Predictors of Optical Coherence Tomography-Defined Calcified Nodules in Patients With Acute Coronary Syndrome　― A Substudy From the TACTICS Registry ―

Abstract

Background: Recent studies suggest that the presence of calcified nodules (CN) is associated with worse prognosis in patients with acute coronary syndrome (ACS). We investigated clinical predictors of optical coherence tomography (OCT)-defined CN in ACS patients in a prospective multicenter registry.

Methods and Results: We investigated 695 patients enrolled in the TACTICS registry who underwent OCT assessment of the culprit lesion during primary percutaneous coronary intervention. OCT-CN was defined as calcific nodules erupting into the lumen with disruption of the fibrous cap and an underlying calcified plate. Compared with patients without OCT-CN, patients with OCT-CN (n=28) were older (mean [±SD] age 75.0±11.3 vs. 65.7±12.7 years; P<0.001), had a higher prevalence of diabetes (50.0% vs. 29.4%; P=0.034), hemodialysis (21.4% vs. 1.6%; P<0.001), and Killip Class III/IV heart failure (21.4% vs. 5.7%; P=0.003), and a higher preprocedural SYNTAX score (median [interquartile range] score 15 [11–25] vs. 11 [7–19]; P=0.003). On multivariable analysis, age (odds ratio [OR] 1.072; P<0.001), hemodialysis (OR 16.571; P<0.001), and Killip Class III/IV (OR 4.466; P=0.004) were significantly associated with the presence of OCT-CN. In non-dialysis patients (n=678), age (OR 1.081; P<0.001), diabetes (OR 3.046; P=0.014), and Killip Class III/IV (OR 4.414; P=0.009) were significantly associated with the presence of OCT-CN.

Conclusions: The TACTICS registry shows that OCT-CN is associated with lesion severity and poor clinical background, which may worsen prognosis.

Acute coronary syndrome (ACS) is one of the leading causes of cardiovascular morbidity and mortality.¹ Three major phenotypes of culprit plaque morphology responsible for ACS have been described: plaque rupture (PR), plaque erosion (PE), and calcified nodules (CN).^2,3 Recent studies have shown an association between the presence of CN and worse prognosis in patients with ACS.^4–6 Several clinical characteristics, such as older age and hemodialysis, have been reported to be associated with the presence of CN.^7–9 However, these previous studies were of a retrospective nature and represented a relatively small number of patients with CN.

In the present study, we aimed to investigate the clinical predictors of optical coherence tomography (OCT)-defined CN in patients with ACS in a prospective multicenter registry.

Methods

Study Population

The present study is a substudy of the TACTICS (Tokyo, Kanagawa, Chiba, Shizuoka, and Ibaraki active OCT applications for ACS) registry, which was an investigator-initiated prospective multicenter observational study conducted at 22 hospitals in Japan between November 2019 and April 2021. The study protocol of the TACTICS registry has been registered with the University Hospital Medical Information Network (UMIN) Clinical Trials Registry of Japan (ID: UMIN000039050). The rationale and design of the main study have been reported elsewhere.¹⁰ Briefly, patients with ACS diagnosed within 24 h of symptom onset who had undergone emergency percutaneous coronary intervention (PCI) with OCT guidance were enrolled. ACS diagnoses included ST-segment elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), and unstable angina.¹¹ The presence and severity of concomitant heart failure was assessed according to the Killip classification.¹² The primary endpoint of the main study was to identify the prevalence of underlying causes of ACS, such as PR, PE, CN, and others, using OCT-defined morphological assessment of the culprit lesion.¹⁰ The results of the main study have been reported previously.⁶ In all, 702 patients who underwent emergency PCI with OCT guidance were eligible for inclusion in the TACTICS registry.

In the present study, we investigated 695 patients enrolled in the TACTICS registry who underwent preprocedural OCT assessment of the culprit lesion during emergency PCI. Patient characteristics were compared between those with and without OCT-CN.

Ethics Approval

The study protocol was approved by the institutional ethics committee of each participating hospital. This study was performed in accordance with the principles of the Declaration of Helsinki and all patients provided written informed consent.

