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Patients presenting with previous coronary artery bypass grafting (CABG) exhibit an accelerated progression of atherosclerosis in native coronary arteries following surgical revascularization. When saphenous vein grafts (SVGs) become diseased or occluded, the treatment of the entire native vessels becomes significantly more challenging. Herein, we present a patient who was admitted to our hospital due to heart failure. He had undergone CABG 12 years earlier, with a left internal mammary artery (LIMA) grafted to the left anterior descending (LAD) artery, a saphenous vein graft (SVG) to the first diagonal branch (D1), and another SVG to the right coronary artery (RCA). Furthermore, a stent was implanted in the SVG to the RCA five years ago. During the current admission, angiography identified multiple chronic total occlusion (CTO) lesions in the native proximal LAD and RCA, as well as in the SVG-D1, along with in-stent occlusion of the SVG to RCA. The percutaneous coronary intervention (PCI) strategy primarily focused on recanalization of the CTO in the RCA. We successfully implemented the Stingray-based antegrade dissection reentry (ADR) technique in the LAD CTO lesion to establish a critical channel. Leveraging this channel, we subsequently accomplished retrograde recanalization of the RCA CTO via septal collateral vessels. This case demonstrates that the Stingray-ADR technique can serve as a promising and effective approach in facilitating the recanalization of more complex multi-vessel CTO lesions. Clinical trial number: Not applicable.

Background Despite the inferior patency compared to arterial grafts, a saphenous vein graft (SVG) is widely used for coronary artery bypass grafting (CABG). A lower atherosclerosis rate and higher patency have been reported for SVG obtained via the no-touch technique (NT) than via conventional preparation (CV). Although CV-mediated endothelial dysfunction is implied, the precise mechanism underlying the higher patency with NT is poorly understood. Methods Human residual SVGs during CABG and SVG sections after autopsy were analyzed. The endothelial surface was observed using scanning electron microscopy (SEM) and blindly compared between CV and NT. The endothelial integrity was also analyzed with immunohistochemistry. Results Unexpectedly, the hyperfine structure on SEM was comparable between CV and NT before grafting, and microvillus, a characteristic of endothelium, was indistinguishable between them. Von Willebrand Factor, an endothelial marker, was equally detected throughout the vascular wall in both groups from residual and postmortem sections. Conclusions The morphological integrity of the endothelium was successfully preserved in SVG with CV, even at an ultrastructural level. Although its functionality remains to be addressed, other factors than the endothelium may be involved in the high patency obtained by NT. The present findings suggest that the characteristics of NT and surgical methodology should be reconsidered.

There is higher long‐term failure of the saphenous vein graft (SVG) compared with the left internal mammary artery (LIMA) graft, which is affected by the hemodynamic environment. A comprehensive analysis of postoperative structure‐function changes is important to study the atherogenesis in the SVG. A comparison of morphometric and hemodynamic parameters was carried out between LIMA grafts and SVGs and between different time points postoperatively. Various parameters were obtained from the image reconstruction and flow simulation in patients, who underwent CT exams for ~1 year, 5 and 10 years after revascularization. Morphometric data showed a decrease in lumen size in the entire SVG and anastomosis of different patients in a sequence of ~1 year, 5 and 10 years postoperatively despite negligible changes of LIMA size. Computational results indicated the fourfold increased surface area ratio (SAR) of low time‐averaged wall shear stress (TAWSS) in the SVG and anastomosis at postoperative 10 years than that at postoperative ~1 year. The SAR of high TAWSS gradient (TAWSSG) at the distal anastomosis between SVG and coronary arteries was significantly higher (14 ± 9% vs. 6 ± 8%) than that in the LIMA group at postoperative ~1 year. There were strong correlations between morphometric and hemodynamic parameters in the SVG and distal anastomosis at various time points postoperatively, which showed deterioration relevant to persistent diffuse diseases at postoperative ~10 years. The retrospective study showed morphometric and hemodynamic changes in SVGs and LIMA grafts of 132 patients for ~1 year, 5 and 10 years after revascularization. The findings showed that the vicious cycle of increased SAR‐TAWSS and decreased lumen size with time is a major risk factor for long‐term SVG occlusion albeit SVG arterialization and high SAR‐TAWSSG contribute to the vascular remodeling in the anastomosis within the initial years after grafting.

