Daniel S. Ong

A Combined Optical Coherence Tomography and Intravascular Ultrasound Study on Plaque Rupture, Plaque Erosion, and Calcified Nodule in Patients With ST-Segment Elevation Myocardial Infarction: Incidence, Morphologic Characteristics, and Outcomes After Percutaneous Coronary Intervention.

OBJECTIVES This study sought to evaluate the incidence of plaque rupture (PR), plaque erosion (PE), and calcified nodule (CN) using optical coherence tomography (OCT) in patients with ST-segment elevation myocardial infarction (STEMI); to compare detailed morphologic plaque characteristics of PR, PE, and CN with optical coherence tomography and intravascular ultrasound; and to compare the post-procedure outcomes among PR, PE, and CN. BACKGROUND The incidence and detailed morphologic characteristics of PR, PE, and CN in STEMI patients and their outcome after percutaneous coronary intervention (PCI) are unknown. METHODS A total of 112 STEMI patients who underwent PCI within 24 h [corrected] from symptom onset were included. Both optical coherence tomography and intravascular ultrasound were performed following aspiration thrombectomy. RESULTS The incidence of PR, PE, and CN was 64.3%, 26.8%, and 8.0%, respectively. PE and CN, compared with PR, had more fibrous plaque (p < 0.001 and p < 0.001) and less thin-cap fibroatheroma (p < 0.001 and p < 0.001) as well as smaller plaque burden (p = 0.003 and p = 0.001) and remodeling index (p = 0.003 and p < 0.001). PE had greater plaque eccentricity index than PR and CN (p < 0.001 and p < 0.001). CN had greater calcified arc and shallower calcium than PR (p < 0.001 and p < 0.001) or PE (p < 0.001 and p < 0.001). More than one-half of CN had negative remodeling. PE had a lower incidence of no-reflow phenomenon after PCI than PR (p = 0.011). CONCLUSIONS PE was the underlying mechanism in one-fourth of STEMI. PE was characterized by eccentric fibrous plaque. CN was characterized by superficial large calcium and negative remodeling. PE was associated with less microvascular damage after PCI.

Incidence and Clinical Significance of Poststent Optical Coherence Tomography Findings One-Year Follow-Up Study From a Multicenter Registry

Background— Optical coherence tomography (OCT) was recently introduced to optimize percutaneous coronary intervention. However, the exact incidence and significance of poststent OCT findings are unknown. Methods and Results— A total of 900 lesions treated with 1001 stents in 786 patients who had postprocedure OCT imaging were analyzed to evaluate the incidence of poststent OCT findings and to identify the OCT predictors for device-oriented clinical end points, including cardiac death, target vessel–related myocardial infarction, target lesion revascularization, and stent thrombosis. Patients were followed up to 1 year. Stent edge dissection was detected in 28.7% of lesions, and incomplete stent apposition was detected in 39.1% of lesions. The incidences of smooth protrusion, disrupted fibrous tissue protrusion, and irregular protrusion were 92.9%, 61.0%, and 53.8%, respectively. Small minimal stent area, defined as a lesion with minimal stent area <5.0 mm2 in a drug-eluting stent or <5.6 mm2 in a bare metal stent, was observed in 40.4% of lesions. One-year device-oriented clinical end points occurred in 33 patients (4.5%). Following adjustment, irregular protrusion and small minimal stent area were independent OCT predictors of 1-year device-oriented clinical end points (P=0.003 and P=0.012, respectively). Conclusions— Abnormal poststent OCT findings were frequent. Irregular protrusion and small minimal stent area were independent predictors of 1-year device-oriented clinical end points, which were primarily driven by target lesion revascularization.Background— Optical coherence tomography (OCT) was recently introduced to optimize percutaneous coronary intervention. However, the exact incidence and significance of poststent OCT findings are unknown. Methods and Results— A total of 900 lesions treated with 1001 stents in 786 patients who had postprocedure OCT imaging were analyzed to evaluate the incidence of poststent OCT findings and to identify the OCT predictors for device-oriented clinical end points, including cardiac death, target vessel–related myocardial infarction, target lesion revascularization, and stent thrombosis. Patients were followed up to 1 year. Stent edge dissection was detected in 28.7% of lesions, and incomplete stent apposition was detected in 39.1% of lesions. The incidences of smooth protrusion, disrupted fibrous tissue protrusion, and irregular protrusion were 92.9%, 61.0%, and 53.8%, respectively. Small minimal stent area, defined as a lesion with minimal stent area <5.0 mm2 in a drug-eluting stent or <5.6 mm2 in a bare metal stent, was observed in 40.4% of lesions. One-year device-oriented clinical end points occurred in 33 patients (4.5%). Following adjustment, irregular protrusion and small minimal stent area were independent OCT predictors of 1-year device-oriented clinical end points ( P =0.003 and P =0.012, respectively). Conclusions— Abnormal poststent OCT findings were frequent. Irregular protrusion and small minimal stent area were independent predictors of 1-year device-oriented clinical end points, which were primarily driven by target lesion revascularization. # CLINICAL PERSPECTIVE {#article-title-35}