Coronary Catheterization and PCI Procedure

Emergency PCI with OCT guidance was performed according to the standard technique aiming to achieve prompt recanalization, mostly followed by second- or newer-generation drug-eluting stent implantation. The culprit lesion was identified by the PCI operators based on combined assessment of coronary angiography, electrocardiographic changes, regional left ventricular wall motion abnormalities, and intraluminal thrombus formation identified using OCT images. Thrombus aspiration and/or gentle predilatation using a balloon ≤2.0 mm in diameter were allowed to obtain prompt recanalization and optimal preprocedural OCT image acquisition, if necessary. Onsite quantitative coronary angiography and OCT findings were used to help determine the PCI strategy.

Coronary Angiographic Image Analysis

Coronary cine angiograms were analyzed offline at an independent angiographic core laboratory (Cardiocore Japan, Tokyo, Japan) by the investigators who were blinded to all clinical data and OCT findings. Coronary flow before and after the procedure was assessed according to the Thrombolysis in Myocardial Infarction (TIMI) flow grade.¹³ Lesion complexity was assessed using the American College of Cardiology/American Heart Association classification.¹⁴ Pre- and post-procedural angiographic SYNTAX scores were calculated.¹⁵

OCT Image Acquisition and Analysis

OCT images were acquired with the ILUMIEN OPTIS system (Abbott Vascular Inc., Santa Clara, CA, USA) and the Dragonfly OPTIS or Dragonfly OpStar imaging catheter (Abbott Vascular Inc.). Either contrast medium or low-molecular weight dextran was allowed as a flushing agent for blood displacement during image acquisition. OCT images were analyzed using offline software at an independent OCT core laboratory (Kobe Cardiovascular Core Analysis Laboratory, Hyogo, Japan). Two independent experienced interventional cardiologists performed qualitative analysis of the baseline OCT and assessed culprit plaque morphology; these assessors were blinded to all clinical data except those of the PCI procedure and angiography. In case of discrepancy, a consensus reading was obtained via discussion at a conference attended by least 6 experienced analysts.

Quantitative OCT assessments were performed as previously described.^16–18 PR was identified as the presence of a disrupted fibrous cap overlying a lipid plaque, with or without intraplaque cavity formation. PE was identified as the presence of attached thrombus overlying a visualized plaque without evidence of fibrous cap disruption, evaluated in multiple adjacent frames. CN was defined as calcific nodules erupting into the lumen with disruption of the fibrous cap and an underlying calcified plate. Representative images of OCT-CN are shown in Figure 1. Culprit lesions not meeting the preceding definitions were classified as “others”, which included the following diagnoses: (1) spontaneous coronary artery dissection; (2) ectasia/aneurysm; (3) significant stenosis; (4) vasospasm; and (5) coronary embolism. The underlying plaque characteristics of the culprit lesion, including lipid plaque, thin-cap fibroatheroma, calcification, thrombus, macrophage accumulation, cholesterol crystals, microchannels, and layered plaque, were also assessed.

Figure 1.

Representative images of a patient with optical coherence tomography-defined calcified nodules (OCT-CN). (A) An 82-year-old woman presented to the emergency department and was diagnosed with non-ST-segment-elevation myocardial infarction. Pre-intervention coronary angiography revealed a severe stenotic lesion in the distal right coronary artery (white dotted line). (B) OCT after predilatation using a 2.0-mm balloon revealed the presence of eruptive CN (4–8 o’clock). (C) The patient was successfully treated with implantation of a 4.0-mm×18-mm drug-eluting stent (yellow dotted line). (D) Postintervention OCT image showing stent expansion.

