Culprit Plaques In Patients Research Articles

Fractal geometry of culprit coronary plaque images within optical coherence tomography in patients with acute coronary syndrome vs stable angina pectoris.

The main cause of acute coronary syndrome (ACS) is plaque rupture and thrombus formation. However, it has not been fairly successful to identify vulnerable plaque to rupture using conventional parameters of intravascular imaging modalities. Fractal analysis is one of the mathematical models to examine geometrical features of picture image using a specific parameter called as fractal dimension (FD) which suggests geometric complexity of the image. This study examined FD of the optical coherence tomography (OCT)-derived images of the culprit plaque in patients with ACS vs stable angina pectoris (SAP) to evaluate the feasibility of FD for identifying vulnerable coronary plaques prone to provoke ACS distinguished from stable plaques only provoking SAP. We examined 65 cases (34 ACS patients, 31 SAP patients) in which the culprit lesion was imaged by OCT before percutaneous coronary intervention in patients with ACS and SAP. The culprit plaque lesion in the ACS group had a significantly larger mean lipid arc (203.8 ± 39.4° vs 152.3 ± 34.5°, p < 0.001) and a larger lipid plaque length (12.6 ± 5.1mm vs 7.7 ± 2.7mm, p < 0.001) and a thinner fibrous cap thickness (75.3 ± 22.3μm vs 134.8 ± 53.2μm, p < 0.001) than those in the SAP group. The prevalence of OCT-derived macrophage infiltration (Mph) in the entire culprit coronary vessel as well as that of the OCT-derived thin-cap fibroatheroma (TCFA) at the culprit lesion were significantly greater in the ACS group than those in the SAP group, respectively (Mph: 61.8% vs 35.5%, p = 0.048; TCFA: 44.1% vs 6.4%, p < 0.001). The FD of culprit plaque in the ACS group was significantly greater than in the SAP group (2.401 ± 0.073 vs 2.341 ± 0.051, p < 0.001). In multivariate regression analysis, the presence of Mph was a significant determinant of FD (regression coefficient estimate 0.049, CI 0.018-0.079, p = 0.002). The FD of OCT-derived image of culprit coronary plaque in the ACS group was significantly greater than that in the SAP group, indicating that the culprit plaque in ACS were structurally more complex. Therefore, fractal analysis of coronary OCT images might be clinically useful for identifying coronary plaques prone to provoke ACS.

Predictive value of the serum uric acid to high-density lipoprotein cholesterol ratio for culprit plaques in patients with acute coronary syndrome

BackgroundHyperuricemia and low level of high-density lipoprotein cholesterol (HDL-C) are both risk factors for coronary artery disease (CAD). The uric acid to HDL-C ratio (UHR) has recently been identified as a new inflammatory and metabolic biomarker. However, the relationship between the UHR and coronary culprit plaques has not been fully investigated in patients with acute coronary syndrome (ACS).MethodsA total of 346 patients with ACS were enrolled in this study. Culprit lesion characteristics were assessed by optical coherence tomography (OCT). Logistic regression and linear correlation analyses were performed to assess the association between the UHR and culprit plaques. The predictive value of the UHR was investigated by receiver operating characteristic (ROC) curve analysis.ResultsThe percentages of typical culprit plaques, including ruptures, erosions and thrombi, were greater in the high-UHR subgroup than those in the low-UHR subgroup. A positive relationship was also found between the UHR and diameter stenosis (r = 0.160, P = 0.003) and between the UHR and area stenosis (r = 0.145, P = 0.007). The UHR was found to be independently associated with plaque rupture, erosion and thrombus. Furthermore, ROC analysis suggested that the UHR had a better predictive value than low-density lipoprotein cholesterol.ConclusionsAn elevated UHR level was independently related to the occurrence rate of culprit plaques. The UHR is a simple and easily acquired parameter for detecting culprit plaques in patients with ACS.