Causes, assessment, and treatment of stent thrombosis[mdash]intravascular imaging insights

Stent thrombosis is a rare, but serious, complication of percutaneous coronary intervention and is associated with severe morbidity and mortality. In addition to clinical and pathological studies, intravascular imaging has advanced our understanding of the mechanisms underlying stent thrombosis. In particular, intravascular imaging has been used to study stent underexpansion, malapposition, uncovered struts, and neoatherosclerosis as risk factors for stent thrombosis. Intravascular ultrasonography and optical coherence tomography can be used to guide stent implantation and minimize the risk of stent thrombosis. Additionally, optical coherence tomography offers the unique potential to tailor treatment of stent thrombosis to address the specific mechanism underlying the thrombotic event. Bioresorbable stent technologies have been introduced with the goal of further reducing the incidence of stent thrombosis, and intravascular imaging has had an integral role in the development and assessment of these new devices. In this Review, we present insights gained through intravascular imaging into the causes of stent thrombosis, and the potential utility of intravascular imaging in the optimization of stent deployment and treatment of stent thrombosis events.

Morphological predictors for no reflow phenomenon after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction caused by plaque rupture

Aims Myocardial no reflow after percutaneous coronary intervention (PCI) is associated with poor outcome. Patients with ST-segment elevation myocardial infarction (STEMI) caused by plaque rupture are at high risk for no reflow. However, specific morphologic characteristics associated with no reflow are unknown in this population. The aim of this study is to identify the morphological characteristics of culprit plaques associated with no reflow in patients with STEMI caused by plaque rupture using both optical coherence tomography (OCT) and intravascular ultrasound (IVUS). Methods and results We enrolled 145 patients with STEMI who underwent both OCT and IVUS within 12 h of symptom onset. Among these patients, we excluded those with plaque erosion and calcified nodule and included 72 patients who had plaque rupture as an underlying mechanism for STEMI. Myocardial no reflow, defined as Thrombolysis in Myocardial Infarction flow grade 0–2 and/or myocardial blush grade 0–1 after PCI, was observed in 28 patients (38.9%). Onset to recanalization time was similar between the groups with and without no reflow. Receiver-operating curve analysis revealed OCT-derived lipid index > 3500 [area under curve (AUC) 0.77, P < 0.001] and IVUS-derived plaque burden > 81.5% (AUC 0.70, P = 0.002) were the best discriminators for myocardial no reflow. Conclusion No reflow occurred in nearly 40% of patients with STEMI caused by plaque rupture. Large lipid index and plaque burden were critical morphological discriminators between no reflow and normal flow.

Prevalence and Predictors of Multiple Coronary Plaque Ruptures: In Vivo 3-Vessel Optical Coherence Tomography Imaging Study

