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Background: The multicenter, international, randomized, blinded, sham-controlled RADIANCE-HTN SOLO trial (A Study of the ReCor Medical Paradise System in Clinical Hypertension) demonstrated a 6.3 mm Hg greater reduction in daytime ambulatory systolic blood pressure (BP) at 2 months by endovascular ultrasound renal denervation (RDN) compared with a sham procedure among patients not treated with antihypertensive medications. We report 6-month results after the addition of a recommended standardized stepped-care antihypertensive treatment to the randomized endovascular procedure under continued blinding to initial treatment. Methods: Patients with a daytime ambulatory BP ≥135/85 mm Hg and Results: A total of 69/74 RDN patients and 71/72 sham patients completed the 6-month ambulatory BP measurement. At 6 months, 65.2% of patients in the RDN group were treated with the standardized stepped-care antihypertensive treatment versus 84.5% in the sham group ( P =0.008), and the average number of antihypertensive medications and defined daily dose were less in the RDN group than in the sham group (0.9±0.9 versus 1.3±0.9, P =0.010 and 1.4±1.5 versus 2.0±1.8, P =0.018; respectively). Despite less intensive standardized stepped-care antihypertensive treatment, RDN reduced daytime ambulatory systolic BP to a greater extent than sham (−18.1±12.2 versus −15.6±13.2 mm Hg, respectively; difference adjusted for baseline BP and number of medications: −4.3 mm Hg, 95% confidence interval, −7.9 to −0.6, P =0.024). There were no major adverse events in either group through 6 months. Conclusions: The BP-lowering effect of endovascular ultrasound RDN was maintained at 6 months with less prescribed antihypertensive medications compared with a sham control. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02649426.

Introduction: Contralateral carotid occlusion (CCO) is an established high-risk feature for carotid endarterectomy (CEA) and is a reason to recommend carotid artery stenting (CAS). Recent observational data have called into question whether CCO remains a high-risk feature for CEA. We investigated the clinical impact of CCO among patients undergoing CEA and CAS in a contemporary nationwide registry. Hypothesis: CCO confers an elevated risk of in-hospital adverse events among patients undergoing CEA, but not CAS. Methods: All patients undergoing CEA or CAS from 2005-2019 in the NCDR CARE and PVI registries were included. The primary exposure was the presence of a CCO. The outcome was a composite of in-hospital death, stroke, and myocardial infarction. Analyses were stratified by treatment with CEA or CAS. Multivariable logistic regression models were used to identify factors associated with adverse outcomes. Results: Among 58,423 patients, 4,624 (7.9%) patients had a CCO. Of those, 68.9% (N=3,185) underwent CAS and 31.1% (N=1,439) underwent CEA. The average age of patients with CCO was 69.5±9.7, 32.6% were female, 92.8% were Caucasian, 51.7% had a prior TIA or stroke, and 45.4% had symptomatic disease. Over the study period, there was a 4.3% decline in procedures performed on patients with CCO (p Conclusions: In this contemporary nationwide registry analysis, CCO remains an important predictor of increased risk in patients undergoing CEA, but not CAS. These data support the continued use of CCO to guide carotid revascularization strategy.

Introduction: Contemporary in-hospital mortality rates for patients presenting with acute myocardial infarction (AMI) and cardiogenic shock (CS) remain as high as 50%. The impact of comorbid lower extremity peripheral artery disease (LE-PAD) is unknown. Hypothesis: LE-PAD is associated with higher morbidity and mortality in patients presenting with CS and AMI. Methods: Medicare beneficiaries hospitalized with CS related to AMI from 10/2015-6/2017 were identified. PAD status was defined by the inpatient billing codes present in the year prior to presentation. Outcomes included in-hospital mortality, amputation, peripheral revascularization, and 6-month mortality. Adjusted regression models were used to evaluate outcomes. A subgroup analysis included patients requiring mechanical circulatory support (MCS). Results: Among 45,144 patients, 5.9% (N=2,651) had LE-PAD. The average age was 77.8±7.9, 59.8% were male and 83.0% were white. Cumulative in-hospital mortality was 46.8%, with greater risk among LE-PAD patients (55.2% vs 46.3%; adjusted OR 1.52, 95% CI 1.39-1.65). LE-PAD patients also had greater adjusted risk of in-hospital amputation (1.5% vs 0.2%; OR 3.23, 95% CI: 2.16-4.83), peripheral revascularization rates (1.4% vs 0.4%; OR 1.54, 95% CI: 1.06-2.23), and 6-month mortality (43.2% vs 23.7%; HR 2.06, 95% CI: 1.80-2.35). MCS was less frequently utilized in LE-PAD (20.1% vs. 38.1%, p Conclusions: Comorbid PAD is associated with worse limb outcomes and mortality among patients with AMI and CS. Although MCS was less likely to be used in LE-PAD patients, in-hospital mortality and limb complication rates were comparable to non-LE-PAD MCS patients.

