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Few studies have compared the ability of sodium bicarbonate plus N-acetylcysteine (NAC) and sodium chloride plus NAC to prevent contrast-induced nephropathy (CIN) in diabetic patients with impaired renal function undergoing coronary or endovascular angiography or intervention. Diabetic patients (n = 382) with renal disease (serum creatinine ≥1.1 mg/dl and estimated glomerular filtration rate60 ml/min/1.73 m(2)) were randomly assigned to receive prophylactic sodium chloride (saline group, n = 189) or sodium bicarbonate (bicarbonate group, n = 193) before elective coronary or endovascular angiography or intervention. All patients received oral NAC 1,200 mg 2 times/day for 2 days. The primary end point was CIN, defined as an increase in serum creatinine25% or an absolute increase in serum creatinine ≥0.5 mg/dl within 48 hours after contrast exposure. There were no significant between-group differences in baseline characteristics. The primary end point was met in 10 patients (5.3%) in the saline group and 17 (9.0%) in the bicarbonate group (p = 0.17), with 2 (1.1%) and 4 (2.1%), respectively, requiring hemodialysis (p = 0.69). Rates of death, myocardial infarction, and stroke did not differ significantly at 1 month and 6 months after contrast exposure. In conclusion, hydration with sodium bicarbonate is not superior to hydration with sodium chloride in preventing CIN in patients with diabetic nephropathy undergoing coronary or endovascular angiography or intervention.

Although cilostazol has decreased restenosis and target lesion revascularization (TLR) after drug-eluting stent implantation, it is not known if this effect is durable at 2 years. We analyzed 2 randomized studies (Drug-Eluting stenting followed by Cilostazol treatment reduces LAte REstenosis in patients with DIABETES mellitus and Drug-Eluting Stenting Followed by Cilostazol treatment reduces LAte REstenosis in patients with LONG native coronary lesions trials) in which 900 patients were randomly assigned to triple antiplatelet therapy (aspirin, clopidogrel, and cilostazol; triple group, n = 450) and dual antiplatelet therapy (aspirin and clopidogrel; standard group, n = 450) for 6 months in patients with diabetes or long lesions receiving drug-eluting stents. We evaluated 2-year major adverse cardiac events (MACEs) including death, myocardial infarction (MI), and TLR. Nine-month TLRs and MACEs were significantly decreased in the triple versus standard group. At 2 years, the triple group sowed significantly decreased TLRs (4.2% vs 9.1%, hazard ratio 0.45, 95% confidence interval 0.26 to 0.78, p = 0.004) and MACEs (5.6% vs 10.4%, hazard ratio 0.52, 95% confidence interval 0.32 to 0.84, p = 0.008) compared to the standard group with no differences in death and MI. In subgroup analysis, triple antiplatelet therapy decrease of 2-year TLR was favorable in all subgroups, especially in patients with paclitaxel-eluting stents, diabetes mellitus, small vessels, long lesions, and left anterior descending coronary artery lesions. In conclusion, compared to the standard group, initial benefit in decreases of 9-month TLRs and MACEs in the triple group was sustained at 2 years with no differences in death or MI. Triple antiplatelet therapy decrease of 2-year TLR was favorable in all subgroups, especially in patients with high-risk profiles.

