Biomedical subjects

Gary S Mintz

Publications and source records attributed to Gary S Mintz.

At least 19 recordsLinked to original sources

PubMed2006

Two-year follow-up of the quantitative angiographic and volumetric intravascular ultrasound analysis after nonpolymeric paclitaxel-eluting stent implantation: late "catch-up" phenomenon from ASPECT Study.

OBJECTIVES: This study used serial angiographic and intravascular ultrasound (IVUS) analysis to evaluate the long-term efficacy of a nonpolymeric, paclitaxel-eluting stent coating on intimal hyperplasia (IH) 2 years after implantation. BACKGROUND: Long-term efficacy of patients treated with nonpolymeric paclitaxel-eluting stents beyond 1 year has not been well determined. METHODS: Patients were randomized to placebo or 1 of 2 doses of paclitaxel (low dose, 1.28 microg/mm2; high dose, 3.10 microg/mm2). Complete after-procedure, 6-month, and 2-year angiographic and IVUS data were available in 53 patients (17, 17, and 19 patients, respectively). RESULTS: Baseline characteristics were similar among the 3 groups. Although 6-month minimal luminal diameter (MLD) was significantly smaller in placebo compared with paclitaxel-eluting stent patients (1.9 +/- 0.6 mm in placebo, 2.5 +/- 0.6 mm in low-dose, and 2.6 +/- 0.5 mm in high-dose patients, p = 0.004), the MLDs at 2 years were similar (2.3 +/- 0.6 mm, 2.3 +/- 0.7 mm, and 2.0 +/- 0.8 mm, respectively, p = 0.4). Despite a stepwise reduction in IH accumulation at 6 months (23 +/- 18 mm3 in placebo, 14 +/- 11 mm3 in low-dose, and 10 +/- 12 mm3 in high-dose, p = 0.017), the increase of IH volume from 6 months to 2 years was significantly greater in the high-dose patients (13 +/- 14 mm3 in high-dose vs. 4 +/- 7 mm3 in low-dose patients, p = 0.074; and vs. 1 +/- 13 mm3 in placebo, p = 0.019). Late target lesion revascularization (beyond 1 year) was performed in 2 high-dose patients. CONCLUSIONS: Despite the suppression of IH after non-polymeric paclitaxel-eluting stents compared with bare-metal stents at 6 months, a "late catch-up" IH growth was found in the high-dose patients at 2-year follow-up.

Coronary Angiography↗

PubMed2006

Volumetric intravascular ultrasound assessment of neointimal hyperplasia and nonuniform stent strut distribution in sirolimus-eluting stent restenosis.

The neointimal hyperplasia (IH) distribution pattern of in-stent restenotic lesions after sirolimus-eluting stent (SES) implantation has not been well described. We identified 48 in-stent restenotic lesions (41 patients) after SES implantation and performed volumetric intravascular ultrasound analyses. Lumen area, stent area, and IH area at the minimal lumen area site were 2.7 +/- 1.0, 5.4 +/- 1.9, and 2.7 +/- 1.4 mm(2), respectively. IH area at the minimal lumen site was larger in the group with a stent area > or =5.0 mm(2) than the group with a stent area <5.0 mm(2) (3.7 +/- 1.3 vs 1.9 +/- 0.8 mm(2), p <0.001). There were fewer visualized stent struts in lesions with a minimum stent area > or =5.0 mm(2) at the minimum lumen site compared with those with a stent area <5.0 mm(2) (0.69 +/- 0.25 vs 0.83 +/- 0.16, p = 0.04). When we compared lesions in patients with diabetes mellitus with patients without diabetes, minimum lumen areas, percent IH at minimal lumen area, percent IH, and neointima-free stent length were identical. In conclusion, (1) lesions without SES underexpansion at the minimum lumen site had more IH and greater nonuniform stent strut distribution compared with restenotic SESs that were underexpanded, and (2) the IH response did not appear to be more aggressive in patients with diabetes mellitus than in those without diabetes mellitus.

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PubMed2006

Relation between plaque progression and low-density lipoprotein cholesterol during aging as assessed with serial long-term (> or =12 months) follow-up intravascular ultrasound of the left main coronary artery.

