Initial Balloon Inflation Research Articles

The Efficacy of Whole Blood Resuscitation During Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) to Mitigate Post-occlusion Circulatory Collapse: A Translational Model in Large Swine.

Uncontrolled torso hemorrhage is the primary cause of potentially survivable deaths on the battlefield. Zone 1 Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA), in conjunction with damage control resuscitation, may be an effective management strategy for these patients in the prehospital or austere phase of their care. However, the effect of whole blood (WB) transfusion during REBOA on post-occlusion circulatory collapse is not fully understood. Yorkshire male swine (n = 6 per group, 70-90 kg) underwent a 40% volume-controlled hemorrhage. After a 10-minute hemorrhagic shock period, a REBOA balloon was inflated in Zone 1. Fifteen minutes after inflation, 0, 1, or 3 units (450 mL/unit) of autologous WB was infused through the left jugular vein. Thirty minutes after initial balloon inflation, the balloon was deflated slowly over 3 minutes. Following deflation, normal saline was administered (up to 3,000 mL) and swine were observed for 2 hours. Survival (primary outcome), hemodynamics, and blood gas values were compared among groups. Statistical significance was determined by log-rank test, one-way ANOVA, and repeated measures ANOVA. Survival rates were comparable between groups (P = .345) with 66% of control, 33% of the one-unit animals, and 50% of the 3-unit animals survived until the end of the study. Following WB infusion, both the 1-unit and the 3-unit groups had significantly higher blood pressure (P < .01), pulmonary artery pressure (P < .01), and carotid artery flow (P < .01) compared to the control group. WB transfusion during Zone 1 REBOA was not associated with increased short-term survival in this large animal model of severe hemorrhage. We observed no signal that WB transfusion may mitigate post-occlusion circulatory collapse. However, there was evidence of supra-normal blood pressures during WB transfusion.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) as adjunct treatment in life threatening postpartum hemorrhage: Fourteen years' experience from a single Norwegian center.

Postpartum hemorrhage (PPH) remains a global health problem. The introduction of resuscitative endovascular balloon occlusion of the aorta (REBOA) in 2008 sought to enhance the management of hemorrhagic shock during PPH. In this study, we present a single Norwegian center's experience with REBOA as a supportive treatment in combating life threatening PPH. This is a historical cohort study from St Olav's University Hospital, with data from period 2008-2021. It includes all patients who underwent REBOA as an adjunct treatment due to life threatening PPH, analyzing the outcomes and trends over a 14-year period. A total of 37 patients received REBOA as an adjunct treatment. All procedures were technically successful, achieving hemodynamic stability with an immediate average increase in systolic blood pressure of 36 ± 22 mmHg upon initial balloon inflation. Additionally, a downward trend was noted in the frequency of hysterectomies and the volume of blood transfusions required over time. No thromboembolic complications were observed. Our 14 years of experience at St Olav's Hospital suggests that REBOA serves as a safe and effective adjunct interventional technique for managing life-threatening PPH. Furthermore, the findings indicate that incorporating a multidisciplinary approach to enable rapid aortic occlusion can potentially reduce the necessity for blood transfusions and hysterectomies.

Treatment of Intracranial Pseudoaneurysms With a Novel Covered Stent: A Series of 19 Patients With Midterm Follow-Up

Background: The optimal treatment for intracranial pseudoaneurysm is unclear. This study aims to analyze the outcome of treating intracranial pseudoaneurysm with a novel covered stent.Materials and Methods: The institutional imaging and clinical databases were retrospectively reviewed for patients with intracranial pseudoaneurysms treated with Willis covered stent from January 2017 to December 2019. The clinical presentations, etiology, intraoperative complications, and immediate and follow-up outcomes were analyzed.Results: A total of 19 patients with 20 pseudoaneurysms were enrolled for analysis. Seventeen patients presented with vision loss and two with epistaxis. Nineteen Willis covered stents were used with one for each patient without technical failure. Intraoperative thrombosis was encountered in one patient (5.3%), which was recanalized by tirofiban. During clinical follow-up, no further epistaxis occurred, and visual acuity improved in three (17.6%) patients. Endoleak occurred in seven (36.8%) patients after the initial balloon inflation and persisted in one (5.3%) patient after balloon re-inflation. This endoleak disappeared at 8 month follow-up. Finally, during angiographic follow-up (median 13 months), parent artery occlusion and in-stent stenosis occurred in one (5.3%) patient. No stent-related ischemic event was encountered.Conclusions: The Willis covered stent is feasible, safe, and efficient in treating intracranial pseudoaneurysms.