Drug-eluting stents (DESs) are increasingly used for treatment of acute ST-segment elevation myocardial infarction (STEMI), but there are few comparisons of outcomes of various types of DES. We compared the efficacy and safety of zotarolimus-eluting stents (ZESs), sirolimus-eluting stents (SESs), and paclitaxel-eluting stents (PESs) in primary intervention for STEMI. This multicenter, prospectively randomized ZEST-AMI trial included 328 patients at 12 medical centers who were randomly assigned to ZES (n = 108), SES (n = 110), or PES (n = 110) deployment. The primary end point was major adverse cardiac events (death, MI, and ischemia-driven target vessel revascularization) at 12 months. Secondary end points included the individual components of the primary end point, late loss, angiographic restenosis, and stent thrombosis. Baseline clinical and angiographic characteristics were well matched. In-segment late loss (0.28 +/- 0.42 vs 0.46 +/- 0.48 vs 0.47 +/- 0.50 mm, respectively, p = 0.029) and restenosis rate (2.7% vs 15.9% vs 12.3%, respectively, p = 0.027) at 8 months were lowest in the SES group compared to the ZES and PES groups. At 12 months, cumulative incidence rates of primary end points in the ZES, SES, and PES groups were 11.3%, 8.2%, and 8.2%, respectively (p = 0.834). There were 2 acute (in the SES group) and 5 subacute (2 in the SES group and 3 in the PES group) stent thromboses. Incidence of death, recurrent MI, or ischemia-driven target vessel revascularization did not differ among the 3 groups. In conclusion, despite the difference in restenosis rate, the efficacy and safety of the 3 different DESs showed similar, acceptable results in the treatment of STEMI.

To evaluate the impact of cilostazol on neointimal hyperplasia after drug-eluting stent (DES) implantation for long coronary lesions, we performed a randomized multicenter prospective study comparing triple antiplatelet therapy (aspirin, clopidogrel, and cilostazol; triple group, n = 250) and dual antiplatelet therapy (aspirin and clopidogrel; standard group, n = 250) for 6 months in patients with long lesions (or =25 mm) requiring a long DES (or =32 mm). The primary end point was in-stent late loss at 6-month angiography. The 2 groups had similar baseline clinical and angiographic characteristics. In-stent late loss (0.22 +/- 0.48 mm vs 0.32 +/- 0.51 mm, p = 0.031) and in-segment late loss (0.34 +/- 0.49 mm vs 0.51 +/- 0.49 mm, p = 0.001) at 6-month follow-up angiography were significantly lower in the triple group versus the standard group. There was a trend toward lower rates of in-segment restenosis in the triple group versus the standard group (6.7% vs 11.2%, p = 0.104). Target lesion revascularization (TLR; 2.8% vs 6.8%, p = 0.036) and major adverse cardiac events (2.8% vs 7.6%, p = 0.016), including death, myocardial infarction, and TLR at 9 months were significantly lower in the triple group than in the standard group. At 9 months, the 2 groups had similar rates of stent thrombosis (0.4% vs 0.4%, p = 0.999), death (0% vs 0.8%, p = 0.499), and myocardial infarction (0.4% vs 0.4%, p = 0.999). In conclusion, cilostazol significantly reduced late loss at 6 months after DES implantation and the occurrence of TLR and major adverse cardiac events in patients with long coronary lesions.

Angiographic and clinical outcomes remain relatively unfavorable for diabetic patients even after the use of drug-eluting stent. This prospective, multicenter, randomized study compared the relative efficacy and safety of resolute zotarolimus-eluting stent (R-ZES) and sirolimus-eluting stent (SES) implantation in diabetic patients with coronary artery disease. The primary end point was noninferiority of angiographic in-segment late loss at 9 months. Clinical events were also monitored for at least 12 months. Patient recruitment was prematurely stopped after enrollment of 256 patients (127 in R-ZES group and 129 in SES) because of discontinuing production of SES. The R-ZES was noninferior to the SES for 9-month in-segment late loss (0.34 ± 0.30 vs 0.39 ± 0.43 mm; difference -0.048; 95% confidence interval -0.157 to 0.061; upper 1-sided 95% confidence interval 0.044; p0.001 for noninferiority). In addition, in-stent late loss (0.22 ± 0.29 vs 0.21 ± 0.40 mm, p = 0.849) and the rates of in-segment (1.2% vs 6.7%, p = 0.119) and in-stent (1.2% vs 3.3%, p = 0.621) binary restenoses were similar between the 2 groups. At 12 months, there were no statistical differences between the 2 groups in the incidence of any clinical outcomes (death, myocardial infarction, stent thrombosis, ischemia-driven target lesion revascularization, ischemia-driven target vessel revascularization, and composite outcomes). In conclusion, despite having reduced power because of early study termination, our study suggests that the R-ZES has noninferior angiographic outcomes at 9 months to the SES in diabetic patients with coronary artery disease.