Background: The impact of carotid artery stent fractures on the incidence of adverse clinical events remains unclear. The objective of this study is to report the stent fracture rate and its association with in-stent restenosis and adverse outcomes in the ACT-1 trial (Carotid Angioplasty and Stenting Versus Endarterectomy in Asymptomatic Subjects Who Are at Standard Risk for Carotid Endarterectomy With Significant Extracranial Carotid Stenotic Disease). Methods: ACT-1 is a prospective multicenter trial of patients who have standard surgical risk with severe asymptomatic carotid artery stenosis randomly assigned to carotid artery stenting or carotid endarterectomy (Abbott Vascular). The primary end point was a composite of death, stroke, or myocardial infarction during the 30 days after the procedure or ipsilateral stroke during the 365 days after the procedure. After 771 patients were enrolled, successively randomly assigned patients were required to undergo annual radiographic (x-ray) analysis for stent fracture. Images were independently adjudicated by a core laboratory. Results: Of 1021 patients treated with carotid artery stenting during a mean follow-up of 3.1±1.6 years, 939 had at least 1 x-ray during the follow-up period. Stent fracture was reported in 51 (5.4%) patients. With a maximum follow-up period of 5 years, adverse clinical outcomes occurred in 39 patients with at least 1 x-ray during the follow-up. Of 826 (80.9%) subjects who underwent both duplex ultrasound and x-ray, 822 (99.5%) were interpretable. There was no association between stent fracture and the primary end point ( P =0.86) or with restenosis ( P =0.53). Conclusions: In this large, independently adjudicated, multicenter study, the stent fracture rate was low and not associated with major adverse clinical events or in-stent restenosis. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT00106938.

Background— To evaluate outcomes after carotid artery stenting in larger real-world populations, the Food and Drug Administration mandated that companies conduct postmarketing surveillance (PMS) studies of approved stent systems. Whether PMS studies are representative of carotid artery stenting in routine clinical practice has not been established. Methods and Results— Within the National Cardiovascular Database Registry–Carotid Artery Revascularization and Endarterectomy (NCDR CARE) Registry, we compared patient and procedural characteristics, in-hospital outcomes, and subsequent all-cause mortality after carotid artery stenting in PMS study participants and nonparticipants. We conducted both crude and propensity score–adjusted comparisons for all outcomes between groups. Compared with nonparticipants, participants in PMS studies had lower rates of symptomatic carotid artery disease within the preceding 6 months, prior stroke, and acute evolving stroke at baseline. The PMS study participants had lower unadjusted rates of combined in-hospital death, stroke, or myocardial infarction (2.3% versus 4.1%; P P =0.005) and death (0.3% versus 1.4%; P P =0.04 for in-hospital mortality; and hazard ratio, 0.80; 95% confidence interval, 0.66 to 0.97; P =0.02 for 2-year mortality). Baseline differences in neurological history explained the largest proportion of the difference in outcomes between groups. Conclusions— Participants in PMS studies for carotid artery stenting have different clinical and procedural characteristics and lower mortality compared with nonparticipants. Extrapolating results from PMS studies of carotid artery stenting to larger real-world settings should be done only with great caution.

The primary goal of this American Heart Association renal intervention writing group was to discuss current controversies related to renal interventions and to recommend important areas of clinical research and advocacy initiatives in this peripheral arterial bed. The 4 areas covered in this section include (1) management of asymptomatic renal artery disease, (2) treatment of ischemic nephropathy, (3) prevention and treatment of atheroembolism in renal artery interventions, and (4) treatment of renal in-stent restenosis (ISR). Atherosclerotic renal artery disease is an often unrecognized contributor to refractory hypertension, renal insufficiency, and increased risk of cardiovascular death.1,2 Renal artery disease is associated with increased cardiovascular events (myocardial infarction, stroke, and death), and when associated with symptomatic coronary artery disease, it independently doubles the risk of death.3 Additionally, the presence of bilateral renal artery stenoses is associated with a reduced 4-year survival rate when compared with unilateral disease (47% versus 59%, P

Atherosclerotic renal artery stenosis is commonly present in patients with clinically manifest atherosclerosis in other vascular beds and is independently associated with increased cardiovascular morbidity and mortality. Screening tests such as renal angiography should be selectively applied to patients at high risk for renal artery stenosis who are potential candidates for revascularization. This multispecialty consensus document describes the rationale for patient selection for screening renal angiography at the time of cardiac catheterization.

