Intrarenal Anti-Leptin Treatment Attenuates Ischemia and Reperfusion Injury.

INTRODUCTION: Renal ischemia and reperfusion (IR) injury introduces cellular stress and is the main cause of acute kidney damage. Renal cells exposed to noxious stress induce the expression of the pleiotropic hormone leptin. As we have previously revealed a deleterious stress-related role for leptin expression, these results suggested that leptin is also involved in pathological renal remodeling. The systemic functions of leptin preclude the study of its local effects using conventional approaches. We have therefore designed a method to locally perturb leptin activity in specific tissues without affecting its systemic levels. This study explores whether local anti-leptin strategy is renoprotective in a post-IR porcine kidney model. METHODS: We induced renal IR injury in pigs by exposing kidneys to ischemia and revascularization. Upon reperfusion, kidneys instantly received an intra-arterial bolus of either a leptin antagonist (LepA) or saline solution. Peripheral blood was sampled to assess systemic leptin, IL-6, creatinine, and BUN levels, and postoperative tissue samples were analyzed by hematoxylin and eosin histochemistry and immunohistochemistry. RESULTS: Histology of IR/saline kidneys exhibited extensive necrosis of proximal tubular epithelial cells, as well as elevated levels of apoptosis markers and inflammation. In contrast, IR/LepA kidneys showed no signs of necrosis or inflammation with normal IL-6 and tall-like receptor 4 levels. LepA treatment led to upregulation in mRNA levels of leptin, leptin receptor, ERK1/2, STAT3, and transport molecule Na/H exchanger-3. CONCLUSIONS: Local, intrarenal postischemic LepA treatment at reperfusion prevented apoptosis and inflammation and was renoprotective. Selective intrarenal administration of LepA at reperfusion may provide a viable option for clinical implementation.

Effectiveness, benefit harm and cost effectiveness of colorectal cancer screening in Austria.

BACKGROUND: Clear evidence on the benefit-harm balance and cost effectiveness of population-based screening for colorectal cancer (CRC) is missing. We aim to systematically evaluate the long-term effectiveness, harms and cost effectiveness of different organized CRC screening strategies in Austria. METHODS: A decision-analytic cohort simulation model for colorectal adenoma and cancer with a lifelong time horizon was developed, calibrated to the Austrian epidemiological setting and validated against observed data. We compared four strategies: 1) No Screening, 2) FIT: annual immunochemical fecal occult blood test age 40-75 years, 3) gFOBT: annual guaiac-based fecal occult blood test age 40-75 years, and 4) COL: 10-yearly colonoscopy age 50-70 years. Predicted outcomes included: benefits expressed as life-years gained [LYG], CRC-related deaths avoided and CRC cases avoided; harms as additional complications due to colonoscopy (physical harm) and positive test results (psychological harm); and lifetime costs. Tradeoffs were expressed as incremental harm-benefit ratios (IHBR, incremental positive test results per LYG) and incremental cost-effectiveness ratios [ICER]. The perspective of the Austrian public health care system was adopted. Comprehensive sensitivity analyses were performed to assess uncertainty. RESULTS: The most effective strategies were FIT and COL. gFOBT was less effective and more costly than FIT. Moving from COL to FIT results in an incremental unintended psychological harm of 16 additional positive test results to gain one life-year. COL was cost saving compared to No Screening. Moving from COL to FIT has an ICER of 15,000 EUR per LYG. CONCLUSIONS: Organized CRC-screening with annual FIT or 10-yearly colonoscopy is most effective. The choice between these two options depends on the individual preferences and benefit-harm tradeoffs of screening candidates.

Percutaneous Coronary Intervention Does Not Lower Cardiovascular Outcomes in Patients with Chronic Kidney Disease.

