Risk assessment of slow or no-reflow phenomenon in aortocoronary vein graft percutaneous intervention.

Slow or no-reflow phenomenon (SNR) complicates 10%-15% of cases of percutaneous intervention (PCI) in aortocoronary saphenous vein grafts (SVG). At present, there are no uniform, effective strategies to predict or prevent this common and potentially serious complication. The purpose of our study was to characterize variables correlated with the risk of SNR in SVG PCI in the era of stenting and glycoprotein IIb/IIIa receptor inhibitors. We identified 2,898 consecutive patients who had PCI, of whom 163 underwent PCI of at least one SVG. The clinical and angiographic characteristics of patients who developed SNR (SNR group) were compared with those who did not (no-SNR group). A total of 23 patients experienced SNR and 140 did not. Using a stepwise multivariate logistic regression analysis, four independent predictors for SNR were detected: probable thrombus (OR 6.9; 95% CI, 2.1-23.9; P = 0.001), acute coronary syndromes (OR 6.4; 95% CI, 2.0-25.3; P = 0.003), degenerated vein graft (OR 5.2; 95% CI, 1.7-16.6; P = 0.003), and ulcer (OR 3.4; 95% CI, 0.99-11.6; P = 0.04). The risk of developing SNR could be estimated according to the number of predictors found: low-grade risk (1%-10%) if < or = one variable was present, moderate risk (20%-40%) if two variables were present, and high risk (60%-90%) if three or more variables were present. We identified and quantified current risk factors for SNR and concluded that the risk of developing SNR during PCI in SVG can be predicted by simple clinical and angiographic variables obtained before PCI. This information may be useful when the risk of PCI has to be balanced against alternative strategies such as medical therapy or redo-bypass surgery or in the selection of those patients that will most benefit from the use of protection devices during PCI.

A precise, three-dimensional atlas of myocardial perfusion correlated with coronary arteriographic anatomy.

To map precise myocardial perfusion anatomy, we correlated detailed coronary arteriographic anatomy for every coronary artery and all secondary branches in the heart that had flow-limiting stenosis with corresponding specific, circumscribed, myocardial perfusion defects by positron emission tomography. Eight hundred ninety-five patients with abnormal coronary arteriograms showing any visible coronary artery narrowing of greater than 10% diameter stenosis underwent positron emission tomography perfusion imaging at rest and after dipyridamole stress; the data obtained were processed automatically into 3-dimensional topographic displays of relative radionuclide uptake in anterior, septal, left lateral, and inferior quadrant views, without attenuation artifacts, depth-dependent resolution, or spatial distortion of polar displays. The selection criterion for detailed anatomic analysis was the presence of a discrete, localized, moderate to severe, dipyridamole-induced perfusion defect, defined by automated algorithms as 1 quadrant view outside 2 SDs of healthy control subjects with which a specific stenotic coronary artery and/or its secondary branches could be correlated unequivocally on the coronary arteriogram for mapping precise perfusion anatomy, not for determining sensitivity or specificity. Because the anatomy of myocardial perfusion is inherently not statistical data, the results are presented as a summary atlas and series of individual cases that illustrate myocardial perfusion anatomy. Because the patterns of myocardial perfusion anatomy were derived from a large number of subjects, the atlas provides generalized information, not previously published, that correlates detailed arteriographic anatomy with perfusion anatomy including secondary diagonal, marginal, and posterior descending branches of the coronary arteries.

Percutaneous and surgical interventions for in-stent restenosis: long-term outcomes and effect of diabetes mellitus.

OBJECTIVE: We examined long-term outcomes of patients with in-stent restenosis (ISR) who underwent different percutaneous interventions at the discretion of individual operators: balloon angioplasty (BA), repeat stent or rotational atherectomy (RA). We also examined long-term outcomes of patients with ISR who underwent coronary artery bypass surgery (CABG). BACKGROUND: In-stent restenosis remains a challenging problem, and its optimal management is still unknown. METHODS: Symptomatic patients (n = 510) with ISR were identified using cardiac catheterization laboratory data. Management for ISR included BA (169 patients), repeat stenting (117 patients), RA (107 patients) or CABG (117 patients). Clinical outcome events of interest included death, myocardial infarction, target vessel revascularization (TVR) and a combined end point of these major adverse cardiovascular events (MACE). Mean follow-up was 19+/-12 months (range = 6 to 61 months). RESULTS: Patients with ISR treated with repeat stent had significantly larger average post-procedure minimal lumen diameter compared with BA or RA (3.3+/-0.4 mm vs. 3.0+/-0.4 vs. 2.9+/-0.5, respectively, p < 0.05). Incidence of TVR and MACE were similar in the BA, stent and RA groups (39%, 40%, 33% for TVR and 43%, 40%, 33% for MACE, p = NS). Patients with diabetes who underwent RA had similar outcomes as patients without diabetes, while patients with diabetes who underwent BA or stent had worse outcomes than patients without diabetes. Patients who underwent CABG for ISR, mainly because of the presence of multivessel disease, had significantly better outcomes than any percutaneous treatment (8% for TVR and 23% for MACE). CONCLUSIONS: In this large cohort of patients with ISR and in the subset of patients without diabetes, long-term outcomes were similar in the BA, repeat stent and RA groups. Tissue debulking with RA yielded better results only in diabetic patients. Bypass surgery for patients with multivessel disease and ISR provided the best outcomes.

