Faculty Bibliography

BACKGROUND: The relationship between low hematocrit and contrast-induced nephropathy has not been investigated. METHODS: Of 6,773 consecutive patients treated with percutaneous coronary intervention, contrast-induced nephropathy (an increase of >/=25% or >/=0.5 mg/dL in preprocedure serum creatinine, at 48 hours postprocedure) occurred in 942 (13.9%) patients. RESULTS: Rates of contrast-induced nephropathy steadily increased as baseline hematocrit quintile decreased (from 10.3% in the highest quintile to 23.3% in the lowest quintile) (chi(2) for trend, P < 0.0001). Stratification by baseline estimated glomerular filtration rate (eGFR) and baseline hematocrit showed that the rates of contrast-induced nephropathy were the highest (28.8%) in patients who had the lowest level for both baseline eGFR and hematocrit. Patients with the lowest eGFR but relatively high baseline hematocrit values had remarkably lower rates of contrast-induced nephropathy (15.8%, 12.3%, 17.1%, and 15.4% in 2nd, 3rd, 4th, and 5th quintiles of baseline hematocrit, respectively) (P < 0.0001). The rates of contrast-induced nephropathy increased with increment in change in hematocrit. Patients in the lowest quintile of baseline hematocrit with absolute hematocrit drop >5.9% had almost doubled rates of contrast-induced nephropathy compared with patients with hematocrit change <3.4% (38.1% vs. 18.8%, respectively) (P < 0.0001). By multivariate analysis, lower baseline hematocrit was an independent predictor of contrast-induced nephropathy; each 3% decrease in baseline hematocrit resulted in a significant increase in the odds of contrast-induced nephropathy in patients with and without chronic kidney disease (11% and 23%, respectively). When introduced into the multivariate model instead of baseline hematocrit, change in hematocrit also showed a significant association with contrast-induced nephropathy. CONCLUSION: Lower hematocrit is an important risk factor for contrast-induced nephropathy. Whether correcting the hematocrit prepercutaneous coronary intervention might decrease the rates of contrast-induced nephropathy should be addressed in a prospectively designed trial

Intravascular ultrasound (IVUS) evaluation was performed in 33 lesions with sirolimus-eluting stent (SES) failure: 4 thromboses, 26 in-stent restenoses (including 6 edge stenoses), 4 new stenoses >5 mm proximal to the stent, and 1 patient with no evidence of the implanted SES (presumably because of embolization). A minimum stent area <5.0 mm(2) (stent underexpansion) was observed in 67% of all SES failures (in particular, 67% of intrastent restenosis); negative remodeling was observed in 4 of 6 stent edge restenoses, and new lesions were secondary to an increase in plaque area

OBJECTIVES: We sought to determine the predictors of stent thrombosis after sirolimus-eluting stent (SES) implantation. BACKGROUND: A number of cases of stent thrombosis have been reported after commercial release of the SES in the 'real world,' such that the U.S. Food and Drug Administration issued a warning. METHODS: Fifteen patients who developed stent thrombosis after successful SES implantation were analyzed and compared with 45 matched control patients who had no evidence of stent thrombosis. RESULTS: Minimum stent cross-sectional area (MSA) (4.3 +/- 1.6 mm(2) vs. 6.2 +/- 1.9 mm(2), p < 0.001) and stent expansion (0.65 +/- 0.18 vs. 0.85 +/- 0.14, p < 0.001) were significantly smaller in the stent thrombosis group than in the matched control patients. There was no significant difference in the rate of SES malapposition between the groups. However, the presence of a significant residual reference segment stenosis was more common in the stent thrombosis group compared with the matched control group (67% vs. 9%, p < 0.001). Independent predictors of stent thrombosis were stent underexpansion (p = 0.03) and a significant residual reference segment stenosis (p = 0.02). CONCLUSIONS: Stent underexpansion and residual reference segment stenosis are associated with stent thrombosis after successful SES implantation

We used intravascular ultrasound (IVUS) to assess the accuracy of manufacturers' stent balloon compliance charts. Many interventional cardiologists rely on manufacturers' compliance charts to select stent size and optimize stent diameters according to inflation pressures during percutaneous procedures. We randomly selected 212 patients who had de novo coronary lesions that had been treated with a single, bare metal, > or =3.0-mm stent (Bx velocity, NIR, TETRA/PENTA, S660/S670/S7) under IVUS guidance. Cases of stent overlap and postdilatation with another balloon were excluded. Predicted stent diameters were derived from each manufacturer's compliance charts, and stent size and final maximal deployment pressures were derived from each physician's report. IVUS-measured minimum stent diameters (range 1.4 to 4.0 mm, mean 2.79 +/- 0.48) were smaller than predicted diameters (range 3.1 to 4.57 mm, mean 3.79 +/- 0.44). The ratio of IVUS to predicted diameters ranged from 44% to 97% (mean 74 +/- 10%). This finding was common to all 3 stent sizes: 74 +/- 12% for 3.0 mm, 73 +/- 9% for 3.5 mm, and 74 +/- 9% for 4.0-mm stents (p = 0.9). This finding was also common to all 4 stent manufacturers, 72 +/- 8% for Boston Scientific, 76 +/- 11% for Guidant, 73 +/- 9% for Cordis, and 74 +/- 11% for Medtronic (p = 0.13), and to different stent lengths. Only 3.8% of the stents achieved 90% of the predicted minimum stent diameters, and only 24.6% achieved 80% of the predicted minimum stent diameters. In conclusion, in human coronary arteries, minimal stent diameter measured by IVUS is significantly smaller than that predicted by in vitro compliance charts. These differences are independent of stent manufacturer, length, diameter, and deployment pressure