Use of bilobed partial resuscitative endovascular balloon occlusion of the aorta is logistically superior in prolonged management of a highly lethal aortic injury.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a viable technique for management of noncompressible torso hemorrhage. The major limitation of the current unilobed fully occlusive REBOA catheters is below-the-balloon ischemia-reperfusion complications. We hypothesized that partial aortic occlusion with a novel bilobed partial (p)REBOA-PRO would result in the need for less intraaortic balloon adjustments to maintain a distal goal perfusion pressure as compared with currently available unilobed ER-REBOA. Anesthetized (40-50 kg) swine randomized to control (no intervention), ER-REBOA, or pREBOA-PRO underwent supraceliac aortic injury. The REBOA groups underwent catheter placement into zone 1 with initial balloon inflation to full occlusion for 10 minutes followed by gradual deflation to achieve and subsequently maintain half of the baseline below-the-balloon mean arterial pressure (MAP). Physiologic data and blood samples were collected at baseline and then hourly. At 4 hours, the animals were euthanized, total blood loss and urine output were recorded, and tissue samples were collected. Baseline physiologic data and basic laboratories were similar between groups. Compared with control, interventions similarly prolonged survival from a median of 18 minutes to over 240 minutes with comparable mortality trends. Blood loss was similar between partial ER-REBOA (41%) and pREBOA-PRO (51%). Partial pREBOA-PRO required a significantly lower number of intraaortic balloon adjustments (10 ER-REBOA vs. 3 pREBOA-PRO, p < 0.05) to maintain the target below-the-balloon MAP. The partial ER-REBOA group developed significantly increased hypercapnia, fibrin clot formation on TEG, liver inflammation, and IL-10 expression compared with pREBOA-PRO. In this highly lethal aortic injury model, use of bilobed pREBOA-PRO for a 4-hour partial aortic occlusion was logistically superior to unilobed ER-REBOA. It required less intraaortic balloon adjustments to maintain target MAP and resulted in less inflammation.

Transcatheter mitral valve implantation for inoperable severely calcified native mitral valve disease: A systematic review.

Transcatheter mitral valve implantation (TMVI) for severely calcified native mitral valve disease recently emerged as a treatment option in patients deemed inoperable by conventional techniques. Yet no systematic appraisal currently exists characterizing this novel treatment paradigm. A systematic literature review summarizing the clinical, anatomical, peri- and post-procedural characteristics underscoring the technical feasibility of this procedure was performed. Nine publications describing 11 patients [mean age 68 ± 10 years, 82% female, 82% severe mitral stenosis (MS), 18% severe mitral regurgitation (MR)] were identified. Mean STS score, trans-mitral gradient and effective orifice area were 10.5 ± 4.6%, 12 ± 2.4 mm Hg and 0.93 ± 0.06 cm(2) respectively. All patients had severe, circumferential mitral annular calcification on imaging. Dedicated balloon-expanding transcatheter aortic valves were used in 10/11 cases, with 8/11 cases involving a true percutaneous approach with peri-procedural 3D trans-esophageal echocardiographic guidance; 3/11 cases involved an open left atrial approach. Following initial balloon inflation and valve deployment, procedural success rate was 73%, without residual paravalvular leaks (PVL). Successful immediate re-deployment of a 2nd valve was needed in 2 instances following significant PVL detection. Residual trans-valvular gradients ranged from 3 to 7 mm Hg, with no patient demonstrating >grade 2 MR. All patients survived the procedure, with 2 reported deaths on days 10- and 41 post-TMVI being non-cardiac-related. Mid-term clinical follow-up, reported in 8 patients, revealed 6 patients to be alive at 3-months with much improved functional status. TMVI for native severely calcified mitral valve disease appears technically feasible with acceptable initial acute and mid-term hemodynamic and clinical outcomes. The outcomes of an ongoing, dedicated global Sapien TMVI registry will shed further light on this evolving treatment paradigm.

Intracoronary Adenosine versus Intravenous Adenosine during Primary PCI for ST-Elevation Myocardial Infarction: Which One Offers Better Outcomes in terms of Microvascular Obstruction?

Aims. Previous studies have suggested that intravenous administration of adenosine improves myocardial reperfusion and reduces infarct size in ST-elevation myocardial infarction (STEMI) patients. Intracoronary administration of adenosine has shown conflicting results. Methods. In this retrospective, single-centre, blinded clinical study, we assessed whether selective intracoronary administration of adenosine distal to the occlusion site immediately before initial balloon inflation reduces microvascular obstruction (MVO) as assessed with cardiac magnetic resonance imaging (MRI). Using contrast-enhanced sequences, microvascular obstruction (MVO) was calculated. We found 81 patients presenting with STEMI within 12 h from symptom onset who were eligible for the study. In 80/81 (100%) patients receiving the study drug, MRI was performed on Day 1 after primary angioplasty. Results. The prevalence of MVO was reduced in the patients treated with intracoronary adenosine, (45%) compared to 85% of patients who were administered intravenous adenosine (P = 0.0043). We found that the size of MVO in patients receiving intracoronary adenosine was significantly reduced compared to 0.91 g in the intravenous-treated group (P = 0.027). There was no statistically significant difference in TIMI flow and clinical outcomes after primary PCI. Conclusion. We found significant evidence that selective high-dose intracoronary administration of adenosine distal to the occlusion site of the culprit lesion in STEMI patients results in a decrease in microvascular obstruction.