Laboratory Data Analysis

Laboratory data were obtained before PCI according to established procedures. Estimated glomerular filtration rate (eGFR) was calculated using the equation modified for Japanese patients,¹⁹ as follows:

eGFR (mL/min/1.73 m²) = 194 × Cre^−1.094 × Age^−0.287 × 0.739 (for female patients)

where Cre is creatinine. Chronic kidney disease was defined as eGFR <60 mL/min/1.73 m² for more than 3 months.^19,20

Statistical Analysis

All analyses were performed using R for Windows 4.1.1 (The R Foundation, Vienna, Austria). Categorical data are expressed as absolute frequencies and percentages, and were compared using the Chi-squared test or Fisher’s exact test, as appropriate. Normality of data distribution was assessed by the Shapiro-Wilk test. Normally distributed continuous variables are expressed as the mean±SD, whereas non-normally distributed continuous variables are presented as the median with interquartile range (IQR). Continuous variables were compared using Student’s t-test, one-way analysis of variance, or the Mann-Whitney U test, as appropriate. P values two-tailed <0.05 was considered statistically significant.

Univariable and multivariable logistic regression analyses were performed to determine the clinical predictors of OCT-CN. The covariates used in multivariable analysis were selected using a criterion of P<0.01 in univariable analysis. The area under the curve (AUC) by receiver operating characteristic (ROC) analysis was used to determine the best cut-off value of age for predicting OCT-CN. Three prediction clinical models were used to determine the incremental discriminatory and reclassification performance for identifying the predictors of OCT-CN. Model 1, as the reference model, included age; Model 2 included age and Killip Class III/IV heart failure; and Model 3 included age, Killip Class III/IV heart failure, and hemodialysis. The discriminatory abilities of prediction models were assessed by the reclassification performance of each model using the relative integrated discrimination improvement (IDI) and category-free net reclassification improvement (NRI) values. Paired comparisons between ROC curves were performed using the DeLong method. P values two-tailed <0.05 was considered statistically significant.

Results

Patient Characteristics

In all, 695 patients were investigated in the present study, with OCT-CN detected in 28 (4.0%) patients. The remaining study population consisted of 411 (59.1%) patients with PR, 178 (25.6%) patients with PE, and 78 (11.2%) patients with other causes of ACS, respectively. Baseline patient characteristics are summarized in Table 1. Patients with OCT-CN were older (75.0±11.3 vs. 65.7±12.7 years; P<0.001) and had a higher prevalence of diabetes (50.0% vs. 29.4%; P=0.034), chronic kidney disease (57.1% vs. 34.3%; P=0.023), hemodialysis (21.4% vs. 1.6%; P<0.001), and concomitant heart failure (Killip Class III/IV; 21.4% vs. 5.7%; P=0.003) than patients without OCT-CN. Peak creatine kinase values did not differ significantly between patients with and without OCT-CN. Patients with OCT-CN had lower hemoglobin and creatinine clearance values than patients without OCT-CN. The prevalence of OCT-CN did not differ significantly between patients with and without STEMI (4.7% vs. 3.7%; P=0.511).

Table 1.

Baseline Patient Characteristics

	No OCT-CN (n=667)	OCT-CN (n=28)	P value
Age (years)	65.7±12.7	75.0±11.3	<0.001
Male sex	539 (80.8)	18 (64.3)	0.057
Body mass index (kg/m2)	24.6±4.1	23.0±3.8	0.047
Clinical presentation			0.800
STEMI	422 (63.3)	16 (57.1)
NSTEMI	187 (28.0)	9 (32.1)
Unstable angina	58 (8.7)	3 (10.7)
Killip Class III/IV heart failure	38 (5.7)	6 (21.4)	0.003
Hypertension	433 (64.9)	20 (71.4)	0.613
Dyslipidemia	388 (58.2)	16 (57.1)	1.000
Diabetes	196 (29.4)	14 (50.0)	0.034
Current smoker	235 (35.2)	4 (14.3)	0.024
CKD	229 (34.3)	16 (57.1)	0.023
Hemodialysis	11 (1.6)	6 (21.4)	<0.001
Family history of premature CAD	99 (14.8)	2 (7.1)	0.409
Prior MI	27 (4.0)	2 (7.1)	0.328
Prior PCI	48 (7.2)	4 (14.3)	0.150
Prior CABG	4 (0.6)	1 (3.6)	0.186
Prior stroke	24 (3.6)	7 (25.0)	<0.001
Laboratory data on admission
WBC count (/μL)	8,700 [6,970–10,900]	7,710 [5,800–9,110]	0.079
Hemoglobin (g/dL)	14.5 [13.3–15.7]	13.3 [11.0–14.2]	<0.001
eGFR (mL/min/1.73 m2)	68.5 [55.0–81.3]	56.9 [27.0–68.9]	0.001
LDL-C (mg/dL)	126 [103–150]	103 [80–120]	<0.001
HDL-C (mg/dL)	48 [41–57]	49 [42–58]	0.502
Triglyceride (mg/dL)	114 [73–181]	96 [66–129]	0.084
HbA1c (%)	6.0 [5.7–6.7]	6.4 [5.6–7.2]	0.276
CRP (mg/dL)	0.15 [0.06–0.40]	0.22 [0.08–0.47]	0.473
Peak CK (U/L)	383 [136–1,562]	266 [87–564]	0.095
LVEF (%)	58 [49–63]	59 [52–61]	0.786

