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.