High-dose intracoronary adenosine for myocardial salvage in patients with acute ST-segment elevation myocardial infarction

Previous studies have suggested that intravenous administration of adenosine improves myocardial reperfusion and reduces infarct size in ST-elevation myocardial infarction (STEMI) patients. Intracoronary administration of adenosine has shown conflicting results. In a prospective, single-centre, double-blind, placebo-controlled clinical study, we assessed whether selective intracoronary administration of adenosine distal to the occlusion site immediately before initial balloon inflation results in myocardial salvage and decreased microvascular obstruction (MVO) as assessed with cardiac magnetic resonance imaging (MRI). Using a combination of T(2)-weighted and contrast-enhanced sequences, myocardial salvage index (MSI) was defined as the percentage of the area at risk that did not become necrotic. We randomized 112 patients presenting with STEMI within 12 h from symptom onset to selective intracoronary administration of adenosine 4 mg or matching placebo. In 100/110 (91%) patients receiving study drug, MRI was performed on Days 2-3. No significant difference in MSI was found between adenosine- and placebo-treated patients: 41.3% (20.8, 66.7) vs. 47.8% (39.8, 60.9) [median (Q1, Q3)] (P = 0.52). The extent of MVO was comparable in both groups, with a trend favouring the placebo group: 2.4 g (0.0, 6.8) vs. 5.9 g (0.0, 12.8) after adenosine (P = 0.07). TIMI flow grade, TIMI frame count, myocardial blush grade, and ST-segment resolution after primary percutaneous coronary intervention were similar between groups. After 4 months, infarct size was similar in both treatment groups. We found no evidence that selective high-dose intracoronary administration of adenosine distal to the occlusion site of the culprit lesion in STEMI patients results in incremental myocardial salvage or a decrease in microvascular obstruction.

Drug-Coated Balloons for the Prevention of Vascular Restenosis

From early in the history of percutaneous cardiovascular intervention, restenosis has been one of the most important clinical and biological measures of success, and a great deal of effort has been put into understanding the mechanisms responsible.1,2 Restenosis is the result of the interaction of a variety of mechanical and biological processes that begin immediately after balloon injury, including early vessel recoil,3,4 negative vascular remodeling,5 and excessive neointimal proliferation.5–7 The most important limitations of balloon angioplasty, abrupt vessel closure resulting from elastic recoil and occlusive plaque dissection, were effectively solved by the introduction of balloon-expandable stents.8 However, in-stent restenosis (ISR), the result of the initial injury and the vascular response to the implanted metallic prosthesis leading to excessive neointimal proliferation, remained as the most important cause of failure of these devices.9,10 Drug-eluting stents (DES) effectively reduced ISR by addressing the biological mechanisms of neointimal proliferation and have become the mainstay of the interventional treatment of coronary atherosclerotic disease.11 However, the demonstrated efficacy of DES is balanced by the small but unpredictable risk of very late stent thrombosis thought to be due to delayed vascular healing resulting from either the initial antiproliferative effect (and associated late acquired incomplete stent apposition) or a hypersensitivity reaction to the drug, polymer coating, or their combination.12,13 Moreover, beyond the coronary vasculature, there has been a paucity of effective therapies to manage restenosis after intervention. In recent years, drug-coated balloons (DCBs) have emerged as a therapeutic alternative in the interventional field.14 With this technology, short-term transfer of antiproliferative drugs to the arterial wall is achieved without the requirement of an implanted drug delivery system, thus potentially reducing the untoward effects associated with polymer-based stent technologies. In small clinical randomized trials, paclitaxel-coated balloons have been shown to be …

Coronary stenting is associated with an acute increase in plasma myeloperoxidase in stable angina patients but not in patients with acute myocardial infarction

Background Myeloperoxidase (MPO) has emerged as a critical mediator in the physiopathology of atherosclerosis from plaque formation and growth until destabilization and rupture leading to acute coronary syndrome (ACS). Using coronary stenting as a model of plaque injury, we aimed to determine the evolution of systemic MPO levels following coronary stenting in stable angina patients and in patients with acute myocardial infarction (AMI). Methods Plasma levels of MPO, lactoferrin, interleukin (IL)-6, C-reactive protein and PMN counts were assessed in 13 patients with Non-ST-elevation myocardial infarction (NSTEMI) (Group A) and in 29 patients with stable angina pectoris (Group B), undergoing coronary stenting. Serial blood samples were taken before angioplasty (baseline) and at 1, 6 and 24 h following initial balloon inflation. Results Following angioplasty, the overall plasma MPO levels significantly increased at 1 h in group B (120.5 ± 79.0 to 166 ± 79.5, p = 0.003) but not in group A (121 ± 63.4 to 124.7 ± 76.9, p = 0.753). In Group B, the increase in MPO levels at 1 h were significantly higher in the presence of complex lesions compared to patients with simple lesions ( p = 0.023). Lactoferrin levels showed no change over time except for a significant decrease at 6 h in group B. Conclusions In stable angina patients, coronary stenting is associated with an acute and transient increase in plasma MPO levels, but not in lactoferrin levels, with an enhanced response in the presence of complex lesions. In contrast, we observed no changes in plasma MPO and lactoferrin levels following stenting in patients with AMI. Given its pro-inflammatory properties, the potential implication of MPO release on clinical outcome in stable patients undergoing stenting needs further investigation.