Because of the clinical benefit of lipid lowering in older patients, we hypothesized that the relation between low-density lipoprotein (LDL) cholesterol serum levels and coronary plaque progression may persist throughout aging. We analyzed serial intravascular ultrasound (IVUS) data of 60 left main stems (18 +/- 9 months apart) and evaluated the relation between LDL cholesterol levels and coronary plaque progression at different ages. The population (n = 60) was divided into 3 groups according to age: tertile 1 (n = 20) was a mean age of 48 +/- 6 years (median 51, range 33 to 55), tertile 2 (n = 20) was a mean age of 58 +/- 2 years (median 59, range 55 to 61), and tertile 3 (n = 20) was a mean age of 66 +/- 6 years (median 65, range 61 to 83). Between groups, there was no significant difference in non-age-related demographics, clinical data, lipid profiles, or medications (e.g., statins). There was a positive linear relation between LDL cholesterol and annual changes in plaque plus media area in all age tertiles, which was statistically significant in tertiles 2 and 3 (r = 0.56, p <0.01; r = 0.50, p <0.02) and showed a strong trend in tertile 1 (r = 0.41, p = 0.07). The estimated LDL cholesterol thresholds, which, as determined by regression analysis, would correspond to no plaque progression, were 74, 60, and 78 mg/dl, respectively, in tertiles 1, 2, and 3. In conclusion, serial IVUS data in left main coronary arteries suggest that the relation between LDL cholesterol serum levels and plaque progression persists during aging.

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PubMed2006

Frequency and severity of plaque prolapse within Cypher and Taxus stents as determined by sequential intravascular ultrasound analysis.

We used intravascular ultrasound to evaluate the incidence, characteristics, and clinical sequel of plaque prolapse within drug-eluting stents. The influence of stent design on plaque prolapse has not been studied. Drug-eluting stents were serially expanded, first at 14 atm and then at 20 atm, with intravascular ultrasound imaging after each inflation. The stent, lumen, and maximum plaque prolapse areas were measured. The residual lumen area and percentage of plaque prolapse burden (maximum plaque prolapse area/stent area) were calculated. Plaque prolapse was divided into grades 1 (<5%), 2 (5% to 10%), and 3 (10% to 20%). Eighty patients (83 lesions, 41 Cypher and 42 Taxus Express stents) were studied. The incidence of plaque prolapse was 41% (17 of 41 lesions) with the Cypher stents versus 24% (10 of 41 lesions) with the Taxus stents after 14 atm (p = 0.096) and 35% (14 of 40) in Cypher stents versus 17.8% (5 of 28) in Taxus stents after 20 atm (p = 0.17). However, the maximum plaque prolapse area was never >20% of the stent area. The frequency and amount of plaque prolapse neither increased nor decreased at higher (20 atm) inflation pressures. Lesions with prolapse were longer (p = 0.004), with a larger external elastic membrane area and greater plaque burden (each p <0.0001) and a larger remodeling index (p = 0.013). Conversely, nonprolapsed plaques had a higher incidence of superficial calcium (p = 0.001). Creatinine kinase-MB elevation was higher with plaque prolapse, and the magnitude of creatinine kinase-MB elevation correlated with the extent of plaque prolapse (r = 0.664, p = 0.002). Multiple logistic regression analysis indicated that a longer lesion length (p = 0.012), and smaller minimal luminal area (p = 0.031) had higher risks of plaque prolapse. In conclusion, plaque prolapse was frequently observed in Cypher and Taxus stents. However, sequential intravascular ultrasound imaging showed that the frequency and amount of plaque prolapse were neither increased nor decreased by additional higher pressure inflations.

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PubMed2006

Effect of plaque volume on subsequent vessel remodeling at edges of sirolimus-eluting stents.

Serial (baseline and 9-month follow-up) intravascular ultrasound analysis was performed at 5-mm reference segments immediately proximal and distal to the sirolimus-eluting stent (SES) in 33 lesions. Proximal and distal reference segments were divided into 1-mm subsegments. Between postintervention and follow-up intravascular ultrasound studies, there were significant decreases in the lumen and increases in plaque & media areas in the subsegment closest to the distal edge, with no change in external elastic membrane area. There was no significant change in external elastic membrane, lumen, and plaque & media areas within the other subsegments. At the nearest 1-mm subsegment from the proximal and distal edges, baseline plaque & media area was associated with subsequent vessel remodeling. In conclusion, a large amount of plaque at the SES edge may be a risk of negative remodeling at follow-up (stent edge restenosis). It supports the importance of "normal-to-normal" SES deployment.