Coronary calcium is intimately associated with coronary atherosclerotic plaque development, although it is controversial as to whether coronary calcium is associated with plaque instability. We analyzed 101 IVUS-detected ruptured plaques and compared them with 101 computer-matched control plaques without evidence of plaque rupture. The arc of calcium was measured every 0.5 mm within 10-mm-long segments that spanned the minimum lumen cross-sectional area, and the number and length of calcium deposits were assessed. Ruptured plaques had a significantly larger number of individual calcium deposits than control plaques (3.5 +/- 1.7 vs 1.8 +/- 1.1, p <0.001). However, the arc of the largest calcium deposit was smaller and the length of the largest calcium deposit in each plaque was shorter in ruptured plaques compared with control plaques (67.3 degrees +/- 41.4 degrees vs 114.9 degrees +/- 77.4 degrees , p <0.001, and 1.6 +/- 1.3 vs 4.0 +/- 2.7 mm, p <0.001, respectively). There was no difference in the number of superficial calcium deposits between the 2 groups, although ruptured plaques had significantly smaller arcs of superficial calcium compared with control plaques (56.2 degrees +/- 35.5 degrees vs 95.8 degrees +/- 65.2 degrees , p <0.001). Conversely, the number of deep calcium deposits was significantly larger in ruptured plaques than in control plaques (1.8 +/- 1.4 vs 0.3 +/- 0.6, p <0.001), although the arc of deep calcium was similar in the 2 groups. Ruptured plaques had quantitatively less calcium, especially superficial calcium, but a larger number of small calcium deposits, especially deep calcium deposits. In conclusion, ruptured plaques are associated with a larger number of calcium deposits within an arc of <90 degrees , a larger number of deep calcium deposits, and a remodeling index

Larger final lumen dimensions after percutaneous coronary interventions in native coronary arteries lead to lower restenosis rates. We sought to determine the impact of stent expansion, as assessed by intravascular ultrasound, on clinical results of stent implantation in saphenous vein grafts (SVGs). We identified 226 consecutive patients who underwent intravascular ultrasound-guided stenting of 234 de novo SVG lesions. Patients were divided into 2 groups based on the final stent cross-sectional area (CSA): group I (stent CSA <100% of the reference lumen CSA, n = 176 patients, 182 lesions) and group II (stent CSA >/=100% of the reference lumen CSA, n = 50 patients, 52 lesions). Baseline patient characteristics were similar between the 2 groups with the exception of smaller lesions in group II. More aggressive stent expansion (group II) was associated with (1) increased rates of in-hospital non-Q-wave myocardial infarction (29% vs 17%, p = 0.05), (2) any myocardial infarction (26% vs 8%, p = 0.003) at 1-year follow-up, and (3) no improvement in target vessel revascularization at 1 year (31% vs 26%, p = 0.3). Aggressive stent expansion in SVG lesions resulted in higher myocardial infarction rates and, unlike native arteries, no improvement in target vessel revascularization rate at 1 year. A less aggressive stent implantation strategy in SVGs than in native coronary lesions appears prudent

The purpose of this study was to compare the clinical outcomes of stenting and minimally invasive coronary artery bypass grafting (MIDCAB) in patients with proximal left anterior descending (LAD) coronary artery disease. The Patency, Outcome, Economics of Minimally invasive direct coronary bypass (POEM) study demonstrated that MIDCAB had similar safety and long-term efficacy for LAD revascularization compared with conventional coronary artery bypass grafting. Although LAD stenting is superior to conventional balloon angioplasty, whether it is comparable to MIDCAB is not known. We identified a matched population of 429 consecutive patients with 1-vessel disease who underwent elective proximal LAD stenting and compared their clinical outcomes with those of the 152 patients in the MIDCAB group of the POEM study. The in-hospital event rate was similar in both groups, except for a shorter length of hospital stay with LAD stenting compared with MIDCAB (2.68 vs 4.07 days, p <0.0001). At 6-month follow-up, the incidence of death and Q-wave myocardial infarction or that of cerebrovascular accident was not significantly different between these 2 groups. However, target vessel revascularization was significantly higher with LAD stenting than MIDCAB (13.3% vs 6.6%, p = 0.045). In the subgroup of patients without diabetes, all clinical events were similar in both groups, and the benefit of a shorter hospital stay associated with stenting was maintained. Compared with MIDCAB, LAD stenting is associated with higher repeat revascularization rates but offers the advantage of shorter hospitalization. For nondiabetics with proximal LAD disease, stenting may be the revascularization strategy of choice

We evaluated the outcomes of 177 consecutive patients (43 women, 134 men) <40 years of age with premature atherosclerosis who underwent percutaneous coronary intervention. Women were younger, had more diabetes mellitus (37% vs 10%; p <0.001), but less hyperlipidemia (58% vs 75%; p <0.001) compared with men. In-hospital vascular complications and 1-year mortality rate or Q-wave myocardial infarction (7.9% vs 0.08%, p <0.01) were higher in women. By multivariable regression analysis, female gender was the only independent predictor of vascular complications (odds ratio, 14.1; 95% confidence intervals, 1.59 to 125, p = 0.01) and of 1-year mortality rate or nonfatal myocardial infarction (odds ratio, 12.5; 95% confidence interval, 1.14 to 111, p = 0.03). Women with premature coronary disease had a distinctive risk factor profile relative to men, with a predominance of diabetes and hypercholesterolemia, and were at higher risk of developing vascular and ischemic complications after percutaneous coronary intervention, warranting aggressive risk factor modification and vigilance in this population