Background Clinical studies have suggested that smooth muscle cell (SMC) hyperplasia is the most likely cause of in-stent restenosis. However, pathological data regarding this issue are limited. Specifically, direct evidence of proliferative activity in tissues excised from stenotic stents has not been previously reported. Methods and Results Tissue specimens were retrieved by directional atherectomy from 10 patients in whom in-stent restenosis complicated percutaneous revascularization of peripheral artery disease. Analysis of cellular composition was performed quantitatively after cell-specific immunostaining. For specimens preserved in methanol (7 of 10), cellular proliferation was evaluated by use of antibodies to proliferating cell nuclear antigen (PCNA), cyclin E, and cdk2. TUNEL staining for apoptosis was performed on 8 paraformaldehyde-preserved specimens. Each of the 10 specimens contained extensive foci of hypercellularity composed predominantly of SMCs (mean±SEM, 59.3±3.0%). Evidence of ongoing proliferative activity was documented in all 7 methanol-preserved specimens: 24.6±2.3% of SMCs were PCNA-positive, 24.8±3.1% were cyclin E–positive, and 22.5±2.2% were cdk2-positive. Apoptotic cells were detected in all 8 specimens that had been appropriately preserved to permit DNA nick-end labeling. Macrophages and leukocytes were identified in each of the 10 specimens but accounted for a proportionately smaller number of cells (14.5±1.9% and 9.5±1.4%, respectively). Organized thrombus was observed in 6 of the 10 specimens. Conclusions These findings support the notion that in-stent restenosis results from SMC hyperplasia and suggest that adjunctive therapies designed to inhibit SMC proliferation may further enhance the utility of endovascular stents.

Peripheral Artery Disease: Primary Pharmacological Therapy Is Ineffective for Patients With Critical Limb Ischemia The prognosis for patients with chronic critical leg ischemia, ie, rest pain and/or established lesions that jeopardize the integrity of the lower limbs, is often poor. Psychological testing of such patients has typically disclosed quality-of-life indexes similar to those of patients with cancer in critical or even terminal phases of their illness.1 It has been estimated that in toto,2 150 000 patients per year require lower-limb amputations for ischemic disease in the United States. Their prognosis after amputation is even worse3 : the perioperative mortality for below-knee amputation in most series is 5% to 10% and for above-knee amputation 15% to 20%. Even when they survive, nearly 40% will have died within 2 years of their first major amputation; a major amputation is required in 30% of cases; and full mobility is achieved in only 50% of below-knee and 25% of above-knee amputees. These grim statistics are compounded by the lack of efficacious drug therapy. As concluded in the Consensus Document of the European Working Group on Critical Leg Ischemia,3 “. . .there presently is inadequate evidence from published studies to support the routine use of primary pharmacological treatment in patients with critical leg ischemia. . . .” Evidence for the utility of medical therapy in the treatment of claudication is no better.4 5 Consequently, the need for alternative treatment strategies in such patients is compelling. ### Therapeutic Angiogenesis Is a Novel Strategy for the Treatment of Critical Limb Ischemia The therapeutic implications of angiogenic growth factors were identified by the pioneering work of Folkman6 and other workers more than two decades ago. Beginning a little more than a decade ago,7 a series of polypeptide growth factors were purified, sequenced, and demonstrated to be responsible for natural as well as pathological angiogenesis. More recent investigations have established the feasibility of using recombinant formulations of such angiogenic growth …