Unless indicated otherwise, data are presented as n (%), mean±SD, or median (interquartile range). CABG, coronary artery bypass graft; CAD, coronary artery disease; CK, creatine kinase; CKD, chronic kidney disease; CRP, C-reactive protein; eGFR, estimated glomerular filtration rate; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSTEMI, non-ST-segment elevation myocardial infarction; OCT-CN, optical coherence tomography-defined calcified nodules; PCI, percutaneous coronary intervention; STEMI, ST-segment elevation myocardial infarction; WBC, white blood cell.

Angiographic Findings

Angiographic findings are summarized in Table 2. The culprit lesion of patients with OCT-CN was most frequently located in the right coronary arteries (53.6%), whereas the culprit lesion of patients without OCT-CN was most frequently located in the left anterior descending coronary arteries (36.1%; P=0.030). Median preprocedural angiographic SYNTAX scores were higher for patients with than without OCT-CN (median 15 [IQR 11–25] vs. 11 [IQR 7–19]; P=0.003).

Table 2.

Angiographic Findings

	No OCT-CN (n=667)	OCT-CN (n=28)	P value
Pre-PCI assessment
Culprit vessel			0.030
LM	4 (0.6)	1 (3.6)
LAD	356 (53.4)	12 (42.9)
LCX	66 (9.9)	0 (0.0)
RCA	241 (36.1)	15 (53.6)
AHA/ACC Type B2/C	415 (62.2)	23 (82.1)	0.052
TIMI flow grade 0–1	359 (53.8)	12 (42.9)	0.254
SYNTAX score	11 [7–19]	15 [11–25]	0.003
Multivessel disease	175 (26.2)	11 (39.3)	0.190
Post-PCI assessment
TIMI flow grade 3	643 (96.8)	28 (100.0)	1.000
SYNTAX score	0 [0–6]	7 [0–19]	0.001

Unless indicated otherwise, data are presented as n (%) or the median [interquartile range]. ACC, American College of Cardiology; AHA, American Heart Association; LAD, left anterior descending coronary artery; LCX, left circumflex coronary artery; LM, left main coronary artery; OCT-CN, optical coherence tomography-defined calcified nodules; PCI, percutaneous coronary intervention; RCA, right coronary artery; TIMI, Thrombolysis in Myocardial Infarction.

OCT Findings

OCT findings are summarized in Table 3. The prevalence of thrombus and microchannels did not differ significantly between patients with and without OCT-CN. Patients with OCT-CN had a higher prevalence of calcification and a lower prevalence of lipid plaque, thin-cap fibroatheroma, macrophage accumulation, cholesterol crystals, and layered plaque than those without OCT-CN.

Table 3.

Optical Coherence Tomography Findings

	No OCT-CN (n=667)	OCT-CN (n=28)	P value
Lipid plaque	607 (91.0)	10 (35.7)	<0.001
TCFA	396 (59.4)	5 (17.9)	<0.001
Calcification	394 (59.1)	28 (100.0)	<0.001
Thrombus	584 (87.6)	27 (96.4)	0.236
Macrophage accumulation	613 (91.9)	19 (67.9)	<0.001
Cholesterol crystals	364 (54.6)	9 (32.1)	0.032
Microchannels	318 (47.7)	8 (28.6)	0.073
Layered plaque	480 (72.0)	10 (35.7)	<0.001

Unless indicated otherwise, data are presented as n (%). OCT-CN, optical coherence tomography-defined calcified nodules; TCFA, thin-cap fibroatheroma.

