Coronary Artery Plaque In Patients Research Articles

The Association of Lipoprotein(a) and Neutrophil-to-Lymphocyte Ratio Combination with Atherosclerotic Cardiovascular Disease in Chinese Patients.

The association of lipoprotein(a) [Lp(a)] with atherosclerotic cardiovascular disease (ASCVD) risk can be modified by chronic systemic inflammation. The neutrophil-to-lymphocyte ratio (NLR) is a reliable and easily available marker of immune response to various infectious and non-infectious stimuli. The purpose of this study was to assess the combined effects of Lp(a) and NLR in predicting the ASCVD risk and coronary artery plaque traits. This study included 1618 patients who had coronary computed tomography angiography (CTA) with risk assessment of ASCVD. CTA was used to evaluate the traits of coronary atherosclerotic plaques, and the association of ASCVD with Lp(a) and NLR was assessed by multivariate logistic regression models. Plasma Lp(a) and NLR were significantly increased in patients having plaques. High Lp(a) was defined as the plasma Lp(a) level > 75 nmol/L and high NLR as NLR > 1.686. The patients were grouped into four categories according to normal or high NLR and plasma Lp(a) as nLp(a)/NLR-, hLp(a)/NLR-, nLp(a)/NLR+ and hLp(a)/NLR+. The patients in the latter three groups had higher risk of ASCVD compared to the reference group nLp(a)/NLR-, with the highest ASCVD risk in the hLp(a)/NLR+ group (OR = 2.39, 95% CI = 1.49-3.83, P = 0.000). The occurrence of unstable plaques was 29.94% in the hLp(a)/NLR+ group, which was significantly higher than groups nLp(a)/NLR+, hLp(a)/NLR- and nLp(a)/NLR- with 20.83%, 26.54% and 22.58%, respectively, and there was a significantly increased risk of unstable plaque in the hLp(a)/NLR+ group compared to the nLp(a)/NLR- group (OR = 1.67, 95% CI = 1.04-2.68, P = 0.035). The risk of stable plaque was not significantly increased in the hLp(a)/NLR+ group compared to the nLp(a)/NLR- group (OR = 1.73, 95% CI = 0.96-3.10, P = 0.066). The concomitant presence of elevated Lp(a) and higher NLR is associated with increased unstable coronary artery plaques in patients with ASCVD.

Role of lncRNAs in Remodeling of the Coronary Artery Plaques in Patients with Atherosclerosis.

Cardiovascular diseases (CVDs) are the leading cause of death worldwide according to World Health Organization (WHO) data. Atherosclerosis is considered as a chronic inflammatory disease that develops in response to damage to the vascular intima-media layer in most cases. In recent years, epigenetic events have emerged as important players in the development and progression of CVDs. Since noncoding RNA (ncRNAs) are important regulators in the organization of the pathophysiological processes of the cardiovascular system, they have the potential to be used as therapeutic targets, diagnostic and prognostic biomarkers. In this study long noncoding RNA (lncRNA) and mRNA gene expression were compared between coronary atherosclerotic plaques (CAP) and the internal mammary artery (IMA) which has the same genetic makeup and is exposed to the same environmental stress conditions with CAP in the same individual. lncRNA and mRNA gene expressions were determined using the microarray in the samples. Microarray results were validated by RT-qPCR. Differentially expressed genes (DEGs; lncRNAs and mRNAs) were determined by GeneSpring (Ver 3.0) [p values <0.05 and fold change (FC) >2]. DAVID bioinformatics program was used for Gene Ontology (GO) annotation and enrichment analyses of statistically significant genes between CAP and IMA tissue. In our study, 345 DEGs were found to be statistically significant (p<0.05; FC >2) between CAP and IMA. Of these, 65 were lncRNA and 280 were mRNA. Thirty-three lncRNAs were upregulated, while 32 lncRNAs were downregulated. Some of the important mRNAs are SPP1, CYP4B1, CHRDL1, MYOC, and ALKAL2, while some of the lncRNAs are LOC105377123, LINC01857, DIO3OS, LOC101928134, and KCNA3 between CAP and IMA tissue. We also identified genes that correlated with statistically significant lncRNAs. The results of this study are expected to be an important source of data in the development of new genetically based drugs to prevent atherosclerotic plaque. In addition, the data obtained may contribute to the explanation of the epigenetic mechanisms that play a role in the pathological basis of the process that protects the IMA from atherosclerosis.

