Coronary catheterization is usually performed via the transfemoral approach. Transradial access may offer some advantages in comparison with transfemoral access especially under conditions of aggressive anticoagulation and antiplatelet treatment.

Between July 2006 and January 2008, a total of 1,024 patients undergoing coronary catheterization were randomly assigned to the transradial or transfemoral approach. Patients with an abnormal Allen's test, history of coronary artery bypass surgery, simultaneous right heart catheterization, chronic renal insufficiency, or known difficulties with the radial or femoral access were excluded.

Successful catheterization was achieved in 494 of 512 patients (96.5%) in the transradial and in 511 of 512 patients (99.8%) in the transfemoral group (p < 0.0001). Median procedural duration (37.0 min, interquartile range [IQR] 19.6 to 49.1 min vs. 40.2 min, IQR 24.3 to 50.8 min; p = 0.046) and median dose area product (38.2 Gycm², IQR 20.4 to 48.5 Gycm² vs. 41.9 Gycm², IQR 22.6 to 52.2 Gycm²; p = 0.034) were significantly lower in the transfemoral group compared with the transradial access group. A median amount of contrast agent was similar among both groups. Vascular access site complications were higher in the transfemoral group (3.71%) than in the transradial group (0.58%; p = 0.0008)

The findings of the present study show that transradial coronary angiography and angioplasty are safe, feasible, and effective with similar results to those of the transfemoral approach. However, procedural duration and radiation exposure are higher using the transradial access. In contrast to the transfemoral route, the rate of major vascular complications was negligible using the transradial approach.

Transradial approach PCI reduces vascular complications compared with a transfemoral approach (TF). However, the mechanism and predictors of TR-PCI failure have not been well-characterized.

The study population consisted of patients undergoing TR-PCI by low-to-intermediate volume operators with traditional TF guide catheters. Baseline characteristics, procedure details, and clinical outcomes were prospectively collected. Univariate and multivariate analyses were performed to determine independent predictors of TR-PCI failure.

A total of 2,100 patients underwent TR-PCI and represented 38% of PCI volume. Mean age was 64 ± 12 years, and 17% were female. Vascular complications occurred in 22 (1%), and TR-PCI failure was observed in 98 (4.7%) patients. The mechanism of TR-PCI failure included inability to advance guide catheter to ascending aorta in 50 (51%), inadequate guide catheter support in 35 (36%), and unsuccessful radial artery puncture in 13 (13%) patients. The PCI was successful in 94 (96%) patients with TR-PCI failure by switching to TF. On multivariate analysis, age >75 years (odds ratio [OR]: 3.86; 95% confidence interval [CI]: 2.33 to 6.40, p = 0.0006), prior coronary artery bypass graft surgery (OR: 7.47; 95% CI: 3.45 to 16.19, p = 0.0002), and height (OR: 0.97; 95% CI: 0.95 to 0.99, p = 0.02) were independent predictors of TR-PCI failure.

Transradial approach PCI can be performed by low-to-intermediate volume operators with standard equipment with a low failure rate. Age >75 years, prior coronary artery bypass graft surgery, and short stature are independent predictors of TR-PCI failure. Appropriate patient selection and careful risk assessment are needed to maximize benefits offered by TR-PCI.

The transradial access has recently become an alternative to transfemoral cardiac catheterization. A potential caveat of this approach lies in possible sustained physical radial artery (RA) damage.

We studied 30 patients (age 61 ± 11 years) undergoing diagnostic coronary angiography with the transradial access (5-F). Endothelium-dependent, flow-mediated vasodilation (FMD) was measured before and at 6 and 24 h after catheterization of the right-sided RA and BA with high-resolution ultrasound. The left-sided RA served as a control.

Transradial catheterization significantly decreased FMD in the RA (overall mean 8.5 ± 1.7% to 4.3 ± 1.6%) and the upstream BA (overall mean 4.4 ± 1.6% to 2.9 ± 1.6%) at 6 h. Subgroup analysis showed that FMD of both arteries at 6 h was significantly lower in active smokers and that it only remained impaired at 24 h in this group, whereas nonsmoker FMD fully recovered. The degree of BA but not RA FMD dysfunction was related to the number of catheters used, with no change after 2 catheters, 1.9 ± 1.2% decrease (6 h) and recovery (24 h) after 3 catheters, and 3.9 ± 1.2% decrease (6 h) without recovery (24 h) after 4 to 5 catheters. The RA dysfunction correlated with the baseline diameter. The contralateral control RA exhibited no change ruling out systemic effects.

Transradial catheterization not only leads to dysfunction of the RA but also the upstream BA, which is more severe and sustained in smokers and with increasing numbers of catheters.

In randomized trials of PCI, major bleeding and periprocedural myocardial infarction (pMI) have been associated with increased mortality. Whether similar associations exist among un-selected PCI patients is unknown.

We used data from the EVENT (Evaluation of Drug Eluting Stents and Ischemic Events) registry—a multicenter registry of unselected patients undergoing PCI—to examine the association between both in-hospital bleeding and pMI and 1-year mortality. Cardiac enzyme levels were assessed in all patients, and pMI was defined as a peak creatine kinase-MB value ≥3x the upper limit of normal. Post-PCI bleeding was classified by Thrombolysis In Myocardial Infarction criteria.

After excluding patients with elevated pre-PCI creatine kinase-MB values and ST-segment elevation myocardial infarction at presentation (n = 1,626), a total of 5,961 patients were available for evaluation. Rates of post-PCI bleeding and pMI were 3.0% and 7.1%, respectively; 1-year all-cause mortality was 2.8%. After multivariable adjustment, both post-PCI bleeding (adjusted hazard ratio [HR]: 3.83, 95% confidence interval: 2.48 to 5.90, p < 0.001) and pMI (adjusted HR: 1.84, 95% confidence interval: 1.17 to 2.89, p = 0.009) were independently associated with 1-year mortality. Time period-specific analyses demonstrated that the adjusted HR for bleeding was similar for 30-day mortality and mortality between 1 month and 1 year, while the adjusted HR for pMI was greater for 30-day mortality as compared with mortality between 1 month and 1 year.

Among unselected PCI patients, both post-PCI bleeding and pMI are independently associated with increased 1-year mortality. Continued efforts to reduce these complications after PCI are warranted.

While long-term outcomes in PCI patients have been reported previously, limited data are currently available regarding the comparative long-term outcomes in PCI patients who receive enoxaparin versus intravenous unfractionated heparin (UFH).

We conducted a follow-up analysis of clinical outcomes at 1 year in patients enrolled in the STEEPLE (SafeTy and Efficacy of Enoxaparin in Percutaneous coronary intervention patients, an internationaL randomized Evaluation) trial of 3,528 patients undergoing elective PCI. Patients were randomized to receive either intravenous 0.50-mg/kg or 0.75-mg/kg enoxaparin or intravenous UFH during elective PCI procedures. All-cause mortality at 1 year after index PCI was the main outcome measure.

Mortality rates were 1.4%, 2.0%, and 1.5% from 1 month to 1 year, and 2.3%, 2.2%, and 1.9% from randomization to 1 year, after index PCI in patients receiving 0.50 mg/kg enoxaparin, 0.75 mg/kg enoxaparin, and UFH, respectively. Multivariate analysis identified nonfatal myocardial infarction and/or urgent target vessel revascularization up to 30 days after index PCI (hazard ratio: 3.5, 95% confidence interval: 1.7 to 7.3; p < 0.001), and major bleeding within 48 h (hazard ratio: 3.0, 95% confidence interval: 1.1 to 8.5; p = 0.04) as the strongest independent risk factors for 1-year mortality.