Objective: To define the clinical and angiographic follow-up results after implantation of paclitaxel-eluting stents (PESs) in stenotic saphenous vein grafts (SVGs). Design: Prospective multicentre study. Comparison with a control group. Methods: 60 consecutive patients with 65 lesions located in 65 SVGs (mean (SD) age of vein grafts 11.3 (5.7) years) treated with PES (V-Flex Plus, 2.7 μg/mm2 paclitaxel, Cook) and 60 patients with 60 SVG lesions treated with bare metal stent (BMS) were included. Lesions had to be <20 mm in length and in grafts of 2.75–3.5 mm diameter. The 6 month angiographic follow-up was obtained on 51 lesions (79%) of the PES group and on 51 lesions (85%) of the BMS group. Results: Baseline clinical and angiographic characteristics were comparable between both groups. At angiographic follow-up, three vein grafts in the PES group and five vein grafts in the BMS group were occluded. In-stent late lumen loss was lower in PES than in BMS (0.61 (0.81) vs 1.06 (0.72) mm, respectively; p = 0.021). In-stent binary restenosis rates were 12% vs 33%, respectively, (p = 0.012). Linear regression analysis showed BMS to be the only factor with an effect on late lumen loss (p = 0.011). Target-vessel failure rates were 18% in the PES group and 41% in the BMS group (p = 0.019), whereas major adverse cardiac event (MACE) rates at 180 days were 15% and 37%, respectively (p = 0.014). Conclusions: Implantation of non-polymer-based PES in SVG lesions is associated with a lower late lumen loss and restenosis rate than those of BMS. There remains a substantial target-vessel failure rate and MACE rate even at 6 months owing to graft occlusion or new lesions in the graft.

No difference in outcome was observed in patients presenting either <10 or >10 years after CABG. [...]time from CABG does not affect outcome in patients with prior CABG treated with primary PCI for STEMI due to SVG occlusion. [...]the large thrombotic burden markedly complicates the recanalisation of an occluded SVG. [...]of graft age, mechanical reperfusion is often complicated by distal embolisation and no reflow, which is associated with a higher short- and long-term mortality. 1- 3 In elective patients with PCI treated for SVG disease, the Saphenous vein-graft Angiopathy Free of Emboli Randomized Trial showed significant improvement of angiographic outcome (TIMI 3 flow and no reflow), resulting in a reduction in myocardial infarctions, with the use of a distal embolic protection device compared with standard techniques. 5 Interestingly, a substudy of this trial showed that SVG age was not a predictor of clinical outcome, as in our study on patients with STEMI.

Objective: To assess clinically and angiographically the feasibility, safety, and effectiveness of vascular brachytherapy (VBT) in saphenous vein bypass grafts (SVG). Patients and methods: 67 of 1098 (6.1%) consecutive patients of the European registry of intraluminal coronary β brachytherapy underwent treatment for 68 SVG lesions by VBT using a Sr/Y90 source train (BetaCath). Clinical follow up data were obtained for all of them after a mean (SD) of 6.3 (2.4) months and angiographic follow up was performed in 61 patients (91.0%) after 6.9 (2.0) months. Results: 58 (86.6%) patients were men, their mean (SD) age was 66 (10) years, 28 (41.8%) had unstable angina, and 21 (31.3%) had diabetes. Fifty three (77.9%) lesions were in-stent restenosis, 13 (19.1%) de novo lesions, and 2 (3.0%) non-stented restenotic lesions. Mean (SD) reference diameter before the intervention was 4.19 (0.52) mm, mean (SD) lesion length was 23.56 (20.38) mm, and mean (SD) minimum lumen diameter measured 0.73 (0.62) mm. Mean (SD) acute gain was 3.02 (0.88) mm. The prescribed radiation dose was 20.1 (3.2) Gy. Pullback manoeuvres were performed in 17 (25.0%) of cases. Most patients received combined aspirin and thienopyridin treatment for 6 or 12 months after the procedure. Technical success was obtained in 62 (91.2%) treated lesions and in-hospital major adverse cardiac events occurred in 4.5%. At follow up, mean (SD) reference diameter was 4.20 (0.53) mm, minimum lumen diameter 2.94 (1.50) mm, and late loss 0.86 (1.25) mm. The overall major adverse cardiac events rate was 26.7%. Conclusion: VBT of SVG is feasible and safe. At follow up the reintervention rate and cardiac morbidity and mortality seem to be favourable, considering that interventions in SVG usually are associated with the highest risks.

