Plaque In Acute Coronary Syndrome Research Articles

Non-culprit plaque characteristics in acute coronary syndrome patients with raised hemoglobinA1c: an intravascular optical coherence tomography study

BackgroundRaised hemoglobinA1c (HbA1c) is an indicator of pre-diabetes, which is associated with increased risk of coronary artery disease. However, the detailed morphological characteristics of non-culprit plaques in acute coronary syndrome (ACS) patients remain largely unknown.MethodsA total of 305 non-culprit plaques from 216 ACS patients were analyzed by intravascular optical coherence tomography. These patients were divided into three groups according to the serum glycosylated hemoglobin level: normal HbA1c (< 5.7%), pre-diabetes with raised HbA1c (5.7–6.4%) and diabetes mellitus (DM).ResultsPlaques in patients with raised HbA1c had a longer lipid length (17.0 ± 8.3 mm vs. 13.9 ± 7.2 mm, P = 0.004) and greater lipid index (2775.0 ± 1694.0 mm° vs. 1592.1 ± 981.2 mm°, P = 0.001) than those with normal HbA1c but were similar to DM. The prevalence of calcification in patients with raised HbA1c was significantly higher (38.7% vs. 26.3%, P = 0.048) than normal HbA1c but was similar to DM. The percentage of macrophage infiltration in the DM group was higher than that in the normal HbA1c group (20.5% vs. 7.4%, P = 0.005).ConclusionsCompared to patients with normal HbA1c, the non-culprit plaques in ACS patients with raised HbA1c had more typical vulnerable features but were similar to DM.

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

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

Relation Between Superficial Calcifications and Plaque Rupture: An Optical Coherence Tomography Study

BackgroundThere are several forms of calcium deposition, which play different roles in the stability of the coronary artery. It remains unknown whether certain calcification morphological characteristics determine rupture of lipid-rich lesions in the same plaque in acute coronary syndrome (ACS). MethodsWe retrospectively analyzed 550 patients with ACS between May 2008 and October 2014, who had undergone preintervention optical coherence tomography (OCT) imaging examination. A total of 78 patients with 78 culprit lipid-rich lesions having superficial calcifications on OCT images were included in this study, among which 45 were ruptured lesions with calcium and 33 were nonruptured lipid-rich lesion with calcium. The smallest depth of calcium (CAL-DEP) was determined, and the morphology of the calcifications and plaques was analyzed during preintervention OCT imaging. ResultsThe CAL-DEP was significantly thinner in ruptured lesions with calcium than in nonruptured lipid-rich lesion with calcium (median, 50 [interquartile range (IQR), 33-63] μm vs 110 [73-208] μm; P < 0.001) and in myocardial infarction than in unstable angina pectoris patients (median, 57 [IQR, 36-78] μm vs median, 85 [IQR, 43-140] μm; P = 0.045). For lipid-rich calcified plaques, when CAL-DEP was < 63 μm, the lipid-rich lesion was most vulnerable and prone to rupture (sensitivity = 77.8%; specificity = 81.8%; area under the curve: 0.804; P < 0.0001). ConclusionsSmall CAL-DEP in lipid-rich calcified plaques is a morphological characteristic of a vulnerable plaque phenotype. A CAL-DEP ≤ 63 μm is the critical depth of calcification for lipid-rich calcified plaque rupture in patients with ACS.

CLINICAL SIGNIFICANCE OF PROTEIN GROWTH AND INJURY FACTORS IN ACUTE CORONARY SYNDROME

Aim . As fundamentals for current study we layed upon the comparison tasks for concentration of pregnancy associated plasma protein (PAPP-A) and insulin-like growth factor 1 (IGF-1) in blood plasma of patients with acute coronary syndrome (ACS); confirmation of biological role of PAPP-A and IGF-1 as interacting components of intravascular injury and reparation of atherosclerotic plaque; clinical significance of PAPP-A and IGF-1 in ACS patients. Material and methods . We measured concentrations of PAPP-A and IGF-1 in 71 patient with ACS, mean age 57 year old. The study group had a diagnosed myocardial infarction (MI) in 44 patients, and unstable angina in 27; 9 death cases. Synchronically, we measured PAPP-A and IGF-1 in the control and comparison group. Comparison group consisted of 40 arterial hypertension patients and with stable forms of ischemic heart disease. Controls were 20 almost healthy persons. Results . The concentrations of PAPP-A and IGF-1 in ACS patients that were different from controls and comparison. In unstable angina patients PAPP-A is higher than in controls 3,56 times, and in MI 11,6 times. PAPP-A in MI is 3,2 times higher than in unstable angina. In unstable angina the highest found levels of IGF-1 are 1,2 times higher than in controls. The lowest IGF-1 were in lethal cases of MI, and were 1,27 lower than in controls. Conclusion. PAPP-A and IGF-I are new biochemical markers of intravascular injury and reparation of atherosclerotic plaques, and can be applied in urgent cardiology as analyzers of destruction and morphological instability of atherosclerotic plaques in ACS.

