Normal Artery Segments Research Articles

Differential Expression of Circulating Damage-Associated Molecular Patterns in Patients with Coronary Artery Ectasia.

Coronary artery ectasia (CAE) is defined as abnormal dilation of a coronary artery with a diameter exceeding that of adjacent normal arterial segment by >1.5 times. CAE is a pathological entity of the coronary arteries and characterized as a variant of coronary atherosclerosis. CAE frequently coexists with coronary artery disease (CAD). While inflammation appears to be involved, the pathophysiology of CAE remains unclear. Damage-associated molecular patterns (DAMPs), defined as endogenous molecules released from stressed or damaged tissue, are deemed as alarm signals by the innate immune system. Inflammatory agents can generate DAMPs and DAMPs can create a pro-inflammatory state. In a prospective cross-sectional study, we enrolled 29 patients with CAE and non-obstructive CAD, 19 patients with obstructive CAD without CAE, and 14 control subjects with normal (control) coronary arteries age- and sex-matched with the CAE patients, to investigate the differential expression of plasma DAMPs. Patients with CAE and non-obstructive CAD had increased plasma levels of the DAMPs S100B, S100A12, HMGB1, and HSP70, the DAMPs receptor TLR4, and miR328a-3p compared to CAD and controls. Plasma levels of the mir328a-3p target the protective soluble form of the DAMPs receptor for advanced glycation end products (sRAGE), and the antioxidant DJ-1 was decreased in both CAE and CAD compared to controls. In an in vitro human umbilical vein endothelial cells model, circulating levels of S100B, HMGB1, HSP70 as well as CAE patient plasma induced inflammatory responses. The differential expression of the DAMPs S100B, HSP70, HMGB1, and their receptors TLR4 and sRAGE in CAE versus CAD makes them attractive novel biomarkers as therapeutic targets and therapeutics.

Sub-satisfactory stenting recanalization of severe vascular stenosis of the posterior circulation can significantly improve cerebral hemodynamic perfusion

PurposeTo investigate the effect of sub-satisfactory stenting recanalization of severe vascular stenosis of the posterior circulation on cerebral hemodynamic perfusion. Materials and methodsPatients with severe vascular stenosis of the posterior circulation who had undergone three-dimensional cerebral angiography before and after stenting were retrospectively enrolled. Computational fluid dynamic (CFD) analysis of hemodynamic parameters at the stenosis, perforating branch, and normal arterial segments proximal and distal to the stenosis were performed. ResultsSixty-two patients with basilar artery stenosis aged 60.9 ± 9.6 years were enrolled, and stent angioplasty resulted in the reduction of stenosis degree from 85.3 ± 7.2% before to 18.6 ± 6.4% after stenting. After stenting, at the proximal normal artery, the total pressures had significantly (P < 0.05) decreased, whereas all the other parameters (WSS, cell Reynolds number, velocity, vorticity, turbulence intensity, turbulence kinetic energy and dissipation rate) had significantly (P < 0.05) increased. At the stenosis, all hemodynamic parameters had significantly decreased. At the stenosis perforating branch, the WSS, cell Reynolds number, velocity, and vorticity were all significantly decreased, and the total pressure, turbulence intensity, kinetic energy, and dissipation rate were all significantly increased. At the distal normal artery, the total flow pressure (perfusion pressure) and velocity were both significantly (P < 0.05) increased, and the total pressure, WSS, cell Reynolds number, vorticity, turbulence intensity, kinetic energy, and dissipation rate were all significantly (P < 0.05) decreased. The hemodynamic parameters after stenting were closer to those after virtual stenosis repair at all measurements. ConclusionSub-satisfactory recanalization has significantly restored the stenosis and improved the hemodynamic parameters near the stenosis and at the root of the perforating branch, thus significantly improving the cerebral perfusion, similar to the changes of hemodynamic status and cerebral perfusion after virtual removal of the vascular stenosis. This may indicate the good effect of sub-satisfactory stenting recanalization of the vascular stenosis at the posterior circulation.

