Edward M. Kreps

Contribution of Stent Underexpansion to Recurrence After Sirolimus-Eluting Stent Implantation for In-Stent Restenosis

Background—We used intravascular ultrasound (IVUS) to evaluate recurrence after sirolimus-eluting stent (SES) implantation treatment of in-stent restenosis (ISR). Methods and Results—Forty-eight ISR lesions (41 patients with objective evidence of ischemia) were treated with SES. Recurrent ISR was identified in 11 lesions (all focal); repeat revascularization was performed in 10. These were compared with 16 patients (19 lesions) without recurrence as documented by angiography. Nine of 11 recurrent lesions had a minimum stent area (MSA) <5.0 mm2 versus 5 of 19 nonrecurrent lesions (P =0.003); 7 of 11 recurrent lesions had an MSA <4.0 mm2 versus 4 of 19 nonrecurrent lesions (P =0.02); and 4 of 11 recurrent lesions had an MSA <3.0 mm2 versus 1 of 19 nonrecurrent lesions (P =0.03). A gap between SESs was identified in 3 of 11 recurrences versus 1 of 19 nonrecurrent lesions. Conclusions—Stent underexpansion is a significant cause of failure after SES implantation treatment of ISR.

Intravascular ultrasound assessment of ulcerated ruptured plaques: a comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes.

Background—It is not clear why some plaque ruptures lead to acute coronary syndromes (ACS) but others do not. Methods and Results—We analyzed 80 plaque ruptures in 74 patients and compared culprit lesions of ACS patients with nonculprit lesions of ACS patients and lesions of non-ACS patients; both culprit and nonculprit plaque ruptures were studied in 6 of 54 ACS patients. Intravascular ultrasound findings suggesting thrombus were observed more frequently in culprit lesions of ACS patients (n=35) compared with nonculprit lesions of ACS patients (n=19) and lesions of non-ACS patients (n=26): 60% versus 32% versus 8% (P <0.001). At the minimal lumen site, smaller lumen areas (3.3±1.5 versus 5.4±2.6 versus 6.1±2.0 mm2, P <0.001) and greater area stenosis (61±15% versus 50±14% versus 46±18%, P =0.002) and plaque burden (80±8% versus 71±8% versus 69±10%, P <0.001) were observed in culprit lesions of ACS patients compared with nonculprit lesions of ACS patients and lesions of non-ACS patients. Lesions were longer (18.7±6.4 versus 154.9±6.1 versus 12.0±4.9 mm, P <0.001) and rupture site remodeling indices were greater (1.26±0.21 versus 1.24±0.21 versus 1.09±0.05, P =0.002). Independent predictors of culprit plaque ruptures in ACS patients were smaller minimum lumen areas (P =0.02) and presence of thrombus (P =0.01). Conclusions—Ruptured plaques in culprit lesions of ACS patients have smaller lumens; greater plaque burdens, area stenosis, and remodeling indices; and more thrombus. Plaque rupture itself does not lead to symptoms. The association of plaque rupture with a smaller lumen area and/or thrombus formation causes lumen compromise and leads to symptoms.

Nonuniform Strut Distribution Correlates With More Neointimal Hyperplasia After Sirolimus-Eluting Stent Implantation

Background—Little is known about causes of intimal hyperplasia (IH) after sirolimus-eluting stent (SES) implantation. Methods and Results—Intravascular ultrasound was performed in 24 lesions with intra-SES restenosis and a comparison group of 25 nonrestenotic SESs. To assess stent strut distribution, the maximum interstrut angle was measured with a protractor centered on the stent, and the visible struts were counted and normalized for the number of stent cells. In SES restenosis patients, minimum lumen site was compared with image slices 2.5, 5.0, 7.5, and 10.0 mm proximal and distal to this site. The minimum lumen site had a smaller IVUS lumen area at follow-up (2.7±0.9 versus 6.2±1.9 mm2; P<0.01), larger maximum interstrut angle (135±39° versus 72±23°; P<0.01), larger IH area (3.4±1.5 versus 0.6±1.1 mm2; P<0.01) and thickness (0.7±0.3 versus 0.1±0.2 mm; P<0.01) at maximum interstrut angle, and fewer stent struts (4.9±1.0 versus 6.0±0.5; P<0.01) even when normalized for the number of stent cells (0.78±0.15 versus 0.97±0.07; P<0.01). Compared with nonrestenotic SES, the restenosis lesions also had a smaller minimal lumen area, larger IH area, thicker IH at maximum interstrut angle, fewer stent struts, and larger maximum interstrut angle. Multivariate analysis identified the number of visualized stent struts normalized for the number of stent cells and maximum interstrut angle as the only independent IVUS predictor of IH cross-sectional area (P<0.01 and P<0.01), minimum lumen area (P<0.01 and P<0.01), and IH thickness (P<0.01 and P<0.01). Conclusions—The number and distribution of stent struts affect the amount of neointima after SES implantation.

