Stable Coronary Plaques Research Articles

The role of endothelial shear stress, shear stress gradient, and plaque topography in plaque erosion

Background and aimsPlaque erosion is a common underlying cause of acute coronary syndromes. The role of endothelial shear stress (ESS) and endothelial shear stress gradient (ESSG) in plaque erosion remains unknown.We aimed to determine the role of ESS metrics and maximum plaque slope steepness in plaques with erosion versus stable plaques. MethodsThis analysis included 46 patients/plaques from TOTAL and COMPLETE trials and Brigham and Women's Hospital's database who underwent angiography and OCT. Plaques were divided into those with erosion (n = 24) and matched stable coronary plaques (n = 22). Angiographic views were used to generate a 3-D arterial reconstruction, with centerlines merged from angiography and OCT pullback. Local ESS metrics were assessed by computational fluid dynamics. Among plaque erosions, the up- and down-slope (Δ lumen area/frame) was calculated for each culprit plaque. ResultsCompared with stable plaque controls, plaques with an erosion were associated with higher max ESS (8.3 ± 4.8 vs. 5.0 ± 1.9 Pa, p = 0.02) and max ESSG any direction (9.2 ± 7.5 vs. 4.3 ± 3.11 Pa/mm, p = 0.005). Proximal erosion was associated with a steeper plaque upslope while distal erosion with a steeper plaque downslope. Max ESS and Max ESSG any direction were independent factors in the development of plaque erosion (OR 1.32, 95%CI 1.06–1.65, p = 0.014; OR 1.22, 95% CI 1.03–1.45, p = 0.009, respectively). ConclusionsIn plaques with similar luminal stenosis, plaque erosion was strongly associated with higher ESS, ESS gradients, and plaque slope as compared with stable plaques. These data support that ESS and slope metrics play a key role in the development of plaque erosion and may help prognosticate individual plaques at risk for future erosion.

Pericoronary Adipose Tissue Attenuation in Patients With Acute Coronary Syndrome Versus Stable Coronary Artery Disease.

Pericoronary adipose tissue (PCAT) attenuation has been associated with coronary inflammation and can be evaluated with coronary computed tomography angiography. The aims of this study were to compare the PCAT attenuation across precursors of culprit and nonculprit lesions of patients with acute coronary syndrome versus stable coronary artery disease (CAD). In this case-control study, patients with suspected CAD who underwent coronary computed tomography angiography were included. Patients who developed an acute coronary syndrome within 2 years after the coronary computed tomography angiography scan were identified, and patients with stable CAD (defined as any coronary plaque ≥30% luminal diameter stenosis) were 1:2 propensity score matched for age, sex, and cardiac risk factors. The mean PCAT attenuation was analyzed at lesion level and compared between precursors of culprit lesions, nonculprit lesions, and stable coronary plaques. In total, 198 patients (age 62±10 years, 65% male) were selected, including 66 patients who developed an acute coronary syndrome and 132 propensity matched patients with stable CAD. Overall, 765 coronary lesions were analyzed (culprit lesion precursors: n=66; nonculprit lesion precursors: n=207; and stable lesions: n=492). Culprit lesion precursors had larger total plaque volume, fibro-fatty plaque volume, and low-attenuation plaque volume compared to nonculprit and stable lesions. The mean PCAT attenuation was significantly higher across culprit lesion precursors compared to nonculprit and stable lesions (-63.8±9.7 Hounsfield units versus -68.8±10.6 Hounsfield units versus -69.6±10.6 Hounsfield units, respectively; P<0.001), whereas the mean PCAT attenuation around nonculprit and stable lesions was not significantly different (P=0.99). The mean PCAT attenuation is significantly increased across culprit lesion precursors in patients with acute coronary syndrome, compared to nonculprit lesions of these patients and to lesions of patients with stable CAD, which may suggest a higher intensity of inflammation. PCAT attenuation on coronary computed tomography angiography may be a novel marker to identify high-risk plaques.