Abstract TP89: Ldl Levels May Correlate With Intracranial Atherosclerotic Plaque Enhancement

Introduction: The enhancement of atherosclerotic plaques after the intravenous administration of gadolinium (Gd) has been correlated with the presence of culprit plaques in patients with acute strokes due to underlying intracranial atherosclerosis (ICAS). A new method to objectively quantify Gd-enhancement was used to monitor plaques over time after an acute stroke. Currently there is no imaging method to accurately monitor atherosclerotic activity. Methods: Patients with stroke or transient ischemic attack caused by ICAS were included. Every patient was started on high-dose statins after ictus. 7T MRI images were obtained at baseline and after at least 6 months. LDL levels were obtained at the time of the event and at follow-up. Culprit plaques were identified based on degree of stenosis, presence of positive remodeling and Gd-enhancement. Arterial 3D enhancement maps in the territory of the culprit plaque were generated. Orthogonal signal intensity (SI) probes were expanded into the plaque and parent vessel to generate 3D enhancement color maps. Arterial segment variance (ASV) (SD 2 Arterial segment Baseline T1+Gd - SD 2 Arterial segment Follow up T1+Gd ) was used to compare the plaque and parent vessel enhancement. Results: Five patients underwent baseline and follow-up imaging. The median time between scans was 13.3 (IQR=13.3) months. ASV was strongly correlated with changes in LDL (Rho=0.9, p=0.037). Additionally, Gd-enhancement and plaque burden correlated with levels of LDL (Figure): Gd uptake (Rho=0.7, p=0.22) and plaque burden (Rho=0.67, p=0.22). Conclusion: This pilot study demonstrates that high-resolution imaging can be used in determining the response to statins in patients with high atherosclerotic burden. Gd-enhancement and plaque burden correlated with serum values of LDL. 3D enhancement maps and histogram analysis of atherosclerotic plaques are promising tools for evaluating disease activity and response to medical therapy.

Relationship between the stroke mechanism of symptomatic middle cerebral artery atherosclerotic diseases and culprit plaques based on high-resolution vessel wall imaging.

PurposeFor patients with symptomatic middle cerebral artery (MCA) atherosclerotic stenosis, identifying the potential stroke mechanisms may contribute to secondary prevention. The purpose of the study is to explore the relationship between stroke mechanisms and the characteristics of culprit plaques in patients with atherosclerotic ischemic stroke in the M1 segment of the middle cerebral artery (MCA) based on high-resolution vessel wall imaging (HR-VWI).MethodsWe recruited 61 patients with acute ischemic stroke due to MCA atherosclerotic stenosis from Shenzhen Bao'an District People's Hospital. According to prespecified criteria based on infarct topography and magnetic resonance angiography, possible stroke mechanisms were divided into parent artery atherosclerosis occluding penetrating artery (P), artery-to-artery embolism (A), hypoperfusion (H), and mixed mechanisms (M). The correlation between the characteristics of MCA M1 culprit plaque and different stroke mechanisms was analyzed using HR-VWI. The indicators included plaque surface irregularity, T1 hyperintensity, location, plaque burden (PB), remodeling index (RI), enhancement rate, and stenosis rate.ResultsParental artery atherosclerosis occluding penetrating artery was the most common mechanism (37.7%). The proposed criteria showed substantial to excellent interrater reproducibility (κ, 0.728; 0.593–0.863). Compared with the P group, the surface irregularity, T1 hyperintensity, and obvious enhancement of the culprit plaque in the A group were more common (p < 0.0125). Compared with the other stroke mechanisms, positive remodeling of culprit plaques was more common (p < 0.0125), the RI was greater (p < 0.05), and the PB was the smallest (p < 0.05) in the P group. The enhancement ratio (ER) was smaller in the P group (p < 0.05). Compared with the A group, T1 hyperintensity of the culprit plaque was more common in the H group (p < 0.0125), and the stenosis rate was greater (p < 0.05). After adjustment for clinical demographic factors in the binary logistic regression analysis, the enhancement level (odds ratio [OR] 0.213, 95% CI (0.05–0.91), p = 0.037) and PB of culprit plaque (OR 0, 95% CI (0–0.477), p = 0.034) were negatively associated with P groups.ConclusionThe culprit plaque characteristics of patients with symptomatic MCA atherosclerotic in different stroke mechanisms may be evaluated using HR-VWI. The plaque characteristics of different stroke mechanisms may have clinical value for the selection of treatment strategies and prevention of stroke recurrence.Clinical trial registrationIdentifier: ChiCTR1900028533.

