In-Hospital Outcomes of Chronic Total Occlusion Percutaneous Coronary Intervention in Patients With Chronic Kidney Disease

Abstract: Objectives. The effect of chronic kidney disease (CKD) on in-hospital outcomes of chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has received limited study. Methods. We evaluated the prevalence of CKD and its impact on CTO-PCI outcomes in 1979 patients who underwent 2040 procedures between 2012 and 2017 at 18 centers. CKD was defined as preprocedural estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m². Results. Compared with patients without CKD (n = 1444; 73%), patients with CKD (n = 535; 27%) had more comorbidities (hypertension, diabetes mellitus, heart failure, peripheral arterial disease, prior myocardial infarction, PCI, coronary artery bypass graft surgery, and stroke), and more severe calcification and proximal vessel tortuosity. Patients with and without CKD had similar technical success rates (84% vs 86%; P=.49) and procedural success rates (83% vs 84%; P=.44). Patients with CKD had higher in-hospital mortality rate (1.9% vs 0.3%; P<.001) and in-hospital major adverse cardiovascular event (MACE) rate (4.3% vs 2.2%; P<.01). In-hospital mortality and MACE rates increased with decreasing eGFR levels (P=.03). In multivariate analysis, an independent association was observed between CKD and in-hospital mortality (adjusted odd ratio, 4.4; 95% confidence interval, 1.2-16.0; P=.02), but not overall MACE (adjusted odds ratio, 1.4; 95% confidence interval, 0.8-2.7; P=.28). Conclusions. CKD is common among patients undergoing CTO-PCI. High success rates can be achieved in patients with decreased glomerular filtration rate, but CKD may be associated with higher in-hospital mortality. 

J INVASIVE CARDIOL 2018;30(11):E113-E121. Epub 2018 September 15.

Key words: chronic kidney disease, chronic total occlusion, percutaneous coronary intervention

Chronic kidney disease (CKD) has been associated with worse in-hospital and long-term outcomes after percutaneous coronary intervention (PCI).^1-7 However, little information exists regarding the effect of CKD on the outcomes of chronic total occlusion (CTO)-PCI.⁷ Patients with CKD often have multiple comorbidities and increased coronary lesion complexity that could adversely affect PCI outcomes. Accordingly, we examined a contemporary multicenter CTO-PCI registry to examine the impact of CKD on the safety and efficacy of CTO-PCI.

Methods

We examined the clinical, angiographic, and procedural characteristics of 1979 patients who underwent 2040 CTO-PCIs and were enrolled in the PROGRESS CTO (Prospective Global Registry for the Study of Chronic Total Occlusion Intervention; NCT02061436) registry between May 2012 and November 2017 at 18 centers in the United States, Europe, and Russia (Appendix 1). The study was approved by the institutional review board of each site. Some centers only enrolled patients during part of the study period due to participation in other studies. 

Renal function assessment. The estimated glomerular filtration rate (eGFR) was calculated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula and the serum creatinine measurement obtained prior to and temporally closest to the index procedure.⁸ Patient classification was based upon the Kidney Disease: Improving Global Outcomes (KDOKI)⁹ and National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF-KDOQI)¹⁰ guidelines: normal or high (G1), ≥90 mL/min/1.73 m²; mildly decreased (G2), 60-89 mL/min/1.73 m²; mildly to moderately decreased (G3a), 45-59 mL/min/1.73 m²; moderately to severely decreased (G3b), 30-44 mL/min/1.73 m²; severely decreased (G4), <29 mL/min/1.73 m²; or kidney failure (G5), <29 mL/min/1.73 m². CKD was defined as eGFR <60 mL/min/1.73 m² (composite of the G3a, G3b, G4, and G5 groups); eGFR ≥60 mL/min/1.73 m² (composite of the G1 and G2 groups) was considered normal. Patients undergoing dialysis were classified in the lowest eGFR group for all analyses. All patients had at least one creatinine measurement performed within 6 months prior to the index procedure. 