Prognostic implications of non-culprit plaques in acute coronary syndrome: non-invasive assessment with coronary CT angiography.

Non-culprit plaques are responsible for a substantial number of future events in patients with acute coronary syndrome (ACS). In this study, we evaluated the prognostic implications of non-culprit plaques seen on coronary computed tomography angiography (CTA) in patients with ACS. Coronary CTA was performed in 169 patients (mean 59 ± 11 years, 129 males) admitted with ACS. Data sets were assessed for the presence of obstructive non-culprit plaques (>50% luminal narrowing), segment involvement score, and quantitative measures of plaque burden, after censoring initial culprit plaques. Follow-up was performed for the occurrence of major adverse cardiovascular events (MACEs) unrelated to the initial culprit plaque; cardiac death, second ACS, or coronary revascularization after 90 days. After a median follow-up of 4.8 (IQR 2.6-6.6) years, MACE occurred in 36 (24%) patients: 6 cardiac deaths, 16 second ACS, and 14 coronary revascularizations. Dyslipidaemia (hazard ratio [HR] 3.1 [95% confidence interval 1.5-6.6]) and diabetes mellitus (HR 4.8 [2.3-10.3]) were univariable clinical predictors of MACE. Patients with remaining obstructive non-culprit plaques (HR 3.66 [1.52-8.80]) and higher plaque burden index (HR 1.22 [1.01-1.48]) had a more risk of MACE. In multivariate analysis, with diabetes, dyslipidaemia, and plaque burden index, obstructive non-culprit plaques (HR 3.76 [1.28-11.09]) remained an independent predictor of MACE. Almost a quarter of the study population experienced a new event arising from a non-culprit plaque during a follow-up of almost 5 years. ACS patients with remaining obstructive non-culprit plaques or high plaque burden have an increased risk of future MACE.

Prognostic implications of non-culprit plaques in acute coronary syndrome: non-invasive assessment with coronary CT angiography

Purpose: Coronary CTA is a reliable non-invasive risk stratification tool for patients with coronary artery disease. However, little is known about the prognostic implications of non-culprit plaques seen on coronary CTA in patients with ACS. In tis study, we sought ou to determine the prognostic value of non-culprit plaques on coronary CT angiography (CTA) in patients with acute coronary syndrome. Methods: Coronary CTA was performed in 169 ACS patients (mean 59±11 years, 129 males) during index admission. Overall residual coronary artery plaque burden was determined using a segment stenosis score for each patient: 0-20% stenosis: score 0, 20-50%: score 1, 50-70%: score 2, >70%: score 3, (maximal score of 48 per patient). Follow-up was performed for the occurrence of major adverse cardiac events (MACE) not related to the initially culprit lesion; cardiac death, recurrent non-fatal myocardial infarction or coronary revascularization after 90 days. Results: Follow-up was completed in 152 (90%) patients with a median follow-up time of 4.8 (IQR 2.6-6.6) years. MACE occurred in 36 (24%) patients, consisting of 6 cardiac deaths, 11 non-fatal myocardial infarctions and 19 coronary revascularisations. A total of 2432 segments were evaluated and 404 were considered non-diagnostic while 172 were censored because of treatment. The median segment stenosis score was higher in patients with MACE (12 [6-16] vs. 7 [3-11], p = 0.005). Non-culprit plaques with a >50% stenose were more often seen in patients with MACE than in those without (83% vs. 52%, p = 0.001). Dyslipidemia (hazard ratio [HR] 3.1 [95% CI 1.4 - 6.6], diabetes mellitus (HR 4.8 [2.3 - 10.3]) and TIMI risk score (HR 1.5 [1.2 - 1.9]) were univariable predictors of MACE, as well as the segment stenosis score (HR 1.09 [1.03 – 1.15]) and >50% stenosis of a non-culprit plaque (HR 3.7 [1.5 - 8.8]). After adjusting for clinical characteristics, >50% stenosis of a non-culprit plaque (HR 3.69 [1.41-9.68]) remained an independent predictor of MACE. Conclusions: Almost a quarter of ACS patients experienced a non-culprit related MACE during 5 years follow-up in this study. Coronary CTA detects non-culprit plaques in ACS patients and identifies those at risk of future non-culprit cardiac events with incremental value over clinical variables.

