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Biomedical subjects

Renu Virmani

Publications and source records attributed to Renu Virmani.

At least 19 recordsLinked to original sources
PubMed2007

Patent foramen ovale: standards for a preclinical model of prevalence, structure, and histopathologic comparability to human hearts.

BACKGROUND: This study evaluated and standardized a Patent Foramen Ovale (PFO) preclinical model in gross anatomic and histopathologic features. METHODS: We examined 150 necropsy-derived domestic porcine hearts, age 4-6 months for PFO prevalence, appearance, and size. Histopathologic preparations were standardized and processed identically to 24 post-mortem human hearts aged 16-62 years. A measurement scheme was developed for PFO atrial openings, tunnel length, and histopathologic features to compare porcine and patient hearts. RESULTS: PFO was found in 32 of the 150 porcine hearts (prevalence 21.3%). Twenty-five porcine PFO underwent standard characterization by tunnel length, and right, and left atrial orifice diameters. Logarithmic regression analysis between porcine PFO tunnel length and left atrial orifice area demonstrated a significant positive relationship (P = 0.0162, R(2) = 0.227). The porcine PFO tunnel length was significantly longer than in humans (12.0 +/- 4.0 mm vs. 7.1 +/- 3.1 mm respectively, P < 0.0001). Histopathologic comparison was made using serial sections perpendicular to the atrial septum and the tunnel long axis. Human and porcine PFO lesions demonstrated strong similarities in tissue cells, connective tissue, and matrix composition. CONCLUSIONS: PFO assessment was standardized in both macroscopically and histopathologically, with quantitative and qualitative comparisons feasible using a porcine preclinical model. PFO prevalence in domestic swine is identical to humans, and microscopic structures very similar to humans. The domestic swine PFO model appears useful to evaluate new interventional closure technologies due to comparability in microscopic features. Tunnel length should be carefully evaluated due to differences across pigs and patients.

Adolescent↗
PubMed2006

Real-time detection and alerting for acute ST-segment elevation myocardial ischemia using an implantable, high-fidelity, intracardiac electrogram monitoring system with long-range telemetry in an ambulatory porcine model.

OBJECTIVES: The purpose of this study was to evaluate feasibility of using real-time, high-fidelity, intracardiac electrogram monitoring from a permanently implantable ischemia detection system (IIDS), with long-range telemetry capability to detect ST-segment shifts associated with acute or subacute coronary occlusion in a porcine model. BACKGROUND: Early identification of coronary occlusion with ST-segment elevation could profoundly accelerate the timing of revascularization and improve clinical outcomes. METHODS: This paper reports the first investigation using real-time, high-fidelity, intracardiac electrogram monitoring from a permanently IIDS, with long-range telemetry capability. This IIDS was tested in an ambulatory porcine model, with acute coronary occlusion precipitated by stent thrombosis. Two overlapping copper stents were implanted in the left anterior descending (n = 3), the circumflex (n = 3), or the right coronary artery (n = 2) of juvenile farm pigs. Monitoring was carried using telemetry from the IIDS. RESULTS: All stented pigs had acute ST-segment elevation event(s) triggering the alerting thresholds of the IIDS. All triggered events were confirmed to be caused by thrombosis of the copper stent(s), and well correlated to infarct age and location. Four of the 8 pigs died from ventricular fibrillation, recorded by the IIDS at a mean time of 70 +/- 121 h after ST-segment alert. The sensitivity and specificity of alerting for ST-segment shift, associated with thrombotic coronary occlusion, were 100% and 100%, respectively. CONCLUSIONS: This study demonstrates the ability of an implantable ischemia detection system to detect ST-segment elevation from coronary occlusion in a porcine model of ST-segment elevation myocardial infarction. ST-segment elevation was sufficient to trigger alerting thresholds in all 3 epicardial coronary distributions. Such a system, with real-time alerting capability, could advance the time frame of reperfusion therapy and potentially prevent, rather than interrupt, acute myocardial infarction in patients with coronary artery disease.