Rationale for different formulations of omega-3 fatty acids leading to differences in residual cardiovascular risk reduction

Rationale for different formulations of omega-3 fatty acids leading to differences in residual cardiovascular risk reduction

Higher levels of serum phosphorus are associated with coronary calcification post heart transplantation

Abstract Background A higher serum phosphorus level, although within the normal range has been linked to coronary artery and aortic calcification in the non-transplant population. Coronary calcification is mostly associated with donor-derived lesions, and is uncommon within the first years after heart transplantation. Purpose We aimed to investigate the association of phosphorus levels with plaque calcification after heart transplantation. Methods A total of 156 patients who underwent virtual histology intravascular ultrasound (VH-IVUS) studies for cardiac allograft vasculopathy (CAV) surveillance and had fasting serum phosphorus levels &amp;lt;4.5 mg/dL, were included in the analyses. IVUS analyses were performed in the proximal left anterior descending artery, and plaque composition of dense calcium (DC) was evaluated using VH-IVUS, and presented as percent DC of total plaque volume. The patients were separated into 3 groups according to tertiles of serum phosphorus levels. Results Mean recipient and donor ages were 54±13 and 31±14 years, respectively. Mean serum phosphorus in recipients was 3.5±0.6 mg/dL, with median time after transplantation at the IVUS studies of 6 (3,10) years. There were no significant differences in %DC between phosphorus tertiles in patients who underwent IVUS within 6 years after transplantation (p=0.11, Fig. 1A). However, beyond 6 years after transplantation, we observed an incremental association between phosphorus levels and the extent of calcification (p=0.02, Fig. 1B). In this group, serum phosphorus levels significantly correlated with %DC (standardized β=0.29, P=0.008), and this correlation remained significant after adjustment for donor age, recipient age, and eGFR (standardized β=0.26, P=0.001). Conclusion Higher serum phosphorus levels were associated with a level-dependent increase in calcified coronary artery plaque in patients starting 6 years post heart transplant. Long-term exposure to higher serum phosphorus, even within the normal range, might promote plaque calcification after heart transplantation. Funding Acknowledgement Type of funding sources: None.

The presence of adverse atherosclerotic coronary plaque features is associated with diabetes

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): The grant was given to the Bioimaging field of Semmelweis University by the Excellence Program of the Ministry of Innovation and Technology in Hungary. On Behalf of Cardiovascular Imaging Research Group (CIRG) Introduction Diabetes mellitus (DM) is associated with increased cardiovascular morbidity and mortality. However, there is a lack of data about the prevalence of high-risk coronary artery plaques in patients with DM. Purpose In our study we aimed to compare the prevalence of adverse atherosclerotic coronary artery plaque features between patients with and without DM. Methods We have analyzed the data of patients who underwent coronary computed tomography angiography (CCTA) between October 2012 and December 2020. Our exclusion criteria were coronary anomaly, congenital or other structural heart disease, previous revascularization or heart transplantation, non-diagnostic image quality and no available data on the presence of DM. Patients were divided into two groups based on the presence of DM. Results In total, 11357 patients (47.6% men) were included in our study. Prevalence of DM was 14.5%. There were significant differences in age (63.2 ± 9.5 vs 58.1 ± 12.2 years, p &amp;lt; 0.001) and major cardiovascular risk factors such as hypertension, dyslipidemia and smoking between the two groups (all p &amp;lt; 0.05). We have measured higher coronary artery calcium score in patients with DM vs. without DM (424.3 ± 744.0 vs 174.2 ± 794.6, p &amp;lt; 0.001). Luminal stenosis &amp;gt;70% was more frequent in the DM group (24.6% vs 10.5%, p &amp;lt; 0.001). While 29.6% of patients without DM had at least one high risk plaque, this rate was 38.9% in those with DM (positive remodeling: 19.6% vs 26.1%, low attenuation: 7.6% vs 10.2%, spotty calcium: 16.9% vs 21.6%, napkin-ring sign: 1.7% vs 2.6%, all p &amp;lt; 0.05). Conclusions The prevalence of severe coronary artery stenosis and coronary plaques with adverse characteristics was higher in patients with DM.

Association of Epicardial Fat Volume With the Extent of Coronary Atherosclerosis and Cardiovascular Adverse Events in Asymptomatic Patients With Diabetes.

