Introduction
Despite remarkable advances in the procedural and clinical outcomes of percutaneous revascularization, chronically occluded coronary arteries represent persistent technical challenges and unresolved clinical dilemmas in interventional cardiology. Although a coronary chronic total occlusion (CTO) is identified in approximately one in every three to five diagnostic cardiac catheterizations, revascularization is attempted in fewer than 10% of instances and overall accounts for less than 8% of all percutaneous coronary interventions (PCI) ( Figure 9-1 ). Such a disparity between their frequency and treatment not only underscores the technical and procedural frustrations associated with these complex lesions but also the clinical uncertainties regarding which patients may benefit from CTO revascularization. Chronic occlusions remain the single most important reason not to attempt PCI in favor of bypass surgery or medical treatment. As an example, in the multivessel PCI versus coronary artery bypass graft (CABG) surgery SYNTAX (SYNergy Between PCI with TAXUS and Cardiac Surgery) study, the prevalence of CTO in the randomized arm was only 10%, yet it was 40% in the CABG registry arm.
Unlike catheter-based revascularization of nonocclusive coronary disease, much of our understanding regarding total occlusions has been further limited by relatively few studies describing the procedural and clinical outcomes among patients undergoing attempted revascularization. Moreover, these investigations are limited by their retrospective, observational design, variability in operator skills, inconsistencies regarding the definition of total occlusions, and bias regarding patient selection. Since the duration of an occluded artery is an independent predictor of procedural outcome, an inability to date these lesions, in addition to their heterogeneous composition, have restricted the evaluation of novel revascularization technologies. Until recently, many of the technologies promoted for the treatment of total occlusions were simply modeled after devices applied to nonocclusive disease, erroneously assuming that the pathophysiology between these lesion subsets was similar.
Anatomic Considerations
The definition of a coronary CTO is reflective of the degree of lumen stenosis, the extent of antegrade blood flow, and the age of the occlusion. In general, a CTO is defined as a high-grade coronary occlusion with reduced antegrade flow (Thrombolysis in Myocardial Infarction [TIMI] grade 0 or 1 flow) with estimated duration of at least 3 months. Without serial angiograms, however, the duration of coronary occlusion is difficult to specify with any certainty and must be estimated from available clinical information related to the timing of the event that caused the occlusion, for example, clinical history of myocardial infarction or a sudden change in angina pattern with electrocardiographic changes consistent with the location of the occlusion. In addition, despite presenting with such advanced disease, less than half of the patients demonstrate a clinical history or electrocardiogram suggestive of prior myocardial infarction. In most patients, the age of the CTO cannot be determined with confidence. Furthermore, the temporal criterion used to define a CTO has varied among registries, trials, and databases, ranging from >2 weeks to >3 months, which in part explains interstudy differences in lesion characteristics and procedural success.
Histopathology of CTOs
Chronic coronary occlusions most often arise from thrombotic occlusion, followed by thrombus organization and tissue aging. Particularly relevant to PCI strategies for CTO recanalization is the histological finding that approximately half of all CTOs are <99% stenotic when observed by histopathology, despite the angiographic appearance of total occlusion with TIMI grade 0 antegrade flow. Moreover, little to no relationship exists between the severity of the histopathological lumen stenosis and either plaque composition or lesion age.
The typical atherosclerotic plaque of a CTO consists of intracellular and extracellular lipids, smooth muscle cells, extracellular matrix, and calcium. Collagens are the major structural components of the extracellular matrix, with predominance of types I and III (and minor amounts of IV, V, and VI) in the fibrous stroma of atherosclerotic plaques. The concentration of collagen-rich fibrous tissue is particularly dense at the proximal and distal ends of the lesion, contributing to a column-like lesion of calcified, resistant fibrous tissue surrounding a softer core of organized thrombus and lipids.
Key histopathological attributes of CTOs include calcification extent, inflammation, and neovascularization. The typical CTO may be classified as “soft,” “hard,” or a mixture of both. Soft plaque consists of cholesterol-laden cells and foam cells with loose fibrous tissue and neovascular channels and is more frequent in younger occlusions (<1 year old). Soft plaque is more likely to allow wire passage either directly through tissue planes or via neovascular channels into the distal lumen. Conversely, hard plaque is characterized by dense fibrous tissue and often contains large fibrocalcific regions without neovascular channels. During percutaneous revascularization, these occlusions are thus more likely to deflect coronary guidewires into the subintimal area, thereby creating dissection planes. Hard plaque is more prevalent with increasing CTO age (>1 year old). Of note, however, areas of calcification frequently occur even in CTOs <3 months of age, although the extent and severity of calcification increase with occlusion duration. This age-related increase in calcium and collagen content of CTOs in part underlies the progressive difficulty during PCI in crossing older occlusions.