We evaluated the influences of minor edge dissections on late angiographic in-stent restenosis in 327 patients with 348 lesions (281 lesions without edge dissection and 67 lesions [19.3%] with edge dissection); the angiographic restenosis rate was 29.9% in the lesions with edge dissections versus 25.3% without edge dissections (p = 0.540). The minor non-flow-limiting dissections at the edge of stents may not be associated with the development of late angiographic in-stent restenosis.

This study evaluates the impact of cilostazol on post-stenting restenosis. Cilostazol is a potent antiplatelet agent with antiproliferative properties. Few data are available about the effect of cilostazol on poststenting restenosis. Four hundred nine patients (494 lesions) who were scheduled for elective stenting were randomized to receive aspirin plus ticlopidine (group I, n = 201, 240 lesions) or aspirin plus cilostazol (group II, n = 208, 254 lesions), starting 2 days before stenting. Ticlopidine was given for 1 month and cilostazol for 6 months. Follow-up angiography was performed at 6 months, and clinical evaluation at regular intervals. Baseline characteristics were similar between the 2 groups. The procedural success rate was 99.6% in group I and 100% in group II. There were no cases of stent thrombosis after stenting. Angiographic follow-up was performed in 380 of the 494 eligible lesions and the angiographic restenosis rate was 27% in group I and 22.9% in group II (p = NS). However, diffuse type in-stent restenosis was more common in group I than in group II (54.2% vs 26.8%, respectively, p0.05). In diabetic patients, the angiographic restenosis rate was 50% in group I and 21.7% in group II (p0.05). Clinical events during follow-up did not differ between the 2 groups. In conclusion, aspirin plus cilostazol seems to be an effective antithrombotic regimen with comparable results to aspirin plus ticlopidine, but it does not reduce the overall angiographic restenosis rate after elective coronary stenting.

The intravascular ultrasound (IVUS) criteria for stent optimization have not been determined in stenting long lesions. We evaluated the predictors of angiographic restenosis and compared it with stent lumen cross-sectional area (CSA) and stent length between short (stent length20 mm) and long (or =20 mm) coronary stenting. IVUS-guided coronary stenting was successfully performed in 285 consecutive patients with 304 native coronary lesions. Six-month follow-up angiogram was performed in 236 patients (82.8%) with 246 lesions (80.9%). Results were evaluated using conventional (clinical, angiographic, and IVUS) methods. The overall angiographic restenosis rate was 22.8% (56 of 246 lesions) (short stent 17.6% vs. long stent 32.2%, p = 0.009). Using multivariate logistic regression analysis, the independent predictors of angiographic restenosis were the IVUS stent lumen CSA (odds ratio 1.51, 95% confidence intervals 1.18 to 1.92, p = 0.001) and stent length (odds ratio 0.95, 95% confidence intervals 0.91 to 1.00, p = 0.039). The angiographic restenosis rate was 54.8% for stent lumen CSA of5.0 mm2 (short stent 37.5% vs. long stent 73.3%, p = 0.049), 27.4% for CSA between 5.0 and 7.0 mm2 (short stent 24.1% vs. long stent 31.7%, p = 0.409), 10.5% for CSA between 7.0 and 9.0 mm2 (short stent 10.0% vs. long stent 12.5%, p = 0.772), and 11.4% for stent lumen CSA ofor =9.0 mm2 (short stent 10.4% vs. long stent 13.3%, p = 0.767) (p = 0.001). Compared with short coronary stenting, long coronary stenting is effective treatment modality to cover long lesions with comparable long-term clinical outcomes in cases of stent lumen CSA ofor =7.0 mm2. Regardless of the stent length, the most important factor determining angiographic restenosis was the IVUS stent lumen CSA in relatively large coronary artery lesions.