Acute Disease↗
PubMed2006

Pioglitazone inhibits in-stent restenosis in atherosclerotic rabbits by targeting transforming growth factor-beta and MCP-1.

OBJECTIVE: Although emerging data from preclinical and clinical studies suggests a reduction of in-stent restenosis with peroxisome proliferator-activated receptor (PPAR)-gamma agonists, the reduction of neointimal growth via anti-inflammatory mechanisms has not been explored. METHODS AND RESULTS: Hypercholesterolemic New Zealand White rabbits (n=45) received bilateral balloon-expandable stents implanted into atherosclerotic iliac arteries. Animals were randomized to oral pioglitazone 3 (low dose) or 10 mg/kg per day (high dose) started on the day of stent implantation; control rabbits received placebo. Tissue harvest was performed 28 days after stenting, and stented segments underwent histology, morphometry, immunostaining for macrophages, and scanning electron microscopy. In selected animals, stented arterial segments were placed in organoid culture for 48 hours, and the conditioned media was assayed for 23 different cytokines. There was a 21% reduction in neointimal area for high-dose pioglitazone treated versus placebo rabbits (P<0.005), which was associated with a significant reduction of neointimal macrophages. Analysis of conditioned media revealed an 82% and 74% reduction in the release of monocyte chemoattractant protein-1 (MCP-1) (P<0.007) and transforming growth factor (TGF)-beta1 (P<0.01), respectively, in stented segments from animals treated with 10 mg/kg per day pioglitazone versus placebo. CONCLUSIONS: Oral pioglitazone suppresses in-stent neointimal growth by limiting local inflammatory pathways and may be useful as an adjunctive therapy in patients undergoing percutaneous interventions.

Administration, Oral↗
PubMed2006

A hypothesis for vulnerable plaque rupture due to stress-induced debonding around cellular microcalcifications in thin fibrous caps.

In this article, we advance a hypothesis for the rupture of thin fibrous cap atheroma, namely that minute (10-mum-diameter) cellular-level microcalcifications in the cap, which heretofore have gone undetected because they lie below the visibility of current in vivo imaging techniques, cause local stress concentrations that lead to interfacial debonding. New theoretical solutions are presented for the local stress concentration around these minute spherical inclusions that predict a nearly 2-fold increase in interfacial stress that is relatively insensitive to the location of the hypothesized microinclusions in the cap. To experimentally confirm the existence of the hypothesized cellular-level microcalcifications, we examined autopsy specimens of coronary atheromatous lesions using in vitro imaging techniques whose resolution far exceeds conventional magnetic resonance imaging, intravascular ultrasound, and optical coherence tomography approaches. These high-resolution imaging modalities, which include confocal microscopy with calcium-specific staining and micro-computed tomography imaging, provide images of cellular-level calcifications within the cap proper. As anticipated, the minute inclusions in the cap are very rare compared with the numerous calcified macrophages observed in the necrotic core. Our mathematical model predicts that inclusions located in an area of high circumferential stress (>300 kPa) in the cap can intensify this stress to nearly 600 kPa when the cap thickness is <65 microm. The most likely candidates for the inclusions are either calcified macrophages or smooth muscle cells that have undergone apoptosis.

Atherosclerosis↗
PubMed2006

Lipoprotein-associated phospholipase A2 protein expression in the natural progression of human coronary atherosclerosis.