Inflammatory cell infiltrates in CTOs consist of macrophages, foam cells, and lymphocytes. Inflammation may exist in the intima, media, and adventitia of CTOs, although it is most predominant in the intima. As fibrotic CTO lesions age, the vessels typically undergo negative remodeling with a decreasing dimension of the external elastic membrane, a phenomenon due to adventitial vascular responses. Less commonly, plaque hemorrhage and inflammation may result in positive remodeling. Notably, although negative remodeling may be initially observed following successful CTO recanalization, serial angiographic surveillance may reveal temporal recovery of normal vessel dimensions.
Another observation common to CTOs is the presence of extensive neovascularization that occurs throughout the extent of the vessel wall. Capillary density and angiogenesis increase with increasing occlusion age. In CTOs <1 year old, new capillary formation is greatest in the adventitia. In CTOs of more advanced duration, the number and size of capillaries in the intima have increased to a similar or greater extent than those present in the adventitia. Relatively large (>250 µm) capillaries are frequently present throughout the CTO vessel wall, even in young occlusions, suggesting that angiogenesis within the CTO is an early event. Frequent co-localization of inflammation and neovascularization within the intimal plaque and adventitia suggests that these findings are closely related, although it is unclear whether inflammation is a cause or an effect of neovascularization in CTOs.
A rich neovasculature network often traverses the CTO vessel wall, arising from the adventitial vasa vasorum across the media and into the lesion intima, suggesting that vessel in-growth proceeds from the adventitia in younger lesions. An autopsy study of subtotal atherosclerotic lesions demonstrated that new intimal vessels originate in the adventitial vasa vasorum of lesions with >70% stenosis but rarely from the coronary lumen. Such microchannels, which can recanalize the distal lumen, may result from thrombus-derived angiogenic stimuli and are suggested on an angiogram of an old CTO without a well-defined proximal cap or stump. In this regard, the distinction should be made between ipsilateral epicardial angiographic “bridging” collateral vessels and true microvascular collaterals. Neochannels may also develop with organization of thrombus, connecting the proximal and distal lumens; this is suggested by a tapered CTO proximal cap on an angiogram. Such channels may serve as a route for a guidewire to reach the distal vessel and hence may have therapeutic value.
Collaterals and CTOs
Collaterals preserve myocardial function and avoid cardiac myocyte death in the distribution of the occluded artery. The most widely used angiographic grading system for collaterals described by Rentrop does not actually characterize the collaterals themselves but rather their contribution to filling the occluded arterial segment. Recently, a grading of collateral connections was introduced specifically for CTOs that may assist in interventional decision making regarding retrograde strategies ( Figure 9-2 ).
Importantly, a common misperception is the unawareness that even well-developed collaterals do not prevent ischemia during exercise. A total occlusion that is well collateralized is functionally equivalent to a 90% stenosis in a non-CTO vessel. When FFR is performed following initial CTO recanalization, the FFR value is persistently ischemic (Pd/Pa < 0.80), and resting ischemia was present in 78% of instances. Ischemia was demonstrated in all CTO cases independent of collateral development or presence of severe regional left ventricular dysfunction. The myocardium remains viable but produces ischemia during periods of increased oxygen demand, and thus patients with these lesions are likely to have exertional angina. Although the risk of a spontaneous acute coronary syndrome due to a chronically occluded lesion is unlikely, infarction in distribution of the CTO may result during instances of increased demand or if the arteries supplying the collaterals become compromised in any way.