Fibrous Cap Thickness Predicts Stable Coronary Plaque Progression: Early Clinical Validation of a Semiautomated OCT Technology.

Imaging-based characteristics associated with the progression of stable coronary atherosclerotic lesions are poorly defined. Utilizing a combination of optical coherence tomography (OCT) and intravascular ultrasound (IVUS) imaging, we aimed to characterize the lesions prone to progression through clinical validation of a semiautomated OCT computational program. Patients with stable coronary artery disease underwent nonculprit vessel imaging with IVUS and OCT at baseline and IVUS at the 12-month follow-up. After coregistration of baseline and follow-up IVUS images, paired 5-mm segments from each patient were identified, demonstrating the greatest plaque progression and regression as measured by the change in plaque burden. Experienced readers identified plaque features on corresponding baseline OCT segments, and predictors of plaque progression were assessed by multivariable analysis. Each segment then underwent volumetric assessment of the fibrous cap (FC) using proprietary software. Among 23 patients (70% men; median age, 67 years), experienced-reader analysis demonstrated that for every 100 μm increase in mean FC thickness, plaques were 87% less likely to progress (P = .01), which persisted on multivariable analysis controlling for baseline plaque burden (P = .05). Automated FC analysis (n = 17 paired segments) confirmed this finding (P = .01) and found thinner minimal FC thickness (P = .01) and larger FC surface area of <65 μm (P = .02) and <100 μm (P = .04) in progressing segments than in regressing segments. No additional imaging features predicted plaque progression. A semiautomated FC analysis tool confirmed the significant association between thinner FC and stable coronary plaque progression along entire vessel segments, illustrating the diffuse nature of FC thinning and suggesting a future clinical role in predicting the progression of stable coronary artery disease.

PCSK9 inhibitors safely and effectively lower LDL after heart transplantation: a systematic review and meta-analysis.

Coronary allograft vasculopathy (CAV) continues to afflict a high number of heart transplant (HT) recipients, and elevated LDL is a key risk factor. Many patients cannot tolerate statin medications after HT; however, data for alternative agents remains scarce. To address this key evidence gap, we evaluated the safety and efficacy of the PCSK9i after HT through systematic review and meta-analysis. We searched Medline, Cochrane Central, and Scopus from the earliest date through July 15th, 2021. Citations were included if they were a report of PCSK9i use in adults after HT and reported an outcome of interest. Outcomes included change in LDL cholesterol from baseline, incidence of adverse events, and evidence of CAV. Changes from baseline and outcome incidences were pooled using contemporary random-effects model methodologies. A total of six studies including 97 patients were included. Over a mean follow-up of 13months (range 3-21), PCSK9i use lowered LDL by 82.61mg/dL (95% CI - 119.15 to - 46.07; I2 = 82%) from baseline. Serious adverse drug reactions were rarely reported, and none was attributable to the PCSK9i therapy. Four studies reported stable calcineurin inhibitor levels during PCSK9i initiation. One study reported outcomes in 33 patients with serial coronary angiography and intravascular ultrasound, and PCSK9i were associated with stable coronary plaque thickness and lumen area. One study reported on immunologic safety, showing no DSA development within 1month of therapy. Preliminary data suggest that long-term PCSK9i therapy is safe, significantly lowers LDL, and may attenuate CAV after HT. Additional study on larger cohorts is warranted to confirm these findings.

PCSK9 Inhibitors Safely and Effectively Lower LDL After Heart Transplantation: A Systematic Review and Meta-Analysis