Prevalence and Angiographic Characteristics of Coronary Ectasia in Adults: A Retrospective Study in a Tertiary Cardiac Centre of Nepal

Background and Aims: Coronary artery Ectasia is a relatively uncommon problem encountered during coronary angiography with the prevalence ranging from 1.2% to 4.9%. Coronary artery Ectasia and aneurysm both denote an arterial segment the dimension of which is larger than normal arterial segment, both have diameter greater than 1.5 times of normal. The length of dilate segment is greater than its width in Ectasia while less in aneurysm. There is an overlap between risk factors of coronary artery Ectasia and atherosclerosis. The clinical relevance in general, and the appropriate medical management of coronary artery Ectasia specifically, is ill defined, as no randomised prospective studies exists. The study was conducted with an aim to estimate the prevalence of coronary artery Ectasia and aneurysm as well as to study the angiographic characteristics of coronary artery Ectasia and aneurysm undergoing in adult patients’ coronary angiography in tertiary cardiac centre of Nepal.&#x0D; Methods: A retrospective study was conducted in Shahid Gangalal national heart centre, Nepal analysing the angiographic records from cardiac catheterization lab. A total of 447 patients who underwent coronary angiography and meet the inclusion criteria from July, 2019 to December, 2019 were included in the study. Any angiographic evidence of coronary Ectasia and aneurysm, coronary artery involved and it’s extent were analysed and recorded in the proforma. In addition, any associated evidence of coronary artery disease was analysed and recorded in the proforma.&#x0D; Results: The findings of our study revealed the overall prevalence of coronary artery Ectasia (CAE) and Coronary artery Aneurysm as 2.6%. Coronary ectasia was most prevalent in left anterior descending (LAD) artery (83.3%), followed by RCA and left main in 66.7% and 16.7% respectively. In contrast, Coronary aneurysm was mostly seen in RCA (66.7%) followed by LCX (33.3%). In addition, the study also showed the frequency of localised Ectasia as 50 % and the association of significant coronary artery disease with coronary artery Ectasia in 66.67%.&#x0D; Conclusion: CAE and aneurysm are rare phenomenon encountered in routine coronary angiography, with LAD and RCA being most commonly involved in CAE and coronary aneurysm respectively. CAE and aneurysm have significant association with the coronary artery disease.

THE RELATIONSHIP BETWEEN THE EXPRESSION LEVELS OF TISSUE INHIBITOR OF METALLOPROTEINASES-3 (TIMP3) AND SEVERITY OF ATHEROSCLEROSIS

Objective: TIMP3 is one of tissue inhibitors of metalloproteinases (TIMPs), which binds to the components of the extracellular matrix, and has crucial roles in atherosclerogenesis and adipose tissue differentiation. In this study, it was aimed to determine the effects of TIMP3 gene expression levels on severity of atherosclerosis in different tissues. Material and Methods: The first group of the study (evaluated for coronary artery disease) were cases classified as high and low plaque scores according to the degree and location of atherosclerotic lesions. In the second group (post-mortem cases) were male cadavers who died due to coronary heart disease (CHD, n=26) and non-cardiac trauma (T-nonP, n=4). The TIMP3 expression levels were examined in leukocyte and peri-coronary epicardial adipose tissues (EAT) samples (n=69 and n=34, respectively) of the first group and EAT and coronary artery samples (n=12 and n=30, respectively) of the second group using quantitative RT-PCR. In addition, the protein expressions of TIMP3 were analysed on artery sections by immunofluorestaining. Results: In the post-mortem study group, the TIMP3 expression levels were found to increase in no plaque segments of arteries of cases with CHD (CHD-nonP) compared to advanced atherosclerotic arteries (CHD-P) and normal arteries of T-nonP cases (p=0.01 and p=0.05, respectively). The TIMP3 expressions in EATs and leukocytes were not statistically significant between the study groups. In addition, TIMP3 protein was detected in normal arteries, peri-coronary EATs and mostly in macrophages-rich areas in advanced atherosclerotic arteries. Conclusion: TIMP3 expression levels increase in normal coronary arterial segments of cases with CHD, which depict a protective role of TIMP3 in development of atherosclerosis.

Epidemiology and contemporary management of abdominal aortic aneurysms.