OBJECTIVE: Although lipoprotein-associated phospholipase A2 (Lp-PLA2) has received recent attention as a biomarker of inflammation and risk for acute coronary events, its relative expression in coronary plaque phenotypes, including unstable lesions, has not been established. METHODS AND RESULTS: Coronary segments (n=30) were prospectively collected from 25 sudden coronary death patients for immunolocalization of Lp-PLA2. Lesion morphologies were classified as pathologic intimal thickening, fibroatheromas, thin-cap fibroatheromas (fibrous cap thicknesses <65 microm), and rupture. The expression of Lp-PLA2 was detected using a specific monoclonal antibody. Apoptosis was identified by DNA end-labeling using terminal deoxynucleotidyl transferase (TdT). Lp-PLA2 staining in early plaques was absent or minimally detected. In contrast, thin-cap fibroatheromas and ruptured plaques showed intense Lp-PLA2 expression within necrotic cores and surrounding macrophages including those in the fibrous cap. The degree of macrophage apoptosis was greater in thin-cap fibroatheroma and ruptures compared with less advanced plaques with additional double labeling studies showing Lp-PLA2 present in apoptotic cells in regions of high macrophage density. CONCLUSIONS: Lp-PLA2 is strongly expressed within the necrotic core and surrounding macrophages of vulnerable and ruptured plaques, with relatively weak staining in less advanced lesions. These findings together with the association of Lp-PLA2 in apoptotic macrophages suggest a potential role in promoting plaque instability.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed2006

Statin treatment is not associated with consistent alterations in inflammatory status of carotid atherosclerotic plaques: a retrospective study in 378 patients undergoing carotid endarterectomy.

BACKGROUND AND PURPOSE: Anti-inflammatory qualities are held partially responsible for the reduction of cardiovascular events after statin treatment. We examined the phenotype of carotid atherosclerotic plaques harvested during carotid endarterectomy in relation to the previous use of different statins prescribed in clinical practice. METHODS: Three hundred and seventy-eight patients were included. Atherosclerotic plaques were harvested, immunohistochemically stained and semiquantitively examined for the presence of macrophages (CD68), smooth muscle cells, collagen and fat. Adjacent atherosclerotic plaques were used to study protease activity and interleukin levels. Patients' demographics were recorded and blood samples were stored. RESULTS: Serum cholesterol, low-density lipoprotein, apolipoprotein B, and C-reactive protein levels were lower in patients treated with statins compared with patients without statin treatment. Atheromatous plaques were less prevalent in patients receiving statins compared with patients without statin therapy (29% versus 42%, P=0.04). An increase of CD68 positive cells was observed in patients receiving statins compared with nonstatin treatment (P=0.05). This effect was specifically related to atorvastatin treatment. In patients treated with atorvastatin, the increased amount of CD68 positive cells were not associated with increased protease activity. In contrast, a dose-dependent decrease in protease activity was shown in the atorvastatin group. Interleukin 6 expression was lower in plaques obtained from patients treated with statins (P=0.04). CONCLUSIONS: Statin use may exert pleiotropic effects on plaque phenotype. However, not the presence of macrophages but activation with subsequent protease and cytokine release may be attenuated by statin use.

Antigens, CD↗
PubMed2006

Accuracy of in vivo coronary plaque morphology assessment: a validation study of in vivo virtual histology compared with in vitro histopathology.

OBJECTIVES: The goal of the present study was to compare the accuracy of in vivo tissue characterization obtained by intravascular ultrasound (IVUS) radiofrequency (RF) data analysis, known as Virtual Histology (VH), to the in vitro histopathology of coronary atherosclerotic plaques obtained by directional coronary atherectomy. BACKGROUND: Vulnerable plaque leading to acute coronary syndrome (ACS) has been associated with specific plaque composition, and its characterization is an important clinical focus. METHODS: Virtual histology IVUS images were performed before and after a single debulking cut using directional coronary atherectomy. Debulking region of in vivo histology image was predicted by comparing pre- and post-debulking VH images. Analysis of VH images with the corresponding tissue cross section was performed. RESULTS: Fifteen stable angina pectoris (AP) and 15 ACS patients were enrolled. The results of IVUS RF data analysis correlated well with histopathologic examination (predictive accuracy from all patients data: 87.1% for fibrous, 87.1% for fibro-fatty, 88.3% for necrotic core, and 96.5% for dense calcium regions, respectively). In addition, the frequency of necrotic core was significantly higher in the ACS group than in the stable AP group (in vitro histopathology: 22.6% vs. 12.6%, p = 0.02; in vivo virtual histology: 24.5% vs. 10.4%, p = 0.002). CONCLUSIONS: Correlation of in vivo IVUS RF data analysis with histopathology shows a high accuracy. In vivo IVUS RF data analysis is a useful modality for the classification of different types of coronary components, and may play an important role in the detection of vulnerable plaque.