Target Vessel
Very little data exist regarding the potential for differential benefit of CTO recanalization depending on the target vessel (e.g., left anterior descending [LAD], left circumflex [LCX], or right coronary artery [RCA]). In a large, single-center registry, PCI for CTO of the LAD, but not LCX or RCA, was associated with improved long-term survival. There were 2608 patients included, and the LAD was the target vessel in 936 (36%), the LCX in 682 (26%), and the RCA in 990 (38%) patients. The angiographic success rates were similar across coronary artery distributions (LAD, 77%; LCX, 76%; RCA, 72%). Procedural success compared with failure was associated with improved 5-year survival in the LAD (88.9% vs. 80.2%, p < 0.001) group but not in the LCX (86.1% vs. 82.1%, p = 0.21) and RCA (87.7% vs. 84.9%, p = 0.23) groups. In multivariable analysis, CTO PCI success in the LAD group remained associated with decreased mortality risk (hazard ratio [HR] 0.61; 95% confidence interval [CI], 0.42 to 0.89). In addition to other clinical characteristics, this information may assist in selecting patients for attempted CTO PCI.
Indications
In general, when the CTO represents the only significant lesion in the coronary tree, PCI is warranted when the following three conditions are all present: (1) the occluded vessel is responsible for the patient’s symptoms of chest pain or heart failure, or the vessel is responsible for a reduced ventricular function (PCI may also be considered in selected cases of silent ischemia if a large myocardial territory at risk is demonstrable); (2) the myocardial territory supplanted by the occluded artery is viable; and (3) the likelihood of success is moderate to high (>60%), with an anticipated major complication rate of death <1% and myocardial infarction <5%. If the PCI attempt is unsuccessful, further management will depend on the symptomatic status and the extent of jeopardized ischemic myocardium. Repeated PCI following initial failure (typically with an allowance of several weeks for vessel healing in the case of dissection) or surgical revascularization may be warranted if a large myocardial territory is ischemic or the patient is very symptomatic. Alternatively, conservative therapy may be appropriate if repeated PCI is unlikely to be successful and the patient’s symptoms can be controlled with antianginal medications.
Despite the intuitive benefit of an open artery, the rationale for CTO PCI is mistakenly challenged by a singular trial demonstrating no clinical benefit with revascularization of subacute total occlusions following recent myocardial infarction. Differences in the indication and pathophysiology notwithstanding, it is noteworthy that unlike the clinical characteristics of patients included in the Occluded Artery Trial (OAT), CTO patients selected for attempted PCI often represent a very different patient population characterized by features systematically excluded from the OAT trial, including symptoms refractory to medical therapy, abnormal left ventricular function, multivessel coronary disease, and/or extensive ischemia demonstrated by noninvasive testing. Performance of CTO revascularization based on these indications is also in accord with recent multidisciplinary committee recommendations regarding appropriateness of PCI in specific patient and lesion subsets.
Recently, consensus recommendations regarding appropriateness of PCI in general have highlighted disparate conclusions related to percutaneous revascularization depending on the stenosis severity. The 2011 American College of Cardiology/American Heart Association PCI guidelines endorse CTO PCI with a class IIA recommendation, citing that PCI of a CTO in patients with appropriate clinical indications and suitable anatomy is reasonable when performed by operators with appropriate expertise. Similarly, the 2010 European Society of Cardiology states that similar to nonchronically occluded vessels, revascularization of a CTO may be considered in the presence of angina or ischemia related to the corresponding territory. In contrast, the 2012 statement on Appropriate Use Criteria for Coronary Revascularization provided a lower level recommendation for CTO PCI compared with patients having one- or two-vessel coronary disease and without a CTO in 10 of 36 clinical scenarios assessed. In particular, for both symptomatic and asymptomatic patients, several instances exist for which PCI may be considered “appropriate” or “uncertain” for a non-CTO lesion but downgraded for the same respective indications to “uncertain” or “inappropriate” for a CTO lesion. Although it is likely that such endorsements are based on both evidence and opinion, the reasons for differing recommendations are not provided. Further, establishing unconditional treatment recommendations regarding CTO revascularization for any individual patient is especially challenging given that the risk/benefit balance may vary considerably depending on the symptoms, the extent of ischemia or left ventricular dysfunction, the presence of multivessel disease, or additional comorbidities that increase procedural risk (e.g., chronic kidney disease). Therefore, for consideration of CTO PCI, the document should be considered a guideline for treatment rather than an absolute standard, and the presence of a CTO should not have an impact on revascularization decision making with the caveat that appropriate expertise in CTO PCI is locally available.