The 1-year mortality rates were low and comparable between patients receiving enoxaparin and UFH during elective PCI. Periprocedural ischemic or bleeding events were the strongest independent predictors of 1-year mortality. (The STEEPLE Trial; NCT00077844)

Clopidogrel is a prodrug that is biotransformed by the cytochrome P450 enzymes CYP2C19, 2C9, and 3A4, 2B6, 1A2. The CYPC219*2 loss of function variant has been associated with a reduced antiplatelet response to clopidogrel and a 3-fold risk of stent thrombosis.

Forty patients on standard maintenance dosage clopidogrel (75 mg), for 9.4 ± 9.2 weeks, were enrolled into a dose escalation study. Platelet function was assessed at baseline and after 1 week of 150 mg once daily using the VerifyNow platelet function analyzer (Accumetrics Ltd., San Diego, California). Genomic DNA was hybridized to a BioFilmChip microarray on the INFINITI analyzer (AutoGenomics Inc., Carlsbad, California) and analyzed for the CYP19*2, *4, *17, and CYP2C9*2, *3 polymorphisms.

Platelet inhibition increased over 1 week, mean +8.6 ± 13.5% (p = 0.0003). Carriers of the CYP2C19*2 allele had significantly reduced platelet inhibition at baseline (median 18%, range 0% to 72%) compared with wildtype (wt) (median 59%, range 11% to 95%, p = 0.01) and at 1 week (p = 0.03). CYP2C19*2 allele carriers had an increase in platelet inhibition of (mean +9 ± 11%, p = 0.03) and reduction in platelet reactivity (mean –26 ± 38 platelet response unit, p = 0.04) with a higher dose. Together CYP2C19*2 and CYP2C9*3 loss of function carriers had a greater change in platelet inhibition with 150 mg daily than wt/wt (+10.9% vs. +0.7%, p = 0.04).

Increasing the dose of clopidogrel in patients with nonresponder polymorphisms can increase antiplatelet response. Personalizing clopidogrel dosing using pharmacogenomics may be an effective method of optimizing treatment.

The safety and efficacy of DES in patients undergoing SVG intervention is controversial.

The STENT (Strategic Transcatheter Evaluation of New Therapies) registry is a multicenter U.S. registry evaluating outcomes with DES. Our study population includes patients undergoing PCI of SVG lesions with DES (n = 785) or BMS (n = 343) who completed 9-month or 2-year follow-up. Outcomes were adjusted with propensity analyses.

The DES patients had fewer emergent procedures but had smaller vessels and longer lesions. The DES patients had less death or myocardial infarction at 9 months (hazard ratio [HR]: 0.52, 95% confidence interval [CI]: 0.33 to 0.83, p = 0.006) and less death at 2 years (HR: 0.60, 95% CI: 0.36 to 0.98, p = 0.041). Target vessel revascularization (TVR) was less with DES at 9 months (7.2% vs. 10.0%, HR: 0.36, 95% CI: 0.22 to 0.61, p < 0.001) but was no different by 2 years (18.3% vs. 16.9%, p = 0.86), although adjusted TVR rates were lower (HR: 0.60, 95% CI: 0.40 to 0.90, p = 0.014). The DES reduced TVR at 9 months in SVG lesions with diameter <3.5 mm (8.0% vs. 17.2%, p = 0.013) but not ≥3.5 mm (6.0% vs. 6.6%, p = 0.74).

Treatment of SVG lesions with DES vs. BMS is effective in reducing TVR at 9 months, although most of this advantage is lost at 2 years. The DES seem safe with less death or myocardial infarction, although selection bias might have affected these results. Our data suggest that DES might have short-term advantages over BMS in SVG lesions with diameter <3.5 mm.

Contrast-induced AKI is a serious consequence of cardiac catheterizations and percutaneous coronary interventions (PCI). Despite recent supporting evidence for combination therapy, not enough has been done to prevent the occurrence of contrast-induced AKI prophylactically.

Published randomized controlled trial data were collected from OVID/PubMed, Web of Science, and conference abstracts. The outcome of interest was contrast-induced AKI, defined as a ≥25% or ≥0.5 mg/dl increase in serum creatinine from baseline. Secondary outcome was renal failure requiring dialysis.

Ten randomized controlled trials met our criteria. Combination treatment of NAC with intravenous NaHCO₃ reduced contrast-induced AKI by 35% (relative risk: 0.65; 95% confidence interval: 0.40 to 1.05). However, the combination of N-acetylcysteine plus NaHCO₃ did not significantly reduce renal failure requiring dialysis (relative risk: 0.47; 95% confidence interval: 0.16 to 1.41).

Combination prophylaxis with NAC and NaHCO₃ substantially reduced the occurrence of contrast-induced AKI overall but not dialysis-dependent renal failure. Combination prophylaxis should be incorporated for all high-risk patients (emergent cases or patients with chronic kidney disease) and should be strongly considered for all interventional radio-contrast procedures.

The impact of a CTO in a non–infarct-related artery (IRA) on prognosis after STEMI is unknown.

Between 1997 and 2005, we admitted 3,277 STEMI patients treated with primary percutaneous coronary intervention. Patients were categorized as single-vessel disease (SVD), multivessel disease (MVD) without CTO, and MVD with a CTO in a non-IRA. We performed a "landmark survival analysis" to 5 years follow-up with a landmark set at 30 days. Additionally, we analyzed the evolution of LVEF within 1 year.

Of the patients, 2,115 (65%) had SVD, 742 patients (23%) had MVD without CTO, and 420 patients (13%) had a concurrent CTO. Presence of a CTO was a strong and independent predictor for 30-day mortality (hazard ratio [HR]: 3.6, 95% confidence interval [CI]: 2.6 to 4.7, p < 0.01), whereas MVD without CTO was a weak predictor (HR: 1.6, 95% CI: 1.2 to 2.2, p = 0.01). In 30-day survivors, CTO remained a strong predictor (HR: 1.9, 95% CI: 1.4 to 2.8, p < 0.01), and MVD lost its independent prognostic value (HR: 1.1, 95% CI: 0.8 to 1.5, p = 0.45). Furthermore, CTO was associated with LVEF ≤40% immediately after STEMI (odds ratio: 1.9, 95% CI: 1.3 to 2.8, p < 0.01) and a further decrease in LVEF within the first year (odds ratio: 3.5, 95% CI: 1.6 to 7.8, p < 0.01).

The presence of a CTO and not MVD alone is associated with long-term mortality even when early deaths are excluded from analysis. The presence of a CTO is associated with reduced LVEF and further deterioration of LVEF.

Successful percutaneous recanalization of coronary CTOs results in improved long-term outcomes. The recanalization of CTOs in native coronary arteries no doubt represents one of the most technically challenging of interventional procedures.

A total of 224 consecutive patients (mean age 61 ± 9 years; 86.2% men) were enrolled in this prospective multicenter registry. This technique combines the simultaneous use of antegrade and retrograde approaches. A subintimal dissection is created in both antegrade and retrograde fashion, thereby limiting the extension of the subintimal dissection within the CTO portion.

Of 224 CTO lesions (>3 months in duration) undergoing attempted recanalization using the CART technique, 145 cases (64.7%) had undergone previous CTO recanalization attempts. The success rates of crossing in a retrograde fashion with a wire and a balloon were 87.9% and 79.9%, respectively. The overall technical and procedural success rates achieved in this registry were 92.4% and 90.6%, respectively.

A bilateral approach for CTO lesions using the CART technique is feasible, safe, and has a higher success rate than previous approaches. These results indicate that a bilateral technique can solve a major dilemma that commonly affects CTO procedures.

The OSIRIS trial showed a significant reduction of angiographic restenosis with an oral adjunctive sirolimus treatment for in-stent restenosis. The long-term efficacy of oral sirolimus therapy is unknown.

