A novel fiber-optic based 0.014″ pressure wire: Designs of the OptoWire™, development phases, and the O2 first-in-man results.

OBJECTIVES: To review the technical limitations of available pressure-wires, present the design evolution of a nitinol fiber-optic pressure wire and to summarize the First-in-Man (FIM) O2 pilot study results. BACKGROUND: Despite increasing use of physiology assessment of coronary lesions, several technical limitations persist. We present technical details, design evolution and early clinical results with a novel 0.014" nitinol fiber-optic based pressure-wire. METHODS AND RESULTS: The 0.014' OptoWire™ (Opsens Medical, Quebec, Canada) was designed to combine improved handling properties compared to standard pressure-wires and to offer extremely reliable pressure recording and transmission due to fiber-optic properties compared to piezo-electric sensors and electrical wires. In vitro assessment showed that OptoWire™ steerability, pushability and torquability properties were closer to regular PCI wires than standard electrical pressure wires. In the First-in-Man O2 study, 60 patients were recruited at 2 centers in Canada. A total of 103 lesions were assessed with the OptoWire™ and OptoMonitor™, 75 lesions at baseline and 28 lesions post-PCI (without disconnection). In all crossed lesions (n = 100, 97%), mean Pd/Pa and FFR could be adequately measured. In 11 cases assessed successively with OptoWire™ and Aegis™ (Abbott Vascular, USA) bland-Altman analysis showed a mean difference of 0.002 ± 0.052 mmHg (p = .91) for Pd/Pa and 0.01 ± 0.06 for FFR calculation (p = .45). There was no device-related complication. Upon these initial results, several design changes aimed to improve overall performance including torquability, stiffness, resistance to kink and pressure drift were completed. CONCLUSION: The novel 0.014" fiber-optic OptoWire™ provides superior wire handling with reduced risk of pressure drift allowing reliable pre- and post-PCI physiology assessment.

Prehospital diagnosis and triage of ST-elevation myocardial infarction by paramedics without advanced care training.

BACKGROUND: Prehospital triage of ST-elevation myocardial infarction (STEMI) for primary percutaneous coronary intervention (PCI) reduces treatment times. Prehospital triage and transport of STEMI patients have traditionally been undertaken in emergency medical service systems with Advanced Care Paramedics (ACPs). However, ACPs are not available in many regions. A pilot study was conducted to determine the feasibility of prehospital STEMI triage in a region with only Primary Care Paramedics. METHODS: Hemodynamically stable patients with chest pain and suspected STEMI were brought directly to a catheterization laboratory for primary PCI. End points included accuracy of prehospital STEMI identification, complications during transfer, and treatment times. RESULTS: One hundred thirty-four consecutive patients with suspected STEMI were triaged for primary PCI. Only 1 patient developed complications during transport (rapid atrial flutter) that required ACP skills. One hundred thirty-three patients underwent urgent angiography, and 105 patients underwent PCI. Based on physician interpretation of the prehospital electrocardiogram, there was agreement with triage decision for 121 (90%) of the 134 cases. The final diagnosis based on the angiogram and cardiac markers was true STEMI for 106 patients and false positive for 28 patients. The median first medical contact to balloon time was 91 (81-115) minutes. CONCLUSIONS: Hemodynamically stable patients with suspected STEMI can be safely and effectively transported directly for primary PCI by paramedics without advanced care training. Prehospital STEMI triage for primary PCI can be extended to regions that have few or no paramedics with advanced care training.

The sPLA2 Inhibition to Decrease Enzyme Release after Percutaneous Coronary Intervention (SPIDER-PCI) trial.