<h3>Purpose</h3> Coronary allograft vasculopathy (CAV) continues to afflict a majority of heart transplant (HT) recipients, and elevated LDL is a key risk factor. Many patients cannot tolerate statin medications after HT, however data for alternative agents remains scarce. To address this key evidence gap, we evaluated the safety and efficacy of the PCSK9i after HT through systematic review and meta-analysis. <h3>Methods</h3> We searched Medline, Cochrane Central, and Scopus from the earliest date through July 15^th, 2021. Citations were included if they were a report of PCSK9i use in adults after HT and reported an outcome of interest. Outcomes included change in LDL cholesterol from baseline, incidence of adverse events, and evidence of CAV. Changes from baseline and outcome incidences were pooled using contemporary random-effects model methodologies. <h3>Results</h3> `A total of six studies including 97 patients were evaluated, most of which either had statin intolerance or refractory hyperlipidemia. Over a mean follow up of 13 months (range 3-21), PCSK9i use lowered LDL by 82.61 mg/dL (95% CI -119.15 to -46.07; <i>I²</i>=82%) (<b>Figure 1</b>) from baseline. Serious adverse drug reactions were rarely reported, and none were attributable to the PCSK9i therapy. Three studies reported stable calcineurin inhibitor levels during PCSK9i initiation. One study reported outcomes in 33 patients with serial coronary angiography and intravascular ultrasound, and PCSK9i were associated with stable coronary plaque thickness and lumen area. No studies reported on immunologic safety (i.e. development of DSA), hence this endpoint cannot be assessed. <h3>Conclusion</h3> Preliminary data suggest that long-term PCSK9i therapy is safe, significantly lowers LDL, and may attenuate CAV after HT. Additional study on larger cohorts is warranted to confirm these findings.

TH1 lymphocytes in the perivascular adipose tissue correlate with plaque composition and increase the risk of intraplaque haemorrhages in coronary arteries: an autopsy study

Abstract Background Inflammation in the perivascular adipose tissue (PvAT) might play a role in coronary artery disease. The T helper 1 (Th1) lymphocytes are the most popular T helper (Th) lymphocytes in atherosclerotic plaques and are proatherogenic. However, the association between the Th1 and Th lymphocytes in the PvAT with coronary atherosclerosis composition was not previously investigated in humans. Purpose We investigated the correlation between Th CD4+ and Th1 CD4+CXCR3+ lymphocytes in the PvAT with atherosclerotic plaque composition. Methods Human coronary arteries were freshly dissected with adjacent PvAT. The most important atherosclerotic plaque was selected of the main coronary arteries and was stained with hematoxylin-eosin, Masson's trichrome, and Verhöeff. We calculated the percentage of arterial obstruction, intima-media thickness, the minimum fibrous cap thickness, and the percentual of collagen, smooth muscle cells (SMC), fibrous cap, calcification, lipid, necrosis, and intraplaque hemorrhage. The atherosclerotic plaques were classified in stable and unstable plaques (hemorrhages and thrombus). The density of Th lymphocytes (CD4+), Th1 (CD4+CXCR3+), and the ratio of Th1/Th were detected using the immunohistochemistry double staining technique. The densities and the ratio Th1/Th were correlated with plaque composition using linear, negative binomial, or Poisson regressions models with clustering for multiple measures in the same individual and adjusted for age, sex, hypertension, diabetes, body mass index, sedentary lifestyle, smoking, and alcohol consumption. Results We evaluated a sample of 126 coronary arteries from 58 subjects. The individuals were older (70.4±14.3 years old), sex was equally distributed, 74% had hypertension, and 40% diabetes. In multivariate analysis, the Th lymphocytes were negatively correlated with calcification content (β=−0.21, 95% CI: −0.41; −0.006, p=0.043). The Th1 lymphocytes were not correlated with plaque composition; however, the increase of Th1 density in relation to Th lymphocytes was negatively correlated with SMC (β=−35.6, 95% CI: −68.5; −2.83, p=0.03) and the fibrous cap content (β=−11.6, 95% CI: −19.1; −4.05, p=0.003). Additionally, the higher proportion of Th1/Th lymphocytes increased the risk of intraplaque haemorrhages compared to stable coronary plaques (OR=15.5, 95% CI: 1.23; 196.4, p=0.03). Conclusions The increase of pro-inflammatory Th1 lymphocytes in the PvAT was correlated to the decrease of components in atherosclerotic plaques related to plaque stabilization, such as SMC and fibrous cap content. Additionally, the increase in the proportion of pro-inflammatory Th1 lymphocytes in the PvAT also increases the risk of intraplaque haemorrhages in coronary arteries. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): São Paulo Research Foundation (FAPESP) Figure 1Figure 2

