severity of the coronary dissection. The condition ranges from asymptomatic state to the development of unstable angina, acute myocardial infarction, ventricular arrhythmia, and sudden cardiac death. There is no definite guideline on how to manage patients with SCAD [5]. In this report, we describe two patients with myocardial infarction caused by SCAD who were treated with percutaneous coronary intervention (PCI).

This report illustrated two cases of myocardial infarction caused by SCAD in middle-aged males who were treated with percutaneous coronary angioplasty.

The incidence of SCAD is low, reportedly 0.07% to 1.10% among patients referred for coronary angiography. It occurs most often in young females (aged < 40 years) and frequently in the peripartum period. Although our cases were more unusual in that they involved SCAD in the LAD of middle-aged males, SCAD is reported to predominantly involve the LAD in females and right coronary artery in males. It has rarely been associated with connective tissue disease, vasculitis, inflammatory disorders, oral contraceptive use, exercise, prolonged sneezing, and cocaine abuse. Thus, it should be suspected in a young patient without major cardiovascular risk factors or in a patient in the peripartum period presenting with acute coronary syndrome or sudden cardiac death [6-10]. Our patients had no underlying conditions, and their SCAD can be considered idiopathic. In addition, SCAD seemed to persist for more than 10 years after myocardial infarction in the first patient. While a weak association between smoking and hypertension has been reported, classic risk factors seem unlikely to be related to SCAD [6]. Coronary atherosclerosis is known to be the most common pathology associated with SCAD. In atherosclerotic arteries, plaques play a central role in the pathogenesis of dissection. Plaques may bleed or rupture, leading to dissection of the adventitia from the media and subsequent rupture of the media. They may also cause intimal tears that progress into the media.

Coronary angiography is essential in the diagnosis of SCAD. The typical appearance is the presence of a thin, longitudinal radiolucent line representing an intimal medial flap with flow in two or more separate lumens. Additional IVUS and optical coherence tomography imaging may provide detailed information on the location and extent of the dissection. Typical IVUS features of SCAD are the presence of an intramural hematoma in the outer third of the media compressing the true lumen with minimal or no atherosclerosis [5,10]. There are two types of SCAD. One is an intimal tear and propagation of medial dissection that can be recognized angiographically, as shown in our cases. The other is medial dissection with hematoma formation, but no intimal tear. Computed tomography coronary angiography can be useful in the follow-up of conservatively managed patients.

Treatment of SCAD is often challenging and may include medical therapy, PCI, or coronary artery bypass graft surgery (CABG). Ongoing ischemia and the disease extent are important considerations when making a decision regarding the most appropriate treatment modality. Medical treatment is a reasonable option in patients with stable hemodynamics, single-vessel SCAD affecting a limited territory, or Thrombolysis In Myocardial Infarction (TIMI) of grade 2 or 3 flow. In patients with completed infarctions without residual ischemic symptoms, medical therapy is reportedly associated with a good long-term outcome. Coronary intervention can be considered as the first-line approach for SCAD complicated by occlusion or significantly slowed flow, especially in cases of proximal dissection or TIMI of grade 0 or 1 f low [3,4,6,10]. CABG may be an optimal treatment choice in multivessel disease or left main vessel disease. In our patients, PCI was performed because both had chest pain suggestive of ongoing ischemia and flow-limiting LAD lesions. During coronary intervention, the surgeon should be cautious about wiring the false lumen because vessel perforation or distal propagation of the dissection may occur; it is important to confirm wiring of the true lumen under intravascular imaging such as IVUS or optical coherence tomography [4,5]. In the present cases, we performed percutaneous coronary angioplasty and stent deployment without complications in patients presenting with myocardial infarction under IVUS. Recent developments in stenting and PCI techniques will make the role of PCI more important in treating SCAD.

In conclusion, SCAD should be considered in patients presenting with acute coronary syndrome with few conventional coronary risk factors. Prompt diagnosis and patient-tailored management may reduce morbidity and mortality in this population.