A limited increase in collateral flow and the high prevalence of coronary steal during stress underscore the functional limitation of collaterals in CTOs without prior Q-wave MI. Even presumably 'well-collateralized' CTOs may benefit from a revascularization.

We could demonstrate that coronary steal in man is mainly due to a hemodynamically significant donor artery lesion, but can also occur due to an impaired vasodilatory reserve of the microcirculation in the absence of a donor artery lesion. Coronary steal may have an adverse influence on the preservation of myocardial function by collaterals.

DC (dendritic cells) play an important role in the immune system. They invade peripheral tissues to detect harmful antigens, inducing a local immune response. Studies suggest that DCPs (dendritic cell precursors) might be reduced in AMI (acute myocardial infarction); however, the reason for their reduction is unknown yet. In the present study, circulating mDCPs (myeloid DCPs), pDCPs (plasmacytoid DCPs), tDCPs (total DCPs) and serum levels of TNFα (tumour necrosis factor α), IL (interleukin)-2, -4, -5, -6, -10 and -12 were analysed by flow cytometry in blood of patients with NSTEMI [non-STEMI (ST-segment elevation myocardial infarction)] (n=44) and STEMI (n=34) compared with controls with excluded CAD (coronary artery disease) (n=45). Post-mortem myocardial specimens of patients with AMI (n=12) and healthy myocardium of accident victims (n=10) were immunostained for mDCs (myeloid dendritic cells) T-cells and macrophages. Compared with controls, in patients with AMI a significant decrease in circulating mDCPs, pDCPs and tDCPs was observed (each P<0.0001). The extent of the decrease was higher in STEMI than NSTEMI patients. Serum levels were significantly higher in patients with AMI compared with controls for IL-6, -10, -12 and TNFα (each P<0.03). Immunostaining revealed significantly higher number of DCs, T-cells and macrophages (each P<0.002) in infarcted than control myocardium. We show that circulating DCPs are significantly reduced in AMI, with a pronounced reduction in STEMI patients. This was accompanied by a significant increase of inflammatory serum cytokines in patients with AMI. Immunohistochemical analysis unravelled that the reduction of circulating DCPs might be due to recruitment into the infarcted myocardium.

RDW is elevated in overweight and reflects the inflammatory state. RDW potentially represents an additional and cost-effective tool to indicate inflammation. Future studies are needed to understand the differential influences of nutrition and overweight on RDW.

No abstract

In this cross-sectional study the well-established parameter BMI was shown to have the best predictive power to identify metabolic syndrome, its components and markers for low-grade inflammation. Newly developed parameters did not provide superior values. Future longitudinal studies are needed to compare these anthropometrical markers in larger cohorts, incorporating different age groups and ethnic backgrounds.

Atherosclerosis is a chronic inflammatory disease of the arterial wall in which presentation of autoantigens by dendritic cells (DCs) leads to the activation of T cells. Anti-inflammatory cells like Tregs counterbalance inflammation in atherogenesis. In our study, human carotid plaque specimens were classified as stable (14) and unstable (15) according to established morphological criteria. Vessel specimens (n = 12) without any signs of atherosclerosis were used as controls. Immunohistochemical staining was performed to detect different types of DCs (S100, fascin, CD83, CD209, CD304, and CD123), proinflammatory T cells (CD3, CD4, CD8, and CD161), and anti-inflammatory Tregs (FoxP3). The following results were observed: in unstable lesions, significantly higher numbers of proinflammatory cells like DCs, T helper cells, cytotoxic T cells, and natural killer cells were detected compared to stable plaques. Additionally, there was a significantly higher expression of HLA-DR and more T cell activation (CD25, CD69) in unstable lesions. On the contrary, unstable lesions contained significantly lower numbers of Tregs. Furthermore, a significant inverse correlation between myeloid DCs and Tregs was shown. These data suggest an increased inflammatory state in vulnerable plaques resulting from an imbalance of the frequency of local pro- and anti-inflammatory immune cells.

AimsChronic hypertension may cause left ventricular hypertrophy (LVH). The role of matrix metalloproteinases (MMPs), tissue inhibitors of matrix metalloproteinases (TIMPs), and tenascin-C (Tn-C) splice variants in concentric vs. eccentric left ventricular remodelling has not been investigated. Methods and resultsSerum levels of B or C domain containing Tn-C, MMP-9, TIMP-1, -2, and -4 were determined in concentric (left ventricular posterior wall thickness .13 mm and intraventricular septum .13 mm, n ¼ 61) and eccentric (end-diastolic left ventricular diameter .55 mm or end-systolic left ventricular diameter .40 mm, n ¼ 34) LVH by enzyme-linked immunoassays. Levels of B domain containing Tn-C were higher in patients with LVH than in normal volunteers (P ¼ 0.020) and higher in eccentric LVH (EH) compared with concentric LVH (CH) (P ¼ 0.003). A cut-off value of 900 ng/mL might discriminate between these different forms of LVH. Matrix metalloproteinase-9 was higher in patients with LVH than in normal volunteers (P ¼ 0.042), and levels were decreased in EH compared with CH (P ¼ 0.028). Patients with LVH had higher levels of TIMP-1 (P ¼ 0.059), TIMP-2 (P ¼ 0.043), and TIMP-4 (P ¼ 0.163) than normal volunteers, but there were no differences between the LVH groups. ConclusionOur data suggest that myocardial remodelling in LVH is associated with changes in serum levels of MMP-9, TIMP-1, -2, -4, and Tn-C splice variants. In addition, B domain containing Tn-C discriminated EH from CH and might be suggested as a potential diagnostic marker.--