Definitions. Coronary CTOs were defined as coronary lesions with Thrombolysis in Myocardial Infarction (TIMI) grade flow 0 of at least 3-month duration. Estimation of the occlusion duration was based on first onset of anginal symptoms, prior history of myocardial infarction in the target-vessel territory, or comparison with a prior angiogram. Calcification was assessed by angiography as mild (spots), moderate (involving ≤50% of the reference lesion diameter), or severe (involving >50% of the reference lesion diameter). Moderate proximal vessel tortuosity was defined as the presence of at least 2 bends >70° or 1 bend >90° and severe tortuosity as 2 bends >90° or 1 bend >120° in the CTO vessel. Interventional collaterals were defined as collaterals deemed amenable to crossing by a guidewire and a microcatheter by the operator. The J-CTO score was calculated as described by Morino et al,¹¹ the PROGRESS CTO score as described by Christopoulos et al,¹² and the PROGRESS CTO Complication score as described by Danek et al.¹³Technical success of CTO-PCI was defined as successful CTO revascularization with achievement of <30% residual diameter stenosis within the treated segment and restoration of TIMI grade 3 antegrade flow. Procedural success was defined as achievement of technical success with no in-hospital major adverse cardiac event (MACE). In-hospital MACE included any of the following adverse events prior to hospital discharge: death, myocardial infarction (MI), recurrent symptoms requiring urgent repeat target-vessel revascularization with PCI or coronary artery bypass graft (CABG) surgery, tamponade requiring either pericardiocentesis or surgery, and stroke. Periprocedural and late in-hospital MI were defined according to the Third Universal Definition of Myocardial Infarction.¹⁴Bleeding was defined according to the National Cardiovascular Data Registry CathPCI database, and included suspected/confirmed bleeding occurring within 72 hours of the procedure and associated with any of the following: (1) hemoglobin drop of ≥3 g/dL; (2) transfusion with whole blood or packed red blood cells; or (3) procedural intervention/surgery at bleeding site to reverse or correct the bleed. Procedure time was calculated from administration of local anesthetic for vascular access to removal of the last catheter. 

Statistical analysis. Categorical variables were described using percentages and compared between groups using Pearson’s Chi-squared test or the Cochran-Armitage test for trend. Continuous variables were described as mean ± standard deviation or median (interquartile range [IQR]) and compared using the Student’s t-test or Wilcoxon rank-sum test. Multivariable logistic regression was used to examine the association between eGFR/dialysis and MACE after adjusting for confounding variables selected on the grounds of (1) univariable association in the present study (P<.10); or (2) previously established links with MACE. Such variables included age, gender, body mass index, diabetes mellitus, hypertension, peripheral arterial disease, chronic lung disease, history of heart failure, MI, stroke, PCI or CABG, occlusion length, degree of lesion calcification, proximal cap morphology, and utilization of a retrograde approach. The group with the highest eGFR (≥90 mL/min/1.73 m²) was used as reference category for renal function. Stepwise backward elimination was used to form the final model. A two-sided P-value of <.05 was considered statistically significant. All statistical analyses were performed with JMP 13.0 (SAS Institute).

Results

The prevalence of CKD was 27% (535 of 1979 patients). Patients with CKD were more likely to be older and female, and to have hypertension, diabetes mellitus, heart failure, peripheral arterial disease, prior MI, PCI, CABG and stroke, and had lower left ventricular ejection fraction, but were less likely to be active smokers (Table 1). The most common CTO target vessel was  the right coronary artery (54%), followed by the left anterior descending (24%) and the circumflex (21%) arteries. CKD patients were more likely to have lesions with moderate or severe calcification, proximal vessel tortuosity, and diseased distal target vessel. They also had more complex lesions with higher J-CTO scores (2.6 ± 1.3 vs 2.4 ± 1.3; P=.01) and PROGRESS CTO scores (1.4 ± 1.1 vs 1.3 ± 1.0; P=.03) (Table 2).