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PubMed2006

Relation between lipoprotein(a) and fibrinogen and serial intravascular ultrasound plaque progression in left main coronary arteries.

OBJECTIVES: Patients with elevated lipoprotein(a) [Lp(a)] and fibrinogen levels have an increased risk of coronary heart disease and adverse cardiovascular events. There is evidence that coronary plaque progression is linked to a higher risk for future cardiovascular events. BACKGROUND: There are no data demonstrating a relation between Lp(a), fibrinogen, and directly measured coronary plaque progression over time. METHODS: We performed a retrospective analysis of serial intravascular ultrasound (IVUS) studies of 60 left main stems (18 +/- 9 months apart) to evaluate plaque progression in relation to Lp(a) and fibrinogen levels and association with adverse cardiovascular events. RESULTS: There was a positive correlation between Lp(a) (r = 0.58; p < 0.0001), fibrinogen (r = 0.48; p < 0.0001), and changes in plaque-plus-media area. Patients with plaque progression (n = 41) had higher Lp(a) (30 +/- 26 mg/dl vs. 14 +/- 9 mg/dl; p < 0.0012) and fibrinogen (295 +/- 88 mg/dl vs. 240 +/- 72 mg/dl; p = 0.019) levels than patients with plaque regression (n = 19). Multivariate linear regression analysis showed Log Lp(a) (regression coefficient = 9.45; p = 0.0008) but not fibrinogen to be independently associated with plaque progression. A total of 19 patients suffered from adverse cardiovascular events; they had higher Lp(a) (44 +/- 30 mg/dl vs. 16 +/- 12 mg/dl; p < 0.0001) and fibrinogen (342 +/- 73 mg/dl vs. 248 +/- 76 mg/dl; p < 0.0001) levels. Multivariate logistic regression analysis showed Log Lp(a) (odds ratio 10.20, 95% confidence interval 2.36 to 44.13; p = 0.0019) and fibrinogen (odds ratio 1.01, 95% confidence interval 1.00 to 1.03; p = 0.018) were independently associated with adverse cardiovascular events. CONCLUSIONS: Serial IVUS showed a positive correlation between Lp(a) and fibrinogen levels and plaque progression. Lp(a), but not fibrinogen, remains independently associated with plaque progression. In addition, the present data suggest a considerable incremental value of Lp(a) in predicting cardiovascular risk.

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PubMed2006

Intravascular ultrasound in the drug-eluting stent era.

Intravascular ultrasound (IVUS) has become an indispensable part of all drug-eluting stent (DES) studies; findings must be put into context with the IVUS findings in bare metal stents. Unfortunately, there is not yet a complete picture of either the Cypher (Cordis, Miami, Florida) or the Taxus (Boston Scientific, Maple Grove, Minnesota) stent (the two U.S. Food and Drug Administration-approved devices). Intimal hyperplasia volume in DES is reduced to <15% of stent volume, but stent underexpansion continues to be a consistent finding in DES failures (restenosis and thrombosis). The utility of IVUS to assure adequate stent expansion may be more important whenever there are clinical risk factors for DES failure.

Cardiology↗

PubMed2006

Negative remodeling and calcified plaque in octogenarians with acute myocardial infarction: an intravascular ultrasound analysis.

OBJECTIVES: The goal of this study was to use intravascular ultrasound (IVUS) to compare octogenarians versus patients <65 years of age with regard to culprit lesion morphology in acute myocardial infarction (MI). BACKGROUND: Although octogenarians represent the fastest-growing segment of our population and have a higher risk profile, they are underrepresented in therapeutic trials. METHODS: Between 2002 and 2005, 42 octogenarians and 52 patients <65 years of age underwent pre-intervention IVUS within 2 days from onset of an MI. Qualitative and quantitative measurements were performed at the lesion site and at the proximal and distal references. Positive remodeling was defined as a remodeling index (lesion/mean reference arterial area) > or =1. RESULTS: Elderly patients mostly (71%) presented with non-ST-segment elevation myocardial infarction (NSTEMI), whereas patients <65 years of age presented almost equally with ST-segment elevation myocardial infarction (STEMI) and NSTEMI (56% vs. 44%). The frequency of rupture/dissection was greater in the <65-year-old group (32% vs. 9%, p = 0.009), and culprit lesions contained more thrombus in this group (14% vs. 2%, p = 0.04). Conversely, in octogenarians, lesions were predominantly calcified (57% vs. 10%, p < 0.001) and longer (20.9 +/- 7.8 mm vs. 16.6 +/- 6.1 mm, p = 0.004) with less positive remodeling (19% vs. 56%, p < 0.001). On multivariant logistic regression analysis, age was the only independent predictor of calcified plaque (p = 0.02) and remodeling (p = 0.005). CONCLUSIONS: Negative remodeling and calcified plaque with rare plaque ruptured were common in elderly people with acute MI. These findings may contribute to the difference in clinical presentation and may suggest a different pathophysiologic mechanism of MI in octogenarians.