BACKGROUND: Secretory phospholipase A(2) (sPLA(2)) may play a role in myonecrosis after elective percutaneous coronary intervention (PCI). Inhibition of this enzyme may have a beneficial effect. The central hypothesis of this study was that treatment with varespladib, a small-molecule inhibitor of sPLA(2) would reduce postprocedural release of cardiac biomarkers after elective percutaneous coronary intervention. METHODS AND RESULTS: Between October 2007 and June 2009, 144 stable patients were randomized in a phase II trial to receive varespladib 500 mg PO BID or placebo 3 to 5 days before and for 5 days after elective percutaneous coronary intervention. The primary end point was elevation of troponin I or creatine kinase-MB above the upper limit of normal at 6 to 8 or 18 to 24 hours after percutaneous coronary intervention. Mean age was 63±10 and 64±10 years, with 38% and 42% with diabetes mellitus and 29% and 28% with prior myocardial infarction for the varespladib and placebo groups, respectively. The primary end point occurred in 75% of varespladib and 63% of placebo patients (P=0.14). Troponin I 3 times the upper limit of normal was observed in 57% and 50% (P=0.39) and creatine kinase-MB 2 times the upper limit of normal in 14% and 3% (P=0.018). Median (first and third quartiles) change in high-sensitivity C-reactive protein in these 2 groups was 0.65 mg/L (-0.18 and 1.48) and 0.70 mg/L (0.00 and 1.50) at 18 to 24 hours (P=0.81) and 0.20 mg/L (-0.70 and 1.40) and 0.60 mg/L (-0.12 and 1.72) at 3 to 5 days (P=0.23), whereas change in sPLA(2) activity at 3 to 5 days in a subset was -2.85 ng/ml (-3.40 and -1.85) and 0.25 ng/ml (-0.20 and 0.85) (P<0.001). CONCLUSIONS: Inhibition of sPLA(2) by varespladib administered for 3 to 5 days before the procedure does not reduce periprocedural myonecrosis associated with elective percutaneous coronary intervention. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00533039.

Comparison of bivalirudin versus heparin on radial artery occlusion after transradial catheterization.

BACKGROUND: Anticoagulant therapy is required to prevent radial artery occlusion (RAO) after transradial catheterization. There is no data comparing bivalirudin to standard heparin. METHODS: We studied 400 consecutive patients. In case of diagnostic angiography-only (n = 200), they received an intravenous bolus of heparin (70 U kg(-1)) immediately before sheath removal whereas in case of angiography followed by ad hoc percutaneous coronary intervention (n = 200), they received bivalirudin (bolus 0.75 mg kg(-1), followed by infusion at 1.75 mg/kg/h). RAO was assessed 4-8 weeks later using two-dimensional echography-doppler and reverse Allen's test with pulse oximetry. RESULTS: At follow-up, 21 of the 400 (5.3%) patients were found to have RAO with no significant difference between the two groups (3.5% bivalirudin vs. 7.0% heparin, P = 0.18). Patients with RAO had a significantly lower weight compared to patients without RAO (78 ± 13 kg vs. 86 ± 18 kg, P = 0.011). By multivariate analysis, a weight <84 kg (OR: 2.78, 95% CI 1.08-8.00, P = 0.032) and a procedure duration ≤20 min (OR: 7.52, 95% CI 1.57-36.0, P = 0.011) remained strong independent predictors of RAO. All cases of radial occlusion were asymptomatic and without clinical sequelae. CONCLUSION: Delayed administration of bivalirudin or heparin for transradial catheterization provides similar efficacy in preventing RAO. Because of its low cost, a single bolus of heparin can be preferred in case of diagnostic angiography whereas bivalirudin can be contemplated in case of ad hoc percutaneous coronary intervention. © 2010 Wiley-Liss, Inc.

Impact of Bleeding and Myocardial Infarction on Mortality in All-Comer Patients Undergoing Percutaneous Coronary Intervention.

BACKGROUND: Bleeding and myocardial infarction (MI) after percutaneous coronary intervention are independent risk factors for mortality. This study aimed to investigate the association of all-cause mortality after percutaneous coronary intervention with site-reported bleeding and MI, when considered as individual, repeated, or combined events. METHODS: We used the data from the GLOBAL LEADERS trial (GLOBAL LEADERS: A Clinical Study Comparing Two Forms of Anti-Platelet Therapy After Stent Implantation), an all-comers trial of 15 968 patients undergoing percutaneous coronary intervention. Bleeding was defined as Bleeding Academic Research Consortium (BARC) 2, 3, or 5, whereas MI included periprocedural and spontaneous MIs according to the Third Universal Definition. RESULTS: At 2-year follow-up, 1061 and 498 patients (6.64% and 3.12%) experienced bleeding and MI, respectively. Patients with a bleeding event had a 10.8% mortality (hazard ratio [HR], 5.97 [95% CI, 4.76-7.49]; P<0.001), and the mortality of patients with an MI was 10.4% (HR, 5.06 [95% CI, 3.72-6.90]; P<0.001), whereas the overall mortality was 2.99%. Albeit reduced over time, MI and even minor BARC 2 bleeding significantly influenced mortality beyond 1 year after adverse events (HR of MI, 2.32 [95% CI, 1.18-4.55]; P=0.014, and HR of BARC 2 bleeding, 1.79 [95% CI, 1.02-3.15]; P=0.044). The mortality rates in patients with repetitive bleeding, repetitive MI, and both bleeding and MI were 16.1%, 19.2%, and 19.0%, and their HRs for 2-year mortality were 8.58 (95% CI, 5.63-13.09; P<0.001), 5.57 (95% CI, 2.53-12.25; P<0.001), and 6.60 (95% CI, 3.44-12.65; P<0.001), respectively. De-escalation of antiplatelet therapy at the time of BARC 3 bleeding was associated with a lower subsequent bleeding or MI rate, compared with continuation of antiplatelet therapy (HR, 0.32 [95% CI, 0.11-0.92]; P=0.034). CONCLUSIONS: The fatal impact of bleeding and MI persisted beyond one year. Additional bleeding or MIs resulted in a poorer prognosis. De-escalation of antiplatelet therapy at the time of BARC 3 bleeding could have a major safety merit. These results emphasize the importance of considering the net clinical benefit including ischemic and bleeding events. Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01813435.