Overall technical and procedural rates were 85% and 84%, respectively, and were similar in patients with and without CKD (Figure 1). Crossing strategies (Table 3) were similar for patients with and without CKD; however, retrograde techniques were used more frequently as the initial crossing approach in the CKD group (17% vs 13%; P=.04). Left ventricular assist devices were used more commonly in CKD patients (8% vs 4%; P<.001), for either prophylactic cardiac support (5% vs 3%; P<.01) or emergency cardiac support (2% vs 1%; P<.01). Procedures performed in CKD patients had longer procedural times (134 min [IQR, 85-200 min] vs 119 min [IQR, 77-185 min]; P<.01) and fluoroscopy times (48.9 min [IQR, 27.3-79.2 min] vs 41.4 min [IQR, 25.3-70.3 min]; P<.01), similar air kerma patient radiation dose (3.2 Gray [IQR, 2.0-5.2 Gray] vs 3.0 Gray [1.8-4.7 Gray]; P=.14), and lower contrast volume (250 mL [IQR, 180-340 mL] vs 260 mL [IQR, 200-350 mL]; P<.02).

The overall in-hospital MACE rate was 2.7% (54 patients) (Table 4) and was higher among CKD patients (4.3% vs 2.2%; P<.01) (Figure 1), driven by higher in-hospital mortality (1.9% vs 0.3%; P<.001). We observed an inverse graded dose-response relationship between MACE and eGFR (P for trend =.03) (Figure 2); this was largely due to an increase in in-hospital mortality with worsening eGFR. Four patients died in the non-CKD group due to coronary perforation (1 hemothorax, 1 intramural cardiac hematoma, 2 coronary tamponade with subsequent cardiogenic shock), and 10 patients died in the CKD group (4 patients suffered cardiogenic shock after coronary perforation; 1 patient suffered cardiac arrest after new MI; 1 patient died from multiple organ dysfunction; 2 patients died from progressive cardiogenic shock despite use of a left ventricular assist device; 1 patient died from hemorrhagic stroke; and 1 patient died from hemorrhagic shock secondary to a vascular access complication). After adjustment for potential confounders, no independent association was found between renal function/dialysis status and overall MACE rate (Table 5); however, the association between CKD and in-hospital mortality persisted after adjustment (odds ratio [OR], 4.4; 95% confidence interval [CI], 1.2-16.0; P=.02). Bleeding was observed in 22 patients (1.1%), as follows: access site in 14 patients, gastrointestinal in 2 patients, retroperitoneal in 4 patients, genito-urinary in 1 patient, and hemothorax in 1 patient. Bleeding was more frequent among patients with CKD (2.2% vs 0.7%; P<.01). Contrast-induced nephropathy (CIN) was diagnosed in 4 patients (0.4%) during the hospital stay, requiring new dialysis in 1 patient. Acute kidney injury only occurred in patients with decreased kidney function (1.6% vs 0.0%; P<.01).

Forty-five patients (2%) were undergoing dialysis at the time the procedure was performed. Compared with non-dialysis patients, those undergoing dialysis had numerically lower technical success (80% vs 85%; P=.31) and procedural success (78% vs 84%; P=.28) and numerically higher incidence of in-hospital MACE (6.7% vs 2.7%; P=.10). 

Discussion

Our study provides novel insights into the acute outcomes of CKD patients undergoing CTO-PCI, as follows: (1) CKD was common in the CTO-PCI population, with approximately one-third of patients having an eGFR of <60 mL/min/1.73 m²; (2) CKD patients, even those with severely reduced renal function (eGFR<30 mL/min/1.73 m²) had similarly high technical success rates vs non-CKD patients; and (3) CKD patients had higher in-hospital mortality rates. 

Several pathophysiological links have been established between renal dysfunction and progression of coronary artery disease, including a pro-inflammatory and hypercoagulable state,¹⁵ homocysteinemia,¹⁶ arterial calcification,¹⁷ and endothelial dysfunction.^18,19 CKD is consistently associated with worse in-hospital^3,6,20 and long-termoutcomes^1,5,21,22 after PCI, but to date, limited information has been published regarding procedural and in-hospital outcomes of patients with CKD undergoing CTO-PCI. 