Angina and Quality of Life
Stress-induced ischemia can typically be elicited in patients with a CTO, especially in the absence of a history of prior myocardial infarction and irrespective of collateral development. The temporal changes in contractility and hyperemic and resting myocardial blood flow in dependent and remote myocardium after PCI of CTOs have been further characterized using cardiovascular magnetic resonance imaging. Three groups were prospectively studied: 17 patients scheduled for CTO PCI, 17 scheduled for PCI of a stenosed but nonoccluded coronary artery (non-CTO), and 6 patients with CTO who were not scheduled for revascularization. Contractility in treated segments was improved at 24 hours and 6 months after CTO PCI but only at 6 months after non-CTO PCI. In both intervention groups, treated segments no longer had reduced myocardial blood flow or contractility compared with remote segments ( Figure 9-3A ). In patients with nonrevascularized CTO segments and treated with medical therapy alone, myocardial blood flow and wall thickening did not improve at follow-up ( Figure 9-3B ).
The majority of patients undergoing CTO PCI have stable or progressive angina, whereas many asymptomatic patients with CTO and minimal or no ischemia by noninvasive imaging are managed medically. In several large databases, only 10% to 15% of patients undergoing angioplasty for CTO were asymptomatic. Conversely, the proportion of patients presenting with unstable angina due to a CTO is also fairly low and of similar prevalence to asymptomatic patients. Patients with medically refractory angina or a moderate to large ischemic burden deserve consideration for percutaneous revascularization, particularly if the symptoms or territory are enough to warrant surgical revascularization as an option. The presence of moderate or severe ischemia is associated with worse clinical outcomes in patients with CTO. In a study of 301 patients who underwent myocardial perfusion imaging before and after CTO PCI, a baseline ischemic burden of >12.5% identified patients most likely to have a significant decrease in ischemic burden post-CTO PCI, indicating that the highest benefit of CTO revascularization is likely to be achieved in patients with a significant baseline ischemic burden.
In a metaanalysis of six observational studies evaluating angina following CTO PCI, patients undergoing successful revascularization experienced a significant reduction in recurrent angina during a 6-year follow-up compared with patients undergoing unsuccessful PCI (odds ratio [OR], 0.45; 95% CI, 0.30 to 0.67). In the Flowcardia’s Approach to Chronic Total Occlusion Recanalization (FACTOR) trial, among patients referred for the CTO PCI (which per protocol required symptoms and/or abnormal stress testing), two thirds of the patients had angina, and one third had no angina. Presence of angina was objectively assessed using the Seattle Angina Questionnaire (SAQ) and defined as angina frequency scores of less than 90. Among those with angina at baseline, the impairment in angina-associated quality of life was significant, and CTO PCI was associated with significant improvement in self-reported angina measures.
The first assessment of the most common angina equivalent (dyspnea) among patients with CTO was reported by Safley and colleagues. In this study, 98 patients with single-vessel CTO were matched with 687 patients undergoing non-CTO PCI. Baseline and post-PCI SAQ and Rose dyspnea scale scores were compared. Dyspnea was present among both CTO and non-CTO patients as reflected in baseline Rose dyspnea scale scores of 1.9 versus 1.7, p = 0.21 (higher scores indicating more dyspnea), in the CTO and non-CTO groups, respectively. Percutaneous CTO revascularization was statistically noninferior to non-CTO PCI in alleviating both dyspnea and angina (p < 0.02 for all domains), suggesting that the clinical benefit was of at least a similar magnitude for both CTO and non-CTO PCI.
Improvement in Left Ventricular Dysfunction
Regional left ventricular systolic function has been demonstrated to improve after CTO PCI. The degree of improvement is especially evident in patients with decreased left ventricular systolic function at baseline, while no change in ejection fraction can be expected when the baseline function is normal. Improvement in left ventricular function is not predicted by a history of myocardial infarction or the duration of occlusion. Further, recovery of impaired ventricular function after revascularization of a CTO is not directly related to the quality of collateral function, as collateral development does not appear to require the presence of viable myocardium. Left ventricular function improvement is dependent on maintenance of CTO target vessel patency and on viability of the perfused myocardial territory.
Reduction in Arrhythmic Events
Although no study has documented a reduction in ventricular arrhythmic events with CTO PCI, the contribution of CTOs to either ischemia-driven or scar-related arrhythmic events has been recently characterized. In the Ventricular Arrhythmia Chronic Total Occlusion (VACTO) study, among 162 patients with ischemic cardiomyopathy who received an implantable cardioverter defibrillator, 44% had at least one CTO. During a median follow-up of 26 months, the presence of CTO was associated with higher ventricular arrhythmia and mortality rates compared with patients without a CTO. In particular, the occurrence of appropriate defibrillator therapy was significantly more common in comparison with patients having multivessel disease but without a CTO.