Myocardial protection with enalaprilat in patients unresponsive to ischemic preconditioning during percutaneous coronary intervention

Cardioprotection due to angiotensin enzyme inhibitors is attributed, at least in part, to the inhibition of bradykinin breakdown and the preconditioning effect of the elevated endogenous bradykinin level. We have previously shown that in patients undergoing percutaneous coronary intervention, one 120-second balloon inflation is insufficient to precondition the heart. The objective of the present study was to examine whether the administration of enalaprilat to these patients results in protection. Twenty patients underwent two 120-second coronary artery occlusions separated by a reperfusion interval of 10 min. Ten patients were given 50 microg x min-1 enalaprilat in an intracoronary infusion between the balloon inflations, whereas the others received an infusion of saline. In the latter control patients, there were no significant differences in ST-segment elevation between the consecutive occlusions (peak ST: 1.61 +/- 0.17 vs. 1.61 +/- 0.16 mV; time to reach 0.5 mV ST elevation: 16 +/- 4 vs. 22 +/- 7 s; mean ST: 1.03 +/- 0.12 vs. 1.02 +/- 0.11 mV). In the patients who received enalaprilat before the second balloon inflation, the ST-segment elevation was significantly less pronounced and slower during the second inflation than during the first (peak ST: 1.80 +/- 0.18 vs. 1.41 +/- 0.19 mV; time to reach 0.5 mV ST elevation: 18 +/- 4 vs. 30 +/- 4 s; mean ST: 1.04 +/- 0.11 vs. 0.85 +/- 0.14 mV). We conclude that enalaprilat administered during percutaneous coronary intervention provides protection to patients who do not have a protective response to the initial balloon inflation.

Abstract 5604: Door-to-Balloon Time - Are We Evaluating the Wrong Metric?

Primary Percutaneous Coronary Intervention (PPCI) for STEMI is a time-sensitive process, commonly assessed by door-to-balloon time (D2B). Indeed, agencies responsible for tracking the success of an institution’s program and those setting reimbursement have established D2B among its core measures of quality. However, reperfusion of the infarct-related artery (IRA) can occur at times other than that of the initial balloon or device deployment. Therefore, we hypothesized that door-to-reperfusion time (D2R) differs significantly from D2B. We studied 68 consecutive patients who presented to our ER with STEMI and underwent PPCI between December 17, 2007 and June 1, 2008. D2B (time from ER arrival to the first use of an intracoronary balloon or thrombectomy device in the IRA) and D2R (time from ER arrival to the first documentation of TIMI 2 or 3 flow in the IRA) were recorded for each patient. All patients received aspirin, unfractionated heparin, and eptifibatide pre-procedure. In our series of 68 consecutive cases, D2R was equal to (11pts) or shorter than (44 pts) D2B in 55 (81%) patients. D2R occurred in a median of 59 min (IQR 49 – 70.5 min) and D2B in a median of 65 min (IQR 53–75.5 min). The difference between D2B and D2R was highly statistically significant (median +3 min, IQR 0 to 8 min, Wilcoxon p &lt; 0.0001). Additional device and/or drug therapy beyond the initial balloon inflation was required to establish TIMI 2–3 flow in 9% (6/68) of cases. D2B was longer than 90 minutes when D2R was less than 90 minutes in 3 of 68 (4%) cases. Our findings indicate that in PPCI, D2B commonly overestimates, and occasionally underestimates, D2R. D2R &lt; D2B was attributable to pre-procedural anticoagulants or guidewire crossing of the occlusion. Considering that coronary reperfusion, which correlates with myocardial salvage, is the goal of PPCI, D2R appears to be the better metric by which to judge quality of care. Use of this more accurate metric may allay an unnecessary and inappropriate force to rush to device therapy.

R-wave amplitude changes measured by electrocardiography during early transmural ischemia

BackgroundChanges in the amplitude of the R wave (RWA) on the electrocardiogram (ECG) have been described during acute myocardial ischemia and infarction. However, this has not been well studied in a controlled setting. We hypothesized that significant increase in RWA occurs during early transmural myocardial ischemia. MethodsWe prospectively evaluated changes in RWA in 50 patients during brief episodes of transmural ischemia induced by first balloon occlusion (mean, 38 seconds at 6-10 atmospheric pressures) during elective percutaneous coronary intervention. We recorded 12-lead ECGs at 20-second intervals before and during balloon inflation in 16 right coronary arteries, 14 left circumflex arteries, and 20 left anterior descending arteries. R wave amplitude was digitally measured in each of the 12 leads in every ECG using the ECG interval editor (General Electric HC, Menomonee Falls, WI). Intracoronary (IC) ECGs were also recorded in 4 patients. The mean of the RWA in each lead before balloon inflation was compared to the mean RWA during balloon inflation. ResultsR wave amplitude significantly increased during balloon inflation from baseline in limb leads I, II, aVL, and all the precordial leads with the exception of lead V1. The RWA increase did not reach statistical significance in leads III, aVF, and V1. Mean RWA increase was consistent in all leads except aVR during the brief episodes of ischemia during initial balloon inflation because of the inverse polarity of this lead. The increase in RWA was seen in most patients (mean, 75%) in whom transmural ischemia was induced by first balloon inflation. Besides, the RWA showed an increase from baseline in 3 patients who had IC-lead recordings. ConclusionR wave amplitude increases significantly in precordial leads (V2-V6) and limb leads (I, II, aVL) of the surface ECG during brief episodes of transmural ischemia. The increase in RWA might be consistent with the expansion of the left ventricular cavity during ischemia and/or alterations in conduction that are intrinsic to the myocardium.