PCSK9 Inhibitors in Heart Transplant Patients: Safety, Efficacy, and Angiographic Correlates

BackgroundStatins are recommended in heart transplant patients, but are sometimes poorly tolerated. Alternative agents are often considered including proprotein convertase subtilisin/kexin type-9 inhibitors (PCSK9i). We sought to investigate the use of PCSK9i after heart transplantation. Methods and ResultsWe identified patients who received a heart transplant from 1999 to 2019 and were started on PCSK9i at our institution. Clinical, laboratory, and coronary angiography with intravascular ultrasound results were compared. Among 65 patients initiated on PCSK9i (48 for statin intolerance and 17 for refractory hyperlipidemia), the median time from transplant was 5.5 years (interquartile range [IQR], 2.8–9.9 years) with a median PCSK9 treatment duration of 1.6 years (IQR, 0.8–3.2 years) and 80% still on treatment. Evolocumab was used in 73.8%, alirocumab in 12.3%, and both in 13.8% owing to insurance coverage. All patients required prior authorization; initial denial occurred in 18.5% and 32.3% had denials in subsequent years. The median low-density lipoprotein cholesterol decreased from 130 mg/dL (IQR, 102–148 mg/dL) to 55 mg/dL (IQR, 35–74 mg/dL) after starting PCSK9i (P < .001), with 72% of patients achieving a low-density lipoprotein cholesterol of <70 mg/dL after treatment. There were also significant reductions of total cholesterol, non–high-density lipoprotein cholesterol, total/high-density lipoprotein cholesterol ratio, and triglycerides, with a modest increase in high-density lipoprotein cholesterol. These changes were durable at latest follow-up. In 33 patients with serial coronary angiography and intravascular ultrasound, PCSK9i were associated with stable coronary plaque thickness and lumen area. ConclusionsAmong heart transplant recipients, PCSK9i are effective in lowering cholesterol levels and stabilizing coronary intimal hyperplasia with minimal side effects. Despite favorable effects, access and affordability remain a challenge.

Density and morphology of coronary artery calcium for the prediction of cardiovascular events: insights from the Framingham Heart Study.

To investigate the association between directly measured density and morphology of coronary artery calcium (CAC) with cardiovascular disease (CVD) events, using computed tomography (CT). Framingham Heart Study (FHS) participants with CAC in noncontrast cardiac CT (2002-2005) were included and followed until 2016. Participants with known CVD or uninterpretable CT scans were excluded. We assessed and correlated (Spearman) CAC density, CAC volume, and the number of calcified segments. Moreover, we counted morphology features including shape (cylindrical, spherical, semi-tubular, and spotty), location (bifurcation, facing pericardium, or facing myocardium), and boundary regularity. In multivariate Cox regression analyses, we associated all CAC characteristics with CVD events (CVD-death, myocardial infarction, stroke). Among 1330 included participants (57.8 ± 11.7years; 63% male), 73 (5.5%) experienced CVD events in a median follow-up of 9.1 (7.8-10.1) years. CAC density correlated strongly with CAC volume (Spearman's ρ = 0.75; p < 0.001) and lower number of calcified segments (ρ = - 0.86; p < 0.001; controlled for CAC volume). In the survival analysis, CAC density was associated with CVD events independent of Framingham risk score (HR (per SD) = 2.09; 95%CI, 1.30-3.34; p = 0.002) but not after adjustment for CAC volume (p = 0.648). The extent of spherically shaped and pericardially sided calcifications was associated with fewer CVD events accounting for the number of calcified segments (HR (per count) = 0.55; 95%CI, 0.31-0.98; p = 0.042 and HR = 0.66; 95%CI, 0.45-0.98; p = 0.039, respectively). Directly measured CAC density does not predict CVD events due to the strong correlation with CAC volume. The spherical shape and pericardial-sided location of CAC are associated with fewer CVD events and may represent morphological features related to stable coronary plaques. • Coronary calcium density may not be independently associated with cardiovascular events. • Coronary calcium density correlates strongly with calcium volume. • Spherical shape and pericardial-sided location of CAC are associated with fewer CVD events.