Three hundred patients with in-stent restenosis were randomly assigned to receive placebo, a cumulative loading dose of 8 mg (usual-dose), or 24 mg (high-dose) of sirolimus over 3 days (2 days before and the day of intervention) followed by maintenance therapy of 2 mg/day for 7 days. The primary outcome of this analysis was the incidence of composite of death, myocardial infarction, and target vessel revascularization at 4-year follow-up. Secondary outcome was the incidence of newly diagnosed malignancies.

No significant differences were observed between placebo, usual-, and high-dose sirolimus treatment groups regarding primary outcome (33.3%, 39.4%, and 31.3%, respectively; p = 0.46), death (5.9%, 9.1%, and 11.1%, respectively; p = 0.41), target vessel revascularization (30.4%, 30.3%, and 22.2%, respectively; p = 0.33), and rate of newly diagnosed malignancies (7.8%, 3.0%, and 11.1%, respectively; p = 0.09).

The benefit in the reduced need for repeat intervention observed at 1 year with high-dose oral sirolimus therapy was attenuated over 4 years. Moreover, this regimen was associated with numerical yet not a significant increase in newly diagnosed malignancies without augmenting the malignancy-induced risk of death. (Oral Sirolimus for In-Stent Restenosis [OSIRUS] trial; NCT00859183)

Recently, genomewide association studies have identified a locus on chromosome 9 (approximately 100 kb in band p21.3) as the strongest genetic factor for coronary heart disease.

We studied the rs7865618, rs1537378, rs1333040, and rs1333049 polymorphisms located on chromosome 9p21.3 in a cohort of 2,028 patients who were treated with percutaneous coronary intervention and implantation of sirolimus- or paclitaxel-eluting stents. Records of 3-year adverse clinical outcomes were obtained from all stented patients. Follow-up angiography at 6 to 8 months after stenting was performed in 1,683 patients (83%).

The polymorphisms were not significantly related with clinical outcomes at 3 years, including death (p ≥ 0.18), myocardial infarction (p ≥ 0.19), repeat revascularization (p ≥ 0.08), and the composite end point of adverse events (death, myocardial infarction, repeat revascularization) (p ≥ 0.34). No association of the polymorphisms was found with angiographic measures at follow-up, including minimal lumen diameter (p ≥ 0.51), diameter stenosis (p ≥ 0.31), late lumen loss (p ≥ 0.05), and binary restenosis (p ≥ 0.31).

Specific polymorphisms in the chromosome 9p21.3 region that were shown to be associated with coronary heart disease in genomewide analyses were not related to the clinical and angiographic outcomes after the placement of drug-eluting stents in coronary arteries.

Treatment delays remain common for patients with primary PCI leading to studies evaluating possible benefit of "facilitated" PCI. In the FINESSE trial, no reduction in the 90-day primary ischemic end point and an increase in bleeding were observed with both facilitated approaches, although modest favorable trends were seen for some patient subgroups.

A total of 2,452 patients with ST-segment elevation myocardial infarction (MI) and anticipated 1 to 4 h delay until catheterization were randomized to reduced-dose reteplase + abciximab, abciximab alone, or placebo, followed by expedited primary PCI. Placebo-treated patients received abciximab in the cath lab. One-year mortality was a pre-specified secondary end point.

One-year mortalities in the 3 groups noted in the preceding text were 6.3%, 7.4%, and 7.0%, respectively (p = NS), representing 1.1%, 1.9%, and 2.5% increments since the 90-day outcome (p = 0.053 for combination treatment vs. primary PCI). A favorable trend with combination treatment was seen for patients with anterior MI (p = 0.09), but no other specified groups benefited or tended to benefit. Independent baseline correlates of 1-year mortality were systolic blood pressure <100 mm Hg, prior MI, age, Killip class >1, anterior MI, body mass index ≤25 kg/m², heart rate >100 beats/min, and no statin use.

These results suggest that widespread utilization of the facilitated approaches tested cannot be justified, but that high-risk patient groups such as patients with anterior MI may deserve further study. (The FINESSE trial; NCT00046228)

The FINESSE (Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events) study failed to demonstrate an improvement in the 90-day composite clinical end point of early treatment with abciximab plus half-dose reteplase (combination-facilitated PCI) or abciximab alone.

We performed a retrospective analysis of 2,452 patients in this double-blind, placebo-controlled study. Patients were stratified by Thrombolysis In Myocardial Infarction (TIMI) risk score for ST-segment elevation myocardial infarction (STEMI), presentation to a spoke (no PCI available) or hub site, and symptom-to-randomization time. Outcomes included the primary composite end point of death, ventricular fibrillation after 48 h, cardiogenic shock, and congestive heart failure through day 90 as well as 1-year mortality.

Mortality for all patients at 1 year was directly related to TIMI risk score (23 of 1,223 = 1.9% in patients with score <3 and 145 of 1,229 = 11.8% with score ≥3, p < 0.001). Patients with TIMI risk score ≥3 and presentation to a spoke site with a symptom-to-randomization time ≤4 h had significantly better 1-year survival if treated with combination-facilitated PCI (hazard ratio [HR]: 0.351, p = 0.01) as well as 90-day composite outcome (HR: 0.45, p = 0.009). A trend for improved survival was also observed in patients with TIMI score ≥3 and spoke site alone (HR: 0.549, p = 0.06).

Facilitation of PCI with a combination of abciximab and half-dose reteplase improved survival at 1 year in high-risk patients presenting to a spoke hospital with symptom-to-randomization time ≤4 h. Further prospective study of facilitated PCI in this subgroup of patients is warranted.

The ASSENT-4 PCI (Assessment of the Safety and Efficacy of a New Treatment Strategy with Percutaneous Coronary Intervention) trial intended to test the hypothesis that in ST-segment elevation myocardial infarction (STEMI) patients an upfront fibrinolytic bolus before PCI ("facilitated PCI") compared with primary PCI would benefit STEMI patients facing a long pre-PCI delay.

Seven hundred forty-nine patients (45%) presented directly to PCIH, 578 (34%) presented to NoPCIH, and 334 (20%) were randomized and initially treated in the PreH setting.

Patients in the PreH-facilitated group had the shortest delays (pain-to-fibrinolytic treatment 125 min) and the lowest 90-day mortality (3.1%). Among patients randomized to primary PCI, the shortest time from pain to first balloon was similarly in the PreH group (223 min). They had the lowest mortality of the primary PCI patient groups (4.1%). The highest mortality (8.4%) was in patients presenting to a PCIH and assigned to the facilitated strategy. Their pain-to-lysis time was 174 min and pain-to-PCI time 266 min (or 92 min after lysis).

Few patients fit the target population, long delays to PCI for whom facilitated PCI was designed. Patients treated early after pain onset in the PreH setting do well after a facilitated approach. Despite limitations of post hoc subgroup analysis, these observations suggest caution in extrapolating the results of the ASSENT-4 trial to the "real world" where many patients might have potentially short pain-to-fibrinolysis time but are facing a long transport time to primary PCI.

Embolization during primary percutaneous coronary intervention (PCI) may result in microvascular obstruction, reduced myocardial perfusion, and impaired prognosis.

Two hundred eight-four patients were randomized to primary PCI with the Proxis system versus primary PCI alone after angiography. The primary end point was the occurrence of complete (≥70%) ST-segment resolution (STR) at 60 min measured by continuous ST-segment Holter.

There was no significant difference in the occurrence of the primary end point (80% vs. 72%, p = 0.14). However, immediate complete STR (at time of last contrast) occurred in 66% of Proxis-treated patients and 50% in control patients (absolute difference, 16.3%; 95% confidence interval: 4.3% to 28.2%; p = 0.009). A significant lower ST-segment curve area (0 to 3 h after primary PCI) was observed in the Proxis arm (5,192 µV/min vs. 6,250 µV/min, p = 0.037). Major adverse cardiac and cerebral events at 30 days occurred with similar frequency in both groups (6 vs. 10).