Aged↗
PubMed2006

Sources of error and interpretation of plaque morphology by optical coherence tomography.

This study was performed to assess the strengths and weaknesses of optical coherence tomography (OCT) intravascular imaging in identifying plaque morphology. Seventy-nine postmortem human coronary arterial sections classified as fibrous-cap atheromas, calcific plaques, fibrous plaques, and complicated lesions were studied. OCT was able to identify 45% of fibrous-cap atheromas (kappa=0.27, p<0.01), 68% of fibrocalcific plaques (kappa=0.40, p<0.001), 83% of fibrous plaques (kappa=0.37, p<0.001), and 100% of complicated lesions (all thrombi; kappa=1, p<0.001). Misinterpretation was caused mainly by the low OCT signal penetration, which could not detect lipid pools or calcium behind thick fibrous caps, and by an inability to distinguish calcium deposits from lipid pools or the opposite. Lesions with thick (>150 microm) caps were histologically identified as 25 thick fibrous-cap atheromas, 8 fibrocalcific plaques, and 5 fibrous plaques; all these lesions were relatively "stable." In contrast, lesions with fibrous caps<150 microm were either vulnerable or stable lesions (11 thin-fibrous-cap atheromas and 11 fibrocalcific plaques). In conclusion, although OCT images may give an indication of the overall composition of large homogenous signal-poor regions, such as lipids or calcified areas, they could be unreliable in differentiating areas with heterogenous compositions. OCT may easily recognize relatively stable lesions.

Artifacts↗
PubMed2006

Pathology of drug-eluting stents in humans: delayed healing and late thrombotic risk.

OBJECTIVES: This study examined human drug-eluting stents (DES) to determine the long-term effects of these stents on coronary arterial healing and identified mechanisms underlying late stent thrombosis (LST). BACKGROUND: Although DES reduce the need for repeat revascularization compared with bare-metal stents (BMS), data suggest the window of thrombotic risk for Cypher (Cordis Corp., Miami Lakes, Florida) and Taxus (Boston Scientific Corp., Natick, Massachusetts) DES extends far beyond that for BMS. METHODS: From a registry of 40 autopsies of DES (68 stents), 23 DES cases of >30 days duration were compared with 25 matched autopsies of BMS implantation. Late stent thrombosis was defined as an acute thrombus within a stent >30 days old. RESULTS: Of 23 patients with DES >30 days old, 14 had evidence of LST. Cypher and Taxus DES showed greater delayed healing characterized by persistent fibrin deposition (fibrin score 2.3 +/- 1.1 vs. 0.9 +/- 0.8, p = 0.0001) and poorer endothelialization (55.8 +/- 26.5%) compared with BMS (89.8 +/- 20.9, p = 0.0001). Moreover, DES with LST showed more delayed healing compared with patent DES. In 5 of 14 patients suffering LST, antiplatelet therapy had been withdrawn. Additional procedural and pathologic risk factors for LST were: 1) local hypersensitivity reaction; 2) ostial and/or bifurcation stenting; 3) malapposition/incomplete apposition; 4) restenosis; and 5) strut penetration into a necrotic core. CONCLUSIONS: The Cypher and Taxus DES result in delayed arterial healing when compared with BMS of similar implant duration. The cause of DES LST is multifactorial with delayed healing in combination with other clinical and procedural risk factors playing a role.

Adult↗
PubMed2006

Pathology of the vulnerable plaque.