Optical coherence tomography assessment of the spatial distribution of culprit ruptured plaques and thin-cap fibroatheromas in acute coronary syndrome

Plaque rupture and subsequent thrombosis is known to be the most important pathology leading to acute coronary syndrome (ACS). We investigated by optical coherence tomography (OCT) whether in ACS there is an association of the location of the culprit plaque in the coronary tree with plaque rupture and/or thin cap fibroatheroma (TCFA). We included 74 patients presenting with ACS that underwent OCT study of the culprit lesion. The distance of the culprit lesion from the ostium was measured angiographically, and the presence of rupture and/or TCFA was assessed by OCT. Sixty-seven patients were analysed. Forty-five ruptured plaques were identified by OCT (67.1%). The distance from the ostium was lower for culprit ruptured plaques versus culprit non-ruptured plaques (p<0.01), particularly in the left anterior descending (LAD) and the left circumflex (LCx) arteries. The majority of culprit ruptured plaques (68.9%) was located in the proximal 30 mm of the coronary arteries. A distance from the ostium of ≤30.54 mm predicted plaque rupture with 71.1% sensitivity and 68.2% specificity. Culprit lesions in the proximal 30 mm are associated with rupture (p<0.05), TCFA (p<0.05), and lower minimal cap thickness (p<0.05). Culprit ruptured plaques in ACS seem to be predominately located in the proximal segments of the coronary arteries.

Increased serum levels of interleukin-6 and von Willenbrand Factor in early phase of acute coronary syndrome in a young and multiethnic Malaysian population

ObjectiveInterleukin-6 (IL6; proinflammatory marker), von Willebrand Factor (vWF; endothelial dysfunction marker) and P-selectin (platelet activation marker), may play important roles in defining the pathogenesis of vulnerable plaques in acute coronary...

The importance of defining serum MMP-9 concentration in diabetics as an early marker of the rupture of atheromatous plaque in acute coronary syndrome

Acute coronary syndrome (ACS) is the main cause of mortality in diabetics. Acute myocardial infarction (AMI) in diabetics is much more often than in non-diabetics. MMP-9 activity could ease the formation of atherosclerosis, destabilization and plaque rupture as well as thrombocyte aggregation. MMP-9 defining in serum in diabetics; the impact of diabetes mellitus on atherosclerosis and MMP-9 level; relation between serum values of MMP-9 and markers of glycoregulation and lipid status, respectively. The greatest concentration of both total and active MMP-9 serum has been noted in diabetics group with ACS. Both total and active MMP-9 values, in group with diabetes and ACS showed significantly important difference regarding the values in control group. Total and active MMP-9 showed statistically important correlation between the values of glycated hemoglobine A1c (HbA1c) and inverse correlations with values of subfraction HDL3.Active MMP-9 showed statistically important inverse correlation with value of HDL cholesterol. According to the results, it has been thought that active MMP-9 shows a certain degree of atherosclerotic changes on blood vessels better than total MMP-9. MMP-9, active one, could present an early marker of atherosclerosis, especially on coronary blood vessels, in diabetics with type 2.

Early Intervention With Rosuvastatin Decreases the Lipid Components of the Plaque in Acute Coronary Syndrome - Analysis Using Integrated Backscatter IVUS (ELAN Study) -

It has recently become possible to analyze coronary plaque characteristics by using integrated backscatter intravascular ultrasound (IB-IVUS). The aim of this study was to use this modality to evaluate the impact of early intervention with rosuvastatin on both the volume and tissue characteristics of non-culprit plaques in acute coronary syndrome (ACS). Patients with ACS underwent IB-IVUS after percutaneous coronary intervention procedure and were administered rosuvastatin. Follow-up IB-IVUS was recorded 6 months later. We analyzed the changes in plaque burden and tissue characteristics in these patients. Plaque components were classified as calcified, fibrous, and lipid according IB-IVUS. We comprehensively analyzed 20 ACS patients. The low-density lipoprotein-cholesterol levels decreased significantly from 117 ± 34 mg/dl to 73 ± 19 mg/dl (P<0.001) after statin therapy. Comparing the baseline images with the follow-up ones revealed a significant reduction in the plaque burden from 98.4 ± 42.1mm(3)/10mm to 80.2 ± 35.8 mm(3)/10mm (P<0.001) and in the lipid volume from 44.1 ± 29.6 mm(3)/10mm to 28.6 ± 17.8 mm(3)/10mm (P<0.001). With respect to the % lipid volume, the reduction rate at follow-up showed a significant correlation with its baseline value (r=-0.498, P=0.024). Early intervention with rosuvastatin in ACS patients enabled significant reduction of the non-culprit plaque during 6 months. This regression was mainly due to the decrease in the lipid component of the plaque.