Improved Tolerance of Ischemic Events
A consistent finding among patients presenting with high-risk acute coronary syndromes has been the association of a CTO with adverse short- and late-term outcome. Potential mechanisms include preexisting left ventricular function, poor tolerance of ischemia secondary to limited collateral supply, and a “double jeopardy” phenomenon associated with simultaneous acute and chronic coronary occlusion in separate coronary artery territories.
Among 3277 patients with ST-segment elevation acute myocardial infarction treated with primary PCI, the presence of a CTO was a stronger and independent predictor for 30-day mortality (HR 3.6; 95% CI, 2.6 to 4.7; p < 0.01) than the presence of multivessel disease without a CTO (HR 1.6; 95% CI, 1.2 to 2.2; p = 0.01) ( Figure 9-4 ). Only presentation of shock was a greater predictor of mortality than presence of a CTO. In a landmark analysis that included surviving patients from 30 days to 5 years, the presence of a CTO remained an independent predictor of mortality that exceeded the risk associated with single-vessel or multivessel disease without CTO ( Figure 9-4 ).
Similarly, in 3283 patients participating in the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-AMI) study, a CTO in a non–infarct-related artery was identified in 8.6% of patients. As with the prior study, CTO in a non–infarct-related artery was an independent predictor of both 30-day mortality (HR 2.88; 95% CI, 1.41 to 5.88, p = 0.004) and day 30 to 3-year mortality (HR 1.98; 95% CI, 1.19 to 3.29; p = 0.009). In comparison, multivessel disease without a CTO was associated with higher 30-day mortality (HR 2.20; 95% CI, 1.00 to 3.06; p = 0.049) but not late (day 30 to 3 years) mortality. Finally, the Thrombus Aspiration in Percutaneous Coronary Intervention in Acute Myocardial Infarction (TAPAS) trial also reported a higher mortality risk among CTO patients presenting with acute myocardial infarction (8% of 1071 total); over a median follow-up period of 2.1 years, mortality was twofold greater for CTO compared with non-CTO patients (HR 2.41; 95% CI, 1.26 to 4.61; p = 0.008).
Despite the consistent association of CTOs with higher risk following presentation with an acute coronary syndrome, limited evidence exists to support a routine strategy of attempted CTO revascularization following myocardial infarction related to a non-CTO target vessel. One small retrospective study demonstrated improved outcomes for patients who underwent successful versus failed CTO PCI after primary PCI for ST-segment elevation acute myocardial infarction. The ongoing EXPLORE (Evaluating Xience V and Left Ventricular Function in Percutaneous Coronary Intervention on Occlusions After ST-Elevation Myocardial Infarction) trial is examining whether PCI of a CTO in a non–infarct-related artery within 1 week after primary PCI can improve left ventricular dimensions and function.
Survival and Completeness of Revascularization
There are no published randomized controlled trials comparing CTO PCI with medical therapy or with surgical revascularization, although comparative study is ongoing ( www.clinicaltrials.gov , identifiers NCT01760083 and NCT01078051). Nevertheless, several issues related to CTO revascularization challenge the conduct of a randomized trial, for example, variability in operator experience, selection and treatment biases, and management of patient crossover and intention to treat. Moreover, although all-cause mortality has been proposed as a singular trial endpoint, the appropriateness of requiring CTO revascularization to achieve a different standard than non-CTO PCI is debated.