Percutaneous intervention in saphenous venous grafts: in-stent restenosis lesions are safer than de novo lesions.

BACKGROUND: The histological appearance of stenosis in de novo saphenous venous grafts (DNSVG) consists of diffuse atherosclerosis that contains blood elements, necrotic debris and limited fibrocollagenous tissue. The friable nature of these lesions complicates percutaneous intervention (PCI) procedures. On the other hand, in-stent restenosis (ISR) of SVG is due primarily to atherosclerotic plaque or fibromuscular hyperplasia, with thrombus formation playing a secondary role. The purpose of this study is to compare the results of PCI in these two types of SVG lesions. METHODS: We reviewed our institutional interventional database from March 1996 through February 2000 and identified all consecutive patients who underwent PCI of at least one SVG. One hundred and ten patients were identified: 89 undergoing DNSVG intervention and 21 patients with ISR lesions. RESULTS: Acute coronary syndromes, degenerated and thrombus-containing lesions were more common in the DNSVG group. "Slow-, no-reflow" complicated 20% of the DNSVG lesions compared to none of the ISR lesions (p = 0.02). Post-procedural myocardial infarction was higher in the DNSVG group (13.5% versus 0%; p = 0.1) and correlated significantly with the occurrence of "slow-, no-reflow" (r = 0.43; p = 0.0001). Utilizing statistical modeling to adjust for baseline differences between the groups, ISR lesions were associated with a low risk of procedural complications (r = 0.22; p = 0.03). CONCLUSION: This study demonstrates that in this relatively high-risk population, PCI is safer in ISR lesions than in de novo SVG lesions.

Endovascular repair of traumatic pseudoaneurysm by uncovered self-expandable stenting with or without transstent coiling of the aneurysm cavity.

Various surgical options for internal carotid or subclavian artery pseudoaneurysm repair have been reported; however, in general they have resulted in poor outcomes with high morbidity and mortality rates. Recently, these open surgical procedures have been partly replaced by percutaneous transluminal placement of endovascular devices. We evaluated the potential for using flexible self-expanding uncovered stents with or without coiling to treat extracranial internal carotid, subclavian and other peripheral artery posttraumatic pseudoaneurysm. Three patients with posttraumatic pseudoaneurysm were treated by stent deployment and coiling (two cases) of the aneurysm cavity. In one case, a 5.0 x 47 mm Wallstent (Boston Scientific) was positioned to span the neck of the 9 x 5 mm size pseudoaneurysm (left internal carotid artery) and deployed. Angiography demonstrated complete occlusion of the pseudoaneurysm without coiling. In the second patient, a 5.0 x 31 mm Wallstent (Boston Scientific) was positioned to span the neck of the 9 x 7 mm size pseudoaneurysm (right internal carotid artery) and deployed. A total of six coils (Guglielmi Detachable Coils, Boston Scientific) were deployed into the pseudoaneurysm cavity until it was completely obliterated. In the third case, an 8.0 x 80 mm SMART (Cordis) stent was advanced over the wire, positioned to span the neck of the 10 x 7 mm size pseudoaneurysm of the left subclavian artery, and deployed. Fourteen 40 x 0.5 mm Trufill (Cordis) pushable coils were deployed into the pseudoaneurysm cavity until it was completely obliterated. At long-term follow-up (6-9 months), all patients were asymptomatic without flow into the aneurysm cavity by Duplex ultrasound. We conclude that uncovered endovascular flexible self-expanding stent placement with transstent coil embolization of the pseudoaneurysm cavity is a promising new technique to treat posttraumatic pseudoaneurysm vascular disease by minimally invasive methods, while preserving the patency of the vessel and side branches.

High prevalence of myocardial perfusion abnormalities on positron emission tomography in asymptomatic persons with a parent or sibling with coronary artery disease.

