The Effect of Clinical Risk Factors on the Atherosclerotic Plaque Characteristics of Intra- and Extracranial Arteries: A retrospective Study.

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.

We sought to compare the morphological features of non-culprit plaques with >50% diameter stenosis in patients with acute coronary syndromes (ACS) with those of culprit plaques in patients with ACS and stable angina pectoris (SAP) using optical coherence tomography (OCT) and integrated backscatter intravascular ultrasound (IB-IVUS). A total of 150 culprit and non-culprit coronary plaques (non-culprit vessels) in 150 patients with coronary artery disease were interrogated by OCT before percutaneous coronary intervention (PCI). Patients were categorized as follows: 73 culprit plaques in patients with ACS (ACS-C), 32 non-culprit plaques in patients with ACS (ACS-NC), and 45 culprit plaques in patients with SAP. The fibrous cap thickness was thinner in the ACS-C and ACS-NC groups than in the SAP group and was thinnest in the ACS-C group (ACS-C vs. ACS-NC vs. SAP, 60 vs. 82 vs. 114 μm, P < 0.001). IB-IVUS sub-analysis of 95 patients demonstrated that % lipid volume was greater and % fibrous volume was lower in the ACS-NC group than those in the SAP group (ACS-C vs. ACS-NC vs. SAP, 56.3 ± 11.0 vs. 59.9 ± 11.2 vs. 50.1 ± 13.9%, P < 0.05 and 39.5 ± 9.0 vs. 35.0 ± 9.0 vs. 43.9 ± 11.3%, P < 0.01, respectively). Plaques of non-culprit vessels in patients with ACS had a thinner fibrous cap and a higher percentage of lipid content than culprit plaques in patients with SAP. However, the fibrous cap thickness was thinner in the culprit lesions in patients with ACS than in the non-culprit lesions in patients with ACS, while plaque compositions were not significantly different between the groups.

BackgroundAlthough atherosclerosis (AS) can affect multiple vascular beds, previous studies have focused on the analysis of single-site AS plaques.ObjectiveThe aim of this study is to explore the differences or similarities in the characteristics of atherosclerotic plaque found in the internal carotid artery, cerebral artery, and coronary artery between patients with atherosclerotic cardiovascular disease (ASCVD) and those without events.MethodsPatients aged ≥ 18 years who underwent both high-resolution vessel wall imaging (HR-VWI) and coronary computed tomography angiography (CCTA) were retrospectively collected and categorized into the ASCVD group and the non-event group. The plaques were then categorized into culprit plaques, non-culprit plaques, and non-event plaques. Plaque morphological data such as stenosis, stenosis grades, plaque length (PL), plaque volume (PV), minimal lumen area (MLA), enhancement grade, and plaque composition data such as calcified plaque volume (CPV), fibrotic plaque volume (FPV), fibro-lipid plaque volume (FLPV), lipid plaque volume (LPV), calcified plaque volume ratio (CPR), fibrotic plaque volume ratio (FPR), fibro-lipid plaque ratio (FLPR), lipid plaque volume ratio (LPR), intraplaque hemorrhage volume (IPHV), and intraplaque hemorrhage volume ratio (IPHR)were recorded and analyzed.ResultsA total of 44 patients (mean age 66 years, SD 9 years, 28 men) were included. In cervicocephalic plaques, the ASCVD group had more severe stenosis grades (p = 0.030) and demonstrated significant differences in LPV, LPR, and CPV (p = 0.044, 0.030, 0.020) compared with the non-event group. In coronary plaques, the ASCVD group had plaques with greater stenosis (p &amp;lt; 0.001), more severe stenosis grades (p &amp;lt; 0.001), larger volumes (p = 0.001), longer length (p = 0.008), larger FLPV (p = 0.012), larger FPV (p = 0.002), and higher FPR (p = 0.043) compared with the non-event group. There were significant differences observed in stenosis (HR-VWI, CCTA: p &amp;lt; 0.001, p &amp;lt; 0.001), stenosis grades (HR-VWI, CCTA: p &amp;lt; 0.001, p &amp;lt; 0.001), plaque length (HR-VWI, CCTA: p = 0.028, p &amp;lt; 0.001), and plaque volume (HR-VWI, CCTA: p = 0.013, p = 0.018) between the non-event plaque, non-culprit plaque, and culprit plaque. In the image analysis of HR-VWI, there were differences observed between IPHR (p &amp;lt; 0.001), LPR (p = 0.001), FPV (p = 0.011), and CPV (p = 0.015) among the three groups of plaques. FLPV and FPV were significantly different among the three different plaque types from the coronary artery (p = 0.043, p = 0.022).ConclusionThere is a consistent pattern of change in plaque characteristics between the cervicocephalic and coronary arteries in the same patient.