In our study, 27% of patients undergoing CTO-PCI had an eGFR of <60 mL/min/1.73 m², a finding consistent with previous reports.^7,23,24 Declining renal function did not significantly affect the technical success of CTO-PCI despite being associated with several comorbidities, such as prior MI and prior CABG, which have been associated with technical failure in other studies.²⁵ Moreover, patients with CKD were more likely to have moderate or severe calcification and proximal tortuosity that could also hinder coronary revascularization.^12,25 Although overall in-hospital MACE increased significantly and incrementally with decreasing renal function, this association was no longer present on multivariable analysis. However, in-hospital mortality was significantly higher in patients with CKD, an association that persisted after multivariable adjustment. This finding, which is in line with previous reports of outcomes after non-CTO PCI and CTO-PCI in patients with CKD, should be incorporated in the decision-making process for patients with a CTO and CKD. Current prediction models for technical success and adverse events of CTO-PCI, such as the PROGRESS CTO score¹² and PROGRESS CTO Complications score,¹³ do not include CKD.

In a single-center study, Stahli et al examined long-term outcomes after CTO-PCI among 2002 patients stratified by the patients’ baseline eGFR.⁷ During a median follow-up of 2.6 years, higher eGFR was associated with lower all-cause mortality (hazard ratio [HR], 0.98; 95% CI, 0.98-0.99; P<.001). However, patients with failed CTO-PCI had worse long-term survival, regardless of whether they had CKD (eGFR <60 mL/min/1.73 m²; HR, 1.59; 95% CI, 1.08-2.32; P=.02) or preserved renal function (eGFR >60 mL/min/1.73 m²; HR, 1.73; 95% CI, 1.15-2.60; P<.01). Stahli et al reported significantly different procedural success rates for CTO-PCI in patients with different stages of renal dysfunction (range, 69%-86%; P for trend <.001); however, in our study, the procedural outcomes were similar in patients with various degrees of renal dysfunction (range, 78%-85%; P for trend =.69). 

Dialysis patients are known to have worse in-hospital and long-term outcomes after PCI,³ as was also observed in our study. This is likely related to higher angiographic complexity (especially more severe calcification) and more comorbidities that may predispose to complications (such as bleeding) or decrease the tolerance of a complication. If feasible, CABG might provide good long-term outcomes in dialysis patients.^26-28

Prior publications of CTO-PCI in CKD patients focused mostly on the incidence of CIN (6.2%-9.4%) (Table 6).^23,24,29-33 Liu et al compared patients with renal failure (defined as creatinine clearance of <90 mL/min/1.73 m²) who did (n = 359) or did not undergo CTO-PCI (n = 142), and reported that high technical success (89%) and improved long-term outcomes could be achieved in the former group, without increasing the risk for CIN (adjusted OR, 0.88; 95% CI, 0.41-1.93).²⁴ Liu et al developed a risk-stratification model for predicting CIN from a cohort of 728 patients: age ≥75 years, left ventricular ejection fraction <40%, and baseline serum creatinine >1.5 mg/dL were identified as independent predictors for CIN.³³ Bataille et al investigated the interaction between CKD and CTO in a non-infarct related artery on short-term (30-day) and long-term (1-year) outcomes after PCI for ST-segment elevation acute MI,³¹ and found that the prevalence of CTOs was twice as high in CKD patients as compared with patients who did not have CKD. Lee et al evaluated the effect of CTO-PCI with periprocedural MI on long-term outcomes of 1058 patients who underwent successful CTO revascularization.³⁴ During a median follow-up of 4.4 years, CKD was independently associated with higher all-cause mortality (HR, 3.39; 95% CI, 1.48-7.75; P<.01). 

Study limitations. First, this was a retrospective, observational study, and is subject to all the limitations of such studies. Second, eGFR calculations were made using only a single creatinine measurement performed closest to the procedure that was recorded as part of the study; data on urine albumin, or specific functional and structural indicators for CKD, were not collected. Given these limitations, CKD classification in our group could be subject to selection bias; however, the prevalence of CKD in our study is in line with prior studies. Third, there was no core laboratory adjudication of angiograms and no clinical event adjudication. Fourth, limited data were available on the incidence of CIN and new need for in-hospital dialysis due to the shorter data collection period. Fifth, no data were available on preprocedural hydration, other interventional or diagnostic procedures that were performed prior to PCI, or the type of contrast agent utilized. 