The majority of patients with acute coronary syndromes (ACS) present with unstable angina, acute myocardial infarction, and sudden coronary death. The most common cause of coronary thrombosis is plaque rupture followed by plaque erosion, whereas calcified nodule is infrequent. If advances in coronary disease are to occur, it is important to recognize the precursor lesion of ACS. Of the three types of coronary thrombosis, a precursor lesion for acute rupture has been postulated. The non-thrombosed lesion that most resembles the acute plaque rupture is the thin cap fibroatheroma (TCFA), which is characterized by a necrotic core with an overlying fibrous cap measuring <65 microm, containing rare smooth muscle cells but numerous macrophages. Thin cap fibroatheromas are most frequently observed in patients dying with acute myocardial infarction and least common in plaque erosion. They are most frequently observed in proximal coronary arteries, followed by mid and distal major coronary arteries. Vessels demonstrating TCFA do not usually show severe narrowing but show positive remodeling. In TCFAs the necrotic core length is approximately 2 to 17 mm (mean 8 mm) and the underlying cross-sectional area narrowing in over 75% of cases is <75% (diameter stenosis <50%). The area of the necrotic core in at least 75% of cases is < or =3 mm2. These lesions have lesser degree of calcification than plaque ruptures. Thin cap fibroatheromas are common in patients with high total cholesterol (TC) and high TC/high-density lipoprotein cholesterol ratio, in women >50 years, and in those patients with elevated high levels of high sensitivity C-reactive protein. It has only recently been recognized that their identification in living patients might help reduce the incidence of sudden coronary death.

Angina, Unstable↗
PubMed2006

Progressive vascular smooth muscle cell defects in a mouse model of Hutchinson-Gilford progeria syndrome.

Children with Hutchinson-Gilford progeria syndrome (HGPS) suffer from dramatic acceleration of some symptoms associated with normal aging, most notably cardiovascular disease that eventually leads to death from myocardial infarction and/or stroke usually in their second decade of life. For the vast majority of cases, a de novo point mutation in the lamin A (LMNA) gene is the cause of HGPS. This missense mutation creates a cryptic splice donor site that produces a mutant lamin A protein, termed "progerin," which carries a 50-aa deletion near its C terminus. We have created a mouse model for progeria by generating transgenics carrying a human bacterial artificial chromosome that harbors the common HGPS mutation. These mice develop progressive loss of vascular smooth muscle cells in the medial layer of large arteries, in a pattern very similar to that seen in children with HGPS. This mouse model should prove valuable for testing experimental therapies for this devastating disorder and for exploring cardiovascular disease in general.

Animals↗
PubMed2006

Adventitial microvessel formation after coronary stenting and the effects of SU11218, a tyrosine kinase inhibitor.

OBJECTIVES: The aim of this study was to delineate the temporal profile of adventitial microvessel (Ad-MV) formation after stenting, its relationship to arterial wall hypoxia, and the effects of a tyrosine kinase inhibitor (TKI), SU11218, on Ad-MV and in-stent intimal hyperplasia (IH). BACKGROUND: Adventitial microvessels have been reported after arterial injury; however, the underlying stimulus for this response and its relationship to IH is unknown. METHODS: Coronary stenting was performed in 40 pigs randomized to SU11218 (n = 20) or placebo (n = 20). Vessel wall hypoxia was assessed by pimonidazole adducts and hypoxia-inducible factor (HIF)-1 alpha expression. Adventitial microvessels were quantified by three-dimensional microscopic computed tomography (3D micro CT). Intimal hyperplasia was measured by intravascular ultrasound (IVUS), 3D micro CT, and morphometry. The effects of SU11218 were assessed in vitro on smooth muscle cell (SMC) and endothelial cell (EC) functions and in vivo on Ad-MV and IH. RESULTS: Hypoxia was evident in the vessel wall at 48 h and persisted for four weeks. Adventitial microvessels increased significantly at one week (24 +/- 7 microvessels/segment) and four weeks (23 +/- 7 microvessels/segment) compared with uninjured arteries (16 +/- 2 microvessels/segment; p < 0.001) and correlated with IH (r = 0.77, p < 0.001). The TKI SU11218 inhibited platelet-derived growth factor receptor-beta phosphorylation, EC and SMC DNA synthesis, and migration in a dose-dependent manner in vitro and significantly inhibited Ad-MV (16 +/- 5 vs. 23 +/- 7 microvessels/segment in placebo, p < 0.001) and produced approximately 80% reduction in IH (0.52 +/- 0.51 mm2 vs. 2.47 +/- 1.66 mm2 in placebo, p < 0.001) at four weeks in vivo. CONCLUSIONS: Arterial stenting causes arterial wall hypoxia followed by Ad-MV formation. The TKI SU11218 inhibits both Ad-MV formation and IH and represents a promising therapeutic agent to prevent in-stent restenosis.