Nevertheless, several observational studies have compared late-term survival among patients undergoing successful versus failed CTO PCI. Despite limitations in study design, a remarkable consistency across such studies is the association of improved survival with successful CTO revascularization. For example, in a single-center observational study of 6996 patients undergoing elective PCI, 836 (11.9%) CTO procedures were attempted, of which 69.6% were successful. Baseline characteristics were similar between cohorts except for a higher frequency of prior revascularization in failed CTO PCI cases. Intraprocedural complications were also more common in unsuccessful cases but did not influence in-hospital major adverse cardiac events. Through 5 years, all-cause mortality was 17.2% for unsuccessful CTO patients and 4.5% for successful CTO patients (p < 0.0001; Figure 9-5A ). Also, the need for coronary bypass surgery was reduced following successful CTO PCI (3.1% versus 22.1%; p < 0.0001; Figure 9-5B ). Multivariate analysis demonstrated that procedural success was independently predictive of reduced mortality (HR 0.32; 95% CI, 0.18 to 0.58), which persisted following propensity score adjustment (HR 0.28; 95% CI, 0.15 to 0.52). In a metaanalysis of 13 observational studies, mortality over a weighted average follow-up of 6 years was 14.3% among 5056 patients with successful CTO recanalization compared with 17.5% among 2232 patients with failed CTO recanalization (OR 0.56; 95% CI, 0.43 to 0.72).
Whether following bypass surgery or PCI, incomplete coronary revascularization has been associated with worse clinical outcomes compared to complete revascularization, and the presence of a CTO is one of the major reasons for incomplete revascularization. While such observations are suggestive but do not establish that CTO revascularization improves patient outcome, it is notable that as angiographic disease complexity increases, completeness of revascularization measured by the residual SYNTAX score paradoxically decreases. Among patients with multivessel coronary disease including a CTO, complete revascularization (i.e . , that included successful CTO PCI) was associated with improved cardiovascular survival compared with incomplete revascularization. Recently, the impact of CTOs on incomplete revascularization and its clinical implications were described from the SYNTAX trial. In this study, the prevalence of a CTO was 26.3% and 36.4% in the PCI and bypass surgery groups, respectively. Nearly 70% of all CTOs were localized to the proximal or midsegment of a major coronary artery, indicating at least moderate territory at ischemic risk, and the CTO PCI success rate was low in this trial (49.4%). The presence of a CTO was the most significant predictor of incomplete revascularization after PCI (HR 2.70; 95% CI, 1.98 to 3.67; p < 0.001). At 4-year follow-up, incomplete revascularization was associated with significantly higher mortality and major adverse cardiac and cerebrovascular events independent of treatment assignment to PCI or bypass surgery.
Procedural Outcomes and Fundamentals
In parallel with outcomes data indicating benefit following CTO revascularization and the successes of drug-eluting stents (DES) in maintaining target-vessel patency is the stark reality that any potential advantage of CTO PCI is handicapped from the outset by the commonality of procedural failure. The technical and procedural success rates of PCI in CTOs have steadily increased over the last 20 years because of greater operator experience and improvements in equipment and procedural techniques. Despite this observation, CTOs remain the lesion subtype in which angioplasty is most likely to fail, and until recently, both attempt and procedural success rates remained relatively stagnant. In recent contemporary series, procedural success rates have ranged from approximately 50% to more than 80%, with the variability reflecting differences in operator technique and experience, availability of advanced guidewires, CTO definition, and case selection. The most common PCI failure mode for CTOs is inability to successfully pass a guidewire across the lesion into the true lumen of the distal vessel.
Predictors of Procedural Outcome
Most historical studies have consistently reported that increasing age of the occlusion, greater lesion length, presence of a nontapered proximal stump, origin of a side branch at the occlusion site, excessive vessel and lesion tortuosity, calcification, ostial occlusion, and lack of visibility of the distal vessel course negatively affect the ability to successfully cross a CTO. However, performance of advanced methods, with newer guidewire developments, has in many instances overcome the historical predictors associated with CTO procedural failure (e.g., CTO length, calcification, side branch involvement). In a more contemporary series, selected clinical and angiographic variables have been incorporated into a model to predict procedural time and success rates. Specifically, the multicenter Japanese CTO (J-CTO) registry surveyed approximately 500 CTO PCI attempts, identifying five independent predictors of crossing time within 30 minutes and overall procedural success : (1) calcification, (2) bending >45° in the CTO segment, (3) a blunt proximal cap, (4) the length of the occluded segment >20 mm, and (5) a previously failed attempt. A scoring model was developed applying 1 point for each of these independent variables when present. The CTO case complexity was further stratified into easy (J-CTO score = 0), intermediate (score = 1), difficult (score = 2), and very difficult (score = 3-5). However, more advanced techniques including retrograde and hybrid strategies were underrepresented in the J-CTO registry. In a more recent evaluation to externally validate the J-CTO model that included such methods, a single-center study reported that the J-CTO score demonstrated excellent discrimination for predicting crossing time within 30 minutes; however, using a hybrid antegrade and retrograde approach and dissection reentry techniques, the overall angiographic recanalization success rate was not affected by the score.