Epicardial adipose tissue has a paracrine effect, enhancing coronary artery atherosclerotic plaque development. This study evaluated epicardial fat volume (EFV), adipokines, coronary atherosclerosis, and adverse cardiovascular events in a cohort of asymptomatic patients with type 2 diabetes mellitus (T2DM). Epicardial fat volume was calculated using data from computed tomography coronary angiograms. Adipokines and inflammatory cytokines were also assayed and correlated with EFV. Epicardial fat volume was also assessed as a predictor of coronary artery calcium (CAC) score, number of coronary artery plaques, and significant plaque (>50% luminal stenosis). Data from the EFV analysis were available for 221 (85.7%) participants. Median EFV was 97.4 cm3, mean body mass index was 28.1 kg/m2, and mean duration of T2DM was 13 years. Statistically significant, but weak, correlations were observed between several adipokines, inflammatory cytokines, and EFV. Epicardial fat volume was a significant univariate (P = .01), but not multivariate, predictor of the number of coronary plaques, but not of CAC score or significant plaque. After a mean follow-up of 22.8 months, 12 adverse cardiovascular events were reported, exclusively in participants with EFV >97.4 cm3. Epicardial fat volume has limited utility as a marker of coronary artery plaque in patients with T2DM and is weakly correlated with adipokine expression.

Quantification of atherosclerotic plaque volume in coronary arteries by computed tomographic angiography in subjects with and without diabetes.

BackgroundDiabetes mellitus (DM) is considered a cardiovascular risk factor. The aim of this study was to analyze the prevalence and volume of coronary artery plaque in patients with diabetes mellitus (DM) vs. those without DM.MethodsThis study recruited consecutive patients who underwent coronary computed tomography (CT) angiography (CCTA) between October 2016 and November 2017. Personal information including conventional cardiovascular risk factors was collected. Plaque phenotypes were automatically calculated for volume of different component. The volume of different plaque was compared between DM patients and those without DM.ResultsAmong 6381 patients, 931 (14.59%) were diagnosed with DM. The prevalence of plaque in DM subjects was higher compared with nondiabetic group significantly (48.34% vs. 33.01%, χ2 = 81.84, P < 0.001). DM was a significant risk factor for the prevalence of plaque in a multivariate model (odds ratio [OR] = 1.465, 95% CI: 1.258–1.706, P < 0.001). The volume of total plaque and any plaque subtypes in the DM subjects was greater than those in nondiabetic patients significantly (P < 0.001).ConclusionThe coronary artery atherosclerotic plaques were significantly higher in diabetic patients than those in non-diabetic patients.

The randomized study of preventive revascularization of vulnerable coronary artery plaques in patients with stable coronary artery disease

Background. Today, a number of unresolved issues remain regarding vulnerable coronary plaques, one of which is the need for preventive revascularization.Aim. Evaluation of the appropriateness of preventive revascularization of functionally insignificant lesions of the coronary arteries with signs of vulnerability according to the virtual histology of intravascular ultrasound in patients with stable coronary artery disease.Methods. The prospective randomized study includes patients with stable coronary artery disease and isolated intermediate-grade coronary stenosis. The first step in patients is measured fractional flow reserve to confirm the hemodynamic insignificance of stenosis. Then an intravascular ultrasound is performed to verify signs of plaque vulnerability: a thin-cap fibroatheroma and / or minimum lumen area &lt;4 mm2 and/or plaque burden &gt;70%. After that, patients are randomized into two groups: preventive revascularization or optimal medical therapy. After 12 months, patients undergo repeated intravascular ultrasound and end-point analysis.Results. So far, 10 patients have been included in the study (6 in the preventive revascularization group and 4 in the optimal medical therapy group). No endpoints and complications were recorded in both groups in 30-days follow-up.Conclusion. Intravascular imaging methods can identify vulnerable coronary plaques, which allows you to use a personalized approach in determining treatment tactics, one of which can be preventive revascularization.