Abdominal aortic aneurysm (AAA) is most commonly defined as a maximal diameter of the abdominal aorta in excess of 3 cm in either anterior-posterior or transverse planes or, alternatively, as a focal dilation ≥1.5 times the diameter of the normal adjacent arterial segment. Risk factors for the development of AAA include age >60, tobacco use, male gender, Caucasian race, and family history of AAA. Aneurysm growth and rupture risk appear to be associated with persistent tobacco use, female gender, and chronic pulmonary disease. The majority of AAAs are asymptomatic and detected incidentally on various imaging studies, including abdominal ultrasound, and computed tomographic angiography. Symptoms associated with AAA may include abdominal or back pain, thromboembolization, atheroembolization, aortic rupture, or development of an arteriovenous or aortoenteric fistula. The Screening Abdominal Aortic Aneurysms Efficiently (SAAAVE) Act provides coverage for a one-time screening abdominal ultrasound at age 65 for men who have smoked at least 100 cigarettes and women who have family history of AAA disease. Medical management is recommended for asymptomatic patients with AAAs <5 cm in diameter and focuses on modifiable risk factors, including smoking cessation and blood pressure control. Primary indications for intervention in patients with AAA include development of symptoms, rupture, rapid aneurysm growth (>5 mm/6 months), or presence of a fusiform aneurysm with maximum diameter of 5.5 cm or greater. Intervention for AAA includes conventional open surgical repair and endovascular aortic stent graft repair.

Expansive arterial remodeling of the carotid arteries and its effect on atherosclerotic plaque composition and vulnerability: an in-vivo black-blood 3T CMR study in symptomatic stroke patients.

BackgroundBased on intravascular ultrasound of the coronary arteries expansive arterial remodeling is supposed to be a feature of the vulnerable atheroslerotic plaque. However, till now little is known regarding the clinical impact of expansive remodeling of carotid lesions. Therefore, we sought to evaluate the correlation of expansive arterial remodeling of the carotid arteries with atherosclerotic plaque composition and vulnerability using in-vivo Cardiovascular Magnetic Resonance (CMR).MethodsOne hundred eleven symptomatic patients (74 male/71.8 ± 10.3y) with acute unilateral ischemic stroke and carotid plaques of at least 2 mm thickness were included. All patients received a dedicated multi-sequence black-blood carotid CMR (3Tesla) of the proximal internal carotid arteries (ICA). Measurements of lumen, wall, outer wall, hemorrhage, calcification and necrotic core were determined. Each vessel-segment was classified according to American Heart Association (AHA) criteria for vulnerable plaque. A modified remodeling index (mRI) was established by dividing the average outer vessel area of the ICA segments by the lumen area measured on TOF images in a not affected reference segment at the distal ipsilateral ICA. Correlations of mRI and clinical symptoms as well as plaque morphology/vessel dimensions were evaluated.ResultsSeventy-eight percent (157/202) of all internal carotid arteries showed atherosclerotic disease with AHA Lesion-Type (LT) III or higher. The mRI of the ICA was significantly different in normal artery segments (AHA LT I; mRI 1.9) compared to atherosclerotic segments (AHA LT III-VII; mRI 2.5; p < 0.0001). Between AHA LT III-VII there was no significant difference of mRI. Significant correlations (p < 0.05) of the mRI with lumen-area (LA), wall-area (WA), vessel-area (VA) and wall-thickness (WT), necrotic-core area (NC), and ulcer-area were observed. With respect to clinical presentation (symptomatic/asymptomatic side) and luminal narrowing (stenotic/non-stenotic) no relevant correlations or significant differences regarding the mRI were found.ConclusionExpansive arterial remodeling exists in the ICA. However, no significant association between expansive arterial remodeling, stroke symptoms, complicated AHA VI plaque, and luminal stenosis could be established. Hence, results of our study suggest that expansive arterial remodeling is not a very practical marker for plaque vulnerability in the carotid arteries.

Piecewise Pulse Wave Imaging (pPWI) for Detection and Monitoring of Focal Vascular Disease in Murine Aortas and Carotids In Vivo.