There was no significant difference in complete STR at 60 min in this proof-of-concept study. However, we observed a significant difference in immediate complete STR in Proxis-treated patients, better STR at later time points, and a reduction of electrocardiogram injury current over time, compared with control patients. The results suggest that primary PCI with the Proxis system may lead to better immediate microvascular flow in ST-segment elevation myocardial infarction patients. (The PREPARE Study; ISRCTN71104460)

Whether backup cardiac surgery improves outcomes among NSTEMI patients or is simply a marker of better adherence to guideline recommendations is unknown.

The NRMI (National Registry of Myocardial Infarction) enrolled 100,071 NSTEMI patients from 2004 to 2006. Outcomes were evaluated in the population as a whole and in propensity-matched analyses in the entire population and in the subset of patients undergoing PCI.

In-hospital mortality was significantly lower at OHS hospitals (5.0% vs. 8.8%, p < 0.001). Patients presenting to OHS hospitals were significantly more likely to receive aspirin, beta-blockers, and statins (p < 0.05 for all) and to undergo PCI (38.4% vs. 14.1%, p < 0.001). In the propensity-matched model, the difference in mortality remained significant (5.9% vs. 8.5%, p < 0.001). After adjusting for differences in medications administered within 24 h of arrival and hospital characteristics, the difference in mortality was nearly attenuated (hazard ratio: 0.89, 95% confidence interval: 0.79 to 1.00, p = 0.050). When the propensity-matched model was restricted to patients undergoing PCI, there was no significant difference in mortality (1.3% vs. 1.0%, p = 0.51).

NSTEMI patients presenting to No-OHS hospitals have significantly higher mortality. This appears to be due to both modifiable (lower use of guideline-recommended medications) and nonmodifiable factors (hospital size, myocardial infarction volume). In a propensity-matched analysis of patients undergoing PCI for NSTEMI, there was no significant difference in mortality.

Diabetes mellitus has been shown to be a risk factor for adverse events and a major determinant in selection of a revascularization strategy in patients with multivessel or LMCA disease.

A total of 1,474 patients with unprotected LMCA stenosis who received DES (n = 784) or underwent CABG (n = 690) were examined. We compared the effects of these 2 treatments on long-term clinical outcomes (death; the composite of death, Q-wave myocardial infarction [MI], or stroke; and target vessel revascularization [TVR]), according to diabetic status.

After adjustment of covariates, the risk of death (hazard ratio [HR]: 0.95, 95% confidence interval [CI]: 0.62 to 1.46, p = 0.83) and the composite of death, Q-wave MI, or stroke (HR: 0.96, 95% CI: 0.65 to 1.42, p = 0.85) at 3 years were similar in the DES and CABG groups. However, the rate of TVR was significantly higher in the DES group (HR: 4.31, 95% CI: 2.28 to 8.15, p < 0.001). These trends were consistent in both diabetic and nondiabetic patients. We also did not observe a diabetes-associated excess risk of death (p_interaction = 0.90 and 0.16), or a composite of death, Q-wave MI, or stroke (p_interaction = 0.68 and 0.93), or TVR (p_interaction = 0.23 and 0.92), between patients receiving either treatment.

The prognostic impact of diabetes on long-term treatment with DES or CABG for patients with unprotected LMCA disease was minimal.

Percutaneous coronary intervention (PCI) in diabetic patients is associated with increased rates of restenosis-related end points compared with PCI in nondiabetic patients. Although ZES has been associated with similar clinical efficacy compared with PES in the overall trial population of the ENDEAVOR IV trial, whether these results are maintained in the higher-risk restenosis subgroup of patients with DM has not been determined.

Clinical and angiographic outcomes were compared according to randomized treatment assignment to either ZES or PES.

Baseline characteristics were similar among ZES (n = 241) and PES (n = 236) diabetic patients, with slightly longer lesion lengths in PES-treated patients (12.9 mm vs. 14.0 mm, p = 0.041). Among the 86 DM patients assigned to routine angiographic follow-up (18% of the overall DM cohort), in-stent percent diameter stenosis at 8 months was greater among ZES-treated patients (32.9 vs. 21.1, p = 0.023), with a trend toward higher in-stent late loss. One-year clinical outcomes were similar among DM patients treated with either ZES or PES (target vessel failure: 8.6% vs. 10.8%, p = 0.53; target lesion revascularization: 6.9% vs. 5.8%, p = 0.70; target vessel revascularization: 8.6% vs. 9.4%, p = 0.87). There were no significant interactions between DM status and stent type with respect to the outcomes measured, and the relative efficacy/safety of ZES and PES were similar among insulin- and noninsulin-requiring subgroups.

One-year clinical outcomes were similar among DM patients treated with ZES and PES in the ENDEAVOR IV trial. These findings parallel the overall trial results, which demonstrated similar efficacy and safety of ZES and PES for single de novo coronary lesions.

Revascularization benefits associated with current drug-eluting stents are often diminished in the presence of complex coronary lesions and in certain patient cohorts. Resolute uses a new proprietary polymer coating that extends the duration of drug delivery to match the longer healing duration often experienced in more complex cases.

The RESOLUTE trial was a prospective, nonrandomized, multicenter study of the Resolute stent in 139 patients with de novo coronary lesions with reference vessel diameters ≥2.5 and ≤3.5 mm and lesion length ≥14 and ≤27 mm. The primary end point was 9-month in-stent late lumen loss by quantitative coronary angiography. Secondary end points included major adverse cardiac events (MACE) at 30 days, 6, 9, and 12 months; acute device, lesion, and procedure success; and 9-month target vessel failure (TVF), target lesion revascularization (TLR), stent thrombosis, neointimal hyperplastic (NIH) volume, and percent NIH volume obstruction.

The 9-month in-stent late lumen loss was 0.22 ± 0.27 mm. Cumulative MACE were 4.3%, 4.3%, 7.2%, and 8.7% at 30 days, 6, 9, and 12 months, respectively. Acute lesion, procedure, and device success rates were 100.0%, 95.7%, and 99.3%, respectively. At 9 months, TLR was 0.0%, TVF was 6.5%, stent thrombosis was 0.0%, NIH volume was 6.55 ± 7.83 mm³, and percent NIH volume obstruction was 3.73 ± 4.05%.

In this feasibility study, the Resolute stent demonstrated low in-stent late lumen loss, minimal neointimal hyperplastic ingrowth, low TLR, no stent thrombosis, and acceptable TVF and MACE. (The RESOLUTE Clinical Trial; NCT00248079)

Although SES has significantly reduced in-stent restenosis by inhibiting neointimal hyperplasia, insufficient neointimal coverage after stenting might result in adverse outcomes.

We evaluated 28 SES lesions with both angioscopy and intravascular ultrasound (IVUS). Quantitative assessments of the lesions and stent expansion were performed by IVUS at the time of stent implantation, and degree of neointimal coverage was judged by angioscopy at follow-up (11 ± 6 months) whether the stent struts were embedded by the neointima ("complete/incomplete" neointimal coverage).

"Complete" coverage was identified in 10 (36%), and "incomplete" coverage was identified in 18 (64%). Time from the stenting to angioscopy as well as the lesion and procedural characteristics were similar between the complete and incomplete coverage groups. The IVUS parameters were also similar, except for the final minimum stent cross-sectional area (CSA) (7.0 ± 1.8 mm² in complete vs. 5.3 ± 1.9 mm² in incomplete, p = 0.02) and lumen CSA at the distal reference site (6.1 ± 1.4 mm² in complete vs. 4.9 ± 1.2 mm² in incomplete, p = 0.02). The ratio of the stent area to the vessel area was significantly larger in the complete coverage than in the incomplete coverage group (0.52 ± 0.11 vs. 0.39 ± 0.09, p = 0.002).

Adequate stent sizing relative to the vessel size might contribute to the angioscopically complete neointimal coverage after SES implantation.