Relation of Coronary Artery Lumen with Baseline, Post-angioplasty Coronary Circulating Pro-Inflammatory Cytokines in Patients with Coronary Artery Disease

Background: Atherogenic progression in Coronary Artery Disease (CAD) involves a chronic inflammatory process, where local production or release of pro-inflammatory mediators into coronary circulation has a main role. Proinflammatory cytokines IL-6, TNFα and IL1β have been particularly related with the atheroma plaque and CAD severity. Aim: To explore whether characteristics of the coronary artery affected by atheroma plaque were related with coronary circulating pro-inflammatory cytokines and their modifications after angioplasty. Methods: Patients with CAD and stable coronary plaque, submitted to coronary angiography and stenting. Coronary artery lumen diameter at the site of the main atherogenic lesion was measured by intravascular ultrasound, whereas IL-6, TNFα and IL1β concentration in coronary and peripheral blood samples, either before or after angioplasty were determined by multiplexing assay. Baseline distribution of coronary cytokines, or its modification after angioplasty, was evaluated according to the diameter of the lumen of coronary artery (subgroups divided by cutoff value 3.5 mm). Results: Coronary lumen diameter <3.5 mm was related to higher baseline coronary concentrations of IL-1β; as well as to the significant increase in coronary concentrations of TNF-α and IL-6, after angioplasty. Baseline cytokines at peripheral blood did were not modified by coronary lumen diameter; however, coronary lumen <3.5 mm was associated to a peripheral increase in IL-1β, after angioplasty. Conclusion: Coronary lumen diameter, possibly implying plaque characteristics, affects baseline and post-angioplasty coronary concentrations of pro-inflammatory cytokines in patients with CAD.

The diagnosis of coronary plaque stability by multi-slice computed tomography coronary angiography.

Coronary computed tomographic angiography is a robust non-invasive method to assess coronary artery disease (CAD) and analyze coronary plaque stability, especially for the non-calcified plaques. The aim of this study was to investigate the differential characteristics between the unstable coronary plaques and the stable coronary plaques using multi-slice computed tomography (MSCT). Sixty patients with coronary heart disease (37 unstable plaques and 31 stable plaques) were included. The napkin ring thickness, napkin-ring sign, plaque CT attenuation and degree of lumen stenosis were retrospectively analyzed. The diagnostic performances of MSCT were determined to predict the unstable plaques. The difference was statistically significant if P<0.05. The napkin ring thickness of the unstable plaques was thinner than that of the stable plaques (P<0.05). The napkin-ring sign was more frequently observed in the unstable group (89.2%) than the stable group (22.6%, P<0.05). The average CT value of the unstable plaques (26.8±17.8 HU) was lower than that of the stable plaques (68.5±25.5 HU, P<0.05). The unstable plaques had more severe lumen stenosis or occlusion (70.3%) than the stable plaques (41.9%, P<0.05). The measurable napkin ring thickness of the plaques with a cutoff value of 0.8 mm and an accuracy of 89.5% was one independent factor to predict unstable plaques. The optimal combined threshold of the napkin-ring sign and/or the plaque CT value of 53 HU with an accuracy of 80.9% was to predict unstable plaques. The optimal combined threshold of the napkin-ring sign and/or the plaque CT value ≤53 HU may be a good indicator to predict the unstable plaques in patients with CAD. The subgroup of measurable napkin ring thickness of the non-calcified plaques may also be an independent factor to predict the unstable plaques in patients with CAD.