Intravascular ultrasound assessment of the incidence and predictors of edge dissections after drug-eluting stent implantation.

OBJECTIVES We used intravascular ultrasound (IVUS) to assess incidence, predictors, morphology, and angiographic findings of edge dissections after drug-eluting stent (DES) implantation. BACKGROUND DES implantation strategies differ compared with bare-metal stenting; coronary dissections after DES implantation have not been well studied. METHODS We studied 887 patients with 1,045 non-in-stent restenosis lesions in 977 native arteries undergoing DES implantation with IVUS imaging. RESULTS 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 mm(2) vs. 5.2 +/- 3.0 mm(2), 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 > or =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 mm(2) vs. 8.9 +/- 4.6 mm(2), 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). CONCLUSIONS 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.

Comparison of Angiographic and Intravascular Ultrasonic Detection of Myocardial Bridging of the Left Anterior Descending Coronary Artery

The purpose of this study was to determine the incidence, location, and clinical features of myocardial bridging (MB) detected by intravascular ultrasound (IVUS) and to compare IVUS-detectable versus angiographically detectable MBs. IVUS images were analyzed in 331 consecutive patients with de novo coronary lesions located in the left anterior descending coronary artery (LAD). MB was defined as a segment of coronary artery having systolic compression and echocardiographically lucent muscle surrounding the artery (IVUS) or systolic milking (angiography). Although angiography detected MB in only 3% of patients (11 of 331), 75 MB segments (23%, 75 of 331, p <0.001) were identified by IVUS. Maximum plaque burden within the MB segment measured only 25 +/- 7%, and abnormal intimal thickness (defined as >or=0.5 mm) was not observed within the bridged segment of any patient with MB, although the study population had advanced atherosclerosis. Vessel and lumen areas in the MB segment were significantly smaller than those in adjacent proximal and even distal reference segments. Angiographically detectable MB was significantly longer, located more proximally in the LAD, and had more severe systolic compression by IVUS. Angiographically silent MB more often occurred in the presence of an adjacent proximal stenosis and lower left ventricular ejection fraction. In conclusion, IVUS may provide useful anatomic information for the accurate diagnosis of MBs that are largely angiographically silent. IVUS-detectable MBs were observed in approximately 1/4 of patients undergoing LAD imaging at our center.

Relation between single tomographic intravascular ultrasound image parameters and intracoronary Doppler flow velocity in patients with intermediately severe coronary stenoses

BACKGROUND Intravascular ultrasound (IVUS) imaging parameters have been suggested as criteria to determine coronary lesion significance before intervention. However, there has not been a systematic examination of combined anatomic and physiologic data in the same patients with coronary artery disease. METHODS AND RESULTS To examine the relation between coronary flow reserve and IVUS parameters, 41 patients with intermediately severe coronary artery stenoses had measurements of coronary flow velocity (0.014-inch Doppler flow wire), coronary flow velocity reserve (CVR) (hyperemic/basal mean flow), IVUS imaging (2.9F, Cardiovascular Imaging Systems, Inc.), and quantitative coronary angiography before intervention. Correlations between physiologic and anatomic parameters were performed by simple regression. Results were also examined by patient subgroups with CVR > 1.8 or < 1.8 to assess differences in IVUS parameters. The angiographic percent diameter stenosis was 52% +/- 17% (range 18% to 95%). Mean CVR was 1.88 +/- 0.56 (range 0.9 to 3.18). IVUS minimal luminal diameter (r = 0.312, p = 0.047) and angiographic percent stenosis (r = 3.05, p = 0.052) were weakly related to poststenotic CVR. Comparing patients with CVR < 1.8, IVUS reference segment area, IVUS lumen area, and angiographic percent diameter stenosis was higher (17.7 +/- 0.3 vs 12.9 +/- 4.4 mm2, p < 0.05; 6.20 +/- 3.76 vs 4.34 +/- 2.00 mm2, p < 0.05; and 60% +/- 14% vs 46% +/- 17%, p < 0.01, respectively) than in the group with CVR > 1.8. CONCLUSIONS Despite a precise determination of cross-sectional vessel areas and absolute dimensions by IVUS, single tomographic measurements did not correlate well with coronary physiologic responses. These data suggest that the physiologic data may be complementary to anatomic quantitative IVUS, enhancing information for coronary interventional decision making.