Conclusion

CKD is common among patients undergoing CTO-PCI. High procedural success rates can be achieved in CKD patients, but they may have increased risk for in-hospital death. 

Acknowledgments. The PROGRESS CTO Registry has received funding from the Abbott Northwestern Hospital Foundation, Minneapolis, Minnesota.

Study data were collected and managed using REDCap electronic data capture tools.³⁵ REDCap (Research Electronic Data Capture) is a secure, web-based application designed to support data capture for research studies, providing (1) an intuitive interface for validated data entry; (2) audit trails for tracking data manipulation and export procedures; (3) automated export procedures for seamless data downloads to common statistical packages; and (4) procedures for importing data from external sources. 

References

1.    Lemos PA, Arampatzis CA, Hoye A, et al. Impact of baseline renal function on mortality after percutaneous coronary intervention with sirolimus-eluting stents or bare metal stents. Am J Cardiol. 2005;95:167-172.

2.    Saltzman AJ, Stone GW, Claessen BE, et al. Long-term impact of chronic kidney disease in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention: the HORIZONS-AMI (Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction) trial. JACC Cardiovasc Interv. 2011;4:1011-1019.

3.    Best PJ, Lennon R, Ting HH, et al. The impact of renal insufficiency on clinical outcomes in patients undergoing percutaneous coronary interventions. J Am Coll Cardiol. 2002;39:1113-1119.

4.    Latif F, Kleiman NS, Cohen DJ, et al. In-hospital and 1-year outcomes among percutaneous coronary intervention patients with chronic kidney disease in the era of drug-eluting stents: a report from the EVENT (Evaluation of Drug Eluting Stents and Ischemic Events) registry. JACC Cardiovasc Interv. 2009;2:37-45.

5.    Baber U, Giustino G, Sartori S, et al. Effect of chronic kidney disease in women undergoing percutaneous coronary intervention with drug-eluting stents: a patient-level pooled analysis of randomized controlled trials. JACC Cardiovasc Interv. 2016;9:28-38.

6.    Gupta T, Paul N, Kolte D, et al. Association of chronic renal insufficiency with in-hospital outcomes after percutaneous coronary intervention. J Am Heart Assoc. 2015;4:e002069.

7.    Stahli BE, Gebhard C, Gick M, et al. Outcomes after percutaneous coronary intervention for chronic total occlusion according to baseline renal function. Clin Res Cardiol. 2018;107:259-267.

8.    Levey AS, Stevens LA, Schmid CH, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150:604-612.

9.    Group KDIGOKCW. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3:1-150.

10.    Inker LA, Astor BC, Fox CH, et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for the evaluation and management of CKD. Am J Kidney Dis. 2014;63:713-735.

11.    Morino Y, Abe M, Morimoto T, et al. Predicting successful guidewire crossing through chronic total occlusion of native coronary lesions within 30 minutes: the J-CTO (Multicenter CTO Registry in Japan) score as a difficulty grading and time assessment tool. JACC Cardiovasc Interv. 2011;4:213-221.

12.    Christopoulos G, Kandzari DE, Yeh RW, et al. Development and validation of a novel scoring system for predicting technical success of chronic total occlusion percutaneous coronary interventions: the PROGRESS CTO (Prospective Global Registry for the Study of Chronic Total Occlusion Intervention) score. JACC Cardiovasc Interv. 2016;9:1-9.

13.    Danek BA, Karatasakis A, Karmpaliotis D, et al. Development and validation of a scoring system for predicting periprocedural complications during percutaneous coronary interventions of chronic total occlusions: the Prospective Global Registry for the Study of Chronic Total Occlusion Intervention (PROGRESS CTO) Complications score. J Am Heart Assoc. 2016;5.

14.    Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circulation. 2012;126:2020-2035.

15.    Shlipak MG, Fried LF, Crump C, et al. Elevations of inflammatory and procoagulant biomarkers in elderly persons with renal insufficiency. Circulation. 2003;107:87-92.

16.    Muntner P, Hamm LL, Kusek JW, Chen J, Whelton PK, He J. The prevalence of nontraditional risk factors for coronary heart disease in patients with chronic kidney disease. Ann Intern Med. 2004;140:9-17.