DES implantation strategies differ compared with bare-metal stenting; coronary dissections after DES implantation have not been well studied.

We studied 887 patients with 1,045 non–in-stent restenosis lesions in 977 native arteries undergoing DES implantation with IVUS imaging.

Eighty-two dissections were detected; 51.2% (42 of 82) involved the proximal and 48.8% (40 of 82) the distal stent edge. Residual plaque area (8.0 ± 4.3 mm² vs. 5.2 ± 3.0 mm², p < 0.0001); plaque burden (52.2 ± 11.7% vs. 36.2 ± 15.3%, p < 0.0001); plaque eccentricity (8.4 ± 5.5 vs. 4.0 ± 3.4, p < 0.0001); and stent edge symmetry (1.2 ± 0.1 vs. 1.1 ± 0.1, p = 0.02) were larger; plaque burden ≥50% was more frequent (62.0% vs. 17.2%, p < 0.0001); calcium deposits (52.1% vs. 35.2%, p = 0.03) more common; and lumen-to-stent-edge-area ratio (0.9 ± 0.2 vs. 1.0 ± 0.2, p < 0.0001) was smaller in the edge dissection group compared with the nondissection group. Intramural hematomas occurred in 34.1% (28 of 82) of dissections. When compared with nonhematoma dissections, residual plaque and media area (6.4 ± 2.5 mm² vs. 8.9 ± 4.6 mm², p = 0.04) was smaller, and stent edges less asymmetric (1.1 ± 0.1 vs. 1.2 ± 0.1, p = 0.009) in the dissection with hematoma group. Independent predictors of any stent edge dissection were residual plaque eccentricity (odds ratio [OR]: 1.4, p = 0.02), lumen-to-stent-edge-area ratio (OR: 0.0, p = 0.007), and stent edge symmetry (OR: 1.2, p = 0.02 for each 0.01 increase).

IVUS identified edge dissections after 9.2% of DES implantations. Residual plaque eccentricity, lumen-to-stent-edge-area ratio, and stent edge symmetry predicted coronary stent edge dissections. Dissections in less diseased reference segments more often evolved into an intramural hematoma.

Treatment of acute myocardial infarction (MI) with BM MNC infusion has shown promise for improving patient outcomes. However, clinical data are conflicting, and demonstrate modest improvements. BM MNCs consist of different subpopulations including stem cells, progenitors, and differentiated leukocytes.

Stem cells (c-kit+) and subsets of mature cells including myeloid lineage, B and T-cells were isolated from bone marrow harvested from isogeneic donor rats. Recipient rats had baseline echocardiography then coronary artery ligation; 1 x 10⁶ cells (enriched subpopulations or combinations of subpopulations of BM MNC) or saline was injected into ischemic and ischemic border zones. Cell subpopulations were either injected fresh or after overnight culture. After 2 weeks, animals underwent follow-up echocardiography. Cardiac tissue was assayed for cardiomyocyte proliferation and apoptosis.

Fractional ventricular diameter shortening was significantly improved compared with saline (38 ± 3.2%) when B cells alone were injected fresh (44 ± 3.0%, p = 0.035), or after overnight culture (51 ± 2.9%, p < 0.001), or after culture with c-kit+ cells (44 ± 2.4%, p = 0.062). B cells reduced apoptosis at 48 h after injection compared with control cells (5.7 ± 1.2% vs. 12.6 ± 2.0%, p = 0.005).

Intramyocardial injection of B cells into early post-ischemic myocardium preserved cardiac function by cardiomyocyte salvage. Other BM MNC subtypes were either ineffective or suppressed cardioprotection conferred by an enriched B cell population.

Rapamycin- and paclitaxel-eluting stents reduce the need for repeat intervention by limiting neointimal hyperplasia but might cause delayed healing, pre-disposing patients to late stent thrombosis. Because inflammation plays a key role in restenosis, pimecrolimus, an anti-inflammatory drug, might reduce restenosis without adversely affecting re-endothelialization.

We evaluated a novel polymeric pimecrolimus-eluting stent covered with a thin parylene C diffusion barrier in a porcine coronary model and in a phase I human clinical trial. The clinical study was a prospective, nonrandomized, first-in-human hypothesis-generating study that enrolled 15 patients who had a single de novo native coronary stenosis.

At 28 days and 3 months in the porcine model, histopathologic indicators predicted safety and biocompatibility when stents coated with polymer only, drug only, and 2 drug-polymer formulations were compared with bare-metal stents (BMS). In the phase I clinical trial, 15 patients had successful implantation of pimecrolimus-eluting stents. By 6 months, no patient suffered death, myocardial infarction, or stent thrombosis. However, the angiographic restenosis (61%), mean late loss (1.44 mm), and repeat target lesion revascularization (53%) were significantly higher than historical BMS controls. Whereas the primary end point was percent volume obstruction, restenosis was so severe that operators performed intravascular ultrasound examination in only 6 patients.

Pimecrolimus-eluting stents induced an exaggerated neointimal hyperplasia at 6 months in comparison with historical controls.

Paravalvular AR might occur after TAVI, but its determinants remain unclear.

Comprehensive echocardiographic examinations were performed in 74 patients who underwent TAVI with a balloon expandable device. Congruence between annulus and device was appraised with the cover index: 100 x (prosthesis diameter – transesophageal echocardiography annulus diameter)/prosthesis diameter.

At baseline aortic valve area was 0.67 ± 0.2 cm², and mean gradient was 50 ± 15 mm Hg. The TAVI used transfemoral approach in 46 patients (62%) and transapical access in 28 (38%). Prosthesis size was 23 mm in 24 patients (34%) and 26 mm in 50 patients (66%). After TAVI, paravalvular AR was absent in 5 patients (7%), graded 1/4 in 53 (72%), 2/4 in 12 (16%), and 3/4 in 4 (5%). Occurrence of AR ≥2/4 was related to greater patient height, larger annulus, and smaller cover index (all p < 0.002) but not to ejection fraction, severity of stenosis, or prosthesis size. AR ≥2/4 was never observed in patients with aortic annulus <22 mm or with a cover index >8%. Significant improvements were observed from the first 20 cases (AR ≥2/4, 40%) to the last 54 (AR ≥2/4, 15%) (p = 0.02). In multivariate analysis, independent predictors of AR ≥2/4 were low cover index (odds ratio: 1.22; per confidence interval: 1.03 to 1.51 per 1% decrease, p = 0.02) and first versus last procedures (odds ratio: 2.24; 95% confidence interval: 1.07 to 5.22, p = 0.03).

Our study shows that the occurrence of AR ≥2/4 is related to prosthesis/annulus discongruence even after adjustment for experience. Hence, to minimize paravalvular AR, appropriate annular measurements and prosthesis sizing are critical.

TAVI is an emerging therapeutic option to treat inoperable/high-risk patients affected by symptomatic AS. However, these patients are also often affected by severe iliac-femoral arteriopathy, rendering the transfemoral approach unemployable for percutaneous revalving procedure.

From among those patients in our department between May 2007 and December 2008, who were refused surgical aortic valve replacement because of high surgical risk and were ineligible for transfemoral percutaneous aortic valve replacement, we scheduled 3 for TAVI by the subclavian approach. Procedures were performed by a combined team of cardiologists, cardiac surgeons, and anesthetists in the catheterization laboratory. The III generation CoreValve Revalving System (CoreValve Inc., Irvine, California) with an 18-F delivery system was introduced in all cases by the left subclavian artery.

Prosthetic valves were successfully implanted in all 3 cases, leading to a fall in transvalvular gradient without significant paravalvular regurgitation. No intraprocedural or periprocedural complications occurred. Two patients developed an atrioventricular block requiring the implantation of a permanent pacemaker. All patients were discharged in asymptomatic status, with good prosthesis performance. No adverse events occurred within the 3-month follow-up.