Atherosclerosis and Abdominal Aortic Aneurysms (AAAs) are two common vascular diseases associated with mechanical changes in the arterial wall. Pulse Wave Imaging (PWI), a technique developed by our group to assess and quantify the mechanical properties of the aortic wall in vivo, may provide valuable diagnostic information. This work implements piecewise PWI (pPWI), an enhanced version of PWI designed for focal vascular diseases. Localized, sub-regional PWVs and PWI moduli ( EPWI ) were estimated within 2-4 mm wall segments of murine normal, atherosclerotic and aneurysmal arteries. Overall, stiffness was found to increase in the atherosclerotic cases. The mean sub-regional PWV was found to be 2.57±0.18 m/s for the normal aortas (n = 7) with a corresponding mean EPWI of 43.82±5.86 kPa. A significant increase ( (p ≤ 0.001)) in the group means of the sub-regional PWVs was found between the normal aortas and the aortas of mice on high-fat diet for 20 ( 3.30±0.36 m/s) and 30 weeks ( 3.56±0.29 m/s). The mean of the sub-regional PWVs ( 1.57±0.78 m/s) and EPWI values ( 19.23±15.47 kPa) decreased significantly in the aneurysmal aortas (p ≤ 0.05) . Furthermore, the mean coefficient of determination (r(2)) of the normal aortas was significantly higher (p ≤ 0.05) than those of the aneurysmal and atherosclerotic cases. These findings demonstrated that pPWI may be able to provide useful biomarkers for monitoring focal vascular diseases.

Innate collateral vessels in the absence of ischemia undergo shear stress similar to normal arterial segments of the same diameter (1079.12)

Some species, including humans, have structural collateral vessels, CV, that can further develop in the presence of coronary stenosis by increasing pressure difference across them. Question is how CV's are maintained in the absence of ischemia.The coronary network of 6 healthy canine hearts was reconstructed in 3D from images obtained with an imaging cryomicrotome after filling with fluorescent replica material (resolution 0.020 mm). CV's were automatically detected. The full coronary network was reconstructed. For all segments, including CV's, diameter and perfused tissue mass, PTM, was derived and shear stress, SS, calculated.Innate collateral connections ranged from 286 to 1015 µm in diameter and were distributed over the myocardial wall with some higher density at the subendocardium: density 2.5 ‐ 5.0 per gram tissue. Highly correlating fractal relations were found between PTM and diameter for normal tree segments and for CV's which fully overlapped. SS in the CV's was equal to neighboring tree segments of similar diameter.Results indicate that collateral segments have the same function in distributing blood, and do so at the same SS, as normal tree segments. Hence, functionally CV's are not different from normal vascular segments and are therefore maintained. CV's form substrate for collateral growth in ischemia.Grant Funding Source: FP7‐ICT‐2007‐224495: euHeart

Prohealing Endothelial Progenitor Cell Capture Stents

Since the early days of percutaneous transluminal angioplasty, it has been recognized that balloon inflation disrupts the endothelial monolayer and injures normal arterial segments.1 This initiates a repair process that is mediated by platelets, inflammatory cells, and circulating progenitor cells that are recruited to sites of injury. There has been recent interest in the prohealing properties of endothelial progenitor cells (EPCs). Early studies identified these cells by expression of the surface antigen CD34 and demonstrated that they promoted reendothelialization after balloon injury.2,3 Because of the fact that these cells are relatively rare in the circulation (0.005%–0.01% of the total white blood cell count), it is not surprising that a stent was designed to capture circulating EPCs and sequester the cells to promote rapid reendothelialization, to decrease thrombogenicity, and to prevent restenosis.4 To accomplish this, the stent incorporated a monoclonal CD34 antibody in a proprietary polysaccharide intermediate coating that was adhered to a stainless steel stent; in 2010, the stent platform was changed to cobalt chromium.5 The safety and efficacy of the EPC capture stent have been studied extensively in clinical registries and randomized trials. The Healthy Endothelial Accelerated Lining Inhibits Neointimal Growth (HEALING) registries established a safety profile for the stent but demonstrated what would become a common theme; the stent did not decrease late lumen loss (LLL) to the same degree observed for drug-eluting stents (DES). This finding was attributed initially to variation in the number of circulating EPCs because of differences in the use …

‘Cold as ice’, why do old coronary arteries pay the price?