Objective—Plaque rupture may be the local expression of a widespread coronary instability. This study aimed to investigate: (1) the prevalence and characteristics of nonculprit plaque rupture; (2) the pancoronary atherosclerotic phenotype in patients with and without nonculprit plaque rupture; and (3) the prevalence and predictors of multiple plaque ruptures. Approach and Results—Six hundred and seventy-five nonculprit plaques from 261 patients (34 acute myocardial infarction, 73 unstable angina pectoris, and 154 stable angina pectoris) were analyzed by 3-vessel optical coherence tomography. Nonculprit plaque ruptures were identified in 51 patients (20%). Patients with nonculprit plaque ruptures had higher prevalence of thin-cap fibroatheroma (51% versus 13%; P<0.001) in the 3 major epicardial coronary vessels. Multiple plaque ruptures were observed in 20% of patients (38% acute myocardial infarction versus 10% unstable angina pectoris versus 19% stable angina pectoris; P=0.042). Thin-cap fibroatheroma, intimal vasculature, and macrophages were independent morphological predictors of multiple plaque ruptures, whereas acute myocardial infarction and chronic kidney disease were independent clinical predictors. Patients with nonculprit plaque ruptures showed higher 1-year rates of nontarget lesion revascularization (11.8% versus 4.4%; P=0.039). Conclusions—Nonculprit plaque ruptures were observed in 20% of patients with coronary artery disease and were associated with pancoronary vulnerability and higher 1-year revascularization rate.

Coronary Calcification and Plaque Vulnerability: An Optical Coherence Tomographic Study.

Background— Spotty superficial calcium deposits have been implicated in plaque vulnerability based on previous intravascular imaging studies. Biomechanical models suggest that microcalcifications between 5 and 65 µm in diameter can intensify fibrous cap stress, promoting plaque rupture. However, the 100- to 200-µm resolution of intravascular ultrasound limits its ability to discriminate single calcium deposits from clusters of smaller deposits, and a previous optical coherence tomographic investigation evaluated calcifications within a long segment of artery, which may not truly reflect the mechanics involved in potentiating focal plaque rupture. Methods and Results— Detailed optical coherence tomographic assessment of coronary calcification at the culprit plaque (10-mm length) was performed in 53 patients with acute ST-segment–elevation myocardial infarction mediated by plaque rupture and 55 patients with stable angina pectoris. The number and longitudinal length of individual calcium deposits were recorded. Cross-sectional images were analyzed every 1 mm for calcium arc and depth, and these quantitative parameters were used to define individual deposits as spotty, large, and superficial. There was no significant difference between ST-segment–elevation myocardial infarction mediated by plaque rupture and stable angina pectoris groups in the number of total ( P =0.58), spotty ( P =0.87), or large calcium deposits ( P =0.27). Minimum calcium depth was similar between groups ( P =0.27), as was the number of superficial deposits ( P =0.35 using a 65-µm depth threshold and P =0.84 using a 100-µm depth threshold). Conclusions— The number and pattern of culprit plaque calcifications did not differ between patients presenting with ST-segment–elevation myocardial infarction mediated by plaque rupture versus stable angina pectoris. The optical coherence tomographic assessment of coronary calcification may not be a useful marker of local plaque vulnerability as previously suspected. Registration Information— URL: . Unique identifier: [NCT01110538][1]. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT01110538&atom=%2Fcirccvim%2F9%2F1%2Fe003929.atomBackground—Spotty superficial calcium deposits have been implicated in plaque vulnerability based on previous intravascular imaging studies. Biomechanical models suggest that microcalcifications between 5 and 65 µm in diameter can intensify fibrous cap stress, promoting plaque rupture. However, the 100- to 200-µm resolution of intravascular ultrasound limits its ability to discriminate single calcium deposits from clusters of smaller deposits, and a previous optical coherence tomographic investigation evaluated calcifications within a long segment of artery, which may not truly reflect the mechanics involved in potentiating focal plaque rupture. Methods and Results—Detailed optical coherence tomographic assessment of coronary calcification at the culprit plaque (10-mm length) was performed in 53 patients with acute ST-segment–elevation myocardial infarction mediated by plaque rupture and 55 patients with stable angina pectoris. The number and longitudinal length of individual calcium deposits were recorded. Cross-sectional images were analyzed every 1 mm for calcium arc and depth, and these quantitative parameters were used to define individual deposits as spotty, large, and superficial. There was no significant difference between ST-segment–elevation myocardial infarction mediated by plaque rupture and stable angina pectoris groups in the number of total (P=0.58), spotty (P=0.87), or large calcium deposits (P=0.27). Minimum calcium depth was similar between groups (P=0.27), as was the number of superficial deposits (P=0.35 using a 65-µm depth threshold and P=0.84 using a 100-µm depth threshold). Conclusions—The number and pattern of culprit plaque calcifications did not differ between patients presenting with ST-segment–elevation myocardial infarction mediated by plaque rupture versus stable angina pectoris. The optical coherence tomographic assessment of coronary calcification may not be a useful marker of local plaque vulnerability as previously suspected. Registration Information—URL: http://www.clinicaltrials.gov. Unique identifier: NCT01110538.