Age Factors↗

PubMed2006

Outcome after acute incomplete sirolimus-eluting stent apposition as assessed by serial intravascular ultrasound.

We investigated the fate of postprocedural incomplete stent apposition (ISA) after sirolimus-eluting stent (SES) implantation by evaluating long-term intravascular ultrasound findings in 168 consecutive patients (182 de novo lesions). Postprocedural ISA was defined as > or = 1 stent strut that was clearly separated from the vessel wall with evidence of blood speckle behind the strut without overlapping a side branch. After SES implantation, there were 61 ISA sites in 46 stents in 31 patients (23 at the proximal edge, 7 at the distal edge, and 31 within the stent body). There were no clinical, procedural, or intravascular ultrasound measurement differences between patients and lesions with versus without ISA. At follow-up, 15 acute ISA sites (25%) in 11 patients completely resolved and 40 sites (75%) in 20 patients persisted, although 32 of 46 persisting ISA sites (70%) decreased. There was a greater decrease in effective lumen area and a greater increase in peristent plaque area in the complete-resolution group than in the persistent-ISA group. No lesion developed stent thrombosis or in-stent restenosis (angiographic diameter stenosis > 50%). Six acute ISA sites were also associated with new, late acquired ISA, only 1 of which resulted in aneurysm formation. Although most ISAs after SES implantation do not resolve completely, the incidence of restenosis or thrombosis is not affected.

Acute Disease↗

PubMed2006

Intravascular ultrasound profile analysis of ruptured coronary plaques.

Angiographic studies have shown that lesions preceding nonfatal acute events are usually not hemodynamically significant. This has led to the concept that plaque ruptures occur at minimal disease sites. We used intravascular ultrasound to create a prerupture "profile" of unstable (vulnerable) plaques. We analyzed 112 ruptured plaques detected by intravascular ultrasound. Reference and lesion external elastic membrane (EEM) and lumen areas were measured to calculate prerupture estimates of plaque area, plaque burden (plaque/EEM area), eccentricity, area stenosis, and remodeling. The narrowest coefficients of variance were for lesion EEM area, maximum plaque thickness, and plaque burden, reference lumen area, and remodeling index (coefficients of variance 0.29, 0.25, 0.12, 0.29, and 0.18, respectively); conversely, there was great variability in measurements of calcification and lumen compromise (minimum lumen area and area stenosis). When using the 5 variables with the narrowest coefficient of variance, we found that 67% of ruptured plaques fit all of following 10th or 90th percentile parameters (> 14.3 mm2 lesion EEM area, > 8.1 mm2 reference lumen area, > 1.6 mm maximum lesion plaque thickness, > 0.63 lesion plaque burden, and > 0.87 remodeling index). Further, 89% of ruptured plaques fit 4 of 5 parameters and 96% fit 3 of 5 parameters. In conclusion, plaque ruptures do not occur at minimal disease sites. Rather, vulnerable (rupture-prone) plaques predictably have significant plaque accumulation and remodeling and occur in larger arteries. It is only the degree of lumen compromise that is variable and often insignificant.

Coronary Artery Disease↗

PubMed2006

Relation between baseline plaque burden and subsequent remodelling of atherosclerotic left main coronary arteries: a serial intravascular ultrasound study with long-term (> or =12 months) follow-up.