BACKGROUND Previous postmortem studies have demonstrated compensatory enlargement of atherosclerotic arteries in animal models and patients. Conclusions regarding these changes were drawn based on a comparison of the dimensions of diseased arteries in one group of subjects with the dimensions of normal arteries in another group. This method admits potential confounding variables, such as demographics and other disease states, which might also have an impact on arterial size. METHODS AND RESULTS Using intravascular ultrasound, we studied a total of 62 paired, adjacent normal and diseased sites in the superficial femoral arteries of 20 patients undergoing peripheral vascular interventions. Morphological assessment was performed using a computer-based image analysis system. Measurements were made of the cross-sectional area of the arterial lumen, the atherosclerotic plaque, and the outer border of the artery. These dimensions were then compared to determine the effects of progressive atherosclerosis on arterial morphology. Luminal cross-sectional area decreased from 21.1 +/- 2.2 mm2 in normal segments to 16.7 +/- 0.8 mm2 (P = .0001) in adjacent atherosclerotic segments. Similarly, minimal luminal diameter decreased from 5.7 +/- 0.2 to 5.0 +/- 0.1 mm2, and maximal luminal diameter decreased from 6.2 +/- 0.2 to 5.7 +/- 0.2 mm2. At these same sites, total arterial area was 32.9 +/- 1.6 and 37.9 +/- 1.9 mm2 (P = .0001) in normal and diseased segments, respectively. Minimal and maximal arterial diameters demonstrated similar increases (7.3 +/- 0.2 to 7.7 +/- 0.2 mm2 [P = .0015] and 7.6 +/- 0.2 to 8.3 +/- 0.2 mm2 [P = .0001], respectively). Regression analysis disclosed correlation of the cross-sectional area of plaque to the total arterial area (R = .70, P = .0001). CONCLUSIONS Human arteries enlarge in response to progressive atherosclerosis. This compensatory mechanism results in an increase in arterial size that is proportionate to the cross-sectional area of plaque that has accumulated in the vessel. Intravascular ultrasound demonstrates that this process is focal compensatory enlargement at discrete sites of atherosclerotic narrowing immediately adjacent to more normal areas in which arterial size is smaller.

Arterial puncture and sheath insertion by use of the modified Seldinger technique has become the standard method by which invasive cardiovascular procedures are performed.1 With improvement in techniques and devices, a significant number of patients with atherosclerotic disease are undergoing invasive vascular procedures. Approximately 7 million invasive cardiovascular procedures are performed worldwide each year, and this number is expected to increase with the aging of the population. The vast majority of these procedures are performed with femoral arterial access. Because the number of cardiovascular procedures performed via the femoral artery approach continues to increase, effective arterial hemostasis techniques are essential to high-quality patient care. In fact, vascular access complications, reported to be as high as 6% in some series, remain the leading cause of morbidity after a cardiac catheterization procedure.2 Manual compression has been considered the traditional technique to achieve closure of the arteriotomy site, requiring close observation and immobilization for success. Arteriotomy closure devices (ACDs) were introduced in 1995 to decrease vascular complications and reduce the time to hemostasis and ambulation. Subsequently, several generations of passive and active ACDs have been introduced that incorporate suture, collagen plug, nitinol clip, and other mechanisms to achieve hemostasis. According to a new Life Science Intelligence report entitled “2008 Global Vascular Closure Device Markets: US, Europe, Rest of World,” the global market for vascular closure devices will reach nearly $1 billion in 2013.3 Despite this widespread use of both passive and active ACDs, there are incomplete data on their safety and efficacy. Additionally, there are few published recommendations regarding the indications for the use of these devices, their comparative effectiveness versus manual compression, and the end points of clinical interest for patients undergoing vascular closure. Therefore, the present scientific statement provides an overview of vascular access and patient risk for …