Clinical Outcomes of Different Calcified Culprit Plaques in Patients with Acute Coronary Syndrome.

Background: Previous studies have found that coronary artery calcification is closely associated with the occurrence of major adverse cardiac events (MACE). This study aimed to investigate the characteristics and clinical outcomes of different calcified plaques in patients with acute coronary syndrome (ACS) by using optical coherence tomography (OCT). Methods: 258 ACS patients with calcified culprit plaques who underwent OCT-guided stent implantation were enrolled. They were divided into three subtypes based on the calcified plaque morphology, including eruptive calcified nodules, calcified protrusion, and superficial calcific sheet. Results: Compared with superficial calcific sheet and calcified protrusion, eruptive calcified nodules had the greatest calcium burden and a higher rate of stent edge dissection (p < 0.001) and incomplete stent apposition (p < 0.001). In a median follow-up period of 2 years, 39 (15.1%) patients experienced MACE (a composite event of cardiac death, target-vessel myocardial infarction, ischemia-driven revascularization), with a significantly higher incidence in the eruptive calcified nodules group (32.1% vs. 10.1% vs. 13.0%, p = 0.001). A multivariate Cox analysis demonstrated that the eruptive calcified nodules (hazard ratio 3.14; 95% confidence interval, 1.64–6.02; p = 0.001) were an independent predictor of MACE. Conclusions: MACE occurred more frequently in ACS patients with eruptive calcified nodules, and the eruptive calcified nodules were an independent predictor of MACE.

Abstract 10824: High Bleeding Risk is Associated with a Higher Prevalence of Severe Calcified Plaque in Patients Requiring Percutaneous Coronary Intervention

Introduction: Optimal revascularization strategy and shorter duration of dual antiplatelet are required in patients with coronary artery disease concomitant with high bleeding risk (HBR). More complex percutaneous coronary intervention (PCI) and subsequent high thrombotic risk in patients with HBR have been also demonstrated. However, the characteristics of culprit plaque in patients with HBR remains to be elucidated. Hypothesis: HBR is associated with more complex plaque in culprit lesion in patients requiring PCI. Methods: A total of 362 consecutive patients with stable coronary disease, who underwent optical coherence tomography (OCT) imaging of the culprit lesion during PCI were included. The characteristics of culprit plaque assessed by OCT were compared between the HBR group (n=196) and the non-HBR group (n=166), which were classified based on the Academic Research Consortium for High Bleeding Risk (ARC-HBR). Results: The prevalence of severe calcified plaque (angle &gt;180 degee, thickness &gt;0.5mm and length &gt;5mm) was significantly higher in the higher HBR group than in the non-HBR group (48 vs. 35%, p =0.016), although other characteristics were comparable (Panel A). Among patients with HBR, the incremental prevalence of severe calcified plaque according to the number of major ARC-HBR criteria met was observed ( p &lt;0.001) (Panel B). Conclusions: HBR was associated with a higher prevalence of severe calcified plaque in culprit lesion in patients with stable coronary disease requiring PCI. The greater number of major ARC-HBR criteria met was associated with a higher prevalence of severe calcified plaque among patients with HBR.