E0436 Clinical Study on Relationship between the Plasma LTB4 levels and Unstable plaque in Acute Coronary Syndrome

ObjectiveTo explore the association between plasma Leukotriene B4 (LT-B4) and the severity of coronary artery lesions in coronary heart disease (CHD) patients.Methods400 patients were divided into CHD group (n=310) and...

Feasibility of FDG Imaging of the Coronary Arteries: Comparison Between Acute Coronary Syndrome and Stable Angina

This study tested the hypothesis that fluorodeoxyglucose (FDG) uptake within the ascending aorta and left main coronary artery (LM), measured using positron emission tomography (PET), is greater in patients with recent acute coronary syndrome (ACS) than in patients with stable angina. Inflammation is known to play an important role in atherosclerosis. Positron emission tomography imaging with (18)F-FDG provides a measure of plaque inflammation. Twenty-five patients (mean age 57.9 +/- 9.8 years, 72% male, 10 ACS, and 15 stable angina) underwent cardiac computed tomographic angiography and PET imaging with (18)F-FDG after invasive angiography. Images were coregistered, and FDG uptake was measured at locations of interest for calculation of target-to-background ratios (TBR). Additionally, FDG uptake was measured at the site of the lesion deemed clinically responsible for the presenting syndrome (culprit) by virtue of locating the stent deployed to treat the syndrome. The FDG uptake was higher in the ACS versus the stable angina groups in the ascending aorta (median [interquartile ranges] TBR 3.30 [2.69 to 4.12] vs. 2.43 [2.00 to 2.86], p = 0.02), as well as the LM (2.48 [2.30 to 2.93] vs. 2.00 [1.71 to 2.44], p = 0.03, respectively). The TBR was greater for culprit lesions associated with ACS than for lesions stented for stable coronary syndromes (2.61 vs. 1.74, p = 0.02). Furthermore, the TBR in the stented lesions (in ACS and stable angina groups) correlated with C-reactive protein (r = 0.58, p = 0.04). This study shows that in patients with recent ACS, FDG accumulation is increased both within the culprit lesion as well as in the ascending aorta and LM. This observation suggests inflammatory activity within atherosclerotic plaques in acute coronary syndromes and supports intensification of efforts to refine PET methods for molecular imaging of coronary plaques.

Update on Clinical Imaging of Coronary Plaque in Acute Coronary Syndrome

Current evidence suggests that understanding coronary artery disease extends beyond identifying and treating traditional risk factors. Progression of coronary plaque contributes to the development of acute coronary syndrome (ACS). In this article, we reviewed current literature for modalities to image coronary plaque as well as discussed the role of emerging techniques that can improve our understanding of the pathophysiology of ACS.

Characterization of culprit lesions in acute coronary syndromes using coronary dual-source CT angiography