BACKGROUND Previous studies regarding the mechanism by which balloon angioplasty increases luminal patency have generally used animal models or postmortem specimens from occasional fatal cases of angioplasty performed in human patients. In either case, conclusions regarding participatory mechanisms have relied exclusively on nonserial, postangioplasty histopathological examination. METHODS AND RESULTS In the present study, intravascular ultrasound examination was performed before and after balloon angioplasty in 40 consecutive patients with iliac artery stenoses. The areas of the arterial wall, plaque, lumen, and areas resulting from angioplasty-induced plaque fractures were measured immediately after angioplasty in vivo and compared with findings recorded immediately before angioplasty. Angioplasty increased luminal cross-sectional area (CSA) from 11.5 +/- 0.6 mm2 before angioplasty to 25.4 +/- 1.2 mm2 after angioplasty (p = 0.0001). CSA of the portion of the postangioplasty neolumen contained within angioplasty-induced plaque fractures measured 10.0 +/- 0.8 mm2; the neolumen excluding the area contributed by these plaque fractures measured 15.4 +/- 0.8 mm2. Thus, the area contained within plaque fractures accounted for 10.0 mm2 (71.9%) of the 13.9-mm2 increase in luminal CSA after angioplasty. Analysis of CSA occupied by atherosclerotic plaque disclosed that plaque CSA decreased from 33.8 +/- 1.8 mm2 before angioplasty to 22.5 +/- 1.5 mm2 after angioplasty (p = 0.0001). Plaque CSA was thus reduced ("compressed") by 11.3 +/- 1.1 mm2. Total artery CSA increased ("stretched") slightly from 45.3 +/- 2.6 mm2 before angioplasty to 47.8 +/- 2.0 mm2 after angioplasty (p = 0.0025). CONCLUSIONS In vivo analysis of iliac stenoses by intravascular ultrasound immediately before and after angioplasty demonstrates that plaque fractures and "compression" of atherosclerotic plaque are the principal factors responsible for increased luminal patency resulting from balloon angioplasty. "Stretching" of the arterial wall provides an additional, but minor, contribution.

BACKGROUND The pathological consequences of cardiovascular laser irradiation have been studied extensively in vitro. Previous in vivo studies of laser-induced injury have included analyses of acute and/or chronic findings in experimental animals. Little information, however, is available regarding the acute effects of laser irradiation of human vascular tissues in vivo. METHODS AND RESULTS To determine the acute pathology resulting from laser irradiation of human vascular tissue in vivo, specimens retrieved from 23 patients by directional atherectomy immediately after laser angioplasty (19 peripheral and four coronary) were examined by light microscopy. Of the 23 patients, three (13.0%) were treated with a metal-capped ("hot-tip") fiber coupled to a continuous-wave neodymium:yttrium-aluminum-garnet (Nd:YAG) laser using up to 18 W power and 18-305 seconds of cumulative exposure time; in all three patients (100%), thermal injury, including frank charring several cell layers thick, was seen along the luminal borders of the atherectomy specimen. In eight of the 23 patients (34.5%), laser angioplasty was performed using a 250-microseconds holmium:YAG laser at fluences up to 2,300 mJ/mm2, a repetition rate of 5 Hz, and 25-200 seconds of cumulative exposure; in seven of eight patients (85.5%), the atherectomy specimen showed signs of vacuolar injury consisting of central and satellite Alcian-blue-negative vacuoles. In two patients (25.0%), there was a "smudged" or "shredded" edge, whereas in one patient, frank signs of thermal injury were observed. Finally, in 12 of the 23 patients (52.2%), laser angioplasty was performed using a 120-nsec excimer laser at fluences up to 60 mJ/mm2, a repetition rate of 25 Hz, and a cumulative exposure time of 21-315 seconds. Pathological findings among these 12 patients were limited to nine patients (75%) in whom a weakly basophilic, smudged, and/or shredded appearance approximately one cell layer thick was observed along the luminal border of the atherectomy specimen and two patients (16.7%) with small foci of vacuolar injury. None of the atherectomy specimens retrieved after excimer laser angioplasty disclosed signs of thermal injury. CONCLUSIONS These findings document that acute pathological alterations resulting from in vivo laser angioplasty are variable, depending on the laser source used, and are similar to that predicted by experimental studies performed previously in vitro. The prognostic implications of these varying pathological features remain to be clarified.

A 19-year-old healthy woman presented with new onset of severe migrainous headache. She did not take medications or use illicit drugs. There was no personal or family history of hypertension. Physical examination revealed a blood pressure of 220/130 mm Hg in both arms. There was no fourth heart sound. She had full and symmetric pulses in the upper and lower extremities with no radial/femoral delay. There were no carotid, subclavian, or abdominal bruits. Fundoscopic examination revealed normal retinal arteries without hypertensive retinopathy. Renal function and serum potassium were normal. Renal artery duplex ultrasonography revealed elevated peak systolic and end-diastolic velocities in the mid to distal portion of the right renal artery, consistent with severe right renal artery stenosis. The left renal artery was normal. The right kidney measured 8.8 cm with atrophy of the right cortical margin. The left kidney was 11.5 cm. There were normal renal resistive indexes …