Animals↗
PubMed2006

A novel paclitaxel-eluting porous carbon-carbon nanoparticle coated, nonpolymeric cobalt-chromium stent: evaluation in a porcine model.

OBJECTIVES: We aimed to evaluate the response of porcine coronary arteries to a novel paclitaxel-eluting porous carbon-carbon nanoparticle coated, nonpolymeric cobalt chromium stent. BACKGROUND: Polymer based drug-eluting stents significantly reduce restenosis. However, the indefinite presence of polymer is thought to initiate and sustain inflammation and contribute to the occurrence of late complications. METHODS: Sixteen carbon-carbon coated, nonpolymeric cobalt chromium stents with two different doses of paclitaxel (eight of each) were implanted in porcine coronary arteries. In addition, eight cobalt chromium stents coated with a biodegradable polymer were also studied. Animals were sacrificed 6 weeks after stent implantation and histomorphometric analysis was performed. Results were compared among the three groups of stents. RESULTS: The cobalt chromium stents coated with carbon-carbon with low and medium doses of paclitaxel both showed acceptable performance characteristics, with respect to endothelialization, neointimal hyperplasia, percentage diameter stenosis, inflammatory response, and tendency to fibrin deposition, when compared to historical data with the Cypher stent. On the other hand, the stents coated with poly(lactide) and poly(lactide-co-glycolide) biodegradable polymers and 0.7 microg/mm2 paclitaxel showed poor performance. There was a significant tendency to poor endothelialization, greater neointimal hyperplasia, percentage diameter stenosis, greater inflammatory response, and tendency to fibrin deposition (P < 0.01 for all parameters). CONCLUSIONS: This preclinical evaluation demonstrates the safety and efficacy of a novel cobalt chromium stent with a carbon-carbon coating and low and medium doses of paclitaxel.

Analysis of Variance↗
PubMed2006

Experimental efficacy of an everolimus eluting cobalt chromium stent.

INTRODUCTION: Rapamycin and its analogs are now being coated on different stent platforms, using different polymer matrices to prevent restenosis by impairing vascular smooth muscle cell proliferation and neointimal formation. METHODS: We evaluated the feasibility and compared the efficacy of biostable polymeric everolimus and sirolimus (CYPHER, Cordis) eluting stents in a porcine coronary model. Cobalt chromium balloon expandable stents (ML VISION, Guidant) were coated with a polymer containing everolimus (190 mug/cm(2)). Twelve pigs underwent placement of 36 oversized sirolimus (n = 12), everolimus (n = 12), and bare metal (cobalt chromium, n = 12) stents in the coronary arteries. RESULTS: At day 28, vessel injury scores were low (<0.25) and similar between each of the three test groups. The mean neointimal thickness was significantly lower in the everolimus- (0.13 +/- 0.07 mm, P = 0.02) and sirolimus-eluting stents (0.13 +/- 0.08 mm, P = 0.04) versus the bare metal stents (0.20 +/- 0.07 mm). The mean percent area stenosis was similar for the everolimus-eluting stents [(20.8 +/- 6.9)%] and the sirolimus-eluting stents [(20.8 +/- 7.6)%], and each was significantly less than that of bare metal stents [(26.1 +/- 7.8)%, P = 0.05]. CONCLUSION: Stent-based delivery of sirolimus and everolimus delivered via durable polymeric matrices are equally effective in the suppression of neointimal formation at day 28 in the porcine coronary model. Further study is necessary to document dose response and long-term comparative effects of these drug-eluting stents.