No/slow reflow may also result from PCI induced microvascular obstruction caused by distal microembolisation and/or microvascular spasm. 5, 6 Because microemboli necessarily stream preferentially to well perfused and viable myocardium, microembolisation kills potentially salvageable myocardium. [...]the vital question is, of course: how much of the coronary no/slow reflow and myocardial hypoperfusion seen after primary PCI reflects the classical no reflow phenomenon caused by necrosis, and how much reflects PCI induced distal microembolisation (and microvascular spasm?) causing more necrosis?

Objective: To identify the incidence and clinical significance of myocardial injury following elective stent implantation. Design: Prospective clinical study with 278 consecutive patients undergoing stenting of de novo coronary or saphenous vein graft lesions. Incidence of periprocedural myocardial injury was assessed by analysis of 12 lead ECG, creatine kinase (CK; upper limit of normal (ULN) 70 IU/l for women, 80 IU/l for men), and cardiac troponin T (cTnT; point of care test; threshold 0.1 ng/ml) before and 6, 12, and 24 hours after the intervention. Major adverse cardiac events (MACE: acute myocardial infarction, bypass surgery, and cardiac death) were recorded during clinical follow up (mean (SD) 7.8 (5.3) months). Results: Following elective stenting, the rate of a positive cTnT status was 17.3%, the rate of CK increase of 1–3× ULN 14.7%, the rate of CK increase of > 3× ULN 1.4%, and the rate of Q wave myocardial infarction 0.4%. Cardiac mortality during follow up was higher in patients with postprocedurally increased CK (7.1% v 1.3%, p = 0.01, log rank) and cTnT (9.1% v 0.9%, p < 0.001, log rank). In addition, postprocedurally increased cTnT was associated with a higher overall incidence of MACE (13.1% v 4.0%, p < 0.01, log rank) and was identified as an independent factor for MACE during follow up (hazard ratio 3.27, 95% confidence interval 1.14 to 9.41, p = 0.028). Conclusions: Following elective stent implantation, a positive cTnT status identified patients at risk of a worse long term outcome. Treatment strategies have to be developed that lead to prognostic improvement by reducing periprocedural myocardial injury.

Fasting preoperative total, low density lipoprotein, and high density lipoprotein cholesterol, triglycerides, glucose, insulin, C reactive protein, haemoglobin A1c, fibrinogen, activated partial thromboplastin time, and white cell count were measured at a government certified laboratory. Table 1 Univariate analysis between clinical factors and the presence of graft non-patency All grafts patent (n = 65) Non-patent graft (n = 15) p Value Clinical data Age (years) 64 (11) 59 (13) 0.09 Men 86% 73% 0.25 Former smoker (<5 years) 22% 13% 0.72 Hypertension 51% 73% 0.15 Hypercholesterolaemia 89% 93% 1.0 Diabetes 43% 46% 1.0 Body mass index (kg/m) 28.1 (3.5) 29.0 (3.6) 0.37 Laboratory data Total cholesterol (mmol/l) 4.0 (0.8) 4.4 (0.9) 0.10 LDL cholesterol (mmol/l) 2.1 (0.7) 2.4 (0.9) 0.32 HDL cholesterol (mmol/l) 1.20 (0.31) 1.17 (0.18) 0.70 Non-HDL cholesterol (mmol/l) 3.2 (0.9) 2.8 (0.8) 0.06 Triglycerides (mmol/l) 1.43 (0.62) 2.03 (0.79) 0.002* Fasting glucose (mmol/l) 7.0 (2.1) 7.3 (2.5) 0.64 Fasting insulin (mU/l) 10.3 (7.0-16.8) 9.7 (6.8-12.5) 0.37 HOMA-R (mmol/l) 2.6 (1.5-5.1) 3.1 (2.0-5.4) 0.47 HOMA-β 3.3 (2.2-6.1) 3.0 (2.1-4.9) 0.34 Haemoglobin A1c (%) 6.6 (1.3) 6.6 (1.1) 0.95 Fibrinogen (mmol/l) 4.1 (0.7) 4.3 (0.8) 0.22 APTT (s) 33.6 (4.0) 31.6 (2.7) 0.07 C reactive protein (mg/l) 23 (13-40) 24 (11-63) 0.66 White cell count (x109/l) 7.0 (1.7) 7.9 (1.4) 0.06 Continuous variables are expressed as mean (SD) for parametric data and median (interquartile range) for non-parametric data.

The routine use of vasodilators in patients with acute coronary syndromes or other groups undergoing percutaneous coronary intervention (PCI) cannot be recommended at present. However, in the event of no-reflow occurring following PCI, intracoronary adenosine or verapamil should be administered