Predictors of OCT-CN

Results of uni- and multivariable logistic regression analyses are presented in Table 4. Multivariable analysis demonstrated that age (odds ratio [OR] 1.072; 95% confidence interval [CI] 1.033–1.116; P<0.001), hemodialysis (OR 16.571; 95% CI 4.946–52.863; P<0.001), and Killip Class III/IV heart failure (OR 4.466; 95% CI 1.472–11.943; P=0.004) were significantly associated with the presence of OCT-CN. The prevalence of OCT-CN according to the presence and absence of these clinical predictors is shown in Figure 2. OCT-CN was frequently detected in patients aged 79 years or older (cut-off value derived from ROC curve analysis) complicated with Killip Class III/IV heart failure (OR 13.220; P<0.001) and patients aged 79 years or older on hemodialysis (OR 39.900; P<0.001). The combination of Killip Class III/IV heart failure and hemodialysis improved risk discrimination for OCT-CN when added to the reference clinical model including age (Table 5). The difference in the AUC of prediction models did not reach statistical significance (Model 1 vs. Model 2, P=0.291; Model 2 vs. Model 3, P=0.088).

Table 4.

Univariable and Multivariable Logistic Regression Analyses for Predicting OCT-CN

	Univariable analysis			Multivariable analysis
	OR	95% CI	P value	OR	95% CI	P value
Age	1.068	1.032–1.109	<0.001	1.072	1.033–1.116	<0.001
Male sex	0.427	0.196–0.983	0.037
Body mass index	0.897	0.803–0.993	0.046
STEMI	0.774	0.362–1.699	0.512
Killip III/IV	4.514	1.588–11.190	0.002	4.466	1.472–11.943	0.004
Hypertension	1.351	0.607–3.304	0.480
Dyslipidemia	0.959	0.449–2.103	0.914
Diabetes	2.403	1.116–5.176	0.024
Current smoker	0.306	0.089–0.804	0.030
CKD	2.550	1.192–5.601	0.017
Hemodialysis	16.264	5.211–47.012	<0.001	16.571	4.946–52.863	<0.001
Hemoglobin	0.556	0.442–0.690	<0.001
eGFR	0.963	0.947–0.978	<0.001
LDL-C	0.980	0.968–0.991	<0.001
HDL-C	1.007	0.983–1.026	0.497
Triglyceride	0.994	0.988–0.999	0.055
HbA1c	1.144	0.834–1.467	0.342
CRP	1.045	0.862–1.171	0.539
LVEF	1.009	0.971–1.053	0.651
RCA culprit	2.040	0.953–4.422	0.066
LAD culprit	0.655	0.299–1.400	0.278

CI, confidence interval; OR, odds ratio. Other abbreviations as in Tables 1,2.

Figure 2.

Prevalence of optical coherence tomography-defined calcified nodules according to the presence and absence of clinical predictors.

Table 5.

Prediction Models for the Presence of OCT-CN

	C statistic	95% CI	Relative IDI		Continuous NRI
			Value	P value	Value	P value
Model 1	0.729	0.630–0.828	Ref.		Ref.
Model 2	0.761	0.670–0.852	0.018	0.105	0.315	0.044
Model 3	0.816	0.738–0.895	0.081	0.007	0.642	<0.001

Model 1 (reference model) included age; Model 2 included age and Killip Class III/IV heart failure; and Model 3 included age, Killip Class III/IV heart failure, and hemodialysis. CI, confidence interval; IDI, integrated discrimination improvement; NRI, net reclassification improvement; OCT-CN, optical coherence tomography-defined calcified nodules.

Subgroup Analysis in Non-Dialysis Patients

In the subgroup of 678 non-dialysis patients, OCT-CN was detected in 22 (3.2%) patients. Multivariable analysis demonstrated that age (OR 1.081; 95% CI 1.035–1.135; P<0.001), diabetes (OR 3.046; 95% CI 1.251–7.594; P=0.014), and Killip Class III/IV heart failure (OR 4.414; 95% CI 1.327–12.709; P=0.009) were significantly associated with the presence of OCT-CN (Table 6).