Prevalence and Predictors of Multiple Coronary Plaque Ruptures

Objective—Plaque rupture may be the local expression of a widespread coronary instability. This study aimed to investigate: (1) the prevalence and characteristics of nonculprit plaque rupture; (2) the pancoronary atherosclerotic phenotype in patients with and without nonculprit plaque rupture; and (3) the prevalence and predictors of multiple plaque ruptures. Approach and Results—Six hundred and seventy-five nonculprit plaques from 261 patients (34 acute myocardial infarction, 73 unstable angina pectoris, and 154 stable angina pectoris) were analyzed by 3-vessel optical coherence tomography. Nonculprit plaque ruptures were identified in 51 patients (20%). Patients with nonculprit plaque ruptures had higher prevalence of thin-cap fibroatheroma (51% versus 13%; P<0.001) in the 3 major epicardial coronary vessels. Multiple plaque ruptures were observed in 20% of patients (38% acute myocardial infarction versus 10% unstable angina pectoris versus 19% stable angina pectoris; P=0.042). Thin-cap fibroatheroma, intimal vasculature, and macrophages were independent morphological predictors of multiple plaque ruptures, whereas acute myocardial infarction and chronic kidney disease were independent clinical predictors. Patients with nonculprit plaque ruptures showed higher 1-year rates of nontarget lesion revascularization (11.8% versus 4.4%; P=0.039). Conclusions—Nonculprit plaque ruptures were observed in 20% of patients with coronary artery disease and were associated with pancoronary vulnerability and higher 1-year revascularization rate.

Incidence and Clinical Significance of Post-Stent OCT Findings: One Year Follow-Up Study From a Multicenter Registry

Background— Optical coherence tomography (OCT) was recently introduced to optimize percutaneous coronary intervention. However, the exact incidence and significance of poststent OCT findings are unknown. Methods and Results— A total of 900 lesions treated with 1001 stents in 786 patients who had postprocedure OCT imaging were analyzed to evaluate the incidence of poststent OCT findings and to identify the OCT predictors for device-oriented clinical end points, including cardiac death, target vessel–related myocardial infarction, target lesion revascularization, and stent thrombosis. Patients were followed up to 1 year. Stent edge dissection was detected in 28.7% of lesions, and incomplete stent apposition was detected in 39.1% of lesions. The incidences of smooth protrusion, disrupted fibrous tissue protrusion, and irregular protrusion were 92.9%, 61.0%, and 53.8%, respectively. Small minimal stent area, defined as a lesion with minimal stent area <5.0 mm2 in a drug-eluting stent or <5.6 mm2 in a bare metal stent, was observed in 40.4% of lesions. One-year device-oriented clinical end points occurred in 33 patients (4.5%). Following adjustment, irregular protrusion and small minimal stent area were independent OCT predictors of 1-year device-oriented clinical end points (P=0.003 and P=0.012, respectively). Conclusions— Abnormal poststent OCT findings were frequent. Irregular protrusion and small minimal stent area were independent predictors of 1-year device-oriented clinical end points, which were primarily driven by target lesion revascularization.Background— Optical coherence tomography (OCT) was recently introduced to optimize percutaneous coronary intervention. However, the exact incidence and significance of poststent OCT findings are unknown. Methods and Results— A total of 900 lesions treated with 1001 stents in 786 patients who had postprocedure OCT imaging were analyzed to evaluate the incidence of poststent OCT findings and to identify the OCT predictors for device-oriented clinical end points, including cardiac death, target vessel–related myocardial infarction, target lesion revascularization, and stent thrombosis. Patients were followed up to 1 year. Stent edge dissection was detected in 28.7% of lesions, and incomplete stent apposition was detected in 39.1% of lesions. The incidences of smooth protrusion, disrupted fibrous tissue protrusion, and irregular protrusion were 92.9%, 61.0%, and 53.8%, respectively. Small minimal stent area, defined as a lesion with minimal stent area <5.0 mm2 in a drug-eluting stent or <5.6 mm2 in a bare metal stent, was observed in 40.4% of lesions. One-year device-oriented clinical end points occurred in 33 patients (4.5%). Following adjustment, irregular protrusion and small minimal stent area were independent OCT predictors of 1-year device-oriented clinical end points ( P =0.003 and P =0.012, respectively). Conclusions— Abnormal poststent OCT findings were frequent. Irregular protrusion and small minimal stent area were independent predictors of 1-year device-oriented clinical end points, which were primarily driven by target lesion revascularization. # CLINICAL PERSPECTIVE {#article-title-35}