Objective We analyzed typical morphological features of coronary atherosclerotic plaques in acute coronary syndromes (ACS) using contrast-enhanced coronary Dual-Source CT angiography (CTA) in comparison to stable coronary lesions. Patients and methods Fifty-five patients with ACS and 55 controls with stable angina pectoris (SAP) with similar atherosclerotic risk profile were studied. CT angiography was performed using a Dual-Source CT scanner (330 ms rotation, 2 × 64 × 0.6 mm collimation, 60–80 mL contrast agent i.v. at 6 mL/s) before invasive catheterization. We analyzed plaque volume (mm 3), mean and minimal CT density (HU), remodeling index, plaque type (calcified/non-calcified/mixed) and presence of “spotty” calcifications as well as presence of contrast rims. Results In patients with ACS and SAP, 28 and 10 lesions showed both calcified and non-calcified components, but in a greater proportion of non-calcified material, 6 and 23 lesions showed a greater proportion of calcified material and 21 and 8 lesions were completely non-calcified, respectively. None of the culprit plaques in ACS and 14 of the lesions in SAP were completely calcified. A “spotty” pattern of calcification within the plaque and a central filling defect surrounded by a rim of contrast were present in 11 and 14 of 55 ACS cases, but never in SAP lesions. For culprit lesions in ACS and for lesions in patients with SAP, mean plaque volumes were 192.8 ± 114.9 mm 3 and 103.8 ± 51.8 mm 3 ( p = 0.001), mean and minimal CT densities were 85.6 ± 45.1 HU and 47.2 ± 33.7 HU versus 143.8 ± 104.1 HU and 95.9 ± 84.0 HU ( p < 0.01) and mean remodeling indices were 1.6 ± 0.4 and 0.97 ± 0.17 ( p < 0.001), respectively. Conclusion Plaques of culprit lesions in ACS show specific morphologic characteristics in non-invasive coronary CT angiography. As compared to stable lesions, culprit lesions in ACS display greater proportion of non-calcified material and presence of “spotty” calcifications/contrast rims as well as larger plaque volumes, lower CT attenuation and higher remodeling indices.

Multislice CT characteristics of coronary atherosclerotic plaques in acute coronary syndrome

Objective To compare the plaque characteristics of acute coronary syndrome (ACS) and stable angina(SA) by muhislice CT(MSCT). Methods MSCT images of 27 patients with ACS and SA were compared. Results The frequency of positive vascular remodeling was significantly different in ACS (19/31) and SA (6/41, X2 = 16. 95, P < 0. 01), the frequency of spotty calcification was significantly higher in ACS (10/34) than in SA (3/48 ,X2 =8.00, P <0. 01), the frequency of eccentric stenosis was significantly different in ACS(29/34) and SA (32/48, X2 = 3.62, P < 0. 05). The mean CT value of non-calcified plaques in ACS [(35.0 ± 15. 1) HU] was lower than in SA [(67. 5 ± 26. 5) HU(t =4. 82,P < 0. 01)]. Conclusion The MSCT characteristics of atherosclerotic plaques in ACS include positive vascular remodeling,low plaque density,spotty calcification,and eccentric stenosis. Key words: Coronary vessel; Atherosclerosis; Tomography; X-ray computed

Pleiotropic Roles of S100A12 in Coronary Atherosclerotic Plaque Formation and Rupture

Macrophages, cytokines, and matrix metalloproteinases (MMP) play important roles in atherogenesis. The Ca(2+)-binding protein S100A12 regulates monocyte migration and may contribute to atherosclerosis by inducing proinflammatory cytokines in macrophages. We found significantly higher S100A12 levels in sera from patients with coronary artery disease than controls and levels correlated positively with C-reactive protein. S100A12 was released into the coronary circulation from ruptured plaque in acute coronary syndrome, and after mechanical disruption by percutaneous coronary intervention in stable coronary artery disease. In contrast to earlier studies, S100A12 did not stimulate proinflammatory cytokine production by human monocytes or macrophages. Similarly, no induction of MMP genes was found in macrophages stimulated with S100A12. Because S100A12 binds Zn(2+), we studied some functional aspects that could modulate atherogenesis. S100A12 formed a hexamer in the presence of Zn(2+); a novel Ab was generated that specifically recognized this complex. By chelating Zn(2+), S100A12 significantly inhibited MMP-2, MMP-9, and MMP-3, and the Zn(2+)-induced S100A12 complex colocalized with these in foam cells in human atheroma. S100A12 may represent a new marker of this disease and may protect advanced atherosclerotic lesions from rupture by inhibiting excessive MMP-2 and MMP-9 activities by sequestering Zn(2+).

Excimer laser debulking for percutaneous coronary intervention in left main coronary artery disease

Excimer laser has been successfully applied to complex atherosclerotic plaques in acute coronary syndromes; however, its role in debulking in left main coronary artery disease has not been fully explored. Details of a series of 20 patients who underwent excimer laser revascularization of a spectrum of left main coronary artery lesions are presented. Twenty symptomatic patients who received excimer laser debulking were examined for procedural outcome and follow up results. The left main coronary artery was characterized as protected, semi-protected, poorly protected, or unprotected, depending on the presence or absence of patent bypass grafts to the left anterior descending (LAD) and circumflex (CX) arteries. A fully protected left main coronary artery (LMCA) was present in only 20% of the patients. The target lesions included 11(55%) distal LMCA stenoses, six (30%) ostial stenoses, and one (5%) mid-portion lesions. Two (10%) patients had in-stent re-stenosis of the entire length of the LMCA. Small (0.7 mm-1.4 mm) excimer laser catheters were mostly used. A relatively high number of laser energy pulses (1,334 +/- 643) were required to achieve adequate debulking. Successful LMCA intervention was performed in 19 (95%) patients, while in-hospital complications occurred in only one (5%) patient. Subacute/late stent thrombosis developed 3 months after the procedure in one patient, and two patients died from non-cardiac causes during follow-up. Lesions in LMCAs can be revascularized in selected patients by laser debulking and adjunct stenting. Inadequate protection by bypass grafts and decreased left ventricular function do not contradict utilization of excimer laser. Small laser catheters and high energy levels are required during laser debulking of stenoses of left main coronary arteries.