AIMS: Glagov's histopathological observation and non-serial intravascular ultrasound studies (IVUS) concluded that compensatory coronary remodelling diminishes as 40% atherosclerotic plaque burden is reached. We tested this hypothesis with serial IVUS. METHODS AND RESULTS: Serial IVUS examinations of 46 atherosclerotic non-stenotic left main stems (18+/-8 months apart) were analysed to assess the relation between baseline plaque burden (=plaque+media area/vessel area) vs. serial remodelling (=vessel area at baseline - at follow-up). There were 25 plaques with baseline plaque burden <40% (30.1+/-6.6%, group A) and 21 plaques with baseline plaque burden > or =40% (46.1+/-5.8%, group B). There was no relation between baseline plaque burden vs. subsequent changes in vessel area overall (r=0.07, P=0.7), for group A (r=0.03, P=0.6), and group B (r=0.01, P=0.8). The frequency of positive serial remodelling (vessel area increase) vs. negative or intermediate serial remodelling (no change or decrease) were similar in group A [17 (68%) vs. 8 (32%)] and group B lesions [18 (86%) vs. 3 (14%)] (P=0.2). CONCLUSION: IVUS demonstrates that serial coronary remodelling is not related to baseline plaque burden. Lesions with baseline plaque burden <40% may subsequently show a lack of compensation or frank arterial shrinkage, whereas lesions with baseline plaque burden >40% may continue to develop compensatory enlargement.

Coronary Artery Disease↗

PubMed2006

Plaque ruptures in stable angina pectoris compared with acute coronary syndrome.

BACKGROUND: Plaque rupture is more frequently observed in patients with acute coronary syndrome (ACS) rather than in patients with stable angina pectoris (SAP). Consequently, studies regarding plaque rupture, which occurred in SAP patients, are rare. Therefore, we evaluated the frequency and axial location of plaque ruptures in SAP patients and compared them with those in ACS patients. METHODS: Three hundred ninety-two patients (231 ACS and 161 SAP patients) who were scheduled for coronary intervention underwent three-vessel intravascular ultrasound (IVUS) study. IVUS criteria for plaque rupture were a plaque contained a cavity that communicated with the lumen with an overlying residual fibrous cap fragment. Using motorized IVUS transducer pullback in all three coronary arteries, the distance between each coronary plaque rupture segment and the respective coronary ostium was measured. RESULTS: Plaque ruptures were detected in 206 of 392 patients who underwent three-vessel intravascular ultrasound examination. At least one plaque rupture in any coronary artery was noted in 48 (30%) SAP and 158 (68%) ACS patients (p<0.001). In both ACS and SAP patients, plaque ruptures were clustered mainly in the proximal segments of the left anterior descending artery and in the proximal and distal segments of the right coronary artery. CONCLUSIONS: At least one plaque rupture in any coronary artery was noted in 30% of SAP patients. Like in ACS patients, plaque ruptures were clustered mainly in the proximal segments of the left anterior descending artery and in the proximal and distal segments of the right coronary artery in SAP patients.

Acute Disease↗

PubMed2006

Effect of simvastatin on coronary lesion site remodeling: a serial intravascular ultrasound study.

BACKGROUND: Direct evidence of coronary artery remodeling can be derived only from serial changes in the external elastic membrane (EEM) and plaque area. The aim of the study was to assess the effect of simvastatin on coronary remodeling in serial intravascular ultrasound (IVUS) studies. METHODS: In 39 male patients ECG-triggered transducer pullback IVUS was performed at baseline, after 3 months on a lipid-lowering diet (control period), and after another 12 months of simvastatin 40 mg/day. The lesion site was the image slice with maximum plaque burden at 3 months. RESULTS: Absolute changes in the EEM area correlated significantly with changes in plaque area during the control period [B = 0.966, r = 0.792 (95% CI 0.71-1.22); p < 0.001] and during simvastatin treatment [B = 0.945, r = 0.822 (95% CI 0.73-1.16); p < 0.001], but there was no significant difference in the slope (delta EEM/delta plaque) between the two time intervals. After 12 months of simvastatin, there was a significant reduction in the lesion EEM area of 4.6% (p = 0.006) and in the lesion plaque area of 5.9% (p < 0.001), but there was no change in reference measurements. As a result, the remodeling index was reduced by simvastatin from 1.01 +/- 0.12 to 0.95 +/- 0.09 (p < 0.001). CONCLUSION: Simvastatin decreases the remodeling index by reducing lesion, but not reference plaque and EEM area. However, simvastatin does not affect direct evidence of remodeling (delta EEM/delta plaque) obtained using serial IVUS studies.