‘Cold as ice’, why do old coronary arteries pay the price?

Endothelial barrier dysfunction in diabetic conduit arteries: a novel method to quantify filtration

The endothelial barrier plays an important role in atherosclerosis, hyperglycemia, and hypercholesterolemia. In the present study, an accurate, reproducible, and user-friendly method was used to further understand endothelial barrier function of conduit arteries. An isovolumic method was used to measure the hydraulic conductivity (L(p)) of the intact vessel wall and medial-adventitial layer. Normal arterial segments with diameters from 0.2 to 5.5 mm were used to validate the method, and femoral arteries of diabetic rats were studied as an example of pathological specimens. Various arterial segments confirmed that the volume flux of water per unit surface area was linearly related to intraluminal pressure, as confirmed in microvessels. L(p) of the intact wall varied from 3.5 to 22.1 × 10(-7) cm·s(-1)·cmH(2)O(-1) over the pressure range of 7-180 mmHg. Over the same pressure range, L(p) of the endothelial barrier changed from 4.4 to 25.1 × 10(-7) cm·s(-1)·cmH(2)O(-1). During perfusion with albumin-free solution, L(p) of rat femoral arteries increased from 6.1 to 13.2 × 10(-7) cm·s(-1)·cmH(2)O(-1) over the pressure range of 10-180 mmHg. Hyperglycemia increased L(p) of the femoral artery in diabetic rats from 2.9 to 5.5 × 10(-7) cm·s(-1)·cmH(2)O(-1) over the pressure range of 20-135 mmHg. In conclusion, the L(p) of a conduit artery can be accurately and reproducibly measured using a novel isovolumic method, which in diabetic rats is hyperpermeable. This is likely due to disruption of the endothelial glycocalyx.

Correlation Between Red Cell Distribution Width and Coronary Ectasia in the Acute Myocardial Infarction

We read with a great interest the article entitled as ‘‘Assessment of red cell distribution width (RDW) in patients with coronary artery ectasia’’ by Dogdu et al that was published online in August 2011 issue of this journal. The authors clearly demonstrated the elevated level of RDW in the isolated coronary ectasia (CE). The RDW is found to be an independent prognostic factor for cardiovascular outcomes and all-cause mortality, even adjustment for multiple potential confounders including anemia. Increased level of RDW reflects chronic inflammatory state which is also revealing in the pathophysiologic mechanism of the CE. In the acute myocardial infarction (AMI), inflammatory markers usually make peak level that may reflect the accelerated inflammatory process. In such a condition, association between RDW and CE was not investigated before. In addition to the results presented by Dogdu et al, we searched the correlation of RDW and CE in the patients with ST-elevation AMI, and we evaluated whether the correlation between RDW and isolated CE is still valid in the patients with AMI. A total of 201 patients with an ST-elevation AMI were evaluated retrospectively. Upon admission, RDW was measured by the automated hematology analyzers Sysmex XT-1800i (Roche Diagnostic, Istanbul, Turkey). The patients’ angiographic data were evaluated from catheter laboratory records and CE was documented for each patients. Coronary ectasia was defined as a localized or diffuse nonobstructive lesion of the epicardial coronary arteries with a luminal dilation exceeding 1.5-fold the diameter of the normal adjacent arterial segment. Then the patients were classified according to the presence of CE, level of RDW, and other clinical and demographic characteristics. The RDW >14.8% was considered as elevated level. All groups were compared by chi-square and Pearson correlation analysis and Mann-Whitney U test according to the presence and distribution of CE. Coronary ectasia was found in the 24 patients and 15 of the ectatic vessels were also infarct-related artery. Although patients with CE did not differ in terms of age, sex, presence of diabetes mellitus, hypertension, previously diagnosed coronary heart disease, and multivessel disease significantly, elevated level of RDW was more common in the patients with CE (P 1⁄4 .01; Table 1). However, isolated ectasia in the infarct-related artery was not correlated with elevated level of RDW (53.3% vs 44.4%; P 1⁄4 .67). Coronary ectasia usually progress on the basis of diffuse atherosclerosis, chronic inflammatory process, and increased oxidative stress. Correlation between elevated level of RDW such mentioned clinical process were also shown with previous studies. Presence of CE may reflect the further exaggeration of the inflammatory response in the AMI, which could explain the correlation between elevated level of RDW and the CE, even adjustment for the AMI. In conclusion, elevated RDW level may also reflect CE in the patients with AMI. There was no significant correlation between elevated RDW level and isolated CE in the infarctrelated artery.