TAVI by subclavian retrograde approach seems safe and feasible in inoperable/high-risk patients with AS and peripheral vasculopathy, who are neither eligible for surgical valve replacement nor transfemoral percutaneous aortic valve implantation. Further studies are needed to evaluate the long-term efficacy of this new therapy.

Procedural technical success remains the major limiting factor for CTO PCI, and has been unchanged over time.

Demographic, procedural, and outcome data were collected on 636 consecutive patients between January 2005 and March 2008 having CTO PCI (514 antegrade, 122 retrograde attempts) at 2 U.S. medical centers. Operators were divided into 2 groups: higher CTO volume, retrograde operators (ROs) (>75 total CTO PCI cases and >20 retrograde attempts during the study period) and lower CTO volume, nonretrograde operators (NROs) to evaluate the impact of CTO-specific operator case volume and retrograde techniques on procedural outcomes.

Two operators met the criteria for RO category and 10 were NRO. ROs performed 395 CTO PCI cases (mean total CTO case experience = 197.5, 60 retrograde) and NROs performed 241 CTO PCI cases (mean total CTO case experience = 24.1, <1 retrograde) during the observed timeframe. The overall technical success was 58.9% for NROs and 75.2% for ROs (p < 0.0001). The technical success rate of NROs did not change, but the technical success for the ROs increased to 90% over time (p < 0.0001 for trend, 94.4% for retrograde and 85.7% for antegrade approaches). Observed major adverse events were similar between ROs and NROs.

Complex antegrade and retrograde "Japanese style" PCI approaches can be applied in the U.S. practice environment with high technical success and low adverse event rates. Higher CTO-specific operator case volume is associated with improved technical success rates.

The most common failure mode of CTO interventions remains the inability to successfully cross the occlusion with a guidewire. Recently, the retrograde approach through collateral channels has been introduced to cross complex CTOs.

Between October 2002 and April 2008, IVUS was performed in 48 de novo CTO lesions after guidewire crossing ± pre-dilation with a 1.5- to 2.0-mm balloon. Twenty-three lesions were treated via the antegrade approach (Ante), and 25 lesions were treated via the retrograde approach (Retro).

Right coronary artery (RCA) CTOs were treated more frequently via the Retro technique. Although the CTO length was much longer in the Retro group (45 ± 26 mm vs. 18 ± 9 mm, p < 0.0001), at the end of the procedure Thrombolysis In Myocardial Infarction flow grade 3 was obtained in all patients. There were no significant differences between the 2 groups in minimum stent area and stent expansion. However, the incidence of the composite end point—subintimal wiring, angiographic extravasation, coronary hematoma, or IVUS-detected coronary perforation—was higher in the Retro group (68% vs. 30%, p = 0.01); and the guidewire was more often subintimal in the Retro group (40% vs. 9%, p = 0.02).

The retrograde approach is a promising option for complex CTO segments, especially long RCA CTOs. Intravascular ultrasound can be a useful tool for the detection of procedure-related vessel damage and subintimal wire tracking.

The mode of SVG failure after stenting has been poorly characterized.

The SOS (Stenting Of Saphenous Vein Grafts) trial enrolled 80 patients with 112 lesions in 88 SVGs who were randomized to a BMS or PES. Angiographic follow-up at 12 months was available in 83% of the patients.

Binary angiographic restenosis occurred in 51% (24 of 47) of BMS-treated lesions versus 9% (4 of 43) of PES-treated lesions (p < 0.0001). Graft occlusion occurred in 9 of the 21 SVGs (43%) that failed in the BMS group and in 2 of 4 SVGs (50%) that failed in the PES group. SVG failure after stenting presented as an acute coronary syndrome in 10 of the 24 patients (42%) (7 of those 10 patients presented with non–ST-segment elevation acute myocardial infarction), stable angina in 9 (37%) patients, and without symptoms in 5 (21%) patients. Of the 19 patients (with 20 grafts) who developed symptomatic graft failure, repeat SVG revascularization was successfully performed in all 13 (100%) subtotally obstructed SVGs but was attempted (and successful) in only 1 of 7 (14%) occluded SVGs. Revascularization of a native coronary artery was performed in an additional 4 of 7 (57%) symptomatic patients with an occluded SVG.

SVG failure after stenting often presents as acute myocardial infarction and with SVG occlusion. Compared with BMS, PES reduce SVG failure.

Stenting of small vessels might be associated with higher rates of adverse events.

"All-comer" patients (n = 1,707) were randomized to BES and SES. Post-hoc–stratified analysis of angiographic and clinical outcomes at 9 months and 1 year, respectively, was performed for vessels with reference diameter ≤2.75 mm versus >2.75 mm.

Of 1,707 patients, 429 patients in the BES group with 576 lesions and 434 patients in the SES group with 557 lesions had only small vessels treated (50.6% of the patient cohort). In patients with small vessels there was no significant difference in overall major adverse cardiac events (MACE) rate (12.1% vs. 11.8%; p = 0.89) or target lesion revascularization (TLR) rate (9.6% vs. 7.4%; p = 0.26) between BES and SES. The MACE and TLR rates in the small-vessel patient population were higher than in the large-vessel population. The TLR rate was 9.6% versus 2.6%, and MACE rate was 12.1% versus 7.1% for small versus large vessels in the BES arm (TLR: hazard ratio [HR] = 3.724, p = 0.0013; MACE: HR = 1.720, p = 0.0412). In the SES arm, TLR was 7.4% versus 5.1%, and MACE was 11.8% versus 10.3% in small versus large vessels (TLR: HR = 1.435, p = 0.2594; MACE: HR = 1.149, p = 0.5546).

Prevalence of small vessel disease is high in an "all-comer" population with higher TLR and MACE rates. The BES and SES seem equivalent in treatment outcomes of small vessels in this "all-comer" patient population.

Anticoagulation strategies used in PPI are based primarily on studies of percutaneous coronary intervention where higher doses of heparin are used usually in combination with a glycoprotein IIb/IIIa inhibitor. There are no studies comparing bivalirudin alone versus low-dose heparin in PPI.

Consecutive patients who underwent PPI at our institution were treated with either bivalirudin or low-dose UFH. Patients were assessed prospectively during index hospital stay for procedural success and bleeding complications. Of 236 patients, 111 were dosed with UFH at 50 U/kg (goal activated clotting time of 180 to 240 s), and 125 were dosed with bivalirudin at 0.75-mg/kg/h bolus followed by a 1.75-mg/kg infusion. Procedural success was defined as <20% post-procedure residual stenosis with no flow-limiting dissections or intravascular thrombus formation and major bleeding as intracranial or retroperitoneal hemorrhage or a fall in hemoglobin ≥5 g/dl. Anticoagulation cost analysis was conducted.

Procedural success and major bleeding rates were similar with bivalirudin versus heparin (98% vs. 99% and 2.4% vs. 0.9%, respectively). There were no differences in minor bleeding, time to ambulation, and length of hospital stay. The hospital cost for bivalirudin was $547 and <$1.22 for heparin (10,000 U). Two activated clotting time levels cost $4.00.

Low-dose UFH is as effective and safe as bivalirudin when used as an anticoagulation strategy in patients undergoing PPI, and low-dose UFH is less costly than bivalirudin. Larger randomized studies are required to further evaluate these findings.

Despite the increasing use of stents for interventional treatment for coarctation of the aorta (CoA) in larger patients, use of large stents is controversial in small children.

Methods included bench testing of large stents, and retrospective review of all patients over 1 year of age who had stent implantation for treatment of CoA. Patients were divided into 2 groups based on weight. Paired comparisons were made before and after stent implantation, and group outcomes were compared.