Vascular Access, Equipment Selection, and Angiography
Decisions regarding femoral or radial vascular access are generally, according to operator’s preference notwithstanding, patient-specific factors that may mandate one or the other method. In general, the relative merits of accommodating larger and possibly more supportive guiding catheters with femoral access can be weighed against the reduction in vascular complications and improved patient comfort with a radial approach. Importantly, among experienced radial CTO operators, procedural success rates applying complex antegrade and retrograde techniques have been demonstrated similar to other contemporary studies employing more traditional femoral access. A guiding principle of vascular access is that operators should utilize access routes that support their typical and optimal technique.
In part based on the vascular access method, selection of the guiding catheter size is commonly limited to 6 Fr (or occasionally sheathless 7 Fr) from the radial approach, compared with 6 Fr to 8 Fr caliber sheaths and guides used in transfemoral CTO PCI. When femoral access is selected, the use of long (45 cm) sheaths is recommended for increased passive support. Guide catheter support and coaxial alignment are essential from the outset, and it is therefore important to avoid accepting satisfactory backup rather than achieving optimal support prior to guidewire engagement in the CTO. In addition, CTO operators should be familiar with adjunctive catheter support methods including balloon anchoring and mother-and-child techniques.
A fundamental of successful CTO PCI is the expert ability to perform diagnostic angiography and its interpretation. Only in rare, selected instances is the performance of contralateral angiography not indicated prior to attempted CTO revascularization. Even in instances in which only ipsilateral collateral supply exists, impaired antegrade flow following the creation of dissections and shearing of vascular tissue planes may result in a preferential collateral shift to retrograde channels otherwise initially inapparent. The performance of the diagnostic angiogram is an opportunity for the CTO operator to delineate collateral supply, identify the proximal and distal CTO cap, and troubleshoot challenges to successful recanalization prior to attempted revascularization. Ad hoc CTO PCI is strongly discouraged; instead, the diagnostic angiogram provides imaging in multiple views and oftentimes with simultaneous contralateral angiography to fully evaluate the coronary anatomy without expenditure of contrast and radiation exposure during the CTO procedure itself.
Guidewires and Microcatheters
Crossing the CTO with a guidewire is the most important and challenging step of the procedure, and it is the most frequent cause for failed PCI of a CTO. There are three separate steps to crossing a CTO: (1) penetrating the proximal fibrous cap, (2) traversing the body of the CTO to reach the distal fibrous cap, and (3) penetrating the distal fibrous cap. Wires designed particularly for treating CTOs can be broadly divided into two major groups: (1) polymer-coated (hydrophilic or lubricious) guidewires and (2) stiffer, nonpolymer (nonhydrophilic, hydrophobic, or nonlubricious) guidewires. The stiffer, nonhydrophilic guidewires are typically more controllable, provide better tactile feel, and are less likely to cause vessel dissection. Hydrophilic wires offer maneuverability in tortuous vessels and may be steered more easily in a true lumen immediately after sharp bends. On the other hand, they are more likely to penetrate beneath plaque and cause subintimal dissections than noncoated wires. Several dedicated CTO guidewires are also designed with a tapered (e.g., 0.009 to 0.010 inch) tip to permit engagement in microchannels and facilitate crossing. Once a specialized CTO guidewire has crossed the occlusion and passed into the distal lumen, the wire should be exchanged with a soft, floppy-tipped wire to minimize the risk of distal wire perforation or dissection.
A microcatheter or an over-the-wire low-profile (e.g., 1.2 or 1.25 mm) balloon catheter can be used for support as well as access for ease of exchanging wires. A balloon catheter also offers the option of treatment with dilation of the vessel as well as added support by using it as an anchor. Several devices are available to create a larger lumen when a balloon catheter is unable to cross expand the lesion. These include the braided stainless steal Tornus catheter (Asahi Intecc, Inc., Nagoya, Japan) and the Corsair catheter (Asahi Intecc, Inc.). The Corsair catheter ( Figure 9-6 ), also known as a channel dilator catheter, is most commonly used in retrograde CTO PCI given its ability to navigate through very angulated and small-caliber collateral channels.
