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
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
The Lipiscan/TVC catheter looks and functions like any standard rotational IVUS
system, but the catheter tip includes near-infrared spectroscopy adjacent to
the IVUS transducer.
Images: Joshua M. Stolker, MD;
reprinted with permission.
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.
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
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For more information:
Joshua M. Stolker, MD, is an associate professor
of medicine at Saint Louis University.
Dr. Stolker reports receiving minor
compensation from InfraReDx for travel costs to present at an interventional