Coronary thrombosis is the most common cause of acute coronary syndromes (ACS), including sudden coronary death (SCD) . Plaque rupture (PRU) in most cases, plaque erosion (PER) uncommonly, and calcified nodule (CaN) rarely have been demonstrated to be the main mechanisms underlying acute coronary thrombosis in both ex vivo and in vivo studies. In postmortem pathologic studies of subjects who died suddenly of coronary heart disease more than two thirds of the fatal events were related to PRU followed by thrombotic occlusion (Fig. 2.1). The acute coronary events were caused by thrombotic occlusion caused by PER (Fig. 2.2) in another third, and CaN was observed in 2–5% of cases [1–4]. Several clinical optical coherence tomography (OCT) studies have confirmed the autopsy data by establishing plaque rupture as the most frequent lesion identified in patients with ACS in vivo [5–10]. Patients with OCT erosion were younger, had a lower frequency of lipid plaque, a thicker fibrous cap, and less severe stenosis. They also presented less frequently with ST-segment elevation myocardial infarction (STEMI) than those with plaque rupture [7, 11]. A combined OCT and intravascular ultrasound (IVUS) study demonstrated that the incidence of PRU, PER, and CaN in 112 patients with acute STEMI was 64%, 27%, and 8%, respectively [9]. PER was characterized by fewer features of plaque vulnerability compared to PRU, including smaller plaque burden, lack of positive remodeling, and lipid richness. In the setting of ACS, high-resolution intravascular imaging with OCT can characterize plaque pathology at the time of intervention and allows better understanding of the etiology of STEMI. Acute events have been broadly classified as associated with ruptured fibrous cap (RFC) or intact fibrous cap (IFC) [12]. A recent OCT study of STEMI patients supports an alternative treatment strategy for patients with OCT-verified plaque erosion wherein nonobstructive lesions might be managed without stenting [13]. However, whether or not distinguishing among different plaque characteristics in STEMI patients undergoing percutaneous coronary intervention (PCI) can help develop personalized treatment strategies leading to improved long-term outcomes remains a matter of debate [14, 15]. Much more data are necessary to develop clinical guidelines regarding the role of OCT in the selection of therapy in patients with STEMI.

Spontaneous coronary artery dissection (SCAD) is a rare but important cause of ACS with an incidence of 0.1–2.1% as reported by angiographic and intravascular imaging studies [8, 9, 12, 16–18]. The majority of SCAD patients are young women manifesting ACS with no risk factors for atherosclerosis. Around a quarter of SCAD cases occurred either postpartum or with use of oral contraceptive [19]. Prompt diagnosis and treatment of patients with SCAD improve survival. The survival rate has been improved up to 95% as a result of advances in imaging modalities and therapy. Therapeutic options include medical therapy, percutaneous coronary intervention, and surgery. Thrombolysis is avoided in patients suspected of SCAD-related myocardial infarction. While diagnostic accuracy of angiography for SCAD is limited, OCT imaging can provide substantial insights into the morphologic features of the condition, including entry point, double lumen, and intramural hematoma [20, 21]. Small dissections or smooth stenoses mostly from an intramural hematoma may not be detected by coronary angiography; this leads to under-reporting of the phenomenon and underestimation the true prevalence of SCAD. Another cause of myocardial infarction in young patients less than 45 years old might be hypercoagulable states characterized by recurrent arterial and venous thrombosis [22]. However, this could be difficult to differentiate from PER. It can also be associated with other autoimmune diseases, for example, systemic lupus erythematosus (SLE) . Patients with SLE have accelerated development of atherosclerosis as a result of nontraditional factors present in SLE in addition to traditional risk factors, and they should be considered as high-risk patients for CAD [23].

Coronary spasm (CS) plays an important role in the pathogenesis of an acute coronary event [12, 24–27]. Because it is a transient phenomenon, morphologic features of CS culprit segments have not been fully understood. Most pathologic reports are case studies of patients presumed to have died from coronary vasospasm. Diagnosis is not always possible with coronary angiography alone. OCT allows detailed in vivo examination of the morphologic characteristics of coronary arteries in patients with CS [28–31]. Coronary segments affected by CS are characterized by diffuse intimal thickening without lipid or calcium accumulation. An additional OCT feature of intima-media separation from adventitia was observed in some CS cases [30, 31].