Sixty patients comprised the entire sample, with 22 patients assigned to group I (<30 kg) and 38 patients assigned to group II (≥30 kg). The mean minimum diameters of the CoA (group I 5.0 to 10.7 mm; group II 8.0 to 15.0 mm) and the ratio of the coarctation diameter to the descending aorta diameter measured at the level of the diaphragm (CoA/DAo ratio) (group I 0.4 to 0.93; group II 0.46 to 0.94) increased significantly in both groups (all p < 0.05). The mean systolic gradient decreased significantly in both groups (group I 23.0 to 2.0 mm Hg; group II 24.0 to 2.8 mm Hg; both p = 0.001). No difference was found between the groups in the CoA/DAo ratio, residual systolic gradients, or the decrease in systolic gradient after stent implantation. There were no significant complications in patients under 30 kg.

As in larger patients, use of large stents for treatment of CoA in small children is effective and safe in the short term. In these patients, stent redilations will be required, and follow-up is ongoing.

Teaching courses focusing on live demonstrations of carotid interventions have been the key educational facility for physicians interested in learning state-of-the-art interventional techniques of carotid stenosis treatment. However, starting with the very first live demonstration of interventional procedures, there has been an ongoing discussion whether patients treated during live transmissions are at higher risk.

Between March 1, 2001, and June 30, 2008, 186 high-grade lesions of the internal carotid artery in 186 patients have been treated by stent implantation during live transmissions to 22 interventional conferences at 3 high-volume centers. Technical success was defined as the ability to perform carotid stent implantation. The combined end point of death, major stroke, minor stroke, or myocardial infarction was defined as primary end point.

The procedure was technically successful in 185 of 186 (99.5%) interventions. Seventeen patients had 1 of the following acute in-hospital complications: major stroke in 2 (1.1%), minor stroke in 3 (1.6%), transient ischemic attack in 11 (5.9%), and amaurosis of the ipsilateral eye due to an occlusion of the retinal artery in 1 (0.5%). None of the patients died, and no myocardial infarctions occurred. The composite primary end point occurred in 6 (3.2%) patients.

In this consecutive series of carotid stent cases performed by expert operators during live demonstration courses, the procedural and 30-day clinical outcomes were similar to the results appearing in the contemporary published data.

The AUTAX registry included patients with 2- or 3-vessel disease, with/without previous percutaneous coronary intervention (PCI) and concomitant surgery.

Patients (n = 441, 64 ± 12 years, 78% men) (n = 1,080 lesions) with possible complete revascularization by PCI were prospectively included. Median clinical follow-up was 753 (quartiles 728 to 775) days after PCI in 95.7%, with control angiography of 78% at 6 months. The primary end point was the composite of major adverse cardiac (nonfatal acute myocardial infarction [AMI], all-cause mortality, target lesion revascularization [TLR]) and cerebrovascular events (MACCE). Potential risk factor effects on 2-year MACCE were evaluated using Cox regression.

Complete revascularization was successful in 90.5%, with left main PCI of 6.8%. Rates of acute, subacute, and late stent thrombosis were 0.7%, 0.5%, and 0.5%. Two-year follow-up identified AMI (1.4%), death (3.6%), stroke (0.2%), and TLR (13.1%), for a composite MACCE of 18.3%. The binary restenosis rate was 10.8%. The median of cumulative SYNTAX score was 23.0 (range 12.0 to 56.5). The SYNTAX score did not predict TLR or MACCE, due to lack of scoring of restenotic or bypass stenoses (29.8%). Age (hazard ratio [HR]: 1.03, p = 0.019) and acute coronary syndrome (HR: 2.1, p = 0.001) were significant predictors of 2-year MACCE. Incomplete revascularization predicted death or AMI (HR: 3.84, p = 0.002).

With the aim of complete revascularization, TAXUS stent implantations can be safe for patients with multivessel disease. The AUTAX registry including patients with post-PCI lesions provides additional information to the SYNTAX (Synergy Between Percutaneous Coronary Intervention With TAXUS and Cardiac Surgery) study. (Austrian Multivessel TAXUS-Stent Registry; NCT00738686)

The SYNTAX score has been developed as a combination of several validated angiographic classifications aiming to grade the coronary lesions with respect to their functional impact, location, and complexity.

Between March 2002 and December 2008, 819 patients with left main coronary artery disease underwent revascularization in 2 Italian centers. We compared clinical outcomes of PCI versus CABG in patients with SYNTAX score ≤34 and patients with SYNTAX score >34.

The rates of 2-year mortality were similar between CABG and PCI in the group of patients with SYNTAX score ≤34 (6.2% vs. 8.1%, p = 0.461). Among patients with SYNTAX score >34, those treated with CABG had lower rates of mortality (8.5% vs. 32.7%, p < 0.001) than those treated with PCI. After statistical adjustment, revascularization by PCI resulted in a similar risk of death compared with CABG in patients with SYNTAX score ≤34 (hazard ratio: 0.81, 95% confidence interval: 0.33 to 1.99, p = 0.64) and in a significantly higher risk in patients with SYNTAX score >34 (hazard ratio: 2.54, 95% confidence interval: 1.09 to 5.92, p = 0.031).

A SYNTAX score threshold of 34 may usefully identify a cohort of patients with left main disease who benefit most from surgical revascularization in terms of mortality.

Following a diagnosis of significant ULMCA stenosis in an individual that is a candidate for surgery, CABG is recommended by the American College of Cardiology/American Heart Association guidelines, whereas PCI is not recommended (Class III).

Databases were searched for clinical studies that reported outcomes after PCI and CABG for the treatment of ULMCA stenosis. Ten studies were identified that included a total of 3,773 patients.

Meta-analysis showed that death, myocardial infarction, and stroke (major adverse cardiovascular or cerebrovascular events) were similar in the PCI- and CABG-treated patients at 1 year (odds ratio [OR]: 0.84 [95% confidence interval: 0.57 to 1.22]), 2 years (OR: 1.25 [95% CI: 0.81 to 1.94]), and 3 years (OR: 1.16 [95% CI: 0.68 to 1.98]). Target vessel revascularization was significantly higher in the PCI group at 1 year (OR: 4.36 [95% CI: 2.60 to 7.32]), 2 years (OR: 4.20 [95% CI: 2.21 to 7.97]), and 3 years (OR: 3.30 [95% CI: 0.96 to 11.33]). There was no difference in mortality in PCI- versus CABG-treated patients at 1 year (OR: 1.00 [95% CI: 0.70 to 1.41]), 2 years (OR: 1.27 [95% CI: 0.83 to 1.94]), and 3 years (OR: 1.11 [95% CI: 0.66 to 1.86]).

Our analysis reveals no difference in mortality or major adverse cardiovascular or cerebrovascular events, for up to 3 years, between PCI and CABG for the treatment of ULMCA stenosis. However, PCI patients had a significantly higher risk of target vessel revascularization. In selected patients with ULMCA stenosis, PCI is emerging as an acceptable option.

CKD is an important predictor of prognosis in the general population. The outcomes of patients with CKD and acute coronary syndromes (ACS) have not been well studied.

In the ACUITY study, 13,819 patients with moderate- and high-risk ACS undergoing an early, invasive strategy were randomly assigned to 1 of 3 antithrombin regimens: a heparin plus a GPI, bivalirudin plus a GPI, or bivalirudin monotherapy. CKD (creatinine clearance <60 ml/min) was present in 2,469 (19.1%) of 12,939 randomized patients with baseline creatinine clearance data.

Patients with CKD had worse 30-day and 1-year clinical outcomes than those with normal renal function. There were no significant differences between bivalirudin monotherapy and heparin plus a GPI in rates of 30-day composite ischemia (11.1% vs. 9.4%, p = 0.27) and net clinical adverse outcomes (16.1% vs. 16.9%, p = 0.65). There was remarkably less major bleeding (6.2% vs. 9.8%, p = 0.008) at 30 days, but no significant difference in 1-year composite ischemia (22.0% vs. 18.9%, p = 0.10) or mortality (7.1% vs. 7.3%, p = 0.96).