Table 6.

Multivariable Analysis for Predicting OCT-CN in the Non-Dialysis Subgroup

	Univariable analysis			Multivariable analysis
	OR	95% CI	P value	OR	95% CI	P value
Age	1.084	1.042–1.134	<0.001	1.081	1.035–1.135	<0.001
Male sex	0.343	0.145–0.849	0.016	0.576	0.230–1.507	0.245
Body mass index	0.897	0.792–1.006	0.078
STEMI	0.688	0.292–1.652	0.390
Killip III/IV	4.921	1.550–13.243	0.003	4.414	1.327–12.709	0.009
Hypertension	0.958	0.404–2.428	0.923
Dyslipidemia	1.023	0.435–2.512	0.959
Diabetes	2.921	1.240–7.031	0.014	3.046	1.251–7.594	0.014
Current smoker	0.290	0.068–0.864	0.049
CKD	1.674	0.697–3.941	0.237
Hemoglobin	0.732	0.600–0.897	0.002
eGFR	0.977	0.955–0.998	0.034
LDL-C	0.984	0.971–0.996	0.011
HDL-C	1.013	0.988–1.031	0.213
Triglyceride	0.994	0.986–1.000	0.071
HbA1c	1.213	0.875–1.566	0.183
CRP	1.041	0.824–1.180	0.625
LVEF	1.011	0.969–1.060	0.617
RCA culprit	2.520	1.071–6.191	0.036
LAD culprit	0.503	0.198–1.190	0.126

CI, confidence interval; OR, odds ratio. Other abbreviations as in Tables 1,2.

Discussion

The principal findings of the present study are as follows: (1) the prevalence of OCT-CN was 4.0% in patients with ACS who underwent emergency PCI with OCT guidance enrolled in the prospective multicenter registry; (2) the presence of OCT-CN was associated with older age, hemodialysis, and concomitant heart failure; (3) patients with OCT-CN had a higher preprocedural angiographic SYNTAX score; and (4) in non-dialysis patients, the presence of OCT-CN was associated with older age, diabetes, and concomitant heart failure.

Prevalence of OCT-CN in Patients With ACS

Pathology studies reported that 5% of fatal acute coronary thrombosis is caused by CN.²¹ Several OCT studies reported that the prevalence of CN ranges from 3% to 8% in patients with ACS.^7–9,22 Our results are in line with the referenced studies and extended these results with a larger number of patients enrolled in the prospective multicenter registry.

Clinical Predictors of OCT-CN

Several factors have been reported to be associated with the presence of CN. Pathology studies reported that CN resulting in sudden cardiac death occur in older individuals and are associated with comorbidities such as diabetes and chronic kidney disease.^3,23 Several OCT studies reported clinical features associated with the presence of OCT-CN, namely patient characteristics such as older age and hemodialysis, as well as lesion characteristics such as severe calcification and hinge movement.^7–9 Our results are in concordance with the referenced studies. Although the differences in characteristics between dialysis and non-dialysis patients with OCT-CN are of interest, no specific features were found in our results, probably due to the small number of patients with OCT-CN developing ACS.

Our findings also demonstrated that the presence of concomitant heart failure, as represented by Killip Class III/IV, was associated with the presence of OCT-CN. The relationship between the presence of OCT-CN and heart failure remains unclear. Previous studies reported relationships between higher Killip class and a higher prevalence of diabetes,^24,25 3-vessel disease,²⁴ and angiographic coronary artery calcification,²⁶ indicating the presence of advanced atherosclerosis. Because OCT-CN is accompanied by underlying calcified plaque, advanced Killip class may be an indicator of OCT-CN. The extent of coronary artery calcification is associated with the incidence of heart failure and regional left ventricular dysfunction even in the absence of overt coronary artery disease.^27,28 These studies imply that patients with CN-derived ACS accompanied by severe coronary artery calcification may have the potential to present with heart failure.