BACKGROUND: We hypothesized that asymptomatic persons with a parent or sibling with coronary artery disease (CAD) have myocardial perfusion defects on positron emission tomography (PET) as markers of early CAD. METHODS AND RESULTS: After medical and family histories were recorded, 90 subjects underwent rest-dipyridamole cardiac PET perfusion imaging, including 18 index cases (a subject with CAD documented by PET and arteriography), 32 asymptomatic adults without known CAD who had a parent or sibling with CAD among these index cases, 30 asymptomatic subjects with comparable coronary risk factors without CAD or a family history of CAD, and 10 volunteer control subjects with no risk factors and no family history. PET perfusion images were quantified with automated software for size of abnormalities as percent of the cardiac image outside 95% CIs of normal controls and for severity as the lowest quadrant average relative activity. Of asymptomatic subjects with a parent or sibling with CAD (first-degree relatives), 50% had dipyridamole-induced myocardial perfusion defects that involved >/=5% of the cardiac image outside normal 95% CIs with or without other risk factors. The size of perfusion defects was larger in first-degree relatives than in control subjects (11+/-13% versus 1+/-1%, P:=0.02) and larger than in asymptomatic subjects with comparable risk factors but no family history of CAD (11+/-13% versus 5+/-6%, P:=0.02). CONCLUSIONS: This study documents the presence of quantitative, statistically significant, dipyridamole-induced myocardial perfusion abnormalities on PET in 50% of asymptomatic persons with a parent or sibling with CAD, independent of other risk factors, indicating preclinical coronary atherosclerosis.

Adenosine use during aortocoronary vein graft interventions reverses but does not prevent the slow-no reflow phenomenon.

Slow or no reflow (SNR) complicates 10-15% of cases of percutaneous intervention (PI) in saphenous vein bypass graft (SVG). To date there have been limited options for the prevention and treatment of this common and potentially serious complication. We evaluated the procedural outcome of 143 consecutive SVG interventions. We compared patients who received pre-intervention intra-graft adenosine boluses with those who did not. In addition we examined the efficacy of adenosine boluses to reverse slow-no reflow events. Angiograms were reviewed and flow graded (TIMI grade) by film readers blinded to the use of any intraprocedural drug or clinical history. Seventy patients received intragraft adenosine boluses before percutaneous intervention (APPI), 73 received no preintervention adenosine (NoAPPI). There were no significant angiographic differences between the two groups at baseline. A total of 20 patients experienced SNR. The incidence of SNR was similar in the two groups (APPI = 14.2% vs. NoAPPI = 13.6%, P = 0.9). SNR was treated with repeated, rapid boluses (24 microg each) of intra-graft adenosine. Reversal of SNR was observed in 10 of 11 patients (91%) who received high doses of adenosine (>/=5 boluses, mean 7.7 +/- 2.6) and in 3 of 9 (33%) of those who received low doses (<5 boluses, mean 1.5 +/- 1.2). Final TIMI flow was significantly better in the high dose than in the low dose group (final TIMI 2.7 +/- 0.6 vs. 2 +/- 0.8, P = 0.04). No significant untoward complications were observed during adenosine infusion. These findings suggest that SNR after PI in SVG is not prevented by pre-intervention adenosine, but it can be safely and effectively reversed by delivery of multiple, rapid and repeated boluses of 24 microg of intra-graft adenosine.

Successful treatment of coronary artery perforation in an abciximab-treated patient by microcoil embolization.

We describe a case of type 2 coronary artery perforation in a 73-year-old man undergoing coronary artery rotablation and stenting with abciximab therapy. The coronary artery perforation was successfully treated by coil embolization with Trufill pushable coils made from platinum alloy and synthetic fibers to promote maximum thrombogenicity.

Restenosis: Relationship with Thrombosis.

Coronary balloon angioplasty was first used in 1977; since then, indications for percutaneous coronary intervention have expanded. However, despite significant advances in reducing the incidence of acute complications, chronic restenosis of dilated lesions remains a serious and frequent problem. The mechanisms of restenosis can be described as a combination of effects involving three main components: vessel recoil and remodeling, hemostatic activation and thrombus formation, and neointimal hyperplasia. Thrombosis is associated with vascular and plaque injury. In animal models thrombus at the injury site is a major determinant of intimal hyperplasia and restenosis. Although the introduction of coronary stenting has limited the effect of vessel recoil and remodeling, no effective therapy is yet available to prevent restenosis. This article reviews the potential role of the hemostatic system in restenosis and those drugs and techniques that may inhibit its effect on the restenotic process.

Causes of early reintervention after successful coronary artery stenting.

Acute reintervention was performed in 26 of 1,620 patients after coronary stenting (1.6%). Half of the patients had stent thrombosis and the other half residual anatomic problems. The mean time for reintervention was shorter in patients with stent thrombosis. All patients with stent thrombosis had a sudden recurrence of chest pain. Electrocardiographic changes were more common with stent thrombosis. Composite end point occurred in 10 patients (77%) with stent thrombosis versus 5 (39%) in the other group (p = 0.04).

