Plaque Rupture: Mechanisms, Imaging, Outcome

Isabel, Meier^*
*Correspondence: Isabel, Meier, Division of Cardiovascular Sciences, Lakeshore University Hospital, Zurich, Switzerland, Email:

Introduction

Myocardial Infarction with Nonobstructive Coronary Arteries, or MINOCA, presents a significant clinical challenge. It's often caused by plaque rupture, even when there isn't obvious significant stenosis. Pinpointing this underlying pathophysiology is absolutely key for accurate diagnosis and delivering management tailored to the individual. We need to clearly differentiate MINOCA stemming from plaque rupture from its other causes to ensure proper patient care [1].

Plaque rupture itself is broadly recognized as the main trigger for the majority of acute coronary syndromes. To truly understand these events, we must examine the intricate mechanisms at play. Factors such as inflammation, the presence of a necrotic core within the plaque, and a thin fibrous cap are identified as crucial determinants that increase plaque vulnerability, ultimately leading to a thrombotic event [2].

Looking beyond the traditional risk factors for atherosclerosis, recent research highlights some less recognized but very important contributors. The perivascular adipose tissue and the perivascular nerves are emerging as significant players in the instability and eventual rupture of atherosclerotic plaques. This really opens up new avenues for how we understand plaque vulnerability and, importantly, how we might target these mechanisms therapeutically in the future [3].

The ability to precisely identify plaque rupture is an essential step in effectively managing acute coronary syndromes. Manual interpretations can be subjective, but now, a novel deep learning algorithm, specifically designed for optical coherence tomography (OCT) images, significantly improves the objective and accurate detection of plaque rupture. This advancement moves us away from reliance on subjective assessment towards more reliable diagnostic tools [4].

While plaque rupture is a common culprit, it is not the only one. Plaque erosion represents another major cause of acute coronary syndromes, and it has distinct mechanisms and visual characteristics. Grasping the pathophysiology, diagnostic methodsâ??often relying on OCTâ??and appropriate management strategies for plaque erosion empowers clinicians to effectively differentiate and treat these two critical forms of plaque instability [5].

Today, advanced imaging technologies are fundamentally changing our capacity to identify high-risk plaques and accurately forecast their potential to rupture. These modalities provide incredibly detailed insights into a plaque's morphology, its exact composition, and its overall vulnerability. Such crucial information guides the development of preventative strategies and ultimately helps improve outcomes for patients dealing with cardiovascular disease [6].

Plaque rupture consistently remains the predominant cause of acute coronary syndrome. It sets off a critical thrombotic cascade, leading directly to myocardial ischemia. To effectively prevent and treat these conditions, it is absolutely fundamental to understand the specific structural features and the unique biochemical environment that makes plaques prone to rupture in the first place [7].

The underlying pathophysiology of atherosclerotic plaque rupture is complex, involving a delicate interplay of several factors. A thin fibrous cap, a large, lipid-rich necrotic core, and localized inflammation all contribute significantly. These combined factors critically weaken the plaque's structure, making it highly susceptible to mechanical stress and eventual rupture, which then precipitates severe acute cardiovascular events [8].

When dealing with acute coronary syndromes, advanced intravascular imaging techniques are proving indispensable. Tools like Optical Coherence Tomography (OCT) and Intravascular Ultrasound (IVUS) are vital for both detecting high-risk plaques and directly identifying actual plaque rupture. These imaging methods guide targeted interventions, which are essential for improving patient prognosis and overall clinical outcomes [9].

Inflammatory cell infiltration plays an undeniably pivotal role in how atherosclerotic plaques progress and become unstable. This infiltration significantly contributes to the weakening of the plaque's fibrous cap and the expansion of its necrotic core. What this really means is that inflammation directly drives plaque vulnerability, ultimately making it far more likely to rupture [10].

Description

Plaque rupture emerges as the primary trigger for the vast majority of acute coronary syndromes (ACS), initiating a thrombotic cascade that directly leads to myocardial ischemia [2, 7]. This fundamental understanding of plaque rupture's role is crucial for developing effective preventative and treatment strategies in cardiovascular medicine [7]. It is also important to note that Myocardial Infarction with Nonobstructive Coronary Arteries (MINOCA) frequently originates from plaque rupture, even when there isn't significant stenosis. Mastering this specific pathophysiology is vital for accurate diagnosis and for tailoring management plans, especially when distinguishing it from other potential causes of MINOCA [1].

The intricate mechanisms behind atherosclerotic plaque rupture involve a complex interplay of several key structural and biological factors [2, 8]. Critical determinants of plaque vulnerability consistently include a thin fibrous cap, a large, lipid-rich necrotic core, and significant localized inflammation [2, 8]. Furthermore, inflammatory cell infiltration plays a pivotal role in accelerating the progression and destabilization of atherosclerotic plaques. This infiltration directly contributes to the weakening of the fibrous cap and the expansion of the necrotic core, substantially increasing the plaqueâ??s susceptibility to rupture [10]. Beyond these established elements, new research sheds light on previously underappreciated contributors: the perivascular adipose tissue and perivascular nerves. These tissues are now recognized as significant players in promoting atherosclerotic plaque instability and rupture, opening new avenues for understanding and potentially targeting plaque vulnerability for therapeutic benefit [3].