Ischemic Preconditioning during the Use of the Percusurge Occlusion Balloon for Carotid Angioplasty and Stenting

Ischemic preconditioning (IP) uses transient ischemia to render tissues tolerant to subsequent, prolonged ischemia. This study sought to evaluate factors that contributed to the development of cerebral ischemia during PercuSurge balloon (Medtronic, Santa Rosa, CA) occlusion in patients undergoing carotid angioplasty and stenting (CAS). The PercuSurge occlusion balloon was used in 43 of 165 patients treated with CAS for high-grade stenosis; 20% were symptomatic. Symptoms of cerebral hypoperfusion during temporary occlusion of the internal carotid artery occurred in 10 of 43 patients and included dysarthria, agitation, decreased level of consciousness, and focal hemispheric deficit. The development of neurologic symptoms after initial PercuSurge balloon inflation and occluded internal carotid artery flow was associated with a decrease in the mean Glasgow Coma Scale (GCS) from 15 to 10 (range 9-14); the GCS returned to normal after occlusion balloon deflation. The mean time to spontaneous recovery of full neurologic function was 8 minutes (range 4-15 minutes). The mean subsequent procedure duration was 11.9 minutes (range 6-21 minutes). No recurrence of neurologic symptoms occurred when the occlusion balloon was reinflated. All 10 patients underwent successful CAS without occlusion, dissection, cerebrovascular accident, or death. Ischemic preconditioning can be used to enable CAS with embolic protection in patients who cannot tolerate initial interruption of antegrade cerebral perfusion by PercuSurge occlusion.

Optimal Catheter Placement During Sonohysterography

To estimate whether the position of the catheter placement into either the uterus or cervix during the saline infusion sonohysterography affected the magnitude of pain. A clinical trial was conducted with women undergoing saline infusion sonohysterogram randomized to intracervical or intrauterine balloon catheter placement. The primary outcome end points were the degrees of pain experienced after initial inflation and then after deflation of the balloon catheter at the completion of the saline infusion sonohysterogram. Pain was quantified with a 10-point visual analog pain scale. Secondary end points included total time for the saline infusion sonohysterogram and the total volume of infused saline necessary for adequate visualization of the endometrial cavity. Thirty-five patients were randomly assigned to intracervical balloon placement and 34 to intrauterine placement. After initial inflation there was significantly less pain with intracervical than intrauterine balloon placement (1.8 compared with 3.0, P=.02), although there was no difference in pain at the end of the procedure after deflation of the balloon (P=.66). Significantly less infused saline was required with intracervical catheter placement (19 mL compared with 40 mL, P=.001). Nulliparous women had significantly more pain than did parous women, both after initial balloon inflation and at completion of the saline infusion sonohysterogram (P<.05). Intracervical catheter placement results in significantly less pain during an saline infusion sonohysterography and also requires half the saline volume to perform the saline infusion sonohysterogram. Therefore, routine intracervical balloon placement should be considered for saline infusion sonohysterogram. ClinicalTrials.Gov, www.clinicaltrials.gov, NCT00534963 I.

Cerebral ischemia associated with PercuSurge balloon occlusion balloon during carotid stenting: Incidence and possible mechanisms

Interruption of antegrade cerebral perfusion results in transient neurologic intolerance in some patients undergoing carotid angioplasty and stenting (CAS). This study sought to evaluate factors that contributed to the development of cerebral ischemia during PercuSurge balloon occlusion and techniques used to allow successful completion of the CAS procedure. The PercuSurge occlusion balloon was used in 43 of 165 patients treated with CAS for high-grade stenosis (mean stenosis, 90%). All 43 patients were at increased risk for endarterectomy (7 restenosis, 3 irradiation, 3 contralateral occlusion, and 30 Goldman class II-III); 20% were symptomatic. Symptoms of cerebral hypoperfusion during temporary occlusion of the internal carotid artery occurred in 10 of 43 and included dysarthria (7/10), agitation (6/10), decreased level of consciousness (5/10), and focal hemispheric deficit (3/10). An incomplete circle of Willis or contralateral carotid artery occlusion, or both, was present in 8 of 10 patients. Symptoms resulting from PercuSurge balloon occlusion were managed by balloon deflation with or without evacuation of blood from the internal carotid artery using the Export catheter. All symptoms resolved completely without deficit after deflation of the occlusion balloon. The development of neurologic symptoms after initial PercuSurge balloon inflation and occluded internal carotid artery flow was associated with a decrease in the mean Glasgow Coma Scale (GCS) from 15 to 10 (range, 9 to 14); the GCS returned to normal after occlusion balloon deflation and remained normal during subsequent reinflation. The mean time to spontaneous recovery of full neurologic function was 8 minutes (range, 4 to 15 minutes). No thrombotic or embolic events were present on cerebral angiography or computed tomography scan. Balloon reinflation was performed after a mean reperfusion interval of 10 minutes after full neurologic recovery (range, 4 to 20 minutes). The mean subsequent procedure duration was 11.9 minutes (range, 6 to 21 minutes). No recurrence of neurologic symptoms occurred when the occlusion balloon was reinflated. All 10 patients underwent successful CAS without occlusion, dissection, cerebrovascular accident, or death. Several factors may contribute to the development of neurologic intolerance during CAS with balloon occlusion. Elucidation of the protective cellular mechanisms that invoke ischemic tolerance after the initial transient ischemic event may enable CAS with embolic protection in patients who cannot tolerate initial interruption of antegrade cerebral perfusion.