17.    Raggi P, Boulay A, Chasan-Taber S, et al. Cardiac calcification in adult hemodialysis patients. A link between end-stage renal disease and cardiovascular disease? J Am Coll Cardiol. 2002;39:695-701.

18.    Blacher J, Safar ME, Guerin AP, Pannier B, Marchais SJ, London GM. Aortic pulse wave velocity index and mortality in end-stage renal disease. Kidney Int. 2003;63:1852-1860.

19.    Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004;351:1296-1305.

20.    Blackman DJ, Pinto R, Ross JR, et al. Impact of renal insufficiency on outcome after contemporary percutaneous coronary intervention. Am Heart J. 2006;151:146-152.

21.    Reinecke H, Trey T, Matzkies F, Fobker M, Breithardt G, Schaefer RM. Grade of chronic renal failure, and acute and long-term outcome after percutaneous coronary interventions. Kidney Int. 2003;63:696-701.

22.    Naidu SS, Selzer F, Jacobs A, et al. Renal insufficiency is an independent predictor of mortality after percutaneous coronary intervention. Am J Cardiol. 2003;92:1160-1164.

23.    Zhang QB, Chen LM, Li M, Cui YQ, Zhao CY, Cui LQ. Influence of chronic kidney disease on the outcome of patients with chronic total occlusion. Am J Transl Res. 2016;8:196-208.

24.    Liu Y, Liu Y, Li H, et al. Percutaneous coronary intervention for chronic total occlusion improved prognosis in patients with renal insufficiency at high risk of contrast-induced nephropathy. Sci Rep. 2016;6:21426.

25.    Alessandrino G, Chevalier B, Lefevre T, et al. A clinical and angiographic scoring system to predict the probability of successful first-attempt percutaneous coronary intervention in patients with total chronic coronary occlusion. JACC Cardiovasc Interv. 2015;8:1540-1548.

26.    Hemmelgarn BR, Southern D, Culleton BF, et al. Survival after coronary revascularization among patients with kidney disease. Circulation. 2004;110:1890-1895.

27.    Marui A, Kimura T, Nishiwaki N, et al. Percutaneous coronary intervention versus coronary artery bypass grafting in patients with end-stage renal disease requiring dialysis (5-year outcomes of the CREDO-Kyoto PCI/CABG Registry Cohort-2). Am J Cardiol. 2014;114:555-561.

28.    Bae KS, Park HC, Kang BS, et al. Percutaneous coronary intervention versus coronary artery bypass grafting in patients with coronary artery disease and diabetic nephropathy: a single center experience. Korean J Intern Med. 2007;22:139-146.

29.    Liu YH, Liu Y, Tan N, et al. Contrast-induced nephropathy following chronic total occlusion percutaneous coronary intervention in patients with chronic kidney disease. Eur Radiol. 2015;25:2274-2281.

30.    Aguiar-Souto P, Ferrante G, Del Furia F, Barlis P, Khurana R, Di Mario C. Frequency and predictors of contrast-induced nephropathy after angioplasty for chronic total occlusions. Int J Cardiol. 2010;139:68-74.

31.    Bataille Y, Plourde G, Machaalany J, et al. Interaction of chronic total occlusion and chronic kidney disease in patients undergoing primary percutaneous coronary intervention for acute ST-elevation myocardial infarction. Am J Cardiol. 2013;112:194-199.

32.    Lin YS, Fang HY, Hussein H, et al. Predictors of contrast-induced nephropathy in chronic total occlusion percutaneous coronary intervention. EuroIntervention. 2014;9:1173-1180.

33.    Liu Y, Liu YH, Chen JY, et al. A simple pre-procedural risk score for contrast-induced nephropathy among patients with chronic total occlusion undergoing percutaneous coronary intervention. Int J Cardiol. 2015;180:69-71.

34.    Lee SW, Lee PH, Kang SH, et al. Determinants and prognostic significance of periprocedural myocardial injury in patients with successful percutaneous chronic total occlusion interventions. JACC Cardiovasc Interv. 2016;9:2220-2228.