Abstract 12976: Higher Triglyceride Level is Associated With Higher Frequency of Macrophage Accumulation in Coronary Plaques

Introduction: The impact of high triglyceride (TG) level on the characteristics of coronary plaque remains to be elucidated. Hypothesis: Higher TG level is associated with higher prevalence of vulnerable coronary plaque in patients with coronary artery disease (CAD). Methods: A total of 865 consecutive patients who underwent optical coherence tomography (OCT) imaging of the culprit lesion were included. Patients were classified into either the higher TG group (non-fasting TG ≥ 200 mg/dL, n=150) or the lower TG group (non-fasting TG &lt; 200 mg/dL, n=715). The morphologies of culprit plaque assessed by OCT were compared between the two groups. Results: The median (interquartile range) of TG in the 2 groups was 265.5 (221.5 – 314.8) mg/dL and 115.0 (84.0 – 152.0) mg/dL, respectively. The frequency of macrophage accumulation was significantly higher in the higher TG group than the lower TG group (41 vs. 33%, p=0.043) (Panel A), whereas the prevalence of other plaque components including thin-cap fibroatheroma (22 vs. 19%, p=0.386), microchannel (24 vs. 25%, p=0.907) and cholesterol crystal (23 vs. 23%, p=0.862) was comparable between the two groups. The incremental frequency of macrophage accumulation according to TG levels was observed (p=0.015, Panel B). Although the frequency of macrophage accumulation was comparable between the 2 groups among patients with a higher HDL cholesterol (HDL-C) level (&gt;35 mg/dL), macrophage accumulation was significantly more frequent in the higher TG group than in the lower TG group (71 vs. 41%, p=0.032) among patients with a lower HDL-C level (≤35 mg/dL). Conclusions: Higher TG level was associated with higher frequency of macrophage accumulation in culprit plaques in patients with CAD. The present results may partly explain the role of TG on the development of culprit plaque in coronary artery.

Frequency, Predictors, Distribution, and Morphological Characteristics of Layered Culprit and Nonculprit Plaques of Patients With Acute Myocardial Infarction: In Vivo 3-Vessel Optical Coherence Tomography Study.

Subclinical atherothrombosis and plaque healing may lead to rapid plaque progression. The histopathologic healed plaque has a layered appearance when imaged using optical coherence tomography. We assessed the frequency, predictors, distribution, and morphological characteristics of optical coherence tomography layered culprit and nonculprit plaques in patients with acute myocardial infarction. A prospective series of 325 patients with acute myocardial infarction underwent optical coherence tomography imaging of all 3 native coronary arteries. Layered plaque phenotype had heterogeneous signal-rich layered tissue located close to the luminal surface that was clearly demarcated from the underlying plaque. Layered plaques were detected in 74.5% of patients with acute myocardial infarction. Patients with layered culprit plaques had more layered nonculprit plaques; and they more often had preinfarction angina, ST-segment-elevation myocardial infarction, higher low-density lipoprotein cholesterol, and absence of antiplatelet therapy. Layered plaques tended to cluster in the proximal segment of the left anterior descending artery and left circumflex artery but were more uniformly distributed in the right coronary artery. As compared with nonlayered plaques, layered plaques had greater optical coherence tomography lumen area stenosis at both culprit and nonculprit sites. The frequency of layered plaque phenotype (P=0.038) and maximum area of layered tissue (P<0.001) increased from nonculprit thin-cap fibroatheromas to nonculprit ruptures to culprit ruptures. Layered plaques were identified in 3-quarters of patients with acute myocardial infarction, especially in the culprit plaques of patients with ST-segment-elevation myocardial infarction. Layered plaques had a limited, focal distribution in the left anterior descending artery, and left circumflex artery but were more evenly distributed in the right coronary artery and were characterized by greater lumen narrowing at both culprit and nonculprit sites. Graphic Abstract: A graphic abstract is available for this article.

Characteristics of non-culprit plaques in acute coronary syndrome patients with calcified plaque at the culprit lesion.