Impact of serum 1,5-anhydro-d-glucitol level on the prediction of severe coronary artery calcification: an intravascular ultrasound study

BackgroundA low 1,5-anhydro-d-glucitol (AG) blood level is considered a clinical marker of postprandial hyperglycemia. Previous studies reported that 1,5-AG levels were associated with vascular endothelial dysfunction and coronary artery disease (CAD). However, the association between 1,5-AG levels and coronary artery plaque in patients with CAD is unclear.MethodsThis study included 161 patients who underwent percutaneous coronary intervention for CAD. The culprit plaque characteristics and the extent of coronary calcification, which was measured by the angle of its arc, were assessed by preintervention intravascular ultrasound (IVUS). Patients with chronic kidney disease or glycosylated hemoglobin ≥ 7.0 were excluded. Patients were divided into 2 groups according to serum 1,5-AG levels (< 14.0 μg/mL vs. ≥ 14 μg/mL).ResultsThe total atheroma volume and the presence of IVUS-attenuated plaque in the culprit lesions were similar between groups. Calcified plaques were frequently observed in the low 1,5-AG group (p = 0.06). Compared with the high 1,5-AG group, the low 1,5-AG group had significantly higher median maximum calcification (144° vs. 107°, p = 0.03) and more frequent calcified plaques with a maximum calcification angle of ≥ 180° (34.0% vs. 13.2%, p = 0.003). Multivariate logistic regression analysis showed that a low 1,5-AG level was a significant predictor of a greater calcification angle (> 180°) (OR 2.64, 95% CI 1.10–6.29, p = 0.03).ConclusionsLow 1,5-AG level, which indicated postprandial hyperglycemia, was associated with the severity of coronary artery calcification. Further studies are needed to clarify the effects of postprandial hyperglycemia on coronary artery calcification.

Association between Lipoprotein(a) and the characteristics of left main coronary artery plaque in patients with stable angina pectoris

Objective: To investigate the relationship between Lipoprotein (LP) (a) level and the characteristics of tissue components of left main coronary artery (LMCA) plaque. Methods: A total of 102 patients with stable angina pectoris who underwent percutaneous coronary intervention (PCI) in the People's Hospital of Henan Province from June 2010 to October 2016 were included. We performed intravascular ultrasound-virtual histology (IVUS-VH) to their LMCAs and evaluated the tissue characteristics, and the blood level of total cholesterol (TC), triacylglycerol (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), ApoB, ApoA1, LP(a) were measured. According to the value of their LP(a) level they were divided into 2 groups (high LP(a) group (>300 mg/L) (n=35) and low LP(a) group (≤300 mg/L) (n=67)), then the relationship between the above lipid values and the tissue characteristics of the LMCA plaque in the patients were evaluated. Results: Patients with a high LP(a) had a larger percentage of fibrolipid volume and a smaller percentage fibrous volume compared to patients with a normal LP(a) (25%±5% vs 13%±6%, P<0.01 and 50%±8% vs 61%±9%, P<0.01). Using multivariate linear regression analysis after adjustment for the above-mentioned confounding factors, LP(a) had a significantly positive correlation with fibrolipid volume percentage (r=0.645, β=0.29, P<0.01), and had a negative correlation with fibrous volume percentage (r=-0.467, β=-0.32,P<0.01), suggesting that the LP(a) was associated with the vulnerability of the LMCA plaque. Conclusion: For the patients with stable angina pectoris, the LP(a) has a significantly positive correlation with the percentage of fibrolipid volume and a negative correlation with the percentage of fibrous volume, suggesting that the LP(a) could predict the vulnerability of the LMCA plaque.

Association of calciprotein particles measured by a new method with coronary artery plaque in patients with coronary artery disease: A cross-sectional study

BackgroundCalciprotein particles (CPPs) have been suggested to be associated with the degree of coronary atherosclerosis, and have also been established as a molecular marker for clinical outcome in patients with chronic kidney disease (CKD). However, there are several concerns with regard to conventional measurement of CPPs. We therefore developed a new CPP measurement system that can detect both smaller and lower-density CPPs. MethodsWe analyzed 71 consecutive patients who underwent percutaneous coronary intervention for acute coronary syndrome (ACS, n=29) and/or stable angina pectoris (AP, n=42) who did not have CKD of stage 4 or greater. CPP measurement was made using an infrared fluorescent bisphosphonate (OsteoSense, PerkinElmer, Waltham, MA, USA) and a gel filtration method. The coronary artery plaque was analyzed by gray-scale intravascular ultrasound (IVUS) and integrated backscatter (IB)-IVUS. ResultsThe median CPP level (interquartile range) was 40,953 (19,171–74,131) arbitrary units (AU). When we divided the CPP level into quintiles, the total and lipid plaque volume were incrementally higher with increasing quintile from lowest to highest (both p<0.02). After adjustment by age, body mass index, and estimated glomerular filtration rate, which factors were correlated with the above-described plaque components, the top quintile of CPP (>86,751AU) had significantly higher total plaque (263mm3 vs. 161mm3; p=0.001) and lipid plaque volume (156mm3 vs. 89mm3; p<0.001) than the other quintiles. However, these associations were not found for the fibrous or calcified plaque volume. The CPP level was higher in the ACS group than the stable AP group (p=0.02), and the total and lipid plaque volume were also higher in the ACS group than the stable AP group (both p<0.05). ConclusionsThe results suggested that a high CPP level, as measured by the novel assay, is a surrogate marker for coronary atherosclerosis, especially in lipid-rich plaques, contributing to an increased risk of plaque vulnerability.