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.

This study aimed to evaluate the difference in wall shear stress (WSS) (axial, circumferential, and 3D) between high-risk and low-risk plaques in patients with moderate carotid artery stenosis and to identify which time points and directions play the dominant roles in determining the risk associated with plaques. Forty carotid arteries in 30 patients were examined in this study. All patients underwent high-resolution vessel wall (HRVW) imaging, diffusion-weighted imaging (DWI), and 4D flow MRI; HRVW imaging and DWI were used to separate low- and high-risk plaque. Twenty-four high-risk plaques and 16 low-risk plaques were enrolled. An independent-sample t-test was used to compare WSS between low- and high-risk plaques in the whole cardiac cycle and at 20 different time points in the cardiac cycle. The study found that patients with high-risk plaques had higher WSS than those with low-risk plaques throughout the entire cardiac cycle (p < 0.05), but the changes varied at the 20 different time points. The number of non-significant differences (p > 0.05) was less in diastole than in systole across different time points. The axial WSS values were higher than the circumferential WSS values; the difference in axial WSS values between high- and low-risk plaques was more significant than the difference in circumferential WSS, whereas 3D WSS values best reflected the difference between high-risk and low-risk plaques because they showed significant differences at every time point. In conclusion, increased WSS, especially during the diastolic period and in the axial direction, may be a signal of a high-risk plaque and may cause cerebrovascular events in patients with moderate carotid artery stenosis. Additionally, WSS can provide hemodynamic information and help clinicians make more appropriate decisions for patients with plaques.

Current imaging modalities underestimate the severity of intracranial atherosclerotic disease (ICAD). High resolution vessel wall imaging (HR-VWI) MRI is a powerful tool in characterizing plaques. We aim to show that HR-VWI MRI is more accurate at detecting and characterizing intracranial plaques compared to digital subtraction angiography (DSA), time-of-flight (TOF) MRA, and computed tomography angiogram (CTA). Patients with symptomatic ICAD prospectively underwent 7T HR-VWI. We calculated: degree of stenosis, plaque burden (PB), and remodeling index (RI). The sensitivity of detecting a culprit plaque for each modality as well as the correlations between different variables were analyzed. Interobserver agreement on the determination of a culprit plaque on every imaging modality was evaluated. A total of 44 patients underwent HR-VWI. Thirty-four patients had CTA, 18 TOF-MRA, and 18 DSA. The sensitivity of plaque detection was 88% for DSA, 78% for TOF-MRA, and 76% for CTA. There's significant positive correlation between PB and degree of stenosis on HR-VWI MRI (p < 0.001), but not between PB and degree of stenosis in DSA (p = 0.168), TOF-MRA (p = 0.144), and CTA (p = 0.253). RI had a significant negative correlation with degree of stenosis on HR-VWI MRI (p = 0.003), but not on DSA (p = 0.783), TOF-MRA (p = 0.405), or CTA (p = 0.751). The best inter-rater agreement for culprit plaque detection was with HR-VWI (p = 0.001). The degree of stenosis measured by intra-luminal techniques does not fully reflect the true extent of ICAD. HR-VWI is a more accurate tool in characterizing atherosclerotic plaques and may be the default imaging modality in clinical practice.

Background: The study of plaque enhancement using high resolution vessel wall imaging can provide useful prognostic data. However, this analysis is hindered by plaque sampling and methodological constrains. We developed a new method to quantify plaque enhancement with 3D map analysis. Methods: Ultra-high resolution (7 Tesla) vessel wall imaging was performed on 41 patients with history of symptomatic atherosclerotic disease. Culprit and non-culprit plaques were analyzed. 3D reconstructions of culprit (N=41) and non-culprit plaques (N=14) was performed on T1 and T1+Gd images. Using an in-house code, orthogonal probes were extended from the lumen of the vessel into the arterial wall (Figure). In this way, the entire wall was sampled with multiple spokes. These values were then normalized to the corpus callosum (CC) to obtain a signal intensity ratio (SI ratio ). Dynamic contrast uptake was quantified as the change in mean SI of the plaque after contrast administration. Results: Forty one culprit and 14 non-culprit plaques (N=55) were analyzed. Culprit plaques enhanced with gadolinium (Gd) more significantly (SI plaque = 0.76 ± 0.28) than non-culprit plaques (SI plaque =0.58 ± 0.14) (p=0.05). In addition, culprit plaques displayed more contrast uptake (ΔSI plaque =0.33±0.25) than non-culprit plaques (ΔSI plaque =0.19 ± 0.08,p=0.01). Conclusion: 3D analysis of plaque enhancement with ultra-high resolution MRI is a promising technique that may be used as a biomarker of culprit intracranial atherosclerotic plaques. In addition, quantifying the dynamic plaque contrast uptake may provide more insight into the biology of these lesions.Figure. Magnified 7T coronal view of a basilar artery plaque pre (A) and post administration of Gd (B). 3D analysis of the dynamic uptake of Gd in T1 (C) and T1 + Gd (D). This plaque had a of 0.49 = highly enhancing.