To investigate the non-culprit plaques (NCPs) characteristics in acute coronary syndrome (ACS) patients with calcified plaques (CP). Recently, a new in vivo classification of calcified culprit plaques in patients with ACS was proposed. Characteristics of NCPs in this group of patients are unknown. A total of 692 NCPs from 492 ACS patients were retrospectively compared based on the culprit plaque phenotype: 71 from CP patients, 383 from plaque rupture (PR) patients, 238 from plaque erosion (PE) patients. NCPs of CP patients had greater maximal calcium thickness, wider calcium arc, longer calcium length, and greater calcium index, compared to PR or PE patients (CP vs. PR: all p < .001, CP vs. PE: all p < .001). Thin-cap fibroatheroma was less prevalent (p = .023), fibrous cap was thicker (p = .035), and mean lipid arc was narrower in CP than in PR (p < .001). In conclusion, NCPs of CP patients had greater calcium burden and less vulnerability. This information may help to better understand the underlying mechanisms of ACS and to develop strategy for tailored management.

Comparison of post-stent optical coherence tomography findings among three subtypes of calcified culprit plaques in patients with acute coronary syndrome.

To compare the postprocedural optical coherence tomography (OCT) findings and in-hospital outcomes among the three subtypes of calcified plaques: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion. Recently, three subtypes of calcified culprit plaques were reported in patients with acute coronary syndrome (ACS). How these subtypes respond to stenting is unknown. ACS patients with calcified plaque at the culprit lesion were selected from our database. OCT findings at baseline and after stent implantation were compared. In the final analysis, 87 cases were included. Preprocedural OCT showed eruptive calcified nodules in 19 (21.8%) cases, superficial calcific sheet in 63 (72.4%), and calcified protrusion in 5 (5.7%). Stent edge dissection (SED) and incomplete stent apposition (ISA) were frequently observed in the eruptive calcified nodules group compared to superficial calcific sheet or calcified protrusion (SED; 47.4% vs. 17.5% vs. 20.0%; p = .032, ISA; 94.7% vs. 58.7% vs. 0.0%; p < .001). The superficial calcific sheet group had the smallest minimal stent area (MSA) among the three groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 6.29 ± 2.41 vs. 4.72 ± 1.37 vs. 6.56 ± 1.13; p = .007). The superficial calcific sheet group had a higher rate of periprocedural myocardial infarction compared to the eruptive calcified nodules group (60.3% vs. 31.6%; p = .028). This study demonstrated eruptive calcified nodules are associated with higher incidence of SED and ISA, whereas superficial calcific sheets are associated with small MSA and higher periprocedural myocardial infarction.

Healed Culprit Plaques in Patients With Acute Coronary Syndromes

BackgroundHealed plaques, morphologically characterized by a layered phenotype, are frequently found in subjects with sudden cardiac death. However, in vivo data are lacking. ObjectivesThe purpose of this study was to determine the prevalence, morphological characteristics, and clinical significance of healed culprit plaques in patients with acute coronary syndromes (ACS) using optical coherence tomography (OCT). MethodsA total of 376 ACS patients (252 ST-segment elevation myocardial infarction [MI] and 124 non–ST-segment elevation acute coronary syndrome) who had undergone pre-intervention OCT imaging of the culprit lesion were enrolled. Patients were stratified according to the presence of layered phenotype, defined as layers of different optical density at OCT. Clinical and laboratory data, OCT characteristics, and 1-year outcome were compared between the 2 groups. ResultsAmong 376 patients, 108 (28.7%) healed plaques were identified. Hyperlipidemia, diabetes, and history of MI were more frequent in patients with healed plaques (44.4% vs. 33.2%; p = 0.041; 35.2% vs. 23.5%; p = 0.021; and 15.7% vs. 6.3%; p = 0.009, respectively). High-sensitivity C-reactive protein was significantly higher in patients with healed plaques (median 4.98 mg/l [interquartile range: 1.00 to 11.32 mg/l] vs. 3.00 mg/l [interquartile range: 0.30 to 10.15 mg/l]; p = 0.029). Plaque rupture (64.8% vs. 53.0%; p = 0.039), thin cap fibroatheroma (56.5% vs. 42.5%; p = 0.016), and macrophage accumulation (81.1% vs. 63.4%; p = 0.001) were common in the layered group. OCT also revealed greater area stenosis in plaques with layered phenotype (79.2 ± 9.5% vs. 74.3 ± 14.3%; p = 0.001). The incidence of major adverse cardiovascular events was similar between the 2 groups, except that the all-cause rehospitalization rate was higher among healed plaques (32.7% vs. 16.5%; p = 0.013). ConclusionsHealed plaques, a signature of prior plaque destabilization, were found at the culprit site in more than one-quarter of ACS patients. Such patients more frequently were diabetic, were hyperlipidemic, or had a history of MI. Healed plaques frequently showed OCT features of vulnerability with evidence of local and systemic inflammation. The combination of plaque vulnerability, local inflammation, and greater plaque burden in addition to systemic inflammation may outweigh the protective mechanism of plaque healing and predispose those plaques to develop occlusive thrombus.