In patients with ACS, CKD is associated with higher 30-day and 1-year adverse event rates. Compared with heparin plus a GPI, the use of bivalirudin monotherapy in patients with CKD results in nonstatistically different ischemic outcomes, but significantly less 30-day major bleeding.

Increasing numbers of patients undergoing CABG have previously undergone PCI.

We analyzed consecutive first-time isolated CABG procedures within the Australasian Society of Cardiac and Thoracic Surgeons Database from June 2001 to May 2008. Logistic regression and propensity score analyses were used to assess the risk-adjusted impact of prior PCI on in-hospital mortality and major adverse cardiac events. Cox regression model was used to assess the effect of prior PCI on mid-term survival.

Of 13,184 patients who underwent CABG, 11,727 had no prior PCI and 1,457 had prior PCI. Mean follow-up was 3.3 ± 2.1 years. Patients without prior PCI had a higher EuroSCORE value (4.4 ± 3.3 vs. 3.6 ± 3.0, p < 0.001), were older, and more likely to have left main stem stenosis and recent myocardial infarction. There was no difference in unadjusted in-hospital mortality (1.65% vs. 1.55%, p = 0.78) or major adverse cardiac events (3.0% vs. 3.0%, p = 0.99) between patients with or without prior PCI. After adjustment, prior PCI was not a predictor of in-hospital (odds ratio: 1.22, 95% confidence interval [CI]: 0.76 to 2.0, p = 0.41) or mid-term mortality at 6-year follow-up (hazard ratio: 0.94, 95% CI: 0.75 to 1.18, p = 0.62).

In this large registry study, prior PCI was not associated with increased short- or mid-term mortality after CABG. Good outcomes can be obtained in the group of patients undergoing CABG who have had previous PCI.

Although the benefits of both SES and PES are well-established, studies comparing these stents directly have yielded conflicting results.

We used data from the EVENT (Evaluation of Drug Eluting Stents and Ischemic Events) registry to compare in-hospital and 1-year outcomes among unselected patients undergoing nonemergent PCI with either SES or PES implantation.

Between July 2004 and June 2006, 6,035 patients underwent PCI with either SES (n = 3,443) or PES (n = 2,592) at 47 U.S. centers. Baseline clinical and angiographic characteristics were generally similar for the 2 stent types. At 1-year, there were no differences in the primary end point of cardiac death or myocardial infarction (MI) between the SES and PES groups (9.1% vs. 10.0%, p = 0.11) or in any individual end points including cardiac death, nonfatal MI, or stent thrombosis. In unadjusted analyses, target lesion revascularization (TLR) was slightly more common with SES than with PES (4.4% vs. 3.3%, p = 0.048), but this difference was no longer apparent after adjusting for baseline characteristics as well as site-related factors (adjusted hazard ratio: 1.09, 95% confidence interval: 0.78 to 1.50).

Among unselected patients undergoing PCI, adjusted rates of both ischemic complications as well as clinically important restenosis were similar for SES and PES. The unexpected finding that TLR was influenced by site characteristics suggests that the correlation between TLR and angiographic restenosis might be weaker than previously described and warrants further study.

The ENDEAVOR IV (Randomized Comparison of Zotarolimus- and Paclitaxel-Eluting Stents in Patients With Coronary Artery Disease) trial was a randomized controlled study of zotarolimus-eluting, phosphorylcholine-coated, cobalt-alloy stents for the treatment of de novo coronary lesions compared with using PES for the same treatment.

Data were obtained from patients with serial (baseline and 8-months follow-up) intravascular ultrasound analysis available (n = 198). Volumetric analysis was performed for vessel, lumen, plaque, stent, and neointima. Cross-sectional narrowing (given as percentage) was defined as neointimal area divided by stent area. Neointima-free frame ratio was calculated as the number of frames without intravascular ultrasound-detectable neointima divided by the total number of frames within the stent. Subsegment analysis was performed at every matched 1-mm subsegment throughout the stent.

At follow-up, the ZES group showed significantly greater percentage of neointimal obstruction (16.6 ± 12.0% vs. 9.9 ± 8.9%, p < 0.01) and maximum cross-sectional narrowing (31.8 ± 16.1% vs. 25.2 ± 14.9%, p < 0.01) with smaller minimum lumen area than the PES group did. However, the incidence of maximum cross-sectional narrowing >50% was similar in the 2 groups. Neointima-free frame ratio was significantly lower in the ZES group. In overall analysis, whereas the PES group showed positive remodeling during follow-up (13.7 ± 4.2 mm³/mm to 14.3 ± 4.3 mm³/mm), the ZES group showed no significant difference (12.7 ± 3.6 mm³/mm to 12.9 ± 3.5 mm³/mm). In subsegment analysis, significant focal positive vessel remodeling was observed in 5% of ZES and 25% of PES cases (p < 0.05).

There were different global and focal vessel responses for ZES and PES. Both drug-eluting stents showed a similar incidence of lesions with severe narrowing despite ZES having a moderate increase in neointimal hyperplasia compared with neointimal hyperplasia in PES. There was a relatively lower neointima-free frame ratio in ZES, suggesting a greater extent of neointimal coverage. (The ENDEAVOR IV Clinical Trial: A Trial of a Coronary Stent System in Coronary Artery Lesions; NCT00217269)

From a patient's perspective, access site management after percutaneous procedures remains challenging.

Patients enrolled in this multicenter, nonblinded trial underwent 6-F diagnostic or interventional procedures were randomly assigned 2:1 to VCD versus MC. The primary efficacy end points were time to hemostasis (TTH) and time to ambulation (TTA), and the primary safety end points were periprocedural and 30-day incidence of arterial access-related complications.

The trial assigned 401 patients (mean age 62.7 ± 10.9 years, 66.1% men) to VCD (n = 267) versus MC (n = 134) after 87 "roll-in" patients treated at 17 participating institutions. The baseline characteristics of the groups were similar. Procedural success was 91.8% in the VCD versus 91.0% in the MC group (p = NS). Mean TTH was 4.4 ± 11.6 min in the VCD versus 20.1 ± 22.5 min in the MC group (95% confidence interval: 19.0 to 12.3; p < 0.0001). Likewise, TTA was significantly shorter in the VCD (2.5 ± 5.0 h) than in the MC (6.2 ± 13.3 h) group (95% confidence interval: 5.5 to 1.9; p = 0.0028). No patient died or suffered a major access-site-related adverse event. Minor adverse events were few among all study groups.

After 6-F percutaneous invasive procedures, TTH and TTA were both significantly shorter in patients assigned to VCD than in patients managed with MC. The 30-day rates of access-site-related complications were remarkably low in all groups. (Safety and Effectiveness Study of the Ensure Medical Vascular Closure Device; NCT00345631)

Circulating EPCs are involved in physiological processes such as vascular re-endothelialization and post-ischemic neovascularization. However, the success of cell therapies depends on the ability to deliver the cells to the site of injury.

Human EPCs were labeled with iron oxide superparamagnetic nanoparticles. Cell viability and differentiation were tested using flow cytometry. Following finite element modeling computer simulations and flow testing in vitro, angioplasty was performed on rat common carotid arteries to denude the endothelium and EPCs were administered with and without the presence of an external magnetic device for 12 min.

Computer simulations indicated successful external magnetic cell targeting from a vessel with flow rate similar to a rat common carotid artery; correspondingly there was a 6-fold increase in cell capture in an in vitro flow system. Targeting enhanced cell retention at the site of injury by 5-fold at 24 h after implantation in vivo.

Using an externally applied magnetic device, we have been able to enhance EPC localization at a site of common carotid artery injury. This technology could be more widely adapted to localize cells in other organs and may provide a useful tool for the systemic injection of cell therapies.