Intracoronary adenosine administered during percutaneous intervention in acute myocardial infarction and reduction in the incidence of "no reflow" phenomenon.

Percutaneous intervention in acute myocardial infarction has been associated with a high incidence of "no reflow," ranging from 11% to 30%, with an increased risk of complications. The role of intracoronary adenosine for the prevention of this phenomenon has not been evaluated fully. We studied the procedural outcomes of 79 patients who underwent percutaneous intervention in the context of acute myocardial infarction. Twenty-eight patients received no intracoronary adenosine, and 51 received intracoronary adenosine boluses (24-48 microg before and after each balloon inflation). Eight patients who were not given adenosine experienced no reflow (28.6%) and higher rates of in-hospital death, while only three of 51 patients (5.9%; P = 0.014) in the adenosine group experienced no reflow. No untoward complications were noted during adenosine infusion. Intracoronary adenosine bolus administration during percutaneous intervention in the context of acute myocardial infarction is easy and safe and may significantly lessen the incidence of no reflow, which may improve the outcome of this procedure.

Timing of coronary stent thrombosis in patients treated with prophylactic tirofiban.

BACKGROUND: Acute and subacute stent thromboses (ASST) are the major thrombotic complications of coronary stenting. The time course of ASST seems to be related to the type of antithrombotic therapy (four days in patients treated with aspirin and coumadin compared to 12 hours with the use of aspirin and ticlopidine). In this report, we compared the timing of ASST in patients treated with aspirin, ticlopidine/clopidogrel, heparin and tirofiban with that in patients treated with the same drugs but without tirofiban. METHODS: Retrospective analysis of the Hermann intervention database between January 1997 and October 1999 was performed. We identified 13 patients who required reintervention in the first week after a successful coronary stenting ( 1 stent). Four patients were treated with tirofiban (Group 1) and 9 were not (Group 2). RESULTS: The median time from stent deployment to ASST was 7 hours (interquartile range, 2.5Eth 33 hours) in group 2 compared to 84.5 hours (interquartile range, 56Eth 124.5 hours) in group 1. The mean time from stent deployment to ASST was 90.3 +/- 43.1 hours in group 1 versus 12.8 +/- 15.3 hours in group 2 (p = 0.0005). All episodes of ASST occurred 3 days in patients treated with tirofiban, whereas they occurred in the first 2 days in all patients not treated with tirofiban. CONCLUSION: Prophylactic tirofiban treatment delays the time to stent thrombosis after successful coronary artery stent implantation for more than two days. Patients at high risk for stent thrombosis treated with short-acting glycoprotein IIb/IIIa platelet receptor inhibitors may warrant close follow-up during the first week after stenting.

Frequency and clinical implications of fluid dynamically significant diffuse coronary artery disease manifest as graded, longitudinal, base-to-apex myocardial perfusion abnormalities by noninvasive positron emission tomography.

BACKGROUND: Diffuse coronary atherosclerosis is the substrate for plaque rupture and coronary events. Therefore, in patients with mild arteriographic coronary artery disease without significant segmental dipyridamole-induced myocardial perfusion defects, we tested the hypothesis that fluid dynamically significant diffuse coronary artery narrowing is frequently manifest as a graded, longitudinal, base-to-apex myocardial perfusion abnormality by noninvasive PET. METHODS AND RESULTS: In this study, 1001 patients with documented coronary artery disease by coronary arteriography showing any visible coronary artery narrowing underwent rest-dipyridamole PET perfusion imaging. Quantitative severity of dipyridamole-induced, circumscribed, segmental PET perfusion defects was objectively measured by automated software as the minimum quadrant average relative activity indicating localized flow limiting stenoses. Quantitative severity of the graded, longitudinal, base-to-apex myocardial perfusion gradient indicating fluid dynamic effects of diffuse coronary artery narrowing was objectively measured by automated software as the spatial slope of relative activity along the cardiac longitudinal axis. CONCLUSIONS: In patients with mild arteriographic disease without statistically significant dipyridamole-induced segmental myocardial perfusion defects caused by flow-limiting stenoses compared with normal control subjects, there was a graded, longitudinal, base-to-apex myocardial perfusion gradient significantly different from normal control subjects (P=0. 001) that was also observed for moderate to severe dipyridamole-induced segmental perfusion defects (P=0.0001), indicating diffuse disease underlying segmental perfusion defects; 43% of patients with or without segmental perfusion defects demonstrated graded, longitudinal, base-to-apex perfusion abnormalities beyond +/-2 SD of normal control subjects, indicating diffuse coronary arterial narrowing by noninvasive PET perfusion imaging.