Effect of continuous quality improvement analysis on the delivery of primary percutaneous revascularization for acute myocardial infarction: A community hospital experience

As time to reperfusion correlates with outcomes, a door-to-balloon time of 90 +/- 30 min for primary percutaneous coronary revascularization (PCI) for the treatment of acute myocardial infarction has been recently established as a guideline by the ACC/AHA. The purpose of this study is to assess the effects of a continuous quality assurance program designed to expedite primary angioplasty at a community hospital. A database of all primary PCI procedures was created in 1998. Two groups of consecutive patients treated with primary PCI were studied. Group 1 represented patients in the time period between 1 June 1998 to 1 November 1998 and group 2 represented patients in the period between 1 January 2000 and 16 June 2000. Continuous quality assurance analysis was performed. Modifications to the primary angioplasty program were initiated in the latter group. Time intervals to certain treatment landmarks were compared between the groups. Significant decreases in the time intervals from emergency room registration to initial electrocardiogram (8.4 +/- 8.2 vs. 3.7 +/- 19.5 min; P < 0.001), presentation to the catheterization laboratory to arterial access (13.5 +/- 12.9 vs. 11.6 +/- 5.8 min; P < 0.001), and emergency room registration to initial angioplasty balloon inflation (132.0 +/- 69.2 vs. 112 +/- 72.0 min; P < 0.001) were achieved. For the subgroup of patients presenting with diagnostic ST elevation myocardial infarction, a large decrease in the door-to-balloon time interval between group 1 and group 2 was demonstrated (114.15 +/- 9.67 vs. 87.92 +/- 10.93 min; P = NS), resulting in compliance with ACC/AHA guidelines. Continuous quality improvement analysis can expedite care for patients treated by primary PCI in the community hospital setting.

Usefulness of creatinine clearance in predicting early and late death after primary angioplasty for acute myocardial infarction

E data have suggested that renal dysfunction is an important predictor of outcome in patients with cardiovascular disease, including acute myocardial infarction (AMI).1–9 Among patients with AMI, those with end-stage renal disease on dialysis are known to have a particularly poor long-term survival.6 Although these patients have usually been excluded from trials of reperfusion therapy, many patients with AMI have evidence of mild or moderate renal insufficiency due to diabetic or hypertensive kidney disease. The degree of renal impairment is often under-recognized, because most clinicians rely on serum creatinine alone as a measure of renal function. Recent studies have shown that even mild or moderate renal impairment is associated with adverse outcomes in patients with hypertension or heart failure, but few data exist regarding this relation in patients with AMI.2–5,8,9 This study investigates the effect of baseline renal function on early and late clinical outcome after primary angioplasty for AMI. • • • Nine hundred patients with AMI presenting within 12 hours of symptom onset were randomized to primary angioplasty or stenting in the Stent Primary Angioplasty in Myocardial Infarction (Stent-PAMI) study.10 All patients had either ST-segment elevation of 1 mm in 2 contiguous electrocardiographic leads or a nondiagnostic electrocardiogram (left bundle branch block or posterior AMI) with documentation of AMI in the catheterization laboratory (with a high-grade stenosis and associated left ventricular wall motion abnormality). Patients with known renal impairment (serum creatinine 2.7 mg/dl) or cardiogenic shock were not eligible for enrollment. Other exclusion criteria have been previously described.10 The catheterization and study procedure have been reported in detail.10 In brief, all patients received aspirin, ticlopidine, and heparin before catheterization. Diagnostic coronary angiography was performed with a low osmolar ionic contrast medium (Ioxaglate, Mallinckrodt, St. Louis, Missouri). After initial balloon inflation, patients were randomized to implantation of a heparin-coated stent or angioplasty alone. The infarct vessel had to be a native vessel with a reference diameter of 3.0 to 4.5 mm and with 1 lesions that could be covered with 1 or 2 stents of 15 mm in length. Administration of glycoprotein receptor antagonists was discouraged. Postprocedural heparin was recommended after primary angioplasty alone. Clinical follow-up was obtained at 6 and 12 months. The baseline serum creatinine on admission was available for 847 patients. Creatinine clearance (CrCl) was calculated using the Cockcroft-Gault formula: CrCl ([140 age] weight)/(72 sCr) , where weight is measured as kilograms and serum creatine (sCr) is measured as milligrams per deciliter.11 CrCl was corrected by a factor of 0.85 for women to account for differences in lean body mass. Major adverse cardiac events (MACEs) were defined as death, nonfatal reinfarction, disabling stroke, and ischemia-driven target vessel revascularization. Reinfarction was defined as the recurrence of clinical symptoms or new electrocardiographic changes accompanied by an increase in creatine kinase-MB levels. Disabling stroke was defined as a stroke that resulted in severe limitation in the ability to perform daily activities or the inability to live independently. An independent clinical events committee adjudicated all events. Data analysis was performed using SAS software (version 6.18, SAS Institute, Cary, North Carolina). Results are expressed as mean SD or percentages. Categorical variables were examined using a Pearson chi-square test or Fisher’s 2-sided exact test. Continuous variables were examined using a Student’s t test. Univariate analysis was performed using serum creatinine and CrCl as continuous and dichotomous variables. For the latter, a serum creatinine of 1.5 mg/dl and CrCl of 75 ml/min were chosen to provide a clinically useful index of renal dysfunction. Multivariate predictors of in-hospital, 6-, and 12-month mortality were identified using stepwise logistic regression analysis. Because there is a strong correlation between age, gender, and the calculated CrCl, we performed models with and without these specific variables. A Kaplan-Meier curve was calculated for freedom from death according to baseline CrCl. A p value of 0.05 was considered statistically significant. From William Beaumont Hospital, Royal Oak, Michigan; Lennox Hill Heart and Vascular Institute, New York, New York; Le Bauer Health Care, Greensboro, North Carolina; Mid Carolina Cardiology, Charlotte, North Carolina; Hospital Gregorio Maranon, Madrid, Spain; Instituto Dante Pazzanese de Cardiologia, San Paulo, Brazil; and L’Institut Cardiovasculaire Paris Sud, Antony, France. Dr. C. Grines’ address is: Division of Cardiology, William Beaumont Hospital, 3601 West 13 Mile Road, Royal Oak, Michigan 48073. E-mail: cgrines@ beaumont.edu. Manuscript received December 27, 2002; revised manuscript received and accepted February 27, 2003.

