Incorporating Fractional Flow Reserve and Instantaneous Wave-Free Ratio in the Management of Intermediate Coronary Lesions

Richard Powell^*
*Correspondence: Richard Powell, Department of Cardiology, University of Chicago, United States, Email:

Introduction

By re-establishing blood flow through stent placement or balloon angioplasty, PCI provides immediate relief from symptoms such as angina and reduces the risk of acute events like myocardial infarction (MI).  Percutaneous coronary intervention (PCI) is a widely used procedure for treating coronary artery disease (CAD), particularly for patients with obstructive lesions in the coronary arteries. However, despite the significant short-term benefits of PCI, patients often face long-term challenges, including restenosis, stent thrombosis, and adverse cardiovascular events. A growing body of evidence suggests that endothelial dysfunction, a condition where the endothelium—the inner lining of blood vessels—fails to perform its normal functions, plays a critical role in determining the long-term outcomes following PCI[1].

The ability to assess endothelial function post-PCI may offer valuable insights into the patient's risk for these long-term complications and help guide post-procedural management. This paper explores the mechanisms underlying endothelial dysfunction following PCI, its impact on long-term cardiovascular outcomes, and its potential as a predictive marker for adverse events in patients undergoing PCI. Endothelial function is an essential component of vascular health and plays a pivotal role in regulating vascular tone, blood flow, and platelet aggregation. After PCI, the integrity of the endothelial layer can be compromised due to mechanical injury from balloon angioplasty or stent implantation. This damage can lead to inflammation, impaired nitric oxide production, and altered vascular reactivity, all of which contribute to the development of restenosis, thrombosis, and the progression of atherosclerosis [2].

Description

The endothelium plays a crucial role in maintaining vascular homeostasis by regulating the balance between vasodilation and vasoconstriction, modulating platelet function, and controlling the inflammatory response. Endothelial dysfunction after PCI is a multifactorial process that involves both mechanical injury and biochemical changes. The physical trauma caused by balloon angioplasty and stent implantation leads to endothelial denudation, which disrupts normal endothelial function and activates the underlying smooth muscle cells. This can cause an imbalance in vasodilatory and vasoconstrictor substances, most notably nitric oxide (NO), which plays a central role in maintaining endothelial health. In healthy vessels, NO induces vasodilation and inhibits platelet aggregation, but in the setting of endothelial dysfunction, NO bioavailability is reduced, contributing to vasoconstriction, thrombosis, and inflammation. This dysfunction is further exacerbated by the stent implantation process, which can induce a pro-inflammatory state, leading to neointimal hyperplasia—the growth of smooth muscle cells and extracellular matrix—ultimately contributing to restenosis and late stent thrombosis [3].

Endothelial dysfunction post-PCI can have significant consequences for long-term patient outcomes. Impaired endothelial function increases the risk of in-stent restenosis (ISR), a process by which the treated artery becomes re-occluded due to neointimal hyperplasia. Restenosis is a well-known complication after PCI, and its prevalence is higher in patients with poor endothelial recovery. Endothelial dysfunction also predisposes patients to stent thrombosis, a potentially life-threatening complication in which blood clots form inside the stent, blocking blood flow and potentially causing acute myocardial infarction. This risk is especially high in the early period following PCI and can be influenced by factors such as inadequate antiplatelet therapy, inflammatory responses, and impaired endothelial healing. Additionally, endothelial dysfunction contributes to the progression of atherosclerosis and increases the risk of recurrent cardiovascular events, including stroke and heart failure. As a result, endothelial dysfunction post-PCI is an important predictor of long-term cardiovascular outcomes, and strategies aimed at improving endothelial function, such as the use of statins, antioxidants, and targeted therapies, may help mitigate these risks  [4].

Following PCI, the assessment of endothelial function has become increasingly important for predicting long-term outcomes. One commonly used method to evaluate endothelial function is flow-mediated dilation (FMD), which assesses the ability of blood vessels to dilate in response to increased blood flow. Reduced FMD is an indicator of endothelial dysfunction and has been associated with an increased risk of restenosis, major adverse cardiovascular events (MACE), and cardiovascular mortality in PCI patients. Other non-invasive methods, such as laser Doppler flowmetry and arterial stiffness measurement, also provide insights into endothelial health by evaluating vascular reactivity and arterial compliance. Moreover, circulating biomarkers such as endothelial progenitor cells (EPCs), soluble vascular cell adhesion molecule-1 (sVCAM-1), and C-reactive protein (CRP) have been implicated in endothelial dysfunction and inflammation post-PCI. These markers can be used in conjunction with functional tests to provide a more comprehensive assessment of vascular health and predict the likelihood of adverse events such as restenosis, thrombosis, and recurrent ischemic events [5].

Conclusion

This dysfunction predisposes patients to a variety of complications, including restenosis, stent thrombosis, and the progression of atherosclerosis, all of which can result in adverse cardiovascular events and poor long-term prognosis. Assessing endothelial function post-PCI through non-invasive methods such as flow-mediated dilation (FMD), along with circulating biomarkers, provides valuable prognostic information that can guide clinical management and inform decisions regarding secondary prevention. Endothelial dysfunction after percutaneous coronary intervention (PCI) plays a pivotal role in determining long-term outcomes in patients with coronary artery disease. The mechanical injury caused by PCI procedures, along with biochemical changes that impair nitric oxide production and promote inflammation, leads to the disruption of normal endothelial function.

Therefore, targeting endothelial dysfunction with pharmacologic interventions, lifestyle modifications, and close follow-up care is essential for improving long-term outcomes. The use of statins, angiotensin-converting enzyme inhibitors (ACE inhibitors), and antioxidants may help restore endothelial health and reduce the risk of adverse events. As our understanding of endothelial dysfunction continues to evolve, it will become increasingly important to incorporate endothelial assessments into routine clinical practice to identify high-risk patients and personalize treatment strategies. Ultimately, improving endothelial function post-PCI holds the promise of enhancing patient outcomes and reducing the burden of cardiovascular disease. Endothelial function is not only a reflection of vascular health but also a predictive marker for future cardiovascular risk. Patients with impaired endothelial function after PCI are at higher risk for restenosis, thrombosis, and recurrent ischemic events.