Impact of chronic obstructive pulmonary disease and dyspnoea on clinical outcomes in ticagrelor treated patients undergoing percutaneous coronary intervention in the randomized GLOBAL LEADERS trial.

AIMS: To evaluate long-term safety and efficacy of ticagrelor monotherapy in patients undergoing percutaneous coronary interventions (PCIs) in relation to chronic obstructive pulmonary disease (COPD) at baseline and the occurrence of dyspnoea reported as adverse event (AE) that may lead to treatment non-adherence. METHODS AND RESULTS: This is a non-prespecified, post hoc analysis of the randomized GLOBAL LEADERS trial (n = 15 991), comparing the experimental strategy of 23-month ticagrelor monotherapy following 1-month dual antiplatelet therapy (DAPT) after PCI with the reference strategy of 12-month DAPT followed by 12-month aspirin monotherapy. Impact of COPD and dyspnoea AE (as a time-dependent covariate) on clinical outcomes was evaluated up to 2 years. The primary endpoint was a 2-year all-cause mortality or non-fatal, centrally adjudicated, new Q-wave myocardial infarction. The presence of COPD (n = 832) was the strongest clinical predictor of 2-year all-cause mortality after PCI [hazard ratio (HR) 2.84; 95% confidence interval (CI) 2.21-3.66; P adjusted = 0.001] in this cohort (n = 15 991). No differential treatment effects on 2-year clinical outcomes were found in patients with and without COPD (primary endpoint: HR 0.88; 95% CI 0.58-1.35; P = 0.562; P int = 0.952). Overall, at 2 years dyspnoea was reported as an AE in 2101 patients, more frequently among COPD patients, irrespective of treatment allocation (27.2% in experimental arm vs. 14.5% in reference arm, P = 0.001). Its occurrence was not associated with a higher rate of the primary endpoint (P adjusted = 0.640) in the experimental vs. the reference arm. CONCLUSION: In this exploratory analysis, COPD negatively impacted long-term prognosis after PCI. Despite higher incidence of dyspnoea in the experimental arm, in particular among COPD patients, the safety of the experimental treatment strategy appeared not to be affected. CLINICAL TRIAL REGISTRATION UNIQUE IDENTIFIER: NCT01813435.

The ACE-DD genotype is associated with endothelial dysfunction in postmenopausal women.

OBJECTIVE: To evaluate the effects of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D), the angiotensinogen M235T and the angiotensin II type 1 receptor A1166C polymorphisms, and hormone therapy used on endothelial function in postmenopausal women without manifestation of coronary artery disease. DESIGN: Sixty-four postmenopausal women (42 hormone therapy users and 22 hormone therapy nonusers) without clinical manifestation of coronary artery disease were evaluated using external vascular ultrasonography to measure endothelium-dependent (hyperemic response, flow-mediated dilatation) and -independent (nitroglycerin) dilatation. Genotypes were determined by polymerase chain reaction amplification. RESULTS: Women with the ACE-DD genotype displayed a lower flow-mediated dilatation compared to those with the ACE-II genotype (8.4% +/- 3.9% vs 12.6% +/- 5.4%, P = 0.04). Endothelial function was not associated with the angiotensinogen M235T and anglotensin II type 1 receptor A1166C polymorphisms. ACE polymorphism seems to modulate endothelial function among postmenopausal women without hormone therapy (8.2% +/- 5.1% vs 18.4% +/- 5.9% for the DD and the II genotype, respectively, P = 0.02). However, in hormone therapy users, flow-mediated dilatation was similar according to the ACE genotypes. CONCLUSIONS: Our findings suggest that ACE-I/D polymorphism is related to endothelial dysfunction in postmenopausal women. Furthermore, a potential interaction between estrogen users and ACE polymorphism on endothelial function may be present.

