In patients with SESs, ISA can fail to heal and even complete apposition can be associated with no neointimal hyperplasia. Incomplete stent apposition without neointimal hyperplasia was significantly associated with the presence of OCT-detected thrombus at follow-up, and may constitute a potent substrate for late stent thrombosis.

Statin treatment induces favorable plaque morphologic changes with an increase in fibrous cap thickness, and decreases in both percentage plaque and lipid volume indexes.

No abstract

Background-Although stent fracture (SF) after sirolimus-eluting stent (SES) implantation has been recognized as one of the predisposing factors of in-stent restenosis, it remains uncertain whether SF can increase the risk of major adverse cardiac events (MACE), especially beyond 1 year after SES implantation. The aim of this study was to assess the impact of SF relative to non-SF on 4-year clinical outcomes after treatment with SES of comparable unselected lesions. Methods and Results-A total of 874 lesions in 793 patients undergoing SES implantation and subsequent angiography 6 to 9 months after index procedure were analyzed. At 6-to 9-month angiographic follow-up, SF was identified in 70 of 874 lesions (8.0%

Deitch EA, Yatani A. Mesenteric lymph duct ligation prevents trauma/hemorrhage shock-induced cardiac contractile dysfunction.

Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp ontrast-induced acute kidney injury (CI-AKI) results from acute tubular necrosis from nephrotoxic iodinated contrast agent administered intra-arterially during a procedure as well as from other homeostatic factors. 1-3 Contrast volume is a key risk factor for CI-AKI and is most crucial in high-risk patients. 3-6Previous studies have demonstrated that the risk of CI-AKI is markedly increased if contrast volume exceeds the weightand creatinine level-adjusted maximum allowable contrast dose (MACD) threshold. 3,7-9 A recent large prospective clinical trial (n=10,065) has shown that exceeding MACD in a patient undergoing percutaneous coronary intervention (PCI) is associated with an increased risk of CI-AKI by 45% for each 50% in excess of MACD, whereas contrast volumes below the threshold hold to a lower plateau risk of CI-AKI. 3 However, CI-AKI remains an adverse outcome for patients even when contrast volume does not exceed MACD. Furthermore, MACD is not exceeded in approximately 80% of the patients undergoing PCI. 3 Thus, it is important to design studies focusing on CI-AKI in patients when contrast volume does not exceed MACD.Elevated blood glucose levels occur commonly in patients with acute myocardial infarction (AMI), and are strongly associated with increased mortality and in-hospital complications. 10-16 Some recent clinical studies have suggested that the pre-procedural glucose level might be a potential and independent risk factor for the development of CI-AKI in patients undergoing coronary angiography for AMI 17 and in patients undergoing primary PCI for ST-segment elevation myocardial infarction. 18 However, the relationship between the pre- The incidence, risk factors, and outcome of contrast-induced acute kidney injury (CI-AKI) in 730 patients with acute coronary syndrome (ACS) undergoing emergency percutaneous coronary intervention (PCI), whose contrast volume was below maximum allowable contrast dose (MACD) was prospectively investigated.

In Japanese STEMI patients, a 3-year follow-up showed that the routine use of SESs reduces the incidence of MACE without increasing the risk of stent thrombosis.

Major burn injury results in impairment of left ventricular (LV) contractile function. There is strong evidence to support the involvement of gut-derived factor(s) transported in mesenteric lymph in the development of burn-related contractile dysfunction; i.e., mesenteric lymph duct ligation (LDL) prevents burn-related contractile depression. However, the cellular mechanisms for altered myocardial contractility of postburn hearts are largely unknown, and the cellular basis for the salutary effects of LDL on cardiac function have not been investigated. We examined contractility, Ca(2+) transients, and L-type Ca(2+) currents (I(Ca)) in LV myocytes isolated from four groups of rats: 1) sham burn, 2) sham burn with LDL (sham + LDL), 3) burn ( approximately 40% of total body surface area burn), and 4) burn with LDL (burn + LDL). Myocytes isolated from hearts at 24 h postburn had a depressed contractility ( approximately 20%) at baseline and blunted responsiveness to elevation of bath Ca(2+). Myocyte contractility was comparable in sham + LDL and sham burn hearts. LDL completely prevented burn-related changes in myocyte contractility. Mechanistically, the decrease in contractility in myocytes from postburn hearts occurred with a decrease in the amplitude of Ca(2+) transients ( approximately 20%) without changes in resting Ca(2+) or Ca(2+) content of the sarcoplasmic reticulum. On the other hand, I(Ca) density was decreased ( approximately 30%) in myocytes from postburn hearts, with unaltered voltage-dependent properties. Thus burn-related myocardial contractile dysfunction is linked with depressed myocyte contractility associated with a decrease in I(Ca) density. These findings also provide strong evidence that mesenteric lymph is involved in the onset of burn-related cardiomyocyte dysfunction.