A new reproducible model of an epidural mass lesion in rodents. Part I: Characterization by neurophysiological monitoring, magnetic resonance imaging, and histopathological analysis.

The goal of this study was to characterize a new model of an epidural mass lesion in rodents by means of neurophysiological monitoring, magnetic resonance imaging, and histopathological analysis. Changes in intracranial pressure (ICP), cerebral perfusion pressure (CPP), and laser Doppler flowmetry (LDF) values, intraparenchymal tissue partial oxygen pressure (PtiO2), and electroencephalography (EEG) activity were evaluated in the rat during controlled, epidural expansion of a latex balloon up to a maximum ICP of 60 mm Hg. The initial balloon inflation was followed by periods of sustained inflation (30 +/- 1 minute) and reperfusion (180 +/- 5 minutes). Histopathological analysis and magnetic resonance (MR) imaging were performed to characterize the lesion. The time to maximum balloon expansion and the average balloon volume were highly reproducible. Alterations in EEG activity during inflation first appeared when the CPP decreased to 57 mm Hg, the LDF value to 66% of baseline values. and the PtiO2 to 12 mm Hg. During maximum compression, the CPP was reduced to 34 mm Hg, the LDF value to 40% of baseline, and the PtiO2 to 4 to 5 mm Hg. The EEG tracing was isoelectric during prolonged inflation and the values of LDF and PtiO2 decreased due to accompanying hypotonia. After reperfusion, the CPP was significantly decreased (p < 0.05) due to the elevation of ICP. Both the LDF value and EEG activity displayed incomplete restoration, whereas the value of PtiO2 returned to normal. Histological analysis and MR imaging revealed brain swelling with a midline shift and a combined cortical-subcortical ischemic lesion beyond the site of balloon compression. This novel model of an epidural mass lesion in rodents closely resembles the process observed in humans. Evaluation of pathophysiological and morphological changes was feasible by using neurophysiological monitoring and MR imaging.

Emergency room administration of eptifibatide before primary angioplasty for ST elevation acute myocardial infarction and its effect on baseline coronary flow and procedure outcomes