BACKGROUND: Chronic kidney disease (CKD) is associated with an increased risk of adverse cardiovascular outcomes, in patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI). However, most studies used bare-metal stents or first-generation drug-eluting stents, and less guideline-directed therapy to reduce cardiovascular risk was reported in CKD patients. This study investigates the impact of moderate-CKD on patients undergoing PCI in the current era. METHODS: Patient level data were pooled from 2 multicenter randomized trials (BIONICS and NIREUS trials) with a near "all-comers" design, comparing PCI with ridaforolimus-eluting stents vs. zotarolimus-eluting stents in patients with CAD. Patients were classified according to the presence or absence of moderate-CKD, defined as creatinine clearance (CrCl) <60 mL/min. We compared baseline characteristics, angiographic findings, and clinical outcomes 1-year post-PCI. RESULTS: 236/2,201 (10.7%) patients had CKD, mean CrCl of 50.3 + 7.8 mL/min. These patients were generally older and more often with hypertension than non-CKD patients, but the use of guideline-directed therapy was similar between the groups. CKD was associated with an increased risk of cardiovascular death (hazard ratio [HR] 6.08; 95% CI 2.11-17.51; p < 0.001), but with a reduced occurrence of repeated revascularization, including ischemia-driven revascularization (HR 0.47; 95% CI 0.24-0.92; p < 0.05). The rate of repeated angiography per severe cardiovascular adverse event was significantly lower in the CKD than the non-CKD group (23/38 [61%] vs. 253/334 [76%], p < 0.05). CONCLUSIONS: Moderate-CKD in patients with CAD was associated with higher rates of all-cause and cardiovascular mortality, yet with a lower risk of revascularization 1-year following PCI. Lack of guideline-directed medical therapy does not explain the adverse outcome of CKD patients.

First-in-Man Experience with a Novel Catheter-Based Renal Denervation System of Ultrasonic Ablation in Patients with Resistant Hypertension.

PURPOSE: To report results of renal denervation (RDN) with the first catheter-based, non-balloon occlusion ultrasonic system in patients with resistant hypertension. MATERIALS AND METHODS: In a multicenter, single-arm trial, 39 patients with resistant hypertension (defined as uncontrolled hypertension while taking ≥ 3 antihypertensive medications) were treated. The cohort consisted of 4 groups: severe resistant hypertension (office systolic blood pressure [OSBP] ≥ 160 mm Hg) treated with a unidirectional catheter (group 1; n = 14); severe resistant hypertension treated with a multidirectional catheter (group 2; n = 18); moderate resistant hypertension (OSBP 140-159 mm Hg) treated with a multidirectional catheter (group 3; n = 5); and recurrent severe resistant hypertension, after an initial response to RF RDN (group 4; n = 2). Blood pressure monitoring was performed for 6 months. RESULTS: Severe adverse events were not noted immediately after the procedure or during follow-up. Treatment time was longer with unidirectional than with multidirectional catheters (36.7 min ± 9.6 vs 11.9 min ± 5.8; P < .001). Mean reductions in office blood pressure (systolic/diastolic) at 1, 3, and 6 months were -26.1/-9.6 mm Hg, -28.0/-9.9 mm Hg, and -30.6/-14.1 mm Hg (P < .01 for all). Per-group analysis showed significant OSBP reduction for groups 1 and 2. Patients with isolated systolic hypertension had a significantly smaller reduction in OSBP after 6 months compared with patients with combined systolic/diastolic hypertension (-16.2 mm Hg ± 18.5 vs -9.9 mm Hg ± 33.4; P < .005). CONCLUSIONS: Use of the RDN system was feasible and safe in this phase I study. Significant blood pressure reductions were observed over 6 months, although less in patients with isolated systolic hypertension.

Distal Radial Fracture Management With an Intramedullary Cage and Fragment Fixation.

PURPOSE: To examine the outcomes associated with the treatment of distal radial fractures with an expandable intramedullary cage and fragment-specific screw fixation. METHODS: A prospective multicenter case series of 100 patients with a fracture of the distal radius treated with the "Cage System" was undertaken. Primary patient outcomes included Disabilities of the Arm, Shoulder, and Hand, Patient-Related Wrist/Hand Evaluation questionnaires, and adverse events associated with the device. Secondary outcomes included wrist range of motion and radiographic findings. RESULTS: Follow-up was performed at intervals of 2 weeks, 4 to 6 weeks, 12 weeks, and 1 year. Ninety-one patients were available for follow-up at 2 weeks, 87 at 4 to 6 weeks, 73 at 3 months, and 61 at 12 months. The mean Disabilities of the Arm, Shoulder, and Hand score at 3 months was 21; at 12 months, it was 9. The mean total Patient-Reported Wrist/Hand Evaluation score at 3 months was 21; at 12 months, it was 11. There were 5 adverse events (5%)-2 involving radial nerve irritation and 3 involving tendon irritation from screws. Four of these 5 patients underwent surgical intervention, a neurolysis in 1 patient and removal of screws in 3. All patients were free of adverse-event symptoms at 3 months' follow-up. Wrist range of motion improved most rapidly in the first 12 weeks following surgery and continued to improve throughout follow-up. The fracture reduction achieved at surgery was maintained throughout the healing process. There was evidence of callus formation at the fracture as early as 2 weeks after surgery with 100% of fractures healed at 3 months. CONCLUSIONS: An expandable intramedullary cage with fragment-specific screw fixation provides maintenance of fracture reduction with a low complication rate. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic IV.