ACE-DD genotype is associated with the occurrence of acute coronary syndrome in postmenopausal women.

The insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE), the A1166C polymorphism in the angiotensin type 1 receptor (AT1R), and the M235T polymorphism of the angiotensinogen gene are associated with cardiovascular disease mostly in men. Few data are available on the effects of these genetic variations in postmenopausal women according to hormone replacement therapy (HRT) use. In this case-control study, we determine the frequency of mutant alleles in the ACE I/D, M235T and A1166C polymorphisms in postmenopausal Caucasian women with and without a diagnosis of acute coronary syndrome (ACS). Data from 198 women with ACS (63+/-10 years) and 149 controls (62+/-7 years) showed that ACE-DD genotype was more prevalent in women with ACS compared to controls (30% vs. 19%, P<0.05). There was no difference in genotype distributions for either the M235T or the A1166C polymorphisms between groups. The difference in ACE genotype distribution between ACS women and controls was driven by current HRT users with 30% of ACS and 15% of controls carrying the ACE-DD genotype (P<0.05). The oligenic combination of ACE-DD and M235T-TT genotypes was higher in ACS compared to controls. Among carriers of M235T-TT, 7% of ACS and 1% of controls also had the ACE-DD genotype, P<0.05. Thus, the ACE-DD genotype may be associated with ACS in postmenopausal women, particularly in HRT users.

Risk scores do not adjust for aggressive, evidence-based changes in percutaneous coronary intervention practice patterns.

AIM: Public reporting of procedural outcomes leads to risk averse behavior because physicians do not believe the scores account for patient risk. We investigated the effects of more aggressive percutaneous coronary intervention (PCI) practice on risk-adjusted mortality. METHODS & RESULTS: 8935 PCI were performed. Risk adjustment was performed with the New York State PCI risk score. The cohort was divided into two eras based on programs implemented to promote more aggressive care. Between eras, overall adjusted mortality ratios rose from 0.66 to 0.90 (observed/predicted, p = 0.02), despite evidence supporting consistent procedural quality. CONCLUSION: Evidence-based changes in PCI practice were associated with worsening risk-adjusted procedural mortality. These data are consistent with physician beliefs regarding risk-adjusted outcome measures.

Coronary Arteriography Should Not Be Routinely Used Postinfarction in Patients Having Received Thrombolytic Therapy.

The use of thrombolytic agents in the context of an acute myocardial infarction has resulted in a significant decrease in postinfarction mortality. However, at this time, little information supporting the routine use of invasive diagnostic and therapeutic interventions in all patients with acute myocardial infarction having received thrombolytic agents is available. Rather, the available data support a conservative strategy, which recommends the judicious use of these techniques in patients with evidence of clinical ongoing ischemia or in patients with a positive predischarge exercise stress test. Several potential explanations have been identified, the most important being the instability of the plaque in the early postinfarction period and the importance of functional capacity as an independent risk factor for subsequent morbidity and mortality. Until studies showing that routine coronary arteriography improves the prognosis of patients with negative predischarge exercise tests, we believe that it will be difficult to justify routine coronary arteriography even in patients with left ventricular dysfunction postinfarction. This more conservative approach should result in significant savings and a more rational use of available resources.

Does hormonal status influence the clinical presentation of acute coronary syndromes in women?