Animals↗
PubMed2006

Protected carotid stenting in high-surgical-risk patients: the ARCHeR results.

BACKGROUND: Carotid endarterectomy is the standard of care for most patients with severe extracranial carotid bifurcation disease. However, its safety and efficacy in patients with significant surgical risk are unclear. The ARCHeR (ACCULINK for Revascularization of Carotids in High-Risk patients) trial was performed to determine whether carotid artery stenting with embolic protection is a safe and effective alternative to endarterectomy in high-surgical-risk patients. METHODS: The ARCHeR trial is a series of three sequential, multicenter, nonrandomized, prospective studies. Forty-eight sites enrolled 581 high-surgical-risk patients between May 2000 and September 2003. Patients with severe carotid artery stenosis (angiographically defined, symptomatic > or =50%, or asymptomatic > or =80%) had an ACCULINK nitinol stent implanted. The ACCUNET filter embolic protection system was added to the procedure in the final 2 studies (422 patients). The primary efficacy end point was a composite of periprocedural (< or =30 days) death, stroke, and myocardial infarction, plus ipsilateral stroke between days 31 and 365. RESULTS: The 30-day rate of death/stroke/myocardial infarction was 8.3% (95% confidence interval [CI], 6.2%-10.8%), and that of stroke/death was 6.9% (95% CI, 5.0%-9.3%). Most (23/32) strokes were minor, of which more than half (12/23) returned to baseline National Institutes of Health Stroke Scale scores within 30 days. The 30-day major/fatal stroke rate was 1.5% (95% CI, 0.7%-2.9%). No hemorrhagic strokes were observed in the study. Ipsilateral cerebrovascular accident occurred in 1.3% between 30 days and 1 year, thus giving a primary composite end point of 30-day death/stroke/myocardial infarction plus ipsilateral stroke at 1 year of 9.6% (95% CI, 7.2%-12.0%), which is below the 14.4% historical control comparator. Target lesion revascularization at 12 months and 2 years was 2.2% and 2.9%, respectively. CONCLUSIONS: The ARCHeR results demonstrate that extracranial carotid artery stenting with embolic filter protection is not inferior to historical results of endarterectomy and suggest that carotid artery stenting is a safe, durable, and effective alternative in high-surgical-risk patients.

Angioplasty, Balloon↗
PubMed2006

Morphological characteristics of coronary atherosclerosis in diabetes mellitus.

The incidence of diabetes is increasing in the general population because of increasing obesity, and is likely to result in a higher incidence of coronary artery disease. It was recently reported that diabetics (types I and II) dying suddenly from coronary artery disease have greater macrophage and T lymphocyte infiltration in atherosclerotic plaques, as well as larger necrotic cores compared with nondiabetics. The inflammatory cell infiltrates showed human leukocyte antigen-DR expression, which was greater in diabetics. The receptors for advanced glycosylation end-products expression, demonstrated by immunohistochemistry, was greater in diabetics than in nondiabetics in macrophages, smooth muscle cells and endothelial cells, and was associated with apoptosis of macrophages and smooth muscle cells, but not of endothelial cells. There is also a higher incidence of healed plaque ruptures and healed myocardial infarct in type II diabetics. Plaque burden is higher in diabetics than in nondiabetics; however, distal plaque burden was only significantly different in type II diabetics compared with nondiabetics. There was greater positive remodelling in diabetic coronary arteries than in nondiabetic ones, which correlated with the per cent necrotic core. Further studies are needed to better understand the mechanisms that govern greater inflammation and plaque burden in diabetics.

Coronary Artery Disease↗