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PubMed2006

Drug-eluting stents in the treatment of intermediate lesions: pooled analysis from four randomized trials.

OBJECTIVES: To address the safety and efficacy of drug-eluting stents (DES) in the treatment of intermediate lesions, we performed a pooled analysis of four randomized DES versus bare-metal stent (BMS) trials and assessed outcomes among patients with intermediate lesions. BACKGROUND: Before the introduction of DES, intermediate coronary lesions were commonly managed based on physiologic or anatomic assessment of lesion severity. The DES may challenge this paradigm. METHODS: The study population involved 167 of 2,478 randomized patients (6.7%) with intermediate lesions (diameter stenosis <50% [mean 44%] by quantitative coronary angiography) from the Sirolimus-coated Bx Velocity Balloon Expandable Stent in the Treatment of Patients with De Novo Coronary Artery Lesions (SIRIUS), TAXUS-IV, and the First and Second First Use to Underscore Restenosis Reduction with Everolimus (FUTURE-I and -II) trials. End points examined included early (in-hospital and 30-day) and late (1-year) major adverse cardiac events (MACE), including cardiac death, myocardial infarction (MI), target vessel revascularization (TVR), stent thrombosis, and follow-up angiographic restenosis. RESULTS: Patients with intermediate lesions randomized to DES versus BMS had low rates of 30-day MACE (1.1% vs. 4.0% respectively; p = 0.22). At one-year follow-up, patients treated with DES versus BMS had similar rates of cardiac death (0% vs. 2.7%, respectively; p = 0.11) and MI (3.4% vs. 5.4%; p = 0.49) but markedly lower rates of TVR (3.4% vs. 20.3%; p = 0.0004), MACE (5.6% vs. 25.4%; p = 0.0003), and binary angiographic restenosis (1.8% vs. 34.0%; p < 0.0001). No patient in either group developed stent thrombosis. CONCLUSIONS: Compared with BMS, treatment of intermediate lesions with DES appears safe and results in a marked reduction in clinical and angiographic restenosis. The efficacy of DES may require a reevaluation of current treatment paradigms for intermediate lesions.

Coronary Restenosis↗

PubMed2006

Dedicated calibration formulas permit correction of differences between measurements by different IVUS devices as demonstrated in atherosclerotic human coronary arteries in vitro.

Serial intravascular ultrasound (IVUS) measurements of coronary vessel dimensions are major endpoints of studies focusing on pharmacological interventions, efficiency of drug eluting stents, and vascular remodeling. In serial studies measurement variability among different IVUS devices may cause substantial misinterpretation and error. We analyzed 33 human coronary plaques in vitro using two different IVUS systems (mechanical IVUS system with a 40 MHz Atlantis SR catheter; solid-state electronic IVUS system with a 20 MHz Invision catheter) and repeatedly measured the total vessel, lumen, and plaque + media cross-sectional area and plaque burden (plaque + media area divided by total vessel area). Between the "raw" measurements made by the two devices, there was a significant difference for both plaque + media area (2.35+/-1.86 mm(2), P < 0.01) and plaque burden (5.39+/-3.68%, P < 0.05). Measurements were then corrected by use of recently introduced calibration formulas; as a result the differences decreased significantly for all IVUS parameters measured ( P < 0.0001). After correction, the remaining differences between the corrected mechanical and solid-state IVUS measurements similar to differences between repeated measurements with the same IVUS device (i.e., the intraobserver variability). Thus, in serial studies the use of different IVUS devices at index and follow-up procedure may introduce a substantial error as a result of system-related differences. The application of dedicated calibration formulas allows for correction for these differences by decreasing such differences to the level of intraobserver variability.

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PubMed2006

Intravascular ultrasound predictors of angiographic restenosis after sirolimus-eluting stent implantation.