BACKGROUND Intravascular ultrasound provides high-resolution images of vascular lumen, plaque, and subjacent structures in the vessel wall; current instrumentation, however, limits the operator to viewing a single, tomographic, two-dimensional image at any one time. Comparative analysis of serial two-dimensional images requires repeated review of the video playback recorded during the two-dimensional examination, followed by a "mind's eye" type of imagined reconstruction. METHODS AND RESULTS Computer-based, automated three-dimensional reconstruction was used to generate a tangible format with which to assess and compare a "stacked" series of two-dimensional images. Three-dimensional representations were prepared from sequential images obtained during intravascular ultrasound examination in 52 patients, 50 of whom were studied before and/or after percutaneous revascularization. Conventional two-dimensional ultrasound images were acquired by means of a systematic, timed pullback of the ultrasound catheter through the respective vascular segments. Images were then assembled in automated fashion to create a three-dimensional depiction of the vessel lumen and wall. Computer-enhanced three-dimensional reconstructions were generated in both sagittal and cylindrical formats. The sagittal format resulted in a longitudinal profile similar to that obtained during angiographic examination; in contrast to angiography, however, the sagittal reconstruction offered 360 degrees of limitless orthogonal views of the plaque and arterial wall as well as the vascular lumen. The cylindrical format yielded a composite view of a given vascular segment, and a hemisected version of the cylindrical reconstruction enabled en face inspection of the reconstructed luminal surface. Sagittal reconstructions facilitated analysis of dissections and plaque fractures resulting from percutaneous revascularization, and the hemisected cylindrical reconstructions enhanced analysis of endovascular prostheses. CONCLUSIONS This preliminary experience demonstrates that computer-based three-dimensional reconstruction may further augment the use of intravascular ultrasound in assessing vascular pathology and guiding interventional therapy.

BACKGROUND Cardiac tamponade after cardiac surgical procedures is often associated with hemodynamically significant localized pericardial effusions. The localized collection of pericardial effusion in the postoperative period and the atypical presentation of cardiac tamponade limit the use of conventional clinical and echocardiographic signs usually seen with a circumferential pericardial effusion. Observation of left ventricular diastolic collapse in the echocardiogram of a patient with postoperative regional cardiac tamponade prompted us to explore the frequency of this sign in regional cardiac tamponade. METHODS AND RESULTS We retrospectively analyzed the echocardiograms of 18 patients with postoperative cardiac tamponade for the following echocardiographic findings: right atrial collapse, right ventricular diastolic collapse, left atrial collapse, and left ventricular diastolic collapse. Three of the 18 patients had circumferential pericardial effusion, and 15 had loculated pericardial effusion; in 10, the effusion was predominantly posterior, and in the other five, it extended laterally or inferiorly. The conventional echocardiographic signs of cardiac tamponade such as right atrial collapse, right ventricular diastolic collapse, and left atrial collapse were present in only 3, 1, and 3 of these 15 patients, respectively, but all exhibited left ventricular diastolic collapse. Increasing pressure within the compartment of a loculated pericardial effusion reaching the limit of pericardial distensibility and consequent transient reversal of transmural left ventricular pressure during diastole are most likely the basis for diastolic collapse of the thick-walled ventricle in a setting of regional cardiac tamponade. CONCLUSIONS We conclude that left ventricular diastolic collapse is a frequent sign of regional cardiac tamponade and could be a useful marker of tamponade in postoperative patients.

Background: In 2007 a consortium of specialty societies developed and published a clinical expert consensus document (CECD) on carotid artery stenting (CAS). This CECD listed suggested indications for CAS based on the presence of symptoms, stenosis severity, and the presence of features that increase the surgical risk of carotid endarterectomy. The National Cardiovascular Data Registry, in conjunction with multiple specialty societies, established the CARE (Carotid Artery Revascularization and Endarterectomy) Registry to provide a comprehensive national database characterizing both forms of carotid revascularization. Methods: CARE employs written definitions, a data dictionary, standardized data collection tools, and quality control checks. We constructed an algorithm that categorized each procedure as conforming to a Recommended Indication (RECC) if it met the indications criteria in the CECD, or as not recommended (NOTRECC) if it didn’t. Patient characteristics and outcomes of these 2 groups were compared. Results: There were 3118 CAS procedures submitted from 107 participating centers for the period 01/2007 through 03/2008. Of these, 2397 (77%) were RECC, while 721 (23%) were NOTRECC. Clinical profiles in the NOTRECC group were more favorable, but overall outcomes were similar. (See Table ) Conclusions: CAS procedures categorized as NOTRECC by CECD criteria accounted for approximately one-fourth of submissions to the CARE Registry. Clinical profiles were different. Outcomes were similar.