Impaired Flow-Mediated Dilation and Severity and Vulnerability of Culprit Plaque in Patients with Coronary Artery Disease.

The association between endothelial function, evaluated using flow-mediated dilatation (FMD), and the severity of coronary artery disease remains to be elucidated.A total of 245 consecutive patients with stable angina were prospectively enrolled. FMD was evaluated in the brachial artery before percutaneous coronary intervention. Patients were divided into 2 groups according to the FMD value (lower FMD group [FMD < 2.0], n = 82; higher FMD group [FMD ≥ 2.0], n = 163). The severity of coronary artery disease was evaluated using findings of angiography and optical coherence tomography, and compared between the 2 groups.The prevalence of left main (LM) disease was significantly higher in the lower FMD group than in the higher FMD group (8.5% versus 2.5%, P = 0.046), although the prevalence of multivessel disease was comparable between the groups. Lower FMD was independently associated with a higher prevalence of LM disease (odds ratio, 3.89; 95% confidence interval, 1.12-15.5; P = 0.033). A general linear model with multiple variables revealed that the minimal lumen area (MLA) in the culprit lesion was significantly smaller in patients with lower FMD than in those with higher FMD (regression coefficient b, -0.249 mm2; 95% confidence interval, -0.479--0.018 mm2; P = 0.035). The prevalence ofvulnerable plaque characteristics was comparable between the 2 groups.Patients with lower FMD had a higher incidence of LM disease and a smaller MLA in the culprit lesion. FMD may be a useful, noninvasive indicator for identifying patients with severe coronary artery disease.

Temporal course and implications of intracranial atherosclerotic plaque enhancement on high-resolution vessel wall MRI.

Little is known about the natural history of intracranial atherosclerotic plaque enhancement and its clinical implications. Our objective was to investigate the value of follow-up high-resolution contrast-enhanced vessel wall MRI (VWMRI) for classifying culprit plaques in patients with intracranial atherosclerotic disease (ICAD). Fourteen patients with symptomatic ICAD (50% females; median age 48years) underwent serial 3T VWMRI. Fifty-five plaques were identified and graded based on the likelihood of having caused the ischemic event (non-culprit, indeterminate, culprit) and degree of enhancement (0, 1, 2) at baseline and follow-up (median follow-up, 140days). For accuracy analysis, plaque enhancement at baseline and stable or increasing plaque enhancement at follow-up was tested to identify a culprit plaque, and areas under the receiver operating characteristic curves (AUCs) were compared. In 37/55 (67.3%) plaques, enhancement grade remained unchanged. Lack of enhancement was only seen in non-culprit plaques at baseline, and none developed enhancement over time. Enhancement never changed more than one grade. Thirty-seven percent (10/27) of non-culprit plaques that enhanced decreased in enhancement grade at follow-up, but no culprit plaques decreased in enhancement. AUC of baseline and follow-up plaque enhancement combined was significantly larger than AUC of baseline plaque enhancement alone to identify culprit plaques (0.733 vs. 0.567, p = 0.0001). Contrast enhancement of ICAD can persist months after the ischemic event. Lack of enhancement at baseline or a decrease in enhancement at follow-up suggests that the plaque is not culprit. Persistent enhancement from baseline to follow-up improves accuracy in identifying culprit plaques.