BACKGROUND: Previous studies suggest that the clinical presentation of acute coronary syndromes (ACS) may differ between women and men. It is not known if different clinical presentations may be explained by hormonal status in women with ACS. Our objective was to compare the clinical presentation of ACS between premenopausal (PRE) women and post-menopausal women with hormone replacement therapy (HRT) and without (POST). METHODS: This was a prospective study of consecutive women admitted with a diagnosis of ACS (myocardial infarction [MI] or unstable angina). All women answered a detailed questionnaire that included a list of 27 clinical symptoms. Symptom results were adjusted for age and current coronary event diagnosis. RESULTS: Seventy-three Caucasian women were studied. No differences were found in terms of the frequency of reported typical symptoms of ACS between PRE (n = 23), HRT (n = 32), and POST (n = 18). However, PRE more often reported atypical chest symptoms than HRT and POST women (57% vs. 31% vs. 22%, PRE vs. HRT vs. POST, respectively, p = 0.05). HRT and POST women experienced substernal chest pain more frequently than PRE (44% vs. 78% vs. 83%, p = 0.03). In contrast, PRE more frequently tended to experience chest pressure (57% vs. 31% vs. 39%, p = 0.2) or chest pain in other locations (22% vs. 3% vs. 6%, p = 0.06). HRT and POST groups reported more frequent indigestion-like pain/discomfort (22% vs. 50% vs. 56%, p = 0.04) and midback pain (35% vs. 63% vs. 72%, p = 0.04) during ACS compared with PRE women. POST experienced sudden fatigue more frequently than PRE and HRT (61% vs. 53% vs. 89%, p = 0.03). CONCLUSIONS: Our results suggest that almost all women admitted with ACS experienced typical chest symptoms but frequently reported both typical and atypical symptoms. Independently of age, atypical chest symptoms occurred more frequently in premenopausal women than in postmenopausal women with or without HRT.

Thrombus formation on guide wires during routine PTCA procedures: a scanning electron microscopic evaluation.

BACKGROUND: Various coatings are used on catheters and guide wires to improve resistance to surface thrombus formation. However, little is known about the thrombogenicity of 0.014" angioplasty guide wires and the protection offered by these coatings. OBJECTIVES: To evaluate the thrombogenicity of five different guide wires used in coronary angioplasty. METHODS: Five different 0.014" guide wire types were evaluated in 50 consecutive angioplasty procedures. At the end of the procedure, the distal part of the guide wire was cut, put in formalin and prepared for scanning electron microscopic evaluation. The condition of each guide wire was then classified into one of three predefined categories: no thrombus, limited thrombus and significant thrombus formation. RESULTS: Silicone (n=10, Guidant, USA), phosphorylcholine polymer (n=8, Biocompatibles, Ireland), hydrophilic polymer (n=8, Scimed, USA) and two Teflon-based coatings (n=16, Schneider, USA; n=8, Cordis, USA) were evaluated. On microscopic examination, 48% of guide wires had a significant amount of thrombus, 18% had limited thrombus formation and 34% had no thrombus. The results were very dissimilar among the groups. Significant thrombus was found on 80% of Guidant guide wires, 69% of Schneider guide wires, 38% of Scimed guide wires and 25% of Cordis guide wires, while none was found on Biocompatibles guide wires (P<0.0001). CONCLUSIONS: Significant thrombus formation on angioplasty guide wires was a frequent finding, occurring in 48% of cases. Resistance to thrombus formation was very dissimilar among coatings, with only the Biocompatibles phosphorylcholine-coated guide wires showing no thrombus formation at all. Whether subclinical thromboembolization occurred in some patients is unknown, and the clinical implications of this study remain to be defined.

Effects of long term cholesterol lowering on coronary atherosclerosis in patient risk factor subgroups: the Simvastatin/enalapril Coronary Atherosclerosis Trial (SCAT).

This study examined the effects of long term cholesterol lowering therapy with simvastatin on progression and regression of coronary atherosclerosis, as determined by quantitative angiographic end points, in subgroups of patients with known coronary risk factors. In this randomized, placebo controlled clinical trial, the effect of simvastatin on coronary atherosclerosis was compared with that of placebo in 394 patients who had paired coronary angiograms taken an average of four years apart. The effects of treatment on the following prespecified subgroups were examined: sex, age (less than 65 years versus at least 65 years), smoking status (current or previous/never), history of diabetes mellitus or hypertension, and severity of coronary artery lesions (diameter at least 50% versus less than 50%). There were significantly smaller decreases in the average minimum diameters, between closeout and baseline angiograms, in all simvastatin-treated subgroups, compared with placebo. Trends toward or significantly smaller decreases in the average of the mean diameters, and similar smaller increases in percentage diameter stenosis were also seen in all subgroups. The slowing of angiographically demonstrable coronary atherosclerotic narrowing supports the contention that this treatment effect is causally related to the reduction of coronary events repeatedly seen in large outcome clinical trials of lipid lowering therapy. Also, this treatment effect occurs in the presence or absence of the traditional coronary risk factors.

Symptoms of disturbed sleep predict major adverse cardiac events after percutaneous coronary intervention.