Precise identification of plaque rupture is an indispensable step for managing acute coronary syndromes effectively [4]. The landscape of detection is being transformed by advanced imaging technologies that significantly enhance our ability to pinpoint high-risk plaques and predict their rupture [6]. Intravascular imaging techniques, notably Optical Coherence Tomography (OCT) and Intravascular Ultrasound (IVUS), are considered indispensable tools for not only detecting high-risk plaques but also for directly identifying actual plaque rupture in patients presenting with ACS. These advanced modalities are critical for guiding targeted interventions aimed at improving patient prognosis [9]. An exciting innovation is the development of a novel deep learning algorithm based on OCT, which substantially improves the objective and accurate detection of plaque rupture, moving beyond the often subjective nature of manual interpretations [4]. Collectively, these advanced imaging techniques offer crucial insights into a plaque's morphology, its exact composition, and its overall vulnerability, thereby informing preventative strategies and ultimately improving patient outcomes in cardiovascular disease [6].

While plaque rupture is a prevalent cause of acute coronary syndromes, it is not the sole mechanism. Plaque erosion represents another significant etiology, possessing distinct mechanisms and characteristic appearances that set it apart from plaque rupture [5]. A comprehensive understanding of plaque erosion's pathophysiology, its diagnostic methodsâ??which often rely on OCTâ??and its appropriate management is paramount for clinicians. This differentiation is critical because it empowers healthcare providers to effectively treat these two unique forms of plaque instability, ensuring tailored and effective interventions for each patient [5].

Conclusion

Plaque rupture is the primary driver of most acute coronary syndromes and a frequent cause of Myocardial Infarction with Nonobstructive Coronary Arteries (MINOCA), even without significant stenosis. Understanding the precise pathophysiology of plaque rupture, characterized by a thin fibrous cap, a large necrotic core, and inflammation, is crucial for accurate diagnosis and effective management. Inflammatory cell infiltration further exacerbates the destabilization of these plaques. Moreover, recent research highlights the previously underappreciated roles of perivascular adipose tissue and nerves as emerging contributors to overall plaque vulnerability. Advanced imaging techniques like Optical Coherence Tomography (OCT) and Intravascular Ultrasound (IVUS) are now vital tools for detecting high-risk plaques and identifying actual rupture events. Novel deep learning algorithms, particularly those integrated with OCT, significantly enhance the objective and accurate detection of plaque rupture, moving diagnosticians beyond subjective manual interpretations. These sophisticated technologies offer invaluable insights into plaque morphology and composition, improving predictive capabilities and guiding preventative strategies effectively. While plaque rupture is the dominant mechanism, plaque erosion is another significant yet distinct cause of acute coronary syndromes, requiring specific diagnostic and management approaches. Differentiating accurately between plaque rupture and plaque erosion, often facilitated by OCT, is absolutely essential for delivering comprehensive and effective patient care. Ultimately, a thorough understanding of all mechanisms of plaque instability combined with advanced diagnostic tools are key to significantly improving cardiovascular patient outcomes.

Acknowledgement

None

Conflict of Interest

None

References

Mohammad RM, Ritu K, Michael CSY. "Myocardial Infarction With Nonobstructive Coronary Arteries (MINOCA): A Comprehensive Review of Pathophysiology, Diagnosis, and Management.".J Clin Med 12 (2023):4458.

Indexed at, Google Scholar, Crossref

Shengkai L, Ruihong D, Lin C. "Pathophysiology and Clinical Management of Plaque Rupture in Patients with Acute Coronary Syndrome.".Curr Probl Cardiol 48 (2023):101784.

Indexed at, Google Scholar, Crossref

Jun-Qing W, Bin X, Yu-Qing H. "New Insights into Atherosclerotic Plaque Rupture: Roles of Perivascular Adipose Tissue and Perivascular Nerve.".Oxid Med Cell Longev 2022 (2022):6430948.

Indexed at, Google Scholar, Crossref

Masafumi N, Atsushi T, Toshiya K. "Plaque rupture detection using a novel optical coherence tomography-based deep learning algorithm.".Eur Heart J 43 (2022):2470-2479.

Indexed at, Google Scholar, Crossref

Satoshi K, Tomoyo S, Akiko M. "Plaque Erosion as a Cause of Acute Coronary Syndromes: Mechanisms, Diagnosis, and Management.".J Clin Med 12 (2023):3861.

Indexed at, Google Scholar, Crossref

Hongming H, Bingbing A, Xiang L. "High-Risk Plaque Detection and Prediction of Plaque Rupture Using Advanced Imaging Modalities.".Front Cardiovasc Med 9 (2022):821935.

Indexed at, Google Scholar, Crossref

Rakesh KS, Arpan R, Sandeep S. "The role of plaque rupture in acute coronary syndrome.".Indian Heart J 73 (2021):65-72.

Indexed at, Google Scholar, Crossref

Atsushi K, Masataka Y, Akiko M. "Pathophysiology of Atherosclerotic Plaque Rupture.".J Clin Med 9 (2020):3372.

Indexed at, Google Scholar, Crossref

Fumihiko K, Masafumi N, Yasushi O. "Imaging for Detection of High-Risk Plaque and Plaque Rupture in Patients With Acute Coronary Syndromes.".JACC Cardiovasc Imaging 13 (2020):827-841.

Indexed at, Google Scholar, Crossref

Elena P, Ofer A, Ronen R. "Inflammatory Cell Infiltration as a Pathogenic Feature of Atherosclerotic Plaque Vulnerability and Rupture.".J Clin Med 12 (2023):5313.

Indexed at, Google Scholar, Crossref