S randomized trials and a meta-analysis have shown the superiority of primary angioplasty over thrombolytic therapy for treatment of ST elevation acute myocardial infarction (AMI).1–4 Two large registries representative of practice in a community setting, however, failed to confirm a significant benefit for primary angioplasty over thrombolytic therapy.5,6 It has been postulated that a major reason for the discrepancy in the randomized trial data and so-called “real-world” primary angioplasty is an increased delay in treatment in the less controlled settings.7 Furthermore, primary angioplasty is not available to many patients due to initial presentation to a hospital without angioplasty or cardiac catheterization facilities. Recently, there has been interest in facilitated primary angioplasty, where patients are treated with fibrinolytic agents, glycoprotein (GP) IIb/IIIa inhibitors, or a combination of these agents before baseline angiography. One potential advantage of these strategies is widening of the therapeutic window for revascularization by the provision of partial reperfusion. The present study evaluates the effects of emergency room administration of the GP IIb/IIIa inhibitor, eptifibatide, before primary angioplasty on baseline coronary flow, procedure results, and in-hospital outcomes. • • • The treatment group (group 1) consisted of 30 consecutive patients who presented to our institution with AMI within 6 hours of symptom onset, were referred for primary angioplasty, and provided informed consent from December 1999 to April 2000. The controls (group 2) included 30 patients who were treated with primary angioplasty, including GP IIb/ IIIa inhibitors at the time of angioplasty, at our institution from January 1999 to November 1999. Group 2 patients were matched 1:1 with group 1 patients for age, AMI location, diabetes, gender, and time from onset of symptoms to presentation in descending order of priority. Eptifibatide was administered as a bolus of 180 mg/kg followed by a 2 mg/kg/min infusion. Patients were then referred to the cardiac catheterization laboratory and the bolus dose of eptifibatide was repeated on arrival. Baseline quantitative angiography was performed using a computer edge detection system (Artrek, Quinton Imaging, Bothell, Washington), and Thrombolysis in Myocardial Infarction (TIMI) flow grade and corrected TIMI frame counts8 were assessed by independent review of the study angiograms by 1 investigator who was blinded to the type of treatment. The primary end point was the percentage of patients with TIMI 2 or TIMI 3 coronary flow at baseline angiography. Secondary end points included percentage of patients with TIMI 3 flow, mean corrected TIMI frame count, time from baseline angiography to first balloon inflation, total procedure time, total fluoroscopy time, and total stent length per lesion. Continuous variables were compared using Student’s t test. Frequencies were compared using the chi-square test or Fisher’s exact test. Mean age was 57 years and 25% of patients were women. Comparative baseline clinical and angiographic characteristics are listed in Tables 1 and 2, respectively. Baseline TIMI 2 or TIMI 3 flow was present in 57% (95% confidence intervals 39% to 74%) of group 1 patients compared with 13% (95% confidence intervals 1% to 26%) of group 2 patients (p ,0.01) (Figure 1). The mean time from baseline angiography to initial balloon inflation and total procedure times were significantly less for group 1 patients. This difference in time to first balloon inflation was also evident for patients with persistent total occlusion of the infarctrelated artery (TIMI grade 0 flow, 11.3% vs 21.6%, p ,0.01). Other procedural outcomes are listed in Table 3 and in-hospital outcomes are shown in Table 4.5 • • • The results of this study show that for patients undergoing primary angioplasty for ST elevation AMI, a strategy of administering the GP IIb/IIIa inhibitor, eptifibatide, early after presentation and before arrival in the cardiac catheterization laboratory provides partial reperfusion and may decrease procedure complexity. Of 30 patients who received eptifibatide administered as a double bolus of 180 mg/kg with the initial bolus given 51 6 27 minutes before baseline angiography, 17 (56.7%) had TIMI 2 or 3 flow. In addition, the time from baseline angiography to first balloon inflation was significantly less for these paFrom the Department of Medicine and Cardiology Unit, University of Rochester Medical Center, Rochester, New York. This study was supported by an educational grant from COR Therapeutics, South San Francisco, California. Dr. Cutlip’s address is: Cardiology Unit, Box 679, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, New York 14642. E-mail: donald_cutlip@urmc.rochester. edu. Manuscript received October 24, 2000; revised manuscript received and accepted February 1, 2001.

Role of intracoronary ultrasound after high-pressure stent implantation

Poststent high-pressure balloon inflation has been shown to improve clinical outcomes. However, it is unknown whether intracoronary ultrasound (ICUS) provides additional clinical guidance after initial high-pressure balloon inflation is used during stent placement. Thus the purpose of this study was to determine if stent deployment techniques are improved with ICUS imaging despite an optimal angiographic result achieved with high-pressure balloon inflation. Prospective data were collected on 96 consecutive patients in whom 151 stents were deployed. Stents and high-pressure balloons were angiographically sized 1:1 by visual estimation. High-pressure (> or =12 atm in all cases) balloon inflations were continued until angiographic completion (<10% residual stenosis), after which index ICUS imaging was performed. Stent apposition, symmetry, and lumen dimensions were evaluated. An optimal ICUS result was defined as full apposition of the stent, symmetry ratio > or =0.80, and acute gain > or =0.80 of the reference lumen area. If inadequate ICUS results were found, further dilations with higher pressures or larger balloons and subsequent stent reevaluation with ICUS were performed. Sixty-nine (46%) stents required additional balloon inflations. Of these stents, 35 (23%) had initial acute gains that were <80% of the reference lumen area. Forty-six (30%) stents were found to have unapposed struts and 24 (16%) had a symmetry ratio <0.80. In patients requiring additional inflations, minimum stent area increased from 7.6 +/- 2.2 mm(2) to 9.2 +/- 2.4 mm(2) (P <.0001). Similarly, complete stent apposition improved from 33% to 68% of total stents (P <.0001). After initial ICUS, higher-pressure dilations were performed in 40 patients, whereas larger balloons greater than or equal to ICUS reference vessel diameter were used in 33 patients. Follow-up was obtained in 95 (99%) patients. The overall major adverse cardiac event rate at 6 months was 9.3%, which consisted of 8 target vessel revascularizations and 1 abrupt closure requiring repeat intervention. Even when poststent high-pressure balloon inflation achieves an optimal angiographic result, ICUS assists in optimizing acute gain, symmetry, and apposition of intracoronary stents in approximately 50% of patients. Moreover, ICUS guidance is associated with low rates for target vessel revascularization and major adverse cardiac events at 6-month follow-up.