Comparison of Kalman-filter-based approaches for block matching in arterial wall motion analysis from B-mode ultrasound

Block matching (BM) has been previously used to estimate motion of the carotid artery from B-mode ultrasound image sequences. In this paper, Kalman filtering (KF) was incorporated in this conventional method in two distinct scenarios: (a) as an adaptive strategy, by renewing the reference block and (b) by renewing the displacements estimated by BM or adaptive BM. All methods resulting from combinations of BM and KF with the two scenarios were evaluated on synthetic image sequences by computing the warping index, defined as the mean squared error between the real and estimated displacements. Adaptive BM, followed by an update through the second scenario at the end of tracking, ABM_KF-K2, minimized the warping index and yielded average displacement error reductions of 24% with respect to BM. The same method decreased estimation bias and jitter over varying center frequencies by 30% and 64%, respectively, with respect to BM. These results demonstrated the increased accuracy and robustness of ABM_KF-K2 in motion tracking of the arterial wall from B-mode ultrasound images, which is crucial in the study of mechanical properties of normal and diseased arterial segments.

Macro-scale phenomena of arterial coupled cells: a massively parallel simulation

Impaired mass transfer characteristics of blood-borne vasoactive species such as adenosine triphosphate in regions such as an arterial bifurcation have been hypothesized as a prospective mechanism in the aetiology of atherosclerotic lesions. Arterial endothelial cells (ECs) and smooth muscle cells (SMCs) respond differentially to altered local haemodynamics and produce coordinated macro-scale responses via intercellular communication. Using a computationally designed arterial segment comprising large populations of mathematically modelled coupled ECs and SMCs, we investigate their response to spatial gradients of blood-borne agonist concentrations and the effect of micro-scale-driven perturbation on the macro-scale. Altering homocellular (between same cell type) and heterocellular (between different cell types) intercellular coupling, we simulated four cases of normal and pathological arterial segments experiencing an identical gradient in the concentration of the agonist. Results show that the heterocellular calcium (Ca(2+)) coupling between ECs and SMCs is important in eliciting a rapid response when the vessel segment is stimulated by the agonist gradient. In the absence of heterocellular coupling, homocellular Ca(2+) coupling between SMCs is necessary for propagation of Ca(2+) waves from downstream to upstream cells axially. Desynchronized intracellular Ca(2+) oscillations in coupled SMCs are mandatory for this propagation. Upon decoupling the heterocellular membrane potential, the arterial segment looses the inhibitory effect of ECs on the Ca(2+) dynamics of the underlying SMCs. The full system comprises hundreds of thousands of coupled nonlinear ordinary differential equations simulated on the massively parallel Blue Gene architecture. The use of massively parallel computational architectures shows the capability of this approach to address macro-scale phenomena driven by elementary micro-scale components of the system.

9333 Fluorescence diagnostics of skin tumors using 5-aminolevulinic acid and its methyl ester

to test the hypothesis that intravascular light could be delivered via a balloon catheter for arterial photodynamic therapy (PDT).pig non-injury model.clinical catheter equipment.large White pigs (15–20 μg) were photosensitised with 5-aminolaevulinic acid (5-ALA) induced protoporphyrin IX (PpIX) at a concentration of 120mg/kg. Arterial biopsies were taken at intervals between 30 mins and 24h and frozen sections analysed using a CCD camera to give a temporal profile of fluorescence in each arterial layer. PDT was given to normal arterial segments via a 4mm transparent PTA balloon inflated so as to occlude flow, but not distend the artery. Animals were culled at 3 and 14 days and the above segments harvested.fluorescence peaked in the adventitia, intima and medial layers at 1.5, 4 and 6h respectively. PDT at all time points produced VSMC depletion compared with controls. The degree of depletion mirrored the fluorescence profile of PpIX.PDT can be delivered via a standard PTA balloon with a transparent channel. This depletes the VSMC population within the arterial wall without complications. Intra-arterial PDT is therefore a potential therapy to reduce the incidence of restenosis post-angioplasty.