Low-Level Laser Therapy to the Bone Marrow Reduces Scarring and Improves Heart Function Post-Acute Myocardial Infarction in the Pig.

OBJECTIVE: Cell therapy for myocardial repair is one of the most intensely investigated strategies for treating acute myocardial infarction (MI). The aim of the present study was to determine whether low-level laser therapy (LLLT) application to stem cells in the bone marrow (BM) could affect the infarcted porcine heart and reduce scarring following MI. METHODS: MI was induced in farm pigs by percutaneous balloon inflation in the left coronary artery for 90 min. Laser was applied to the tibia and iliac bones 30 min, and 2 and 7 days post-induction of MI. Pigs were euthanized 90 days post-MI. The extent of scarring was analyzed by histology and MRI, and heart function was analyzed by echocardiography. RESULTS: The number of c-kit+ cells (stem cells) in the circulating blood of the laser-treated (LT) pigs was 2.62- and 2.4-fold higher than in the non-laser-treated (NLT) pigs 24 and 48 h post-MI, respectively. The infarct size [% of scar tissue out of the left ventricle (LV) volume as measured from histology] in the LT pigs was 3.2 ± 0.82%, significantly lower, 68% (p < 0.05), than that (16.6 ± 3.7%) in the NLT pigs. The mean density of small blood vessels in the infarcted area was significantly higher [6.5-fold (p < 0.025)], in the LT pigs than in the NLT ones. Echocardiography (ECHO) analysis for heart function revealed the left ventricular ejection fraction in the LT pigs to be significantly higher than in the NLT ones. CONCLUSIONS: LLLT application to BM in the porcine model for MI caused a significant reduction in scarring, enhanced angiogenesis and functional improvement both in the acute and long term phase post-MI.

The Leaflex™ Catheter System - a viable treatment option alongside valve replacement? Preclinical feasibility of a novel device designed for fracturing aortic valve.

AIMS: To demonstrate the feasibility of the Leaflex™ Catheter System, a novel percutaneous device for fracturing valve calcification using mechanical impact in order to regain leaflet mobility. METHODS AND RESULTS: Radiographic analysis of calcium patterns in 90 ex vivo human aortic valve leaflets demonstrated that 82% of leaflets had a typical "bridge" or "half-bridge" pattern, which formed the basis for the catheter design. The therapeutic effect was quantified in 13 leaflets showing a reduction of 49±16% in leaflet resistance to folding after treatment. A pulsatile flow simulator was then used with 11 ex vivo valves demonstrating an increase in aortic valve area of 35±12%. Using gross pathology and histology on fresh calcified leaflets, we then verified that mechanical impacts do not entail excessive risk of embolisation. In vivo safety and usability were then confirmed in the ovine model. CONCLUSIONS: We demonstrated preclinically that it is feasible to improve valve function using the Leaflex™ technology. Once demonstrated clinically, such an approach may have an important role as preparation for or bridging to TAVI, as destination treatment for patients where TAVI is clinically or economically questionable and, in the future, maybe even as a means to slow disease progression in asymptomatic patients.

Regulatory T cells and IL-10 levels are reduced in patients with vulnerable coronary plaques.

BACKGROUND: Despite having a similar large extent of atherosclerotic coronary affliction, some patients suffer of recurrent cardiac events, whereas others remain asymptomatic. HYPOTHESIS: We hypothesized the existence of a systemic "signature" that could distinguish "vulnerable" patients with preexisting coronary atherosclerosis from those having similar risk factors and atheromatous burden, but no history of clinically evident plaque rupture/erosion. METHODS: Twenty three patients who had at least two prior myocardial infarctions ("vulnerable group") were matched in respect to their background and coronary atherosclerosis extent with twenty one patients without a history of previous myocardial infarction who underwent routine coronary angiography before valvular surgery. We studied a panel of cytokines, antibodies and hormones including IL-6, IL-10, IL-12, antibodies to ß2 glycoprotein I (ß2GPI), antibodies to oxidized-LDL, adiponectin and resistin, along with levels of circulating EPCs and Tregs. RESULTS: A significantly higher level of Treg cells was present in the control (73.4%±4) than in the "vulnerable patient" group (62.2%±10.7), p<0.001. IL-10 level was also significantly higher in the control than in the vulnerable patients (2.6±1.2 pg/ml versus 0.9±0.1 pg/ml respectively, p=0.03). There was no significant difference in the circulating levels of the other cytokines, hormones or EPCs between the two groups. CONCLUSION: Regulatory T cells and serum IL-10 may discriminate "vulnerable" versus stable patients and may have a protective role against plaque rupture in patients with coronary atherosclerosis.