An omega-3 fatty acid plasma index ≥4% prevents progression of coronary artery plaque in patients with coronary artery disease on statin treatment

Background and aimsHigher blood levels of the omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been associated with fewer cardiovascular events and lower mortality in prospective studies. Our aim was to determine a target level of EPA and DHA to prevent progression of coronary artery plaque. Methods218 subjects with stable coronary artery disease on statins were randomized to high-dose EPA and DHA (3.36 g daily) or no omega-3 for 30 months. Coronary plaque volume was measured by coronary computed tomographic angiography. Plasma phospholipid levels of EPA, DHA and total fatty acids were measured by gas chromatography mass spectrometry. The omega-3 fatty acid index was calculated as EPA+DHA/total fatty acid. ResultsMean (SD) age was 62.9 (7.8) years; mean (SD) LDL-C level 78.6 (27.3) mg/dL and median triglyceride level 122 mg/dL. Subjects assigned to EPA and DHA had increased plasma EPA and DHA levels variably from 1.85% to 13.02%. Plasma omega-3 fatty acid index ≥4% prevented progression of fibrous, noncalcified, calcified and total plaque in nondiabetic subjects whereas those in the lowest quartile (<3.43%) had significant progression of fibrous, calcified and total plaque. No difference was observed in diabetic subjects. ConclusionsEPA and DHA added to statins prevented coronary plaque progression in nondiabetic subjects with mean LDL-C <80 mg/dL, when an omega-3 index ≥4% was achieved. Low omega-3 index <3.43% identified nondiabetic subjects at risk of coronary plaque progression despite statin therapy. These findings highlight the importance of measuring plasma levels of omega-3 fatty acids early and at trial conclusion. Targeting an omega-3 index ≥4% maximizes cardiovascular benefit.

Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients With Coronary Artery Disease: A Randomized Clinical Trial.

BackgroundAlthough statins reduce cardiovascular events, residual risk remains. Therefore, additional modalities are needed to reduce risk. We evaluated the effect of eicosapentaenoic acid and docosahexaenoic acid in pharmacologic doses added to statin treatment on coronary artery plaque volume.Methods and ResultsA total of 285 subjects with stable coronary artery disease on statins were randomized to omega‐3 ethyl‐ester (1.86 g of eicosapentaenoic acid and 1.5 g of docosahexaenoic acid daily) or no omega‐3 (control) for 30 months. Coronary plaque volume was assessed by coronary computed tomographic angiography. Mean (SD) age was 63.0 (7.7) years; mean low‐density lipoprotein cholesterol ≤80 mg/dL. In the intention‐to‐treat analysis, our primary endpoint, noncalcified plaque volume, was not different between groups (P=0.14) but approached significance in the per protocol analysis (P=0.07). When stratified by age in the intention‐to‐treat analysis, younger omega‐3 subjects had significantly less progression of the primary endpoint, noncalcified plaque (P=0.013), and fibrous, calcified and total plaque. In plaque subtype analysis, controls had significant progression of fibrous plaque compared to no change in the omega‐3 ethyl‐ester group (median % change [interquartile range], 5.0% [−5.7, 20.0] versus −0.1% [−12.3, 14.5], respectively; P=0.018). Among those on low‐intensity statins, omega‐3 ethyl‐ester subjects had attenuation of fibrous plaque progression compared to controls (median % change [interquartile range], 0.3% [−12.8, 9.0] versus 4.8% [−5.1, 19.0], respectively; P=0.032). In contrast, those on high‐intensity statins had no difference in plaque change in either treatment arm.ConclusionsHigh‐dose eicosapentaenoic acid and docosahexaenoic acid provided additional benefit to statins in preventing progression of fibrous coronary plaque in subjects adherent to therapy with well‐controlled low‐density lipoprotein cholesterol levels. The benefit on low‐intensity statin, but not high‐intensity statin, suggests that statin intensity affects plaque volume.Clinical Trial Registration URL: http://www.ClinicalTrials.gov. Unique identifier: NCT01624727.