Abstract 21405: Dynamic Enhancement Pattern is Different Between Unstable and Stable Coronary Plaque: Analysis With 320-Row Area Detector Computed Tomography

Introduction: Intraplaque neovascularization is a marker of unstable coronary plaque. We investigated a difference in dynamic enhancement pattern of coronary plaque between stable and unstable angina pectoris, using 320-row area detector computed tomography (CT), which enables whole-heart volumetric acquisition in a single gantry rotation. Hypothesis &amp; Methods: We analyzed 106 coronary plaque segments in 38 patients (mean age 69.8±8.3 years, 32 male) with angina pectoris (13 stable, 25 unstable) who underwent coronary CT and percutaneous coronary intervention (PCI). Coronary plaques were evaluated using 320-row area detector CT with and without contrast enhancement. Culprit plaques (PCI target) of unstable patients were defined as unstable plaque(n=35), whereas culprit plaques of stable patients and non-culprit plaque were defined as stable plaque(n=71). Coronary plaque without contrast enhancement, corresponding to the plaque detected by contrast enhanced CT, was identified using unique calcification as a landmark. The mean Hounsfield unit (HU) in the coronary plaque was measured, and the presence of positive vascular remodeling was evaluated. Coronary artery stenosis was quantified by coronary angiography. Results: Unstable patients were younger than stable patients (66.6±7.2 vs 76.1±6.7 years, p&lt;0.01). Positive vascular remodeling and spotty calcification was more frequently observed in unstable than stable patients (68.4% vs 15.4%, p&lt; 0.01 and 45.5% vs 86.4%, p&lt;0.05 respectively). Coronary artery stenosis was not different between the 2 groups. In CT without contrast enhancement, plaque HU was not different between the 2 groups (unstable: 25.0±32.4 vs stable: 24.9±33.1). With contrast enhancement, plaque HU was significantly elevated in both groups from those without contrast enhancement to 53.9±24.1 (unstable: p&lt;0.01) and to 42.6±33.5 (stable: p&lt;0.01). Unstable plaque showed higher enhancement (delta HU) than stable plaque (28.9±23.5 vs 17.7±25.5, p=0.024). Conclusions: Dynamic enhancement pattern is different between unstable and stable coronary plaque. Compared to stable plaque, unstable plaque shows higher contrast enhancement, suggesting the increased neovascularization in the plaque.

Abstract 21015: Coronary Inflammation in Humans Drives Spatial Changes of Perivascular Adipose Tissue Composition Detectable by a Novel Computed Tomography-Based Technology

Background: Non-invasive detection of vascular inflammation remains an unmet goal. We hypothesized that phenotypic changes in perivascular adipose tissue (PVAT) induced by vascular inflammation can be quantified using a new computed tomography angiography (CTA) methodology. Methods: In Arm 1, human PVAT adipocytes were cultured +/- inflammatory cytokines (n=7) or co-cultured with vascular tissue (+/-Angiotensin-II, n=6) to assess the effects of vascular inflammation on PVAT differentiation. In Arm 2, AT explants (epicardial, subcutaneous and thoracic AT) from 453 cardiac surgery patients were used in histology and gene expression studies to relate the ex vivo images with in vivo CT scan information (n=105) on the biology of the explants. In Arm 3, in 267 patients undergoing diagnostic CTA, PVAT attenuation (Fat Attenuation Index (FAI) defined as the average CT attenuation of AT), was analysed around the proximal right coronary artery. In Arm 4, PVAT FAI around unstable (culprit) and stable coronary plaques was calculated in 22 CAD patients undergoing CTA. Results: In Arm 1, Angiotensin-II (A) and proinflammatory cytokines (B) prevented lipid accumulation and adipocyte differentiation in cultured PVAT. In Arm 2, adipocyte size by histology was inversely correlated with FAI in vivo (C). Both FAI of AT explants (not shown) and FAI in-vivo (n=105) were negatively associated with epicardial AT differentiation as assessed by FABP4 expression (D). In Arm 3, PVAT FAI change over distance from RCA wall was significantly different in CAD compared to no CAD patients (E). In Arm 4, PVAT FAI was significantly increased around unstable plaques (F). Conclusions: Human vessels exert paracrine effects on surrounding PVAT, affecting local intracellular lipid accumulation in preadipocytes, which can then be monitored using a CT imaging approach. This novel methodology can be implemented in clinical practice to detect unstable plaques in the human coronary vasculature.