Heparanase alters arterial structure, mechanics, and repair following endovascular stenting in mice.

Heparan sulfate proteoglycans (HSPGs) are potent regulators of vascular remodeling and repair. Heparanase is the major enzyme capable of degrading heparan sulfate in mammalian cells. Here we examined the role of heparanase in controlling arterial structure, mechanics, and remodeling. In vitro studies supported that heparanase expression in endothelial cells serves as a negative regulator of endothelial inhibition of vascular smooth muscle cell (vSMC) proliferation. Arterial structure and remodeling to injury were also modified by heparanase expression. Transgenic mice overexpressing heparanase had increased arterial thickness, cellular density, and mechanical compliance. Endovascular stenting studies in Zucker rats demonstrated increased heparanase expression in the neointima of obese, hyperlipidemic rats in comparison to lean rats. The extent of heparanase expression within the neointima strongly correlated with the neointimal thickness following injury. To test the effects of heparanase overexpression on arterial repair, we developed a novel murine model of stent injury using small diameter self-expanding stents. Using this model, we found that increased neointimal formation and macrophage recruitment occurs in transgenic mice overexpressing heparanase. Taken together, these results support a role for heparanase in the regulation of arterial structure, mechanics, and repair.

Complication of a closed Colles-fracture: necrotising fasciitis with lethal outcome. A case report.

We report a case of a 77-year-old female patient who died 4 days after a closed colles-fracture of the right wrist because of secondary emerged necrotising fasciitis. At the time of visiting our emergency department, the patient reports about untypical pain and progressive swelling of the entire right arm 3 days following a fall onto the outstretched hand where she sustained a closed distal radius fracture. Within 6 h, the patient developed hypotension and fever leading to cardiac and respiratory failure. The emergent-induced diagnostic presented a severe septic situation in the laboratory examination of the blood samples, an apparent before unknown diabetes mellitus and an unknown bronchial carcinoma with part of post-stenosis pneumonia of the right lung. After initial CPR and stabilisation, the patient underwent an urgent and aggressive surgical debridement with fasciotomies of the muscle compartments of the entire right upper extremity. The microbiological investigation of the intraoperative taken specimens presented plentiful group-A-beta-haemolytic streptococcus. Despite a broad spectrum intravenous antibiotic therapy, intensive care support and a second look operation 12 h later with exarticulation of the right arm in the shoulder joint, the patient died of septic shock and multiorgan failure 34 h after admission.

The PROXIMAL trial: proximal protection during saphenous vein graft intervention using the Proxis Embolic Protection System: a randomized, prospective, multicenter clinical trial.

OBJECTIVES: To determine if outcomes could be further improved, we investigated an embolic protection device placed proximal to the target lesion that could provide protection before lesion instrumentation, allow the use of conventional guidewires, and permit embolic protection in anatomy unfavorable for distal devices. BACKGROUND: Embolic complications during stenting of degenerated saphenous vein coronary bypass grafts are reduced, but not eliminated, by distal protection. METHODS: A total of 594 patients undergoing stenting of 639 saphenous vein grafts were prospectively randomized, using a noninferiority design, to compare 2 treatment strategies: control (distal protection whenever possible) or test (proximal protection when possible, distal when not). RESULTS: The primary composite end point of death, myocardial infarction, or target vessel revascularization at 30 days by intention to treat analysis occurred in 10.0% of control and 9.2% of test patients; difference = -0.8% (95% confidence interval [CI] -5.5% to 4.0%); p for noninferiority = 0.0061. In device specific analysis, this composite end point occurred in 11.7% of distal protection patients and 7.1% of proximal protection patients (difference = -4.6% [95% CI -9.6% to 0.3%]; p for superiority = 0.10, p for noninferiority = 0.001). Finally, in the subset of patients with lesions amenable to treatment with either proximal or distal protection devices (n = 410), the primary composite end point occurred in 12.2% of distal protection patients and 7.4% of proximal protection patients; difference = -4.7% (95% CI -10.4% to 1.0%), p for superiority = 0.14, p for noninferiority = 0.001. CONCLUSIONS: Using proximal embolic protection whenever possible during treatment of diseased saphenous vein grafts produced outcomes similar to those with distal embolic protection.