Our findings showed that the presence of OCT-CN was most prevalent in the right coronary artery and associated with a higher preprocedural angiographic SYNTAX score. Previous studies concordantly reported that CN was frequently located in the right coronary artery,^2,3,9,22,23 whereas the prevalence of CN in the left anterior descending artery varies depending on the study population, ranging from 7.7%²³ to 41.7%.²² A recent pathology study reported that the less calcified segments adjacent to heavily calcified segments are more susceptible to external mechanical forces because of greater movement of the coronary artery during the cardiac cycle, leading to the formation of CN.²³ Our results indicate that lesion complexity, represented by a higher preprocedural angiographic SYNTAX score, may be associated with the presence of OCT-CN.

Clinical Implications

In recent studies, ACS caused by OCT-CN was associated with a worse prognosis.^4,5 The main findings of the TACTICS registry study also demonstrated that the presence of OCT-CN was associated with 1-year major adverse cardiac events (hazard ratio [PE as reference] 4.49; 95% CI 1.35–14.89; P=0.014).⁶ Our results suggest that the likelihood of OCT-CN increases if the patient presenting with ACS is older than 79 years of age and on hemodialysis, or is a non-dialysis patient aged 79 years or older complicated with heart failure. In such patients, special caution should be exercised. The presence of OCT-CN is associated with a higher incidence of target lesion failure.^4,5,29 Appropriate lesion preparation, including the use of debulking devices, such as rotational atherectomy³⁰ and/or intravascular lithotripsy,³¹ during PCI, may need to be considered. Because optimal stent expansion can be hampered by the presence of CN, stentless strategies, such as the combined use of rotational atherectomy and drug-coated balloon angioplasty, can be therapeutic options.³⁰

Study Limitations

This study has some limitations. First, the TACTICS registry was an observational study and the indication for OCT guidance during emergency PCI was at the operator’s discretion; therefore, the present study has an intrinsic risk of selection bias. Second, PCI with OCT guidance was less likely to be performed in patients who were older, had cardiogenic shock and/or renal dysfunction, and had the culprit lesion located in the left main coronary artery or the ostium of the right coronary artery. In a simultaneous parallel observational cohort called the TACTICS Background registry, comprising patients with ACS diagnosed within 24 h of symptom onset who had undergone emergency PCI but not been enrolled in the TACTICS registry, the main clinical reasons for avoiding the use of OCT were cardiogenic shock (14.5%), lesion anatomy (9.6%), and renal failure (6.9%).⁶ Finally, clinical outcomes were not evaluated in the present study.

Conclusions

The TACTICS registry demonstrated the clinical predictors of OCT-CN, which may be associated with worse prognosis. In addition to age and hemodialysis, diabetes, Killip Class III/IV heart failure, and a higher preprocedural angiographic SYNTAX score were significantly associated with the presence of OCT-CN. Our results indicate that OCT-CN may potentially be caused by multiple factors indicating the presence of advanced atherosclerosis.

Acknowledgments

None.

Sources of Funding

The TACTICS registry study was sponsored by Abbott Medical Japan LLC (Tokyo, Japan). Other than financial sponsorship, the company had no role in study protocol development or implementation, management, data collection, or analysis. The authors and their colleagues were solely responsible for the design and execution of this study.

Disclosures

J. Yamaguchi was endowed by Abbott Medical Japan LLC, Boston Scientific Japan K.K., Medtronic Japan Co., Ltd., and Terumo Corporation. T.M. has received consultancy fees from Zeon Medical Inc., research grants from Boston Scientific Japan K.K., and speaker fees from Abbott Medical Japan LLC, CathWorks G.K., and Boston Scientific Japan K.K. T. Shinke has received personal fees and research grants from Abbott Medical Japan LLC. Y.I. is a member of Circulation Journal’s Editorial Board. All other authors have no relationships relevant to the contents of this paper to disclose.

IRB Information

The study protocol was approved by the Institutional Ethics Committee on Human Research of Tsuchiura Kyodo General Hospital (Approval no. 2022FY72).

Data Availability

The deidentified participant data will not be shared.

Supplementary Files

Please find supplementary file(s);

https://doi.org/10.1253/circj.CJ-24-0111

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