Evaluation of MMP-7 and TIMP-1 in patients with coronary atherosclerosis

Objectives: MMP’s are a family of enzymes capable to degrade components from the extracellular matrix; they play an important role in normal physiology such as angiogenesis,wound healing ,embryonic development an also in pathogenic pocesses such as atherosclerosis and atherotrombosis by turning a stable coronary plaque into an unstable one.Their activity is regulated by a group of inhibitors(TIMP’s).

PP.18.10] EVALUATION OF MMP-7 AND TIMP-1 IN PATIENTS OF DIFFERENT AGES WITH CORONARY ARTERY DISEASE

Objective: MMP's are a family of enzymes capable to degrade components from the extracellular matrix; they play an important role in normal physiology such as angiogenesis,wound healing,embryonic development an also in pathogenic pocesses such as atherosclerosis and atherotrombosis by turning a stable coronary plaque into an unstable one. Their activity is regulated by a group of inhibitors (TIMP's). Aim: We tested the possibility of MMP-7 and TIMP-1 to serve as biological markers for plaque instability. Design and method: We have analysed a group of 114 patients (77 men and 27 women) aged 45–73 years old,evaluated for coronary artery disease (CAD) by performing coronarography;47 patients with stable CAD, 31 patients with unstable angina pectoris (UAP), 16 with acute myocardial infarction (AMI), and 17 patients without angiographic evidence of CAD. Blood samples collected from patients were centrifuged at 3000 rpm and serum was kept at −70 C until the assay has been made. Serum MMP-7 and TIMP-1 were determined by ELISA method and statistical analysis has been done using SPSS 15.0. Results: Serum concentration of MMP-7 was increased in patients with UAP/AMI patients compared to patients with stable CAD, the highest levels were obtained in UAP group of patients . The evaluation of TIMP-1 followed a similar trend as MMP-7. The level of MMP-7 and TIMP-1 in controls were in the interval specified by the manufacturer. Conclusions: High serum levels of MMP-7 and TIMP-1 seem to be associated with acute coronary events which may be determined by inflammation and degradation of the extracellular matrix from the atherosclerotic cap.

Angioscopic comparison of arterial repair after second-generation drug-eluting stent implantation into vulnerable and stable coronary plaques

BackgroundArterial repair after intracoronary stenting depends on stent types and plaque vulnerability. The aim of this study was angioscopic comparison of arterial repair after implantation of the second-generation drug-eluting stents (G2-DES) between the stable and vulnerable plaques. MethodsFour types of G2-DES were successfully implanted into stable plaques (n=41) and vulnerable plaques (n=34): 13 and 9 Xience-everolimus-, 7 and 6 Endeavor-zotarolimus-, 15 and 9 Resolute-zotarolimus-, and 6 and 10 Nobori-biolimus-eluting stents (EES, E-ZES, R-ZES, and BES), respectively. Coronary angioscopy at 1-year follow-up revealed in-stent appearance, such as neointimal stent coverage (NSC), presence of yellow plaques (YP), and in-stent mural thrombus (MT). NSC was graded into poor and good coverage. ResultsYellow plaques and mural thrombi were found more frequently in the vulnerable plaques than in the stable plaques (29% vs. 12%, P=0.06; 12 vs. 0%, P=0.02; respectively). In EES, poor NSC was observed more frequently in the vulnerable plaques than in the stable plaques (54% vs. 11%, P=0.04). In BES, YP was observed more frequently in the vulnerable plaques than in the stable plaques (80% vs. 17%, P=0.01). In E-ZES and R-ZES, there were no significant differences with regards to angioscopic parameters between the stable and vulnerable plaques. ConclusionsArterial repair after EES and BES implantation into the vulnerable plaques remained vulnerable even at 1-year follow-up.

