Cardiology

	Joshua M. Stolker

For decades, cardiologists have used the diagnostic coronary angiogram to identify patients most likely to benefit from revascularization. However, in the modern era of multiple risk factors in an aging population, we rarely find a simple, straightforward culprit lesion amenable to PCI. Instead, we are commonly faced with diffuse atherosclerosis and multiple coronary lesions with varying degrees of stenosis, each of which may or may not be responsible for our patient’s ischemic syndrome. Furthermore, some of these lesions may represent “vulnerable plaques” at risk of precipitating a future coronary event, and the recent PROSPECT study demonstrated that some plaque characteristics related to future coronary events may be detected with imaging technologies in the cath lab.

Questions arise as to whether we should just stent all the tight stenoses or bypass all vessels with atherosclerosis; the answer to these questions is a resounding “no.” Clearly, there are patients and lesions that benefit from revascularization and others in which revascularization causes as many problems as it fixes. Although PCI outcomes have improved since the introduction of stents, we remain challenged by complications, including distal embolization, no-reflow, dissection, periprocedural MI, stent thrombosis and restenosis. Intraprocedural events are somewhat difficult to quantify, but periprocedural MI still occurs after 3% to 15% of PCI procedures, while repeat revascularization and short-term readmission rates remain around 10% to 15% despite drug-eluting stents and contemporary medical therapy. With more than 1.2 million PCI procedures performed annually in the United States, these complications contribute significantly to the burden of health care expenses in addition to the adverse effects on each individual patient.

With this background in mind, many investigators have worked to optimize PCI performance based on data obtained during the PCI procedure itself. Treatment of ischemic lesions and avoidance of PCI in nonischemic lesions using fractional flow reserve is one approach to properly select targets for revascularization. IVUS provides information about plaque anatomy and structure (and to a limited degree, plaque composition), and the larger stent lumens achieved by IVUS-guided PCI translate into lower rates of early stent malapposition and, potentially, future complications such as stent thrombosis and restenosis.

Advancement in Imaging

One of the most intriguing new technologies to help evaluate coronary atherosclerosis is near-infrared spectroscopy (NIRS), clinically available as LipiScan or TVC Imaging (InfraReDx). This catheter is used in a manner similar to rotational IVUS, with NIRS acquisition mounted adjacent to an IVUS transducer. NIRS provides real-time information regarding the lipid content of coronary plaques, as a computer algorithm demonstrates the presence (yellow) or absence (red) of significant lipid-core plaque (LCP), which has been previously validated with autopsy specimens of LCP. By identifying LCP during the planning of an interventional procedure, the NIRS data allow a new dimension of atherosclerosis imaging — chemical composition — to augment the physiologic and anatomic determinations derived from FFR and IVUS.

Although the data obtained from NIRS imaging are striking, the TVC catheter brings up an important question for the busy interventional cardiologist: Why do we need chemical composition data during PCI? There are several population-level and patient-specific reasons for considering NIRS imaging.

First, the presence of LCP potentially identifies a higher-risk subset of patients and lesions at higher risk of subsequent coronary events, since autopsy studies suggest that nearly 75% of sudden coronary events are caused by rupture of LCP. Second, PCI within LCP results in higher rates of periprocedural MI, with one multicenter study demonstrating periprocedural MI occurring in 50% of patients with a large, NIRS-identified LCP in the target lesion vs. only 4% of target lesions without LCP. Third, preliminary studies have suggested higher rates of stent-edge complications such as edge dissection or plaque disruption when stents land in LCP (potentially also contributing to stent thrombosis or restenosis during longer-term follow-up), and investigations into these relationships are ongoing.

Ultimately, the identification of risk factors for adverse events can only be useful if these risk factors may be modified. When considering the potential adverse events related to LCP identified prior to PCI, several options may be considered. The mere presence of LCP may trigger intensified secondary prevention therapy for atherosclerosis, or perhaps closer patient follow-up after PCI may be recommended by some clinicians after these vulnerable plaques or vulnerable patients have been identified.

Regarding periprocedural MI, some interventionalists may choose to pre-emptively treat vessels with LCP using vasodilators or other therapies to avoid no-reflow, or perhaps embolic protection devices to minimize damage from distal embolization (currently being evaluated in the CANARY trial). Still, others may alter the stent location or length to help avoid landing the stent edges in LCP, thus redefining the frequently taught rule of “stenting normal to normal” to cover all of the LCP in a given coronary segment (as opposed to only landing stent edges in areas free of stenosis by angiography).

An Illustrative Case

Although the role of NIRS imaging still requires additional clinical outcome studies, we look forward to better defining its role in daily PCI practice as an additional imaging modality to complement the physiologic and structural data acquired from FFR and IVUS.

As an example, we recently brought a patient with anterior STEMI to our hospital’s cath lab and found no obstructive stenosis in the main body of the left anterior descending (LAD) artery. However, mild irregularities were noted in the mid-vessel and a hazy “cut-off” was noted in the apical LAD segment, suggestive of thrombus or another distal embolization event.

We then asked ourselves what happened and whether we should cover the luminal irregularities with a stent. NIRS imaging revealed a small LCP well proximal to the moderately stenotic region in the mid-LAD, and complementary IVUS imaging (on the same catheter) revealed no physical evidence of heterogeneous or ruptured plaque.

While lipid cores are likely thrombogenic and are associated with coronary events, the absence of high-risk findings by both IVUS and NIRS at the site of stenosis led us to treat this patient medically without stent placement, although admittedly we have little data to help guide our clinical decision-making for such patients. We still intensified the patient’s statin dose and treated the patient with dual antiplatelet therapy for 12 months after the event.

Conclusion

This illustrative case, in conjunction with the clinical trial data described above, will hopefully contribute to the continued refinement of PCI techniques with new technologies such as NIRS imaging. Ideally, proper application of these devices and procedural approaches will continue to improve the safety profile of our increasingly complex patient population undergoing PCI.

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For more information:

Joshua M. Stolker, MD, is an associate professor of medicine at Saint Louis University.

Disclosure:

Dr. Stolker reports receiving minor compensation from InfraReDx for travel costs to present at an interventional cardiology meeting.