Local and systemic drug competition in drug-eluting stent tissue deposition properties.

The efficacy of drug-eluting stents (DES) requires delivery of potent compounds directly to the underlying arterial tissue. The commercially available DES drugs rapamycin and paclitaxel bind specifically to their respective therapeutic targets, FKBP12 and polymerized microtubules, while also associating in a more general manner with other tissue elements. As it is binding that provides biological effect the question arises as to whether other locally released or systemically circulating drugs can displace DES drugs from their tissue binding domains. Specific and general binding sites for both drugs are distributed across the media and adventitia with higher specific binding associated with the higher specific binding site densities in the media. The ability of rapamycin and paclitaxel to compete for specific protein binding and general tissue deposition was assessed for both compounds simultaneously and in the presence of other commonly administered cardiac drugs. Drugs classically used to treat standard cardiovascular diseases, such as hypertension and hypercoaguability, displace rapamycin and paclitaxel from general binding sites, possibly decreasing tissue reserve capacity for locally delivered drugs. Paclitaxel and rapamycin do not affect the other's binding to their biologically relevant specific protein targets, but can generally displace each other from tissue at three log order molar excess, decreasing arterials loads by greater than 50%. Local competitive binding therefore should not limit the placement of rapamycin and paclitaxel eluting stents in close proximity.

Vascular neointimal formation and signaling pathway activation in response to stent injury in insulin-resistant and diabetic animals.

Diabetes and insulin resistance are associated with increased disease risk and poor outcomes from cardiovascular interventions. Even drug-eluting stents exhibit reduced efficacy in patients with diabetes. We now report the first study of vascular response to stent injury in insulin-resistant and diabetic animal models. Endovascular stents were expanded in the aortae of obese insulin-resistant and type 2 diabetic Zucker rats, in streptozotocin-induced type 1 diabetic Sprague-Dawley rats, and in matched controls. Insulin-resistant rats developed thicker neointima (0.46+/-0.08 versus 0.37+/-0.06 mm2, P=0.05), with decreased lumen area (2.95+/-0.26 versus 3.29+/-0.15 mm2, P=0.03) 14 days after stenting compared with controls, but without increased vascular inflammation (ED1+ tissue macrophages). Insulin-resistant and diabetic rat vessels did exhibit markedly altered signaling pathway activation 1 and 2 weeks after stenting, with up to a 98% increase in p-ERK (anti-phospho ERK) and a 54% reduction in p-Akt (anti-phospho Akt) stained cells. Western blotting confirmed a profound effect of insulin resistance and diabetes on Akt and ERK signaling in stented segments. p-ERK/p-Akt ratio in stented segments uniquely correlated with neointimal response (R2=0.888, P=0.04) in insulin-resistant and type 1 and 2 diabetic rats, but not in lean controls. Transfemoral aortic stenting in rats provides insight into vascular responses in insulin resistance and diabetes. Shifts in ERK and Akt signaling related to insulin resistance may reflect altered tissue repair in diabetes accompanied by a shift in metabolic:proliferative balance. These findings may help explain the increased vascular morbidity in diabetes and suggest specific therapies for patients with insulin resistance and diabetes.

[A new model of comprehensive data linkage--evaluation of its application in femoral neck fracture]. / Ein neues Modell der sektorübergreifenden Datenzusammenführung und Evaluation am Beispiel der Schenkelhalsfraktur.

Aim of the project was a comprehensive assessment of short- and middle-term outcome of femoral neck fracture by linkage and analysis of available data from routine care. For this purpose, a generic model of data linkage was developed, agreed with the data security officer, and practically applied. Included were all patients of the AOK Westphalia-Lippe, who were treated in a general or trauma surgery hospital in 1995/1999 for a femoral neck fracture (ICD-9: 820). For these patients, the linkage was based on the following sources: the data regarding the initial hospital stay were provided by the office of quality assurance of the chamber of physicians of Westphalia-Lippe; the administrative data were provided by the AOKWestphalia-Lippe; and the data evaluating the nursing needs were obtained from the Medical Services of the Health Insurance of Westphalia-Lippe (MDK). This paper presents the model of data linkage and describes its practical implementation; it also presents medical data demonstrating that femoral neck fractures are associated with high mortality and increase of nursing needs in the course of disease. The benefit of the new model is manifold and can be easily extended to other clinical questions.