TCT-508 The PREDICT (Prognostic Role of coronary artery plaquEs in patients with suspected coronary artery Disease using multislice Computed Tomography) observational comparative outcomes study

TCT-508 The PREDICT (Prognostic Role of coronary artery plaquEs in patients with suspected coronary artery Disease using multislice Computed Tomography) observational comparative outcomes study

Arterial Stiffness Index and Coronary Artery Plaques in Patients with Subclinical Coronary Atherosclerosis.

Arterial stiffness is a physiologic quantitative value used to measure arterial compliance. It is predictive of coronary atherosclerosis in patients with intermediate to high cardiovascular risk. However, a correlation between arterial stiffness and subclinical coronary atherosclerosis has yet to be established. Therefore, the purpose of this study was to evaluate arterial stiffness using an arterial stiffness index (ASI) and investigate its association with coronary artery plaque in patients with subclinical coronary atherosclerosis. Our study enrolled 156 consecutive subjects who underwent health screening using a 64-slice cardiac computed tomography angiography (CCTA). Their arterial stiffness index was assessed noninvasively by CardioVision(®) MS-2000. The atheroma on the coronary vessel walls was analyzed. Of the 156 patients, 53 displayed at least one > 50% stenotic lesion over the coronary arteries in CCTA images. The patients with at least one > 50% coronary stenotic plaque were older and had higher systolic blood pressure and ASI values than patients without > 50% coronary stenotic plaque. After dividing the study population into 2 groups by those patients over and under 50 years of age, the ASI positively correlated with the presentation of at least one > 50% coronary stenotic plaque in patients aged ≥ 50 years (odds ratio = 1.02, 95% confidence interval: 1.00-1.04, p = 0.03). The ASI could play a role in risk stratification systems for coronary artery disease in patients with subclinical coronary atherosclerosis, and is a useful clinical marker for the correlation of early coronary plaque. Arterial stiffness; Arterial stiffness index; Atherosclerosis; Coronary artery plaque.

Effects of Combination of Ezetimibe and Rosuvastatin on Coronary Artery Plaque in Patients with Coronary Heart Disease

In approximately 80% of cardiovascular disease-related deaths, patients suffer from coronary atherosclerotic heart disease. Ezetimibe is the first intestinal cholesterol absorption inhibitor. Its combination with statins for treating coronary atherosclerotic heart disease has attracted attention worldwide. The study group comprised 106 patients with coronary atherosclerotic heart disease and hyperlipidaemia. Each was randomly assigned to one of two groups: (1) Ezetimibe (10mg, once a night) plus rosuvastatin (10mg, once a night) (n=55) or (2) Rosuvastatin alone (10mg, once a night) (n=51). The primary endpoint was new or recurrent myocardial infarction, unstable angina pectoris, cardiac death, and stroke. Blood lipid, high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), and matrix metalloproteinase-9 (MMP-9) levels were measured before treatment and at one, six and 12 months after treatment. Coronary plaque size and compositional changes were determined using intravascular ultrasonography. The combination of ezetimibe plus rosuvastatin decreased total cholesterol, low-density lipoprotein cholesterol, hsCRP, IL-6, and MMP-9 levels at six and 12 months after treatment. Statistical significance was detected between two groups. At 12 months, the plaque burden, plaque cross-sectional area, and percentage of necrotic plaque composition were significantly lower in the combination group than in rosuvastatin alone group (P<0.05). And compared with rosuvastatin alone group, the primary endpoint decreased more effectively in combination group. The combination of ezetimibe and rosuvastatin apparently diminishes lipid levels and plaque burden and improves plaque stability, which may be associated with the potent inhibitory effects of ezetimibe and rosuvastatin on inflammatory cytokines.