Changes in coronary plaque morphology in patients with acute coronary syndrome versus stable angina pectoris after initiation of statin therapy.

ObjectivesThe aim of this study was to examine coronary plaque morphology after initiation of statins and compare changes in plaque morphology in patients presenting with acute coronary syndrome (ACS) versus stable angina pectoris (SAP). BackgroundACS is associated with a pan-inflammatory state, and intraplaque features of inflammation correlate with coronary plaque progression. Statins have known anti-inflammatory properties that may contribute toward their beneficial cardiovascular effects. MethodsSixty-nine statin-naive patients (ACS, n=55; SAP, n=14) underwent baseline imaging with optical coherence tomography and intravascular ultrasound. Repeat imaging was performed at 6 and 12 months. A total of 97 nonculprit plaques were analyzed (ACS, n=74; SAP, n=23). ResultsFibrous cap thickness increased in both ACS and SAP patients (all P<0.001 compared with the baseline); the ACS group showed greater percent change in fibrous cap thickness at 12 months (192.8±148.9% in ACS vs. 128.2±88.7% in SAP, P=0.018). The ACS group also showed a significant decrease in plaque microvessels (44.6% at baseline vs. 26.6% at 12 months, P=0.0386). ConclusionCompared with patients with SAP, patients presenting with ACS show more favorable changes in plaque morphology after starting statin treatment. This supports a potential additive benefit of statins in the inflammatory state of ACS and reaffirms the clinical importance of statin therapy for coronary atherosclerosis.

Associations between the Framingham Risk Score and coronary plaque characteristics as assessed by three-vessel optical coherence tomography.

ObjectivesThis study sought to explore the association between the Framingham Risk Score (FRS) and coronary plaque characteristics assessed by optical coherence tomography (OCT) imaging. BackgroundClinical prediction models are useful for identifying high-risk patients. However, coronary events often occur in individuals estimated to be at low risk. MethodsA total of 254 patients with coronary artery disease who underwent three-vessel OCT were divided into tertiles according to FRS. Nonculprit plaque characteristics were compared among the three groups. ResultsA total of 663 plaques were analyzed. FRS was significantly associated with calcification [37% (low FRS) vs. 46% (intermediate FRS) vs. 70% (high FRS); P<0.001] and neovascularization [39% (low FRS) vs. 41% (intermediate FRS) vs. 56% (high FRS); P<0.001], but not with lipid-rich plaques or thin-cap fibroatheroma (TCFA). On multivariate analysis, FRS was an independent predictor of the presence of both calcification and neovascularization. There were no deaths, two acute myocardial infarctions, and 15 nontarget lesion revascularizations at the 1-year follow-up. The event rate increased progressively across FRS tertiles [2.4% (low FRS) vs. 7.1% (intermediate FRS) vs. 8.6% (high FRS); P=0.186]. The c-statistic for FRS to predict future clinical events was 0.628 (95% confidence interval, 0.500−0.757). The addition of both calcification and TCFA to FRS provided incremental prognostic value [c-statistics: 0.761 (95% confidence interval, 0.631−0.890)]. ConclusionThe present study showed significant associations between FRS and the presence of coronary calcification and neovascularization in nonculprit plaques. The combination of FRS and OCT-detected calcifications and TCFA provides improved prognostic ability in identifying patients with known coronary artery disease who are at risk of recurrent events.