Popliteal Artery Aneurysm: Epidemiology and Modern Management

PAA is a predominantly male disease, more than 90% of affected patients are men. Riskfactors for amputation are poor run-off, use of a synthetic graft, emergency treatment and high age. The frequency of amputation decreased over time in Sweden, which was associated with increased use of preoperative thrombolysis and fasciotomy. Thrombolysis can transform an emergent into an elective situation, and often improves out-flow. The risk of late amputation is low. Operation with a Posterior approach is associated with lower risk of late expansion, and is considered first choice of treatment when a short by-pass is sufficient. Multiple aneurysm disease is common among patients with PAA, in particular among those with bilateral PAA. All patients, irrespective of age, should be included in a life-long surveillance program. Normal arterial segments should be re-examined after three years.

The Effect of Acute Hypoxemia on Coronary Arterial Dimensions in Patients with Coronary Artery Disease

Objectives: To assess the influence of acute hypoxemia on the dimensions of diseased and nondiseased coronary arterial segments in humans. Methods: In 18 subjects (age 53 ± 8 years) with known or suspected coronary artery disease, quantitative coronary angiography was performed before and after being randomly assigned to breathing (1) an inspired oxygen concentration (fraction of inspired oxygen, FIO₂) of 21% (room air, RA) for 20 min (n = 4, controls) or (2) an FIO₂ of 15 and 10% for 10 min each (corresponding to altitudes of 2,500 and 5,500 m, respectively; n = 14). Results: In the control subjects, no hemodynamic, oximetric or angiographic variable changed. In the 14 study subjects, the arterial partial pressure of oxygen averaged 85 ± 13 mm Hg on RA, 65 ± 15 mm Hg on 15% FIO₂ and 44 ± 13 mm Hg on 10% FIO₂. Average arterial segment diameter was 2.52 ± 0.63 mm on RA, 2.55 ± 0.62 mm on 15% FIO₂ (not significant vs. RA) and 2.66 ± 0.66 mm on 10% FIO₂ (p < 0.001 vs. RA). The increase in coronary arterial diameter with 10% FIO₂ occurred only in normal segments (2.74 ± 0.64 vs. 2.97 ± 0.64 mm; p < 0.001), but not in diseased segments (2.34 ± 0.57 vs. 2.38 ± 0.55 mm; not significant). Conclusions: In humans, severe hypoxemia induces vasodilation of angiographically normal coronary arterial segments, whereas it causes no change in diseased segments.

Neuropeptide Y and CGRP concentrations in the rat tail artery: Effects of age and two types of diabetes

The changes in concentrations of two neuropeptides, neuropeptide Y (NPY) and calcitonin gene-related peptide (CGRP) in different segments of the rat tail artery have been investigated (a) after 12 and 16 weeks of streptozotocin (STZ)-induced hyperglycemia that has been induced at the age of 10 weeks, and (b) in 52-week-old Goto-Kakizaki (GK) rats that were intolerant of glucose, and age-matched Wistar controls. In the control animals at 22, 26 and 52 weeks of age, the concentration of CGRP was significantly greater in distal, relative to proximal, segments of normal arteries, and this contrasted with the pattern of distribution of NPY, which was consistently greater in the proximal than the distal segments. STZ-induced diabetes caused significant reductions in the concentrations of NPY and CGRP in the middle and distal segments of the vessel after 12 and 16 weeks of hyperglycemia. In the glucose-intolerant Goto-Kakizaki (GK) rats, the noradrenalin and adrenalin levels increased significantly in the distal segment of the artery relative to controls; in contrast there was a significant fall in dopamine concentration. The only significant change in the level of NPY in 52-week-old GK rats was an increase in the proximal segment, suggesting that in Type II pre-diabetes, noradrenalin and its co-transmitter NPY are affected independently. The concentration of CGRP increased significantly in all segments of the artery of the 12-month-old GK rats relative to controls. The similarities and differences between these measurements in Type I and Type II diabetic models are discussed.