Correlation of coronary arterial remodeling determined by intravascular ultrasound with angiographic diameter reduction of 20% to 60%

Negative remodeling is commonly observed in stenotic coronary lesions. It is unknown whether negative remodeling is an early or late event. This study was designed to elucidate when negative remodeling occurs in the development of coronary stenosis. Remodeling was assessed by preintervention intravascular ultrasound in 104 native coronary lesions with intermediate stenosis (20% to 60% of diameter stenosis measured by quantitative coronary angiography). Positive remodeling was defined as lesion external elastic membrane (EEM) cross-sectional area (CSA) greater than the proximal reference, intermediate remodeling as lesion EEM CSA between those of the proximal and distal references, and negative remodeling as lesion EEM CSA less than the distal reference. Positive, intermediate, and negative remodeling were observed in 18%, 32%, and 50%, respectively, of lesions with intermediate stenosis. Lesions with negative and intermediate remodeling had more hard plaque compared with those with positive remodeling (79% vs 70% vs 42%, p = 0.02). Calcium was more frequent in lesions with negative and intermediate remodeling than in those with positive remodeling (52% vs 55% vs 16%, p = 0.01). Lesions with negative remodeling had smaller EEM CSA (11.5 +/- 5.2 vs. 13.7 +/- 3.4 vs 14.5 +/- 5.6 mm(2), p = 0.03) and less plaque (7.9 +/- 4.6 vs 10.8 +/- 3.4 vs 10.8 +/- 4.9 mm(2), p = 0.004) compared with positive and intermediate remodeling lesions, although lumen CSA (3.7 +/- 1.7 vs 2.8 +/- 0.8 vs 3.6 +/- 1.3 mm(2), p = 0.1) and area stenosis (57 +/- 15% vs 59 +/- 14% vs 56 +/- 10%, p = 0.7) were similar. Negative remodeling is frequently observed in lesions with intermediate stenosis. This suggests that negative remodeling occurs early in lesion formation.

Luminal narrowing due to intramural hematoma shift from left anterior descending coronary artery to left circumflex artery

This case report demonstrates subacute luminal narrowing 20 days after balloon angioplasty in the left anterior descending coronary artery due to an intramural hematoma. Stenting was performed and resulted in side‐branch compromise caused by squeezing the hematoma from the left anterior descending coronary artery into the left circumflex artery. Another stent was deployed to treat the stenosis in the left circumflex artery. Catheter Cardiovasc Interv 2004;62:461–465.

Does genetic polymorphism for platelet glycoprotein illa impact early and long-term outcomes after elective percutaneous coronary interventions?

Background: Genetic polymorphism (PI A2) of the platelet GPllla protein has been associated with increased thrombosis and myocardial infarctnon compared to the Al Al status; the rare A2A2 status confers the greatest risk, while the AlAZ status confers rather modest risk. The association of PI A2 with adverse events after percutaneous coronary intervention (PCI) is unknown. Patients and Methods: We followed 153 consecutive patients with normal baseline CKMB, who underwent elective PCI for symptomatic coronary artery disease for 1 year. All patients were tested for PI A2 polymorphism. Adverse events were recorded and adjudicated by an independent committee blinded to the polymorphism status. All patients received ASA and Clopidogrel for one month post PCI. Results: The normal (AIAI) and heterozygous (Al AZ) variants were found in 106 (70.6%) and 45 (29.4%) of the patients respectively; the homozygous variant was not detected in this population. Baseline patient and lesion characteristics, as well as platelet aggregation assay, maximum activated cloting time value and use of GP Ilb/llla blockers were similar between the 2 groups. There were no differences in outcome between groups (Table). Conclusions: Heterozygous genetic polymorphism PI Al A2 was found in approximately one third of patients undergoing elective PCI and it was not associated with any increase in early or late adverse outcomes after PCI compared to the normal homozygous PI AIAI status.