Calcified Plaques in Patients With Acute Coronary Syndromes

ObjectivesThis study conducted detailed analysis of calcified culprit plaques in patients with acute coronary syndromes (ACS). BackgroundCalcified plaques as an underlying pathology in patients with ACS have not been systematically studied. MethodsFrom 1,241 patients presenting with ACS who had undergone pre-intervention optical coherence tomography imaging, 157 (12.7%) patients were found to have a calcified plaque at the culprit lesion. Calcified plaque was defined as a plaque with superficial calcification at the culprit site without evidence of ruptured lipid plaque. ResultsThree distinct types were identified: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion (prevalence of 25.5%, 67.4%, and 7.1%, respectively). Eruptive calcified nodules were frequently located in the right coronary arteries (44.4%), whereas superficial calcific sheet was most frequently found in the left anterior descending coronary arteries (68.4%) (p = 0.012). Calcification index (mean calcification arc × calcification length) was greatest in eruptive calcified nodules, followed by superficial calcific sheet, and smallest in calcified protrusion (median 3,284.9 [interquartile range (IQR): 2,113.3 to 5,385.3] vs. 1,644.3 [IQR: 1,012.4 to 3,058.7] vs. 472.5 [IQR: 176.7 to 865.2]; p < 0.001). The superficial calcific sheet group had the highest peak post-intervention creatine kinase values among the groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 241 [IQR: 116 to 612] IU/l vs. 834 [IQR: 141 to 3,394] IU/l vs. 745 [IQR: 69 to 1,984] IU/l; p = 0.032). ConclusionsThree distinct types of calcified culprit plaques are identified in patients with ACS. Superficial calcific sheet, which is frequently located in the left anterior descending coronary artery, is the most prevalent type and is also associated with greatest post-intervention myocardial damage. (Identification of Predictors for Coronary Plaque Erosion in Patients With Acute Coronary Syndrome; NCT03479723)

CALCIFIED PLAQUES IN PATIENTS WITH ACUTE CORONARY SYNDROMES

Calcified plaques as an underlying pathology in patients with acute coronary syndromes (ACS) have not been systematically studied. We conducted detailed analysis of calcified culprit plaques in patients with ACS. From 1241 patients with ACS who had undergone pre-intervention optical coherence

Clinical impact of optical coherence tomography findings on culprit plaque in acute coronary syndrome: The OCT-FORMIDABLE study registry.

Aim of this study was to evaluate the clinical impact of the culprit plaque features assessed by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). The OCT-FORMIDABLE register enrolled retrospectively all consecutive patients who perform OCT on culprit plaque in patients with ACS in nine European centres. The primary endpoint was the prevalence of culprit plaque rupture (CPR) in patients experiencing major adverse cardiovascular events (MACEs). Secondary endpoint was the prevalence necrotic core with macrophage infiltrations (NCMI) in the patients experiencing MACEs. Two-hundred and nine patients were included in the study. Mean age was 60.1 ± 12.9 years old, 19.1% were females. Main clinical presentation was ST-elevation myocardial infarction (55%). At OCT analysis, CPR was observed in 71.8% patients, while 31.6% presented NCMI. During follow-up (12.6 ± 14.5 months), 11% of the patients experienced MACEs. The presence of CPR (HR 3.7,1.4-9.8, P < .01) and NCMI (HR 3.3,1.6-6.6, P < .01) were independent predictors for MACEs, while dual antiplatelet therapy with prasugrel/ticagrelor at discharge (HR 0.2,0.1-0.6, P < .01) were protective. The protective impact of new antiplatelet drugs was reported only in patients with CPR while in patients without any of the baseline clinical or procedural features impacted on MACEs. CPR and the presence of NCMI are independent predictors of worse outcome. Patients with CPR seem to benefit more of an intensive therapy, both from a pharmacological and interventional point of view. (NCT02486861).