Expression Levels of Toll-Like Receptor Genes in Coronary Atherosclerotic Lesions of Patients With Acute Coronary Syndrome or Stable Angina Pectoris

The differences between acute coronary syndrome (ACS) and stable angina pectoris (SAP) in Toll-like receptor (TLR) expression levels in coronary plaques are not well known. TLR gene expression levels were examined, not only in peripheral blood mononuclear cells (PBMCs), but also in coronary plaques in ACS and SAP patients. TLR gene expression levels were examined in PBMCs using real-time RT-PCR in 27 ACS patients, 45 SAP patients and 28 control subjects. TLR2 and TLR4 expression levels in the PBMCs were significantly higher in the ACS group than in the SAP group. TLR9 expression levels were not significantly different among the 3 groups. TLR gene expression levels were also measured in directional coronary atherectomy (DCA) samples from 9 ACS and 14 SAP patients. The TLR2 expression levels in the DCA samples did not significantly differ between the 2 groups. The TLR4 expression levels were significantly higher in the ACS group than in the SAP group. The results suggest that TLR4 signaling could be more associated with plaque destabilization than with plaque progression. TLR4 expression control may be a novel target for ACS treatment.

Relationships of adiponectin and matrix metalloproteinase-9 to tissue inhibitor of metalloproteinase-1 ratio with coronary plaque morphology in patients with acute coronary syndrome

Adiponectin, an adipocyte-specific protein, matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) play a crucial role in arteriosclerosis and plaque disruption. The present study was designed to elucidate the relationship of adiponectin and the ratio of MMP-9/TIMP-1 and their effects on the stability of plaque in acute coronary syndrome (ACS). The concentrations of adiponectin, MMP-9, TIMP-1 and interleukin-10 were analyzed using ELISA in 56 consecutive unselected patients divided into two groups, stable angina (n=13) and ACS (n=43), and were compared with 19 healthy control subjects. The 56 patients were also angiographically studied and divided into two groups, simple lesion (n=22) and complex lesion (n=34), based on coronary plaque morphology. The ratio of MMP-9/TIMP-1 showed significantly higher values in the ACS group compared with the control group (0.22+/-0.10 versus 0.11+/-0.03; P<0.001). Adiponectin was negatively correlated with the ratio of MMP-9/TIMP-1 (r=--0.332; P=0.008) and positively correlated with interleukin-10 (r=0.651; P=0.001). Multivariate logistic regression analysis showed that adiponectin (P=0.046) and MMP-9/TIMP-1 (P=0.044) are independent predictors for ACS, and MMP-9/TIMP-1 (P=0.013) is an independent predictor for complex lesion morphology plaques. In the present study, it was found that adiponectin has a negative relationship with the ratio of MMP-9/TIMP-1 in patients with ACS, and that the ratio of MMP-9/TIMP-1 is an independent predictor of the stability of atherosclerotic plaque and the severity of coronary atherosclerosis.

Coronarographic and pathomorphological characteristics of unstable atherosclerotic plaques in acute coronary syndromes

The proximal segments of the main coronary vessels are the most often localization of "soft" unstable atherosclerotic plaques. The maximum number of plaques developed in the anterior descending branch of the left coronary artery. Pathognomonic relationship was found between the type of these plaques (with ulceration, rupture, thrombosis) and certain acute coronary syndrome. It was shown that the criteria of the plaque instability correlated with clinical manifestations of coronary syndromes. The bases and effects of "pathological" vascularization of unstable atherosclerotic plaques on the angioarchitectonics and hemodynamics of the heart were determined. Dissociation between myocardial vascularization degree and myocardial blood supply index was detected, which underlies the development of "unstable" myocardium in patients with acute coronary syndromes.