Acute coronary syndromes without coronary plaque rupture

Abstract

The latest advances in plaque imaging have provided clinicians with opportunities to treat acute coronary syndrome (ACS) and provide individualized treatment recommendations based not only on clinical manifestations, angiographic characteristics, and biomarker data, but also on the findings of plaque morphology. Although a substantial proportion of ACS events originate from plaques with an intact fibrous cap (IFC), clinicians predominantly equate ACS with plaque rupture arising from thin-cap fibroatheromas. In this Review, we discuss the recent advances in our understanding of plaque morphology in ACS with IFC, reviewing contemporary data from intravascular imaging. We also explore whether use of such imaging might provide a roadmap for more effective management of patients with ACS.

A Case of Vasospastic Angina Involving Erosion and Thrombus within the Spastic Segment Detected by Coronary Angioscopy

“…Thrombus formation due to coronary spasms has been reported as one of the mechanisms responsible for ACS without plaque rupture [2][3][4], with the findings of the present case supporting the presence of coronary spasm-induced thrombus formation.…”

“…In cases with coronary plaque rupture, coronary spasm may cause plaque rupture mediated by the external force of the coronary spasm itself; and this relationship was confirmed in an autopsy case report [7]. On the other hand, coronary erosions without plaque rupture are thought to contribute to coronary spasminduced thrombus formation [2][3][4]. Using CAS, Etuda et al [5] reported that intracoronary abnormalities, such as intracoronary hemorrhage, intimal flap, thrombus, or ulcers, were present in 40% of cases with variant angina, which is thought to be a type of angina with a high coronary spasm activity.…”

“…Further, thrombus formation is most commonly caused by plaque rupture [1]. Conversely, ACS without plaque rupture has been reported [2], and coronary spasm has been considered one of the causes of ACS without plaque rupture [2][3][4]. However, a little is known regarding the relationship between coronary spasm and thrombus formation [5,6].…”

The CANTOS Trial

“…Unfortunately, our current experimental models in hypercholesterolemic mice fail to emulate many of the key features of plaque erosion (i.e., endothelial desquamation, neutrophil recruitment, few macrophages, and small necrotic core). 4 However, a recent study found that a combination of vascular injury followed by flow disruption recapitulated many of the characteristics of eroded plaques, a strategy that may be a valuable tool to probe anti-inflammatory therapies moving forward. 5 It is important to note that even if there were a trend toward reduced relative risk of plaque erosion in these patients, plaque rupture of thin-capped fibroatheromas (TCFAs) – also known as “vulnerable plaques” – remains the primary modality for atherosclerosis complications and still requires extensive research focus.…”

“…Estimates on the prevalence of plaque erosion and rupture vary, but even aggressive estimates suggest that rupture remains the primary driver of plaque failure. Indeed, a ruptured fibrous cap is found in ~2/3 of post-mortem samples from patients dying of an acute coronary syndrome 4 and intravascular imaging has shown that plaque rupture accounts for ~71% and 43% of ST and non-STEMI, respectively. 3 Although the PROSPECT study showed that only 5% of TCFAs resulted in a clinical event in 3.4 years, TCFA plaque morphology was the only independent risk factor that was predictive for a future event.…”