Pathologic correlates in stable coronary plaques. Traditional and novel insights from pathology

AbstractCoronary artery disease (CAD) remains the most common cause of death overall and is the leading cause of cardiovascular mortality worldwide . Although huge advances in medical therapy have been made within the last decades, the number of worldwide deaths due to CAD will further increase according to current forecasts . Based on the knowledge and understanding of CAD which cardiovascular research has provided over the last decades, patient care has made substantial progress in daily clinical practice. Although the implementation and further refinement of invasive treatment techniques have paved the way for revolutionary concepts especially in the setting of acute coronary syndromes, a true mortality benefit after percutaneous coronary intervention (PCI) of stable lesions has not been shown to date, which may partly be explained by incomplete understanding of atherosclerotic lesion progression underlying the symptomatic presentation of patients with CAD. Therefore, the following review focuses on traditional knowledge and novel concepts of stable atherosclerotic coronary plaque progression from a pathological point of view, to provide a foundation for future technological refinements and novel therapeutic approaches.Answer questions and earn CME: https://wileyhealthlearning.com/Activity2/4279927/Activity.aspx

Identifying stable coronary plaques with OCT technology

AbstractThis article discusses the current value of optical coherence tomography (OCT) for the assessment of stable coronary lesions. OCT generates intracoronary images with unprecedented image resolution, namely a 10‐fold higher image resolution compared to conventional intravascular ultrasound. OCT is able to visualize a variety of atherosclerotic plaques features that have been associated with rapid lesion progression and clinical events. There is broad agreement that the detailed, easy accessible, and interpretable information of OCT on the presence of atherosclerosis, its extent, lumen narrowing, as well as on the result of any interventional measure can be of clinical value, at least in individual patients and in specific clinical scenarios. Preliminary data indicate that OCT can change the operator's intention‐to‐treat and modify the overall revascularization strategy, potentially avoiding unnecessary interventional procedures. OCT might be efficient in complex interventions including treatment of long lesions, diffuse disease, bifurcations, as well as in all cases of angiographically ambiguous lesions. As such, OCT might emerge, next to its undisputed position in research, as tool of choice in all clinical scenarios where angiography is limited by its nature as two‐dimensional luminogram.Answer questions and earn CME: https://wileyhealthlearning.com/Activity2/4279893/Activity.aspx

Characterizing stable coronary plaques with MSCT angiography

AbstractNoninvasive access to coronary anatomy has long been anticipated and eventually became available with the emergence of multislice computed tomography angiography (MSCTA). MSCTA offers the possibility to identify coronary artery disease already in its preclinical phase. This unprecedented information proves to be useful in clinical practice as it allows the appropriate allocation of preventive therapies such as statin and aspirin.Answer questions and earn CME: https://wileyhealthlearning.com/Activity2/4279884/Activity.aspx

The use of ct coronary angiography as a primary preventative strategy in patients with familial hypercholesterolaemia: A prospective introductory clinical study

Aim: Previously individuals suspected of having familial hypercholesterolaemia (FH) would undergo analysis of serum lipids followed by exercise ECG testing and eventually cardiac catheterisation. Frequently, results of invasive coronary angiography would illustrate stable coronary plaque disease that could be managed with medications only. The aim of this study is to show the benefit of CT coronary angiography in identifying stable plaque disease to initiate early primary prevention strategies and avoid unnecessary invasive procedures.

Optische Kohärenztomografie

Optical coherence tomography (OCT) is an intracoronary imaging system, which produces cross-sectional images of the coronary arteries using near infra-red light with a high resolution (10 – 20 μm). This technique visualizes various patterns of atherosclerotic features of the coronary artery in vivo and may differentiate lipid-rich, calcified and fibrous plaques as well as vulnerable and stable coronary plaques. Moreover, OCT may contribute to an optimization and guidance of percutaneous coronary interventions by detecting several features of inadequate stent implantation, such as stent-malapposition, stent edge dissections, tissue or thrombus protrusion through the stent struts or during follow-up an insuffizient stent endothelialization.