BACKGROUND: Disturbed sleep is associated with atherosclerosis in native coronary arteries and may be associated with adverse cardiac events after percutaneous coronary intervention (PCI). We sought to determine the association between symptoms of disturbed sleep and adverse cardiovascular events after PCI. METHODS: Outpatients who were stable after successful PCI were assessed for symptoms of disturbed sleep with 10 true/false questions. Follow-up was performed at least 4 years after PCI. The primary outcome was a composite of death, myocardial infarction (MI), and repeated revascularization. RESULTS: Three hundred eighty-eight patients (mean age, 66 ± 11 years) reported on average 3.1 ± 2.1 sleep disturbance symptoms. Follow-up was performed on average 4.4 years after the incident PCI. The primary outcome occurred in 25% of patients. An association was seen between the number of sleep disturbance symptoms and the occurrence of the primary end point. Patients with zero symptoms had a 4-year event rate of 12% compared with a 67% event rate for those with 9 symptoms. On multivariable analysis, sleep symptoms, diabetes mellitus, and the number of diseased coronary vessels were independently associated with the primary end point. Each additional sleep symptom was associated with a hazard ratio (HR) of 1.2 (P = 0.001). The results were driven primarily by the association between symptoms of disturbed sleep and the need for repeated revascularization (repeated PCI HR, 1.9; P = 0.003; coronary artery bypass grafting (CABG) HR, 1.5; P = 0.001). CONCLUSIONS: Symptoms of disturbed sleep were associated with increased risk of long-term adverse cardiovascular outcomes after successful PCI.

Inhibition of endothelin-converting enzyme for protection against neointimal proliferation following balloon angioplasty of the rat carotid artery.

Clinical success of percutaneous transluminal coronary angioplasty is limited by restenosis within months of the initial intervention. A number of vasoactive mediators and growth factors have been reported to participate in this process. The aim of the present experiments was to examine the effects of nonselective neutral endopeptidase (NEPi)/endothelin-converting enzyme (ECEi) inhibitors against neointimal proliferation (NIP) following balloon angioplasty of the left carotid artery of Sprague-Dawley rats with the right vessel serving as the uninjured control. The rats were divided in several groups: group 1, nontreated (vehicle); group 2, treated with a selective NEPi i.p.; groups 3-7, treated with nonselective NEPi/ECEi either i.p., s.c., i.v., or p.o. at various doses. After 2 weeks, cross-sectional histopathological and morphometrical examination of the left carotids revealed a severe NIP in vehicle-treated angioplastic rats compared with the control uninjured right carotid of the same rats. The selective NEPi CGS 24592 had no significant effect on restenosis, nor did the dual NEPi/ECEi CGS 26303 at 5 mg x kg(-1) x day(-1) i.p. Both s.c and i.v. NEPi/ECEi treatment (10 mg x kg(-1) x day(-1) b.i.d. s.c. or 10 mg x kg(-1) x day(-1) i.v.) reduced NIP by up to 35%. The prodrug CGS 26393 (p.o.) also attenuated NIP by 23%. Plasma concentrations of these compounds correlated with the degree of inhibition. These data support the participation of the endothelin system in the rat model of balloon angioplasty and suggest that selective ECEi may be effective.

Transradial coronary brachytherapy with the Novoste Beta-Rail system.

We report our initial experience in 10 consecutive patients who underwent transradial coronary brachytherapy for in-stent restenosis using a 90Sr/Y source and the Novoste Beta-Rail system. In all patients, procedures were successfully completed using a right transradial approach. We performed the procedures with the Beta-Rail catheter using 7 Fr (Zuma II, Medtronic, MN; n = 5) or 8 Fr (Cordis, Miami, FL; n = 5) guiding catheters. All lesions were successfully dilated and no additional stent was inserted. We used a 40 mm source (n = 3) or a 60 mm source (n = 7) with manual stepping in four cases. In three cases, we did one stepping, and in one case, we did three steppings. The mean dwell time was 195 plus minus 44 sec. The mean delivered dose was 23 +/- 3 Gy at 2 mm distance from the source. No radiation treatment was interrupted. Mean fluoroscopy time was 26 +/- 13 min. Procedural success was achieved in all patients. Three patients had mild CK elevations (< 3 times upper normal limit). All patients were pretreated with clopidogrel (300 mg) and combined treatment with aspirin + clopidogrel is to be continued for at least 1 year. Clinical follow-up up to 3 months has not yielded any complication and all patients have remained free from angina.