High-resolution vessel wall imaging (HR-VWI) is a powerful tool in diagnosing intracranial vasculopathies not detected on routine imaging. We hypothesized that 7T HR-VWI may detect the presence of atherosclerotic plaques in patients with intracranial atherosclerosis disease initially misdiagnosed as cryptogenic strokes. Patients diagnosed as cryptogenic stroke but suspected of having an intracranial arteriopathy by routine imaging were prospectively imaged with HR-VWI. If intracranial atherosclerotic plaques were identified, they were classified as culprit or nonculprit based on the likelihood of causing the index stroke. Plaque characteristics, such as contrast enhancement, degree of stenosis, and morphology, were analyzed. Contrast enhancement was determined objectively after normalization with the pituitary stalk. A cutoff value for plaque-to-pituitary stalk contrast enhancement ratio (CR) was determined for optimal prediction of the presence of a culprit plaque. A revised stroke cause was adjudicated based on clinical and HR-VWI findings. A total of 344 cryptogenic strokes were analyzed, and 38 eligible patients were imaged with 7T HR-VWI. Intracranial atherosclerosis disease was adjudicated as the final stroke cause in 25 patients. A total of 153 intracranial plaques in 374 arterial segments were identified. Culprit plaques (n=36) had higher CR and had concentric morphology when compared with nonculprit plaques (P≤0.001). CR ≥53 had 78% sensitivity for detecting culprit plaques and a 90% negative predictive value. CR ≥53 (P=0.008), stenosis ≥50% (P<0.001), and concentric morphology (P=0.030) were independent predictors of culprit plaques. 7T HR-VWI allows identification of underlying intracranial atherosclerosis disease in a subset of stroke patients with suspected underlying vasculopathy but otherwise classified as cryptogenic. Plaque analysis in this population demonstrated that culprit plaques had more contrast enhancement (CR ≥53), caused a higher degree of stenosis, and had a concentric morphology.

BackgroundSymptomatic intracranial atherosclerotic stenosis (sICAS) patients had a higher risk of stroke recurrence, and the risk of acute ischemic stroke (AIS) was higher than transient ischemic attack (TIA). Therefore, it is important to explore the risk factors associated with sICAS clinical subtypes and the risk of stroke recurrence. The purpose of this study was to investigate the association between intracranial arterial culprit plaque characteristics with sICAS clinical subtypes and the risk of stroke recurrence.MethodsA total of 206 patients with sICAS were included. Baseline demographic data and relevant serologic indices were collected from all participants. All participants were assessed by high-resolution vessel wall imaging (HR-VWI) for culprit vessel and culprit plaque characteristics. The follow-up method was outpatient or telephone follow-up. Associated factors for sICAS clinical subtypes were analyzed by binary logistic regression. Cox proportional hazard regression analysis were used to analysis the independent risk factors for recurrent stroke.ResultsIn this group, there were 154 patients with AIS, 52 patients with TIA, 124 patients with anterior circulation ischemic symptom (ACiS), and 82 patients with posterior circulation ischemic symptom (PCiS). Male gender [odds ratio (OR) =5.575, 95% confidence interval (CI): 2.120 to 14.658], history of previous statin use (OR =0.309, 95% CI: 0.113 to 0.843) and serum apolipoprotein A/B values (OR =0.363, 95% CI: 0.139 to 0.948) were associated factors for AIS. A total of 24 patients (11.7%) experienced stroke recurrence during the 1-year follow-up period. Hyperintensity on T1 weighted imaging (T1WI) in the culprit plaque [hazard ratio (HR) =3.798, 95% CI: 1.433 to 10.062] was an independent risk factor for stroke recurrence. The incidence of significant enhancement (62.2% vs. 39.5%, χ2=9.681, P=0.002), positive remodeling (69.5% vs. 52.4%, χ2=5.661, P=0.020), and hyperintensity on T1WI (42.7% vs. 22.6%, χ2=16.472, P=0.003) was higher in the posterior circulation than in the anterior circulation.ConclusionsThe characteristics of intracranial arterial culprit plaques were independent risk factors for recurrent stroke, and there were differences in the plaque characteristics of anterior and posterior circulation. Early HR-VWI examination for sICAS patients is of great significance for patient risk stratification and personalized management.