Risk of new aneurysms after surgery for popliteal aneurysm

Conclusion: In patients treated surgically for popliteal artery aneurysm, the development of new aneurysms at other sites during follow-up is common. Summary: Patients with popliteal artery aneurysms (PAA) are known to have a high incidence of concurrent aneurysmal degeneration of the opposite popliteal artery or the abdominal aorta, or both, at the time of discovery of the index PAA. The risk of developing new aneurysms in previously apparently normal arterial segments after PAA repair is, however, unknown. This study sought to determine the incidence of development of new aneurysms in previously nonaneurysmal popliteal arterial segments after repair of an index PAA. The study was based on analysis of the Swedish Vascular Registry. (Every citizen in Sweden has a unique personal identity code that can be used in vascular surgical research.) Between 1987 and 2002, 571 patients (717 legs) in Sweden had a primary operation for PAA. Analysis for this study began in January 2005. Data were crosschecked against the national population registry and indicated 337 patients had undergone PAA repair during the study period and were alive in January 2005. Patients were then assessed for the presence of additional aneurysms at the time of their index PAA repair and were asked to participate in a telephone interview and a re-examination. Of these, 240 patients agreed, and 190 were re-examined by ultrasonography at a medium of 7 years (range, 2.9-18.7 years) after their index PAA repair. At the time of the PAA repair, the number of patients with at least one aneurysm, in addition to the index PAA, was 108 (56.8%) at the index operation, and 131 (68.0%) at re-examination. The number of additional aneurysms increased from 244 to 346 (an increase of 41.8%). Among the 82 patients who had an isolated PAA at the index operation, a new aneurysm was detected in 23 at the time of their follow-up ultrasound study. Patients in whom new aneurysms developed tended to be older (P = .004). The presence of bilateral PAA at the index operation was associated with a later development of an abdominal aortic aneurysm (P = .004). Increased age and hypertension at the time of the index operation were associated with multianeurysmal disease at any time (P = .004 and P = .012 respectively). Venous bypass grafts were used to treat 138 of the legs, and six (4.3%) developed aneurysm degeneration of the venous bypass graft. Within 3 years of the initial PAA repair, no normal arterial segments had developed sufficient aneurysmal degeneration that required surgery. Overall, an additional 102 aneurysms developed in 74 patients, and only 59 of the 190 subjects re-examined did not develop an additional aneurysm. Comment: This study indicates new aneurysm development in patients with PAA is frequent. Because no patient developed a new aneurysm that required surgery ≤3 years of the index operation, it would seem that a practical plan for follow-up would be to reinvestigate patients with PAAs for new aneurysms every 3 years, beginning 3 years after the initial popliteal aneurysm repair.

Risk of new aneurysms after surgery for popliteal artery aneurysm

The risk of developing a new aneurysm after surgery for popliteal artery aneruysm (PAA) is not well known. The aim was to study this risk in a cohort of patients. A total of 571 patients who had primary operation for PAA (717 legs) between 1987 and 2002 were identified from the Swedish Vascular Registry (Swedvasc). Of these, 190 patients were re-examined by ultrasonography after a median of 7 (range 2.9-18.7) years. The number of patients with at least one aneurysm in addition to the PAA was 108 (56.8 per cent) at the index operation and 131 (68.0 per cent) at re-examination. The overall number of aneurysms increased by 41.8 per cent, from 244 to 346. Among the 82 patients who had an isolated PAA at the index operation, 23 developed a new aneurysm; these patients tended to be older (P = 0.004). Bilateral PAA at the index operation was associated with a later development of abdominal aortic aneurysm (P = 0.004). Age (P = 0.004) and hypertension (P = 0.012) at the time of the index operation were associated with multianeurysm disease at any time. Six (4.3 per cent) of 138 legs treated by venous bypass grafts had developed a graft aneurysm by the time of re-examination. No normal arterial segment developed an aneurysm that required surgery within 3 years. The development of new aneurysms was common in patients with a PAA; lifelong surveillance may be warranted.