Chronic coronary disease and resultant chest pain can often be treated with medical therapies to minimise symptoms and improve quality of life. However, the case presented by Volleberg et al. highlights the intrinsic complexities of assessing and treating coronary artery disease in those with intrusive symptoms and failed medical therapy.1 The case provides several insights that reaffirm the importance of using both intra-coronary physiology and imaging in the setting of coronary artery disease. A physiological assessment provides insight into where within the coronary vasculature symptoms may be emanating from. Physiology assessment also indicates whether the chest pain is because of a combination of epicardial coronary disease, and/or microcirculatory or endothelial dysfunction (identified by the adjunctive use of intra-coronary acetylcholine-provoking symptoms and clinical features consistent with coronary vasospasm). Whereas intra-coronary imaging, such as high-definition intravascular ultrasound (IVUS) or optical coherence tomography (OCT), provides unique lesion and vessel morphological information additive to generic angiographic assessment alone. The higher resolution imaging afforded by OCT specifically enables more detailed evaluation than IVUS at the endoluminal level and for the superficial plaque (e.g. in detecting cavity formation of a plaque rupture, thin-cap fibroatheroma and stent architecture). Moreover, OCT also provides higher fidelity identification of sub-optimal percutaneous coronary intervention (PCI) or complications from PCI, such as coronary dissections, tissue protrusions, stent under expansion and malapposition.2 OCT specifically can evaluate neointimal proliferation, neoatherosclerosis, uncovered struts, and persistent/late-acquired stent malapposition, which may be associated with adverse events.3–5
However – frequently – physiology and intra-coronary imaging are used as individual entities and not as the powerful combined tool they could be. In an era where PCI is readily performed in high volumes across the world, we should be seeking to improve and iterate upon current practice. While the basic principles of coronary intervention are derived – and will continue to be – from angiographic assessment of the epicardial arteries, the use of angiographic-only assessment to determine the aetiology of chest pain is sub-standard and should only be considered as a conduit to a more in-depth assessment of coronary pathophysiology by means of physiology and imaging guidance. This more detailed assessment and understanding provides personalisation of care, which is critical in clinical scenarios where co-existing entities are at play. The case highlights the presence of a functionally significant epicardial stenosis (fractional flow reserve [FFR] 0.75) secondary to stent protrusion from a previously implanted diagonal vessel stent and subsequent neo-intimal bridging, along with super-added epicardial vasospasm (identified by acetylcholine-induced vasospasm), in the presence of normal microvascular function (index of microvascular resistance [IMR] 19). This allowed PCI to be performed to alleviate the ischaemia-inducing epicardial lesion while also tailoring medical therapies for potential vasospasm-induced symptoms.
The use of more in-depth physiological indices other than those assessing the functional significance of an epicardial stenosis (FFR and instantaneous wave-free ratio) such as IMR and coronary flow reserve (CFR) remains limited in routine clinical practice. There is an increasing body of evidence highlighting the importance of physiological data in guiding both obstructive and non-obstructive coronary disease. However, further guidance by international guideline committees is required to provide operators with routinely usable cath lab algorithms.
Finally, the case emphasises the undoubted reality that epicardial coronary disease can – and frequently does – co-exist with coronary or microvascular vasospasm and/or microvascular dysfunction. Our collective focus going forward should be to broaden our invasive assessment beyond the epicardial vessel into concepts governing myocardial perfusion and abnormal endothelial function while dovetailing this with intra-coronary imaging to optimise treatment decisions.