P4636Association of isolated low HDL-C level with morphological features of culprit plaques in patients with ST segment elevation myocardial infarction: an optical coherence tomography study

P4636Association of isolated low HDL-C level with morphological features of culprit plaques in patients with ST segment elevation myocardial infarction: an optical coherence tomography study

Data on the lipoprotein (a), coronary atherosclerotic burden and vulnerable plaque phenotype in angiographic obstructive coronary artery disease.

Lipoprotein Lp(a) represents an independent risk factor for coronary artery disease (CAD). However, its association with CAD burden and lipid rich plaques prone to rupture in patients with acute coronary syndrome (ACS) still remains unknown. These data aim to investigate the association among serum Lipoprotein(a) (Lpa) levels, coronary atherosclerotic burden and features of culprit plaque in patients with ACS and obstructive CAD. For his reason, a total of 500 ACS patients were enrolled for the angiographic cohort and 51 ACS patients were enrolled for the optical coherence tomography (OCT) cohort. Angiographic CAD severity was assessed by Sullivan score and by Bogaty score including stenosis score and extent index, whereas OCT plaque features were evaluated at the site of the minimal lumen area and along the culprit segment. In the angiographic cohort, Lp(a) was a weak independent predictor of Sullivan score (p<0.0001), stenosis score (p<0.0001) and extent index (p<0.0001). In the OCT cohort, patients with higher Lp(a) levels (>30 md/dl) compared to patients with lower Lp(a) levels (<30 md/dl) exhibited a higher prevalence of lipidic plaque at the site of the culprit stenosis (P=0.02), a wider lipid arc (p=0.003) and a higher prevalence of thin-cap fibroatheroma (p=0.004)

Edge dissection of calcified plaque as a possible mechanism for acute coronary syndrome

We evaluated the incidence and predictors of edge dissection of the calcified culprit plaque in patients with acute coronary syndrome (ACS) or stable angina (SA). Calcified plaque is not rare in patients with ACS, and compliance mismatch may create edge dissection of the calcified plaque to trigger ACS. However, little data are available on calcium edge dissection in relation to ACS. Pre-intervention intravascular ultrasound data were analyzed in 143 patients with ACS (n = 53) or SA (n = 90). Edge dissection of the calcified plaque was found in 14 patients (9.8%). Patients were divided into two groups based on calcium edge dissection: group I (edge dissection, n = 14) and group II (no edge dissection, n = 129). Clinical and angiographic characteristics were largely similar between the two groups; however, ACS was more common in group I than in group II (64.3 vs. 34.1%, respectively, p = 0.039). Intravascular ultrasound variables did not differ between the two groups except thrombus and reference measurements, with thrombus more frequently observed in group I than in group II (35.7 vs. 8.5%, respectively, p = 0.010). Likewise, proximal and distal reference measurements were larger in group I than in group II. Multivariate analysis showed that ACS was the only independent predictor of calcium edge dissection (odds ratio 3.5, 95% confidence interval 1.1-11.0, p = 0.034). Edge dissection of the calcified plaque was present and more common in ACS patients than in SA patients. Calcium edge dissection may play a role in the pathogenesis of ACS.

Association of metabolic syndrome with coronary artery remodeling of culprit plaque in patients with or without acute coronary syndrome: an intravascular ultrasound study

Association of metabolic syndrome with coronary artery remodeling of culprit plaque in patients with or without acute coronary syndrome: an intravascular ultrasound study