35.    Harris PA, Taylor R, Thielke R, Payne J, Gonzalez N, Conde JG. Research electronic data capture (REDCap) – a metadata-driven methodology and workflow process for providing translational research informatics support. J Biomed Inform. 2009;42:377-381.

From the ¹Minneapolis Heart Institute, Abbott Northwestern Hospital, Minneapolis, Minnesota; ²University of Szeged, Division of Invasive Cardiology, Second Department of Internal Medicine and Cardiology Center, Szeged, Hungary; ³VA North Texas Health Care System and University of Texas Southwestern Medical Center, Dallas, Texas; ⁴Henry Ford Hospital, Detroit, Michigan; ⁵Columbia University, New York, New York; ⁶Massachusetts General Hospital, Boston, Massachusetts; ⁷Baylor Heart and Vascular Hospital, Dallas, Texas; ⁸Beth Israel Deaconess Medical Center, Boston, Massachusetts; ⁹VA San Diego Healthcare System and University of California San Diego, La Jolla, California; ¹⁰Meshalkin Siberian Federal Biomedical Research Center, Ministry of Health of Russian Federation, Novosibirsk, Russian Federation; ¹¹University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; ¹²Medical Center of the Rockies, Loveland, Colorado; ¹³VA Central Arkansas Healthcare System, Little Rock, Arkansas; ¹⁴Korgialeneio-Benakeio Hellenic Red Cross General Hospital of Athens, Athens, Greece; ¹⁵Torrance Memorial Hospital, Torrance, California; ¹⁶VA Minneapolis Healthcare System and University of Minnesota, Minneapolis, Minnesota; and ¹⁷The Heart Hospital Baylor Plano, Plano, Texas.

Clinical Trial Registration: NCT02061436, Prospective Global Registry for the Study of Chronic Total Occlusion Intervention (PROGRESS CTO).

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Alaswad reports consulting fees from Terumo and Boston Scientific; consultant (non-financial) for Abbott Laboratories. Dr Holper reports proctoring and speakers’ bureau income from Boston Scientific. Dr Karmpaliotis reports honoraria from Abbott Vascular and Boston Scientific. Dr Jaffer reports personal fees from Abbott Vascular, Boston Scientific, Philips, and Siemens; research grant from Canon and Siemens. Dr Yeh reports grant support from Abbott Vascular, Abiomed, and Boston Scientific; personal fees from Abbott Vascular, Asahi Intecc, Boston Scientific, Medtronic, and Teleflex. Dr Patel reports speakers’ bureau income from Astra Zeneca. Dr Mahmud reports speakers’ bureau income from Medtronic and Abbott Vascular; advisory board income from Boston Scientific; consulting fees and research support from Abbott Vascular. Dr Burke reports consulting and speaker honoraria from Abbott Vascular and Boston Scientific. Dr Wyman reports honoraria/consulting/speaking fees from Boston Scientific, Abbott Vascular, and Asahi Intecc. Dr Garcia reports consulting fees from Medtronic. Dr Rangan reports research grants from InfraReDx, Inc., and the Spectranetics Corporation. Dr Banerjee reports research grants from Gilead and the Medicines Company; consultant/speaker honoraria from Covidien and Medtronic; ownership in MDCare Global (spouse); intellectual property in HygeiaTel. Dr Brilakis reports consulting/speaker honoraria from Abbott Vascular, Amgen, CSI, Elsevier, GE Healthcare, and Medtronic; grant support from Boston Scientific, Osprey, Regeneron, and Siemens; other income from the American Heart Association (Associate Editor, Circulation), Cardiovascular Innovations Foundation (Board of Directors), and the Society of Cardiovascular Angiography and Interventions (Board of Trustees); shareholder in MHI Ventures. The remaining authors report no conflicts of interest regarding the content herein.

Manuscript submitted June 13, 2018, provisional acceptance given June 18, 2018, final version accepted July 3, 2018.

Address for correspondence: Emmanouil S. Brilakis, MD, PhD, Minneapolis Heart Institute, 920 E. 28th Street #300, Minneapolis, MN 55407. Email: esbrilakis@gmail.com