Oral acetylcysteine as an adjunct to saline hydration for the prevention of contrast-induced nephropathy following coronary angiography. A randomized controlled trial and review of the current literature.

AIMS: To determine laboratory and clinical benefit of oral acetylcysteine, as an adjunct to saline hydration, in chronic renal insufficiency patients undergoing coronary angiography. METHODS AND RESULTS: We prospectively studied 80 patients with chronic renal insufficiency (mean [+/-SD] serum creatinine concentration 2.0+/-0.39mg/dl), who underwent coronary angiography with or without intervention. Patients were randomly assigned to receive either acetylcysteine (600mg orally t.i.d.) or placebo, in addition to intravenous 0.45% saline (1ml/kg of body weight per hour), 12h prior to and after coronary angiography. There was an increase of >/=0.5mg/dl in the serum creatinine concentration 48h after coronary angiography in seven of the 80 patients (9%): in four of the 41 patients (10%) in the acetylcysteine group and in three of the 39 patients (8%) in the placebo group (P=0.52). The incidence of in-hospital adverse clinical events (acetylcysteine, 5% vs placebo, 8%, P=0.47) and the length of hospital stay [acetylcysteine, median (interquartile range) 4 (2-4) days vs placebo, 2 (2-4) days, P=0.44] did not differ significantly between the two treatment groups. CONCLUSION: Our findings do not support routine prophylactic administration of oral acetylcysteine as an adjunct to saline hydration for the prevention of contrast-induced nephropathy in chronic renal insufficiency patients undergoing coronary angiography.

Current smoking, smoking cessation, and the risk of sudden cardiac death in patients with coronary artery disease.

BACKGROUND: Cigarette smoking is a known risk factor for sudden cardiac death (SCD). However, the effect of continued cigarette smoking and smoking cessation on SCD risk in patients with established coronary artery disease (CAD) is subject to controversy. We, therefore, evaluated the effect of cigarette smoking on SCD risk in a large cohort of patients with established CAD. METHODS: The study population was composed of 3122 patients with a previous myocardial infarction or stable angina who participated in the Bezafibrate Infarction Prevention Trial. Patients were prospectively followed up for a mean of 8.2 years. The primary end point was the incidence of SCD according to smoking status. RESULTS: Among the 370 patients who were current smokers, 30 (8.1%) experienced SCD; 83 (4.6%) of the 1821 patients who had quit smoking and 43 (4.6%) of the 931 patients who had never smoked experienced SCD (P =.01). In multivariate analyses, current smoking was associated with a significant increase in the risk of SCD (hazard ratio, 2.47; 95% confidence interval, 1.46-4.19). Patients who had stopped smoking had no significant increase in the risk of SCD compared with patients who had never smoked (hazard ratio, 1.06; 95% confidence interval, 0.70-1.62). CONCLUSIONS: Current cigarette smoking is a powerful independent predictor of SCD risk in patients with CAD. Patients who quit smoking experienced a significant reduction in SCD risk. Thus, efforts to reduce mortality from SCD in patients with CAD should include vigorous smoking cessation strategies.

Subclavian coronary steal syndrome: an obligatory common fate between subclavian artery, internal mammary graft and coronary circulation.

The long-term patency of the left internal mammary artery (IMA) has made it the preferred conduit for myocardial revascularization. The proximal segment of the subclavian artery becomes functionally connected to the coronary circulation as a result of IMA implantation during coronary artery bypass surgery. The subclavian coronary steal syndrome results from stenosis in the left subclavian artery proximal to the IMA, compromising blood flow to the myocardium. We describe 7 patients, aged 55-75 years, 1.7-10.5 years after coronary bypass who presented with recurrent angina due to subclavian artery stenosis. The IMA graft was found open in each patient. A true steal mechanism was not demonstrated, casting doubt on the syndrome's traditional name. Angioplasty and stenting of the subclavian artery resulted in the immediate disappearance of angina and continuous benefit at a follow-up of 3-32 months. The subclavian coronary steal syndrome, although rare, is a severe condition readily treated by angioplasty and stenting.