Background: Higher mortality has been reported in patients admitted with acute myocardial infarction during off-hours, and has been related to a lower use of primary percutaneous coronary intervention (PCI). Methods: We thus conducted a study, where primary PCI is routinely performed in all patients with ST elevation myocardial infarction (STEMI) regardless of the day and time of admission. Patients admitted during on-hours (Monday through Friday 7am–6pm) where compared to off-hours (including weekends). The outcome of in-hospital mortality, cardiogenic shock and recurrent myocardial infarction was explored. The different components of door-to-balloon (DTB) time were examined and compared between both groups. Results: Between 2003 and 2007, 747 STEMI patients (46% on-hours vs. 56% off-hours) underwent primary PCI. Patient baseline demographic characteristics were similar during on-vs. off-hours. Admissions during off-hours were associated with longer DTB times (134 vs. 109 minutes, p Conclusion: 1) This study is the first to show that even when treated equally with primary PCI, off-hours STEMI admissions have higher mortality than on-hours. Longer DTB time during off-hours likely explain our findings. Strategies to optimize hospital protocols, reperfusion therapies, and perhaps a dedicated in-house “STEMI team” during off-hours need to be revised.

A 5-year-old boy with Williams syndrome (WS) presented with a history of diffuse recurrent obstructive vascular disease. At the age of 12 months, he underwent pericardial patch augmentation of the ascending aorta and pulmonary arteries. He subsequently required Dacron patch repair of the ascending aorta and aortic arch at 3 years of age. In the interim, he had undergone percutaneous transluminal angioplasty and stenting for recurrent peripheral pulmonary artery stenoses and aortic recoarctation. On routine follow-up, he was found to have worsening right ventricular hypertension associated with disparate lung perfusion on a nuclear perfusion scan. He was brought to the catheterization laboratory for further investigation. Angiography showed recurrent pulmonary artery in-stent restenosis and aortic recoarctation. Coronary …

BACKGROUND We investigated the hypothesis that an ultrasound transducer positioned within an angioplasty balloon could be used to perform quantitative assessment of arterial dimensions before and after percutaneous transluminal angioplasty (PTA) and to identify certain mechanical alterations consequent to PTA, including vascular wall recoil and the initiation of plaque fractures. METHODS AND RESULTS A combination balloon-ultrasound imaging catheter (BUIC) that houses a 20-MHz ultrasound transducer within and halfway between the proximal and distal ends of an angioplasty balloon was used to perform PTA in 10 patients with peripheral vascular disease. Each PTA site was also evaluated before and after PTA by standard (nonballoon) intravascular ultrasound (IVUS) technique. In eight patients in whom satisfactory images were recorded with the BUIC before PTA, luminal cross-sectional area (XSA) of stenotic sites (0.10 +/- 0.01 cm2) did not differ significantly from measurements of XSA by IVUS (0.09 +/- 0.01 cm2, p = NS). Likewise, minimum luminal diameter (Dmin) measured by BUIC (0.34 +/- 0.02 cm) was similar to that measured by IVUS (0.33 +/- 0.01 cm, p = NS). In nine patients in whom satisfactory images were recorded with the BUIC after PTA, XSA measured by BUIC (0.29 +/- 0.03 cm2) did not differ significantly from XSA measured by IVUS (0.30 +/- 0.03 cm2, p = NS). Dmin measured by BUIC after PTA (0.57 +/- 0.02 cm) was also similar to Dmin measured by IVUS (0.57 +/- 0.03 cm, p = NS). After PTA, XSA and Dmin measured immediately after deflation were significantly less than balloon XSA and diameter at full inflation, indicating significant elastic recoil of the dilated site. For the nine patients in whom post-PTA images were satisfactory for quantitative analysis, including four patients in whom recoil was 39%, 46%, 50%, and 61%, percent recoil measured 28.6 +/- 7.2%. Finally, plaque fractures were identified on-line in six of 10 patients (60%); in each case, initiation of plaque fracture was observed at inflation pressures of 2 atm or less. CONCLUSIONS The results of this preliminary human investigation indicate that an ultrasound transducer positioned within an angioplasty balloon can be used to perform quantitative and qualitative analyses of lumen-plaque-wall alterations immediately preceding, during, and immediately after PTA in patients with peripheral vascular disease.