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.

Real-world data on lipid levels and treatment among adults with diabetes mellitus (DM) are relatively limited. We studied lipid levels and treatment status in patients with DM across cardiovascular disease (CVD) risk groups and sociodemographic factors. In the All of Us Research Program, we categorized DM as (1) moderate risk (≤1 CVD risk factor), (2) high risk (≥2 CVD risk factors), and (3) DM with atherosclerotic CVD (ASCVD). We examined the use of statin and non-statin therapy as well as LDL-C and triglyceride levels. We studied 81,332 participants with DM, which included 22.3% non-Hispanic Black and 17.2% Hispanic. A total of 31.1% had ≤1 DM risk factor, 30.3% had ≥2 DM risk factors, and 38.6% of participants had DM with ASCVD. Only 18.2% of those with DM and ASCVD were on high-intensity statins. Overall, 5.1% were using ezetimibe and 0.6% PCSK9 inhibitors. Among those with DM and ASCVD, only 21.1% had LDL-C < 70 mg/dL. Overall, 1.9% of participants with triglycerides ≥ 150 mg/dL were on icosapent ethyl. Those with DM and ASCVD were more likely to be on high-intensity statins, ezetimibe, and icosapent ethyl. Guideline-recommended use of high-intensity statins and non-statin therapy among our higher risk DM patients is lacking, with LDL-C inadequately controlled.

Recurrent ischemic stroke in patients with symptomatic intracranial atherosclerotic stenosis (sICAS) can be attributed to two main causes: intracranial atherosclerotic stenosis (ICAS) and cerebral small vessel disease (CSVD). This study investigates the potential associations between stroke recurrence and the modified cerebral small vessel disease (mCSVD) burden score, as well as the characteristics of culprit plaques related to intracranial artery high-resolution vessel wall imaging (HR-VWI). A total of 145 patients presenting sICAS underwent intracranial artery HR-VWI and routine cranial MRI at two large Chinese hospitals from December 2019-2022 were participants of this retrospective analysis. Standard MRI scans were used to calculate the mCSVD score. Following a 12-month observation period, the patients were categorized into two distinct groups depending on whether or not they experienced a subsequent stroke. Within 12 months, 32 patients experienced stroke recurrence. The recurrence group's mCSVD score was higher compared to the non-recurrence group (p < 0.001). Their luminal stenosis and culprit plaque thickness and burden were also higher (p < 0.05). Additionally, higher rates of diabetes, T1WI hyperintensity of culprit plaques, and significant plaque enhancement were observed in the recurrence group (p < 0.05). The adjusted Cox regression model indicated that the mCSVD score (HR = 1.730, 95% CI 1.021-2.933, p = 0.042) and T1WI hyperintensity of the culprit plaque (HR = 6.568, 95% CI 1.104-39.059, p = 0.039) remained significantly independent risk variables. The combination of the mCSVD score and T1WI hyperintensity of the culprit plaque demonstrated the highest efficacy in predicting stroke recurrence (z = 2.678, p < 0.05). The mCSVD score, associated with T1WI hyperintensity of culprit plaque, effectively predicts stroke recurrence and can be easily obtained, offering high clinical value.