AIMS: In many countries, drug-eluting stent implantation is the dominant interventional strategy. We evaluated the clinical, angiographic, procedural, and intravascular ultrasound (IVUS) predictors of angiographic restenosis after sirolimus-eluting stent (SES) implantation. METHODS AND RESULTS: SES implantation was successfully performed in 550 patients with 670 native coronary lesions. Six-month follow-up angiography was performed in 449 patients (81.6%) with 543 lesions (81.1%). Clinical, angiographic, procedural, and IVUS predictors of restenosis were determined. Using multivariable logistic regression analysis, the only independent predictors of angiographic restenosis were post-procedural final minimum stent area by IVUS [odds ratio (OR)=0.586, 95% confidence interval (CI) 0.387-0.888, P=0.012] and IVUS-measured stent length (OR=1.029, 95% CI 1.002-1.056, P=0.035). Final minimum stent area by IVUS and IVUS-measured stent length that best separated restenosis from non-restenosis were 5.5 mm2 and 40 mm, respectively. Lesions with final minimum stent area<5.5 mm2 and stent length>40 mm had the highest rate of angiographic restenosis [17.7% (11/62)], P<0.001 compared with other groups. CONCLUSION: Independent predictors of angiographic restenosis after SES implantation were post-procedural final minimum stent area by IVUS and IVUS-measured stent length. The angiographic restenosis rate was highest in lesions with stent area<5.5 mm2 and stent length>40 mm.

Coronary Angiography↗

PubMed2006

Incomplete neointimal coverage of sirolimus-eluting stents: angioscopic findings.

OBJECTIVES: The goal of this study was to use angioscopy to investigate the amount of neointimal coverage after sirolimus-eluting stent (SES) implantation. BACKGROUND: Sirolimus-eluting stents reduce intimal hyperplasia. METHODS: We used angioscopy to evaluate 37 consecutive stented coronary artery lesions (15 SES and 22 bare-metal stents [BMS]) in 25 patients (18 men, 7 women) at 3 to 6 months after stent implantation. Angioscopic evaluation focused on: 1) neointimal coverage of stent struts, and 2) the existence of thrombi. The degree of neointimal coverage was classified as grade 0 when there was no neointimal coverage (similar to immediately after the implantation); grade 1 when stent struts bulged into the lumen, but were covered and still translucently visible; grade 2 when stent struts were visible but not clearly seen (not translucent); and grade 3 when stent struts were not visible because they were embedded in the neointima. RESULTS: Thrombi were identified in eight stented segments, tended to be more common with SES (p = 0.14), but were not seen on angiography. Three of the 15 SES (20%) had grade 0 neointimal coverage, and only 2 SES (13.3%) had complete coverage (grades 2/3). In contrast, all 22 BMS showed complete intimal coverage (grades 2/3). Thrombi were more common in stents with incomplete neointimal coverage (p = 0.09). CONCLUSIONS: The SES had incomplete neointimal coverage three to six months after implantation, and this was associated with subclinical thrombus formation.

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PubMed2006

Serial intravascular ultrasound evidence of both plaque stabilization and lesion progression in patients with ruptured coronary plaques: effects of statin therapy on ruptured coronary plaque.

Using serial intravascular ultrasound (IVUS), we evaluated the natural evolution of non-culprit/non-target lesion ruptured coronary plaques and assessed the impact of statin therapy. Twenty-eight patients with non-stenotic ruptured plaques underwent baseline and 12-month follow-up IVUS studies; half were treated with statins. Standard IVUS analyses were performed. Complete healing of ruptured plaques was observed in four (29%) statin-treated patients and no non-statin-treated patients (p=0.049). Statin-treated patients had an increase in lumen area of 0.4+/-0.8 mm2 (versus a decrease in lumen area of -0.6+/-1.0 mm2 in non-statin-treated patients, p=0.007) and no change in plaque area (versus an increase in plaque area of 0.6+/-0.9 mm2, p=0.051). During 1-year follow-up, target lesion revascularization was performed in three non-statin-treated patients (21%) and no statin-treated patient (p=0.11). Compared to lesions that did not require revascularization, lesions requiring revascularization had a decrease in lumen area (-1.7+/-1.4 mm2 versus 0.1+/-0.8 mm2, p=0.001) as well as an increase in plaque area (1.6+/-1.0 mm2 versus 0.1+/-0.7 mm2, p=0.002). In conclusion, the current observational follow-up IVUS study showed beneficial effects of statin treatment on reduction of revascularization rates and stabilization of non-culprit/non-target lesion plaque ruptures without significant stenosis. Conversely, healing of non-statin-treated non-culprit/non-target lesion plaque ruptures can be responsible for lesion progression requiring revascularization.

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