Unveiling the Causes of Acute and Non-Acute Myocardial Ischemic Syndromes: The Role of Optical Coherence Tomography

Abstract

Despite significant advances in understanding and management, cardiovascular diseases remain the leading cause of mortality worldwide. Historically, diagnostic and therapeutic strategies have typically targeted obstructive coronary arteries. However, growing evidence supports the pivotal role of non-obstructive mechanisms in myocardial ischemia, prompting a new classification that distinguishes Acute Myocardial Ischemic Syndromes from Non-Acute Myocardial Ischemic Syndromes. In this evolving context, Optical Coherence Tomography (OCT) plays an important diagnostic role in the assessment of both obstructive and non-obstructive ischemic mechanisms. In Acute Myocardial Ischemic Syndromes, OCT enables the identification of major plaque destabilization mechanisms and contributes to the diagnosis of Myocardial Infarction with Non-Obstructive Coronary Arteries, helping to differentiate between atherosclerotic and non-atherosclerotic causes. In Non-Acute Myocardial Ischemic Syndromes, OCT assists in evaluating stenosis severity, plaque morphology, vulnerability, and healing, and may contribute to the diagnosis of Ischemia with Non-Obstructive Coronary Arteries, identifying myocardial bridge and epicardial spasm alongside conventional functional assessment of intermediate stenoses. This narrative review outlines the expanding clinical applications of OCT across the full spectrum of ischemic syndromes, emphasizing its role in bridging obstructive and non-obstructive pathophysiology and supporting a more comprehensive diagnostic approach to ischemic heart disease.

Keywords: Acute Myocardial Ischemic Syndromes; Non-Acute Myocardial Ischemic Syndromes; Optical Coherence Tomography; precision medicine; tailored therapy.

Figure 1

Mechanisms of Acute Coronary Syndromes. Panel (A): Plaque rupture: rupture of fibrous cap (white arrow) resulting in a large vessel wall cavity with exposure of highly thrombotic necrotic core to the blood flow without evidence of thrombi. Panel (B): Definite OCT-erosion: presence of thrombus overlying an intact plaque without evidence of fibrous cap rupture. Mixed thrombus at 6–11 ‘o clock (white arrow) with posterior shadowing with an underlying lipid-rich plaque. Panel (C): Eruptive CN with fibrous cap rupture and overlying mixed thrombus (white arrow) in the context of severely calcified in-stent restenosis. The asterisk is indicating the guide wire artifact. All images come from the authors’ personal archive, unless otherwise indicated.

Figure 2

Thrombi. Panel (A): case of in-stent thrombosis in the context of major stent malapposition (the distance between the malapposed struts and the vessel wall is indicated by the double-headed arrow). A red thrombus is visible (high backscattering and posterior shadowing) with attenuation of the underlying plaque (dashed arrow), as well as a white thrombus (low backscattering and without posterior shadowing) (white arrow) Panel (B): mixed thrombus in the context of a lipid-rich plaque (definite OCT-erosion). The asterisk is indicating the guide wire artifact. All images come from the authors’ personal archive, unless otherwise indicated.

Figure 3

Epicardial spasm. Panel (A): coronary angiography showing focal coronary artery spasm after intracoronary acetylcholine administration, with >90% luminal diameter reduction; Panel (B): OCT pullback showing evidence of “short-in-length” luminal area reduction in a segment with intimal thickening; Panel (C): resolution of the spasm after intracoronary nitrate administration. The asterisk is indicating the guide wire artifact. These images are courtesy of Francesco Fracassi, MD, PhD, with permission for use.

Figure 4

Plaque morphology and features. Panel (A): fibrous plaque with loss of typical three-layered structure characterized by a homogeneous region with high-intensity signal and an intimal thickness of ≥600 μm. “Spotty” calcium is indicated (white arrow). Panel (B): thin-cap fibroatheroma, lipid-rich plaque with a lipid arc >90° (signal-poor region with poorly defined borders) and a highly reflective thin fibrous cap (<65 μm). Panel (C): diffuse calcification, characterized by a region with low or heterogeneous intensity and sharply defined borders with an angular extension >90°. Panel (D): macrophages, recognized as confluent “bright spot” with posterior shadowing (white arrow). Panel (E): microvessel, recognized as small, round, low-intensity areas referred to as “small black holes” without contact with intimal layer (white arrows). Panel (F): cholesterol crystal, recognized as thin, linear, sharp-bordered regions with high intensity signal (white arrow). The asterisk is indicating the guide wire artifact. All images come from the authors’ personal archive, unless otherwise indicated.

Figure 5

Healed plaque. Layered structure with an “onion-like” appearance, featuring one or more layers with intense, heterogeneous signals layer of different optical densities (double-headed arrow) and a distinct demarcation from the underlying tissue. The asterisk is indicating the guide wire artifact. All images come from the authors’ personal archive, unless otherwise indicated.

Figure 6

Myocardial bridge. Clinical case of a 74-year-old man with rest angina who underwent coronary angiography. Panel (1): coronary angiography revealed a myocardial bridge of the mid-LAD with the classic “milking effect,” which manifests as systolic compression of the coronary artery with subsequent relaxation during diastole. To better evaluate the bridge and assess for concomitant coronary stenosis, an OCT pullback was performed (Panels (A–D)), showing a long myocardial bridge in the mid-to-distal LAD with the characteristic appearance of “moon-shaped” areas surrounding the adventitia with well-demarcated borders, and a heterogeneous, middle-backscattering signal (dashed curved line). All segments showed a normal three-layered vessel structure with no features of atherosclerosis. Panels (E,F): magnification of the segment most compressed by the bridge, demonstrating significant luminal narrowing with a minimal lumen area of 1.10 mm², shown in both cross-sectional and longitudinal views, with “bumps” and intimal folding caused by external systolic compression. Panel (G): 3D reconstruction of the same vessel segment showing bumps and depressions of the intima, generated by intimal folding during systole due to external compression. All images come from the authors’ personal archive, unless otherwise indicated.