Coronary atherosclerosis is a leading cause of cardiovascular morbidity and mortality worldwide. Plaque complications occur most commonly from plaque rupture, and also from plaque erosion and calcified nodule formation. Over the past years, advanced structural, metabolic and molecular imaging technologies have emerged and offer new windows into atherosclerosis pathophysiology [1–4]. Molecular imaging complements traditional structural plaque imaging through the use of targeted probes that identify specific molecules and/or biological processes in vivo [5]. Preclinical atherosclerosis molecular imaging has successfully identified nearly all established high-risk plaque characteristics including inflammation, thrombosis, neo-vessel formation, apoptosis, and haemorrhage. However, clinical translation of molecular imaging has been slow compared with the rapid growth within the field. Currently, clinical atherosclerosis molecular imaging is dominated by non-invasive PET metabolism/inflammation plaque imaging with fluorine 18 (18F)-fluorodeoxyglucose (FDG). For the past two decades, 18F FDG has been the only fluorine-18 radioligand approved by the US Food and Drug Administration (FDA) for PET imaging. Coronary FDG PET is challenging, in part owing to the small size of coronary vessels and cardiac motion artefacts, but also because of the intense FDG uptake of the adjacent highly metabolic myocardium that obscures the coronary FDG signal. However, with dietary myocardial suppression protocols, detection of FDG PET signal in the left main and proximal coronary artery beds is sometimes achievable. Recently, non-invasive coronary FDG PET activity has been investigated in the stented culprit lesions of 20 subjects with acute coronary syndromes (ACS) versus seven non-ACS subjects within 1 week of stent placement [6]. Using a predetermined FDG target to background ratio of 2.0 or greater to identify FDG-positive lesions, the ACS patients correlated positively with elevated stent FDG signal. However, coronary FDG signal was interpretable in only 50 % of ACS patients, implying the need for further improvements in coronary FDG PET. Apart from 18F FDG coronary imaging, clinically available approaches such as sodium 18F-fluoride (NaF) for PET are emerging. Coronary calcification is a hallmark of advanced atheroma that can be detected with non-invasive NaF PET, which has been used for the past 3 decades to detect cancer bone metastases. As opposed to FDG, background myocardial uptake of NaF is negligible, and therefore NaF can determine coronary osteogenic activity. In a study by Dweck et al. from the University of Edinburgh [7], NaF PET molecular imaging identified sites of active coronary calcification non-invasively by PET and may be a new therapeutic target. The NaF signal was elevated in proportion to coronary CT calcium scores in 119 subjects, except in those with the highest calcium scores that may represent end-stage calcified plaques. From the same research group, Joshi et al. [8] recently (Lancet November 2013) studied coronary plaque imaging using two different radioactive tracers: 18F-NaF and 18F-FDG. The Scottish study included 40 patients with acute myocardial infarction (AMI) and 40 patients with stable angina. All patients underwent PET-CT, invasive coronary angiography, CT coronary angiography, and CT calcium scoring. Among the 40 patients with AMI, 18F-NaF PET uptake was 34 % higher in the culprit ruptured plaque compared with non-culprit plaques. Nearly all patients (93 %) had increased 18F-NaF uptake in the culprit plaque. With 18F-FDG, however, no differences in uptake between culprit and non-culprit plaques were observed. Among the 40 patients with stable angina, 45 % had plaques with increased 18F-NaF uptake. These plaques were mostly non-obstructive at coronary angiography and contained more high-risk features on intravascular ultrasound compared with plaques without tracer uptake. Consequently, 18F-NaF PET may become an effective tool for predicting an AMI, which would have a great impact for patients with coronary atherosclerosis. Early detection of the atherosclerotic ‘danger zones’ could include immediate instalment of drugs such as statins or aspirin, drastic changes in lifestyle and even inserting stents into the affected coronary artery. The use of 18F-NaF PET-CT offers the first non-invasive imaging method to identify and localise ruptured and high-risk coronary plaques. A next step is to show that increased 18F-NaF predicts future adverse clinical events. Further studies are therefore needed to evaluate whether the detection of risky plaques before rather than after an AMI has the potential to save lives. To summarise, the addition of newer molecular imaging tools such as NaF PET-CT will continue to strengthen our understanding of the in vivo biology of high-risk plaques [9, 10]. They are increasingly being translated into clinical use, and in combination with structural imaging they provide more comprehensive information to build risk-prediction tools. Ongoing efforts to improve non-invasive coronary imaging strategies must be pursued. Overall, with continued advances in molecular and structural atherosclerosis imaging, high-risk coronary atherosclerotic plaques will be brightened as never before. The recent study in the Lancet at least suggests that molecular imaging using PET-CT scanning may provide an answer in identifying ‘ticking time bomb’ patients at risk of an AMI.

Limitation of Angiography to Identify the Culprit Plaque in Acute Myocardial Infarction With Coronary Total Occlusion: Utility of Coronary Plaque Temperature Measurement to Identify the Culprit Plaque

Atherosclerosis is an inflammatory process, and vulnerable plaques are characterized by an increased inflammatory infiltrate that generates heat. Intracoronary thermography (ICT) is a catheter-based technique for the functional imaging of atherosclerotic plaques, with the ability to identify potential vulnerable and culprit plaques in patients with coronary artery disease (CAD). ICT is able to detect thermal heterogeneity, which has been shown to be present more often in unstable coronary plaques, and positively correlated to vulnerable plaque morphology characteristics and serum markers of systemic inflammation. ICT has also been shown to have a good predictive value for clinical events after percutaneous coronary intervention and has been used to assess response to statin therapy in patients with CAD. ICT has several important limitations and is yet to be validated in large prospective trials, but may be used in the future to detect vulnerable or culprit plaques and thus used to direct local and/or systemic therapy in patients with CAD.