TCT-614: Prognostic Role of coronary artery plaquEs in patients with suspected coronary artery Disease using multislice Computed Tomography (PREDICT

TCT-614: Prognostic Role of coronary artery plaquEs in patients with suspected coronary artery Disease using multislice Computed Tomography (PREDICT

Abstract 3725: Myocardial Microvascular Obstruction in Sudden Death from Acute Myocardial Infarction Occurs more often in Coronary Plaque Erosion than in Plaque Rupture

Epicardial coronary artery thrombosis is associated with myocardial microvascular obstruction (MVO) and microemboli. Clinical consequences include acute myocardial infarction and sudden cardiac death from myocardial MVO and myocyte necrosis. We thus characterized myocardial histopathology and morphometry and related these findings to epicardial coronary artery plaque in patients dying from coronary artery occlusion. Hearts from patients with proven sudden coronary death from acute coronary artery occlusion underwent histopathologic characterization for MVO, cardiac microemboli, and epicardial coronary artery plaque. Immunohistochemistry was performed on microvascular thrombus to evaluate for platelet and fibrin content. Forty four cases were studied (mean age at death 51 ± 15 yrs). All emboli and MVO thrombus stained for both fibrin and platelets, and occurred in 54% of all patients, mean 4.5 microemboli/heart. Of all occluded microvessels, 89% were less than 120 um diameter (39% were &lt; 30 um dia), and only 4% were greater than 200 um diameter. Microvascular obstruction and emboli occurred more often in epicardial plaque erosion (74% vs 40% of cases with MVO), and was most common in the LAD territory. Histopathologic epicardial coronary stenosis severity was (mean) 74% in those with emboli and 75% in those without (p=ns). Microemboli and microvascular obstruction are very common in patients dying of acute coronary artery thrombosis. Plaque erosion may be most likely to cause such emboli, with accumulation in sub-200 micron vessels. These emboli and microvessel obstruction have a prominent clinical role due to associated myonecrosis. Interventional strategies for eliminating MVO may be useful to limit myocardial damage and prevent long term sequelae.

Implication of Plaque Color Classification for Assessing Plaque Vulnerability: A Coronary Angioscopy and Optical Coherence Tomography Investigation

The purpose of this study was to assess the relationship between plaque color evaluated by coronary angioscopy and fibrous cap thickness estimated by optical coherence tomography (OCT) in vivo. Yellow color intensity of coronary plaque evaluated by coronary angioscopy might be associated with plaque vulnerability. Seventy-seven coronary artery plaques in patients with acute coronary syndrome were observed by angioscopy and OCT. Plaque color was graded as white, light yellow, yellow, or intensive yellow. There were significant differences among the groups classified by plaque color with respect to the fibrous cap thickness estimated by OCT: 389 +/- 74 mum in white plaques, 228 +/- 51 microm in light yellow plaques, 115 +/- 28 microm in yellow plaques, and 59 +/- 14 microm in intensive yellow plaques (p < 0.0001). In Spearman rank-order correlation analysis, there was a significant negative correlation between yellow color intensity and fibrous cap thickness (p < 0.0001). Furthermore, 80% of intensive yellow plaques were thin cap fibroatheroma with a cap thickness of < or =65 microm. The plaque color in coronary angioscopy was determined by the fibrous cap thickness, which was assessed by OCT. Although coronary angioscopy remains a specialized research tool, it might allow us to evaluate plaque vulnerability.

Elevation of Plasma Matrix Metalloproteinase-9 in the Culprit Coronary Artery in Patients With Acute Myocardial Infarction Clinical Evidence From Distal Protection

Although the elevation of circulating plasma matrix metalloproteinase (MMP)-9 levels in patients with acute myocardial infarction (AMI) has been documented, the origin of MMP-9 remains unclear. Plasma MMP-9 levels in both the peripheral circulation and coronary arteries were measured in patients with AMI (n=23) and with stable angina pectoris (SAP, n=10) during percutaneous coronary intervention (PCI) with a distal protection device. Blood samples were collected from the femoral artery (FA) and the coronary artery before (Initial) and after (Second) dilation of the culprit lesion. Coronary sinus blood samples were obtained immediately after PCI (n=7). Coronary artery plaque fragments were aspirated in patients with AMI (n=20) and compared with those from patients with SAP who underwent directional atherectomy (n=10). MMP-9 levels in Initial and Second were significantly higher in patients with AMI than in patients with SAP (p<0.01). In AMI patients MMP-9 levels were significantly higher in Initial than in the FA (p<0.05), and were further increased in Second (p<0.0001), whereas those in the coronary sinus were similar to the FA. Immunohistochemistry revealed augmented MMP-9 expression in the coronary artery plaque fragments from AMI patients. MMP-9 is mainly released into the coronary circulation from the coronary artery plaque in patients with AMI.