Coronary functional assessment in non-obstructive coronary artery disease: Present situation and future direction

Abstract

Non-obstructive coronary artery disease (CAD), which is defined as coronary stenosis <50%, has been increasingly recognized as an emerging entity in clinical practice. Vasomotion abnormality and coronary microvascular dysfunction are two major mechanisms contributing to the occur of angina with non-obstructive CAD. Although routine coronary functional assessment is limited due to several disadvantages, functional evaluation can help to understand the pathophysiological mechanism and/or to exclude specific etiologies. In this review, we summarized the potential mechanisms involved in ischemia with non-obstructive coronary arteries (INOCA) and myocardial infarction with non-obstructive coronary arteries (MINOCA), the two major form of non-obstructive CAD. Additionally, we reviewed currently available functional assessment indices and their use in non-obstructive CAD. Furthermore, we speculated that novel technique combined anatomic and physiologic parameters might provide more individualized therapeutic choice for patients with non-obstructive CAD.

Pathophysiology and Outcomes of Endothelium Function in Coronary Microvascular Diseases: A Systematic Review of Randomized Controlled Trials and Multicenter Study

“…Patients who experienced this clinical condition are termed INOCA, a syndrome reflecting the well-specified role of CMD which is sustained by a different aetiology with symptoms and signs of myocardial ischaemia [ 37 , 38 , 39 ]. Several recently published studies using multimodal protocols to comprehensively study coronary physiology have revealed that a marked percentage of patients in whom INOCA occurs differ in the underlying form of the coronary microvascular disease [ 23 , 40 , 41 , 127 ].…”

“…To the best of our knowledge, CMD is a pathophysiological entity, known as ischaemia and no obstructive CAD (INOCA), in which coexist ischaemia and no obstructive CAD are linked, the disease results in chest pain that develops over time, leading to further progression and is characterized by the presence or absence of coronary macrovascular disorder responsible to evoke an epicardial obstructive CAD [ 37 , 38 , 39 ]. Despite patients with INOCA from CMD experiencing steadily high prevalence and important prognostic course and consideration in both genders, it occurs, especially in women [ 20 , 21 , 22 , 23 , 24 , 25 , 26 ].…”

Diffuse non-obstructive coronary artery disease: two clinical faces of the same disease—a case report

“…It is important to acknowledge the weakness of coronary angiography to assess lumen geometry, plaque components, and presence of thrombus. 6 Indeed, plaque rupture has been identified using intravascular ultrasound in 40% of the MINOCA cases. 7 Our case confirms that OCT can definitely identify the morphologic hallmark of STEMI including plaque rupture and thrombus.…”

Chemokine Fractalkine and Non-Obstructive Coronary Artery Disease—Is There a Link?

“…Interestingly, inflammatory response is not limited to the ruptured plaque and the adjacent myocardium, but may affect the entire heart, leading to severe consequences, such as cardiomyocyte death. Moreover, spontaneous thrombolysis, a recognized factor in NO-CAD, may be responsible for ischemia/reperfusion injury, resulting in: an increase in ROS, exacerbation of inflammation and even cell death via mechanisms such as necrosis, apoptosis, or ferroptosis [62]. A recent clinical trial confirmed this thesis, wherein the concentration of high sensitivity C-reactive protein (hsCRP), an inflammatory marker, emerged as a stronger predictor of future cardiovascular events and mortality than cholesterol concentration [63].…”