Loss of alpha-globin genes in human subjects is associated with improved nitric oxide-mediated vascular perfusion.

Alpha thalassemia is a hemoglobinopathy due to decreased production of the α-globin protein from loss of up to four α-globin genes, with one or two missing in the trait phenotype. Individuals with sickle cell disease who co-inherit the loss of one or two α-globin genes have been known to have reduced risk of morbid outcomes, but the underlying mechanism is unknown. While α-globin gene deletions affect sickle red cell deformability, the α-globin genes and protein are also present in the endothelial wall of human arterioles and participate in nitric oxide scavenging during vasoconstriction. Decreased production of α-globin due to α-thalassemia trait may thereby limit nitric oxide scavenging and promote vasodilation. To evaluate this potential mechanism, we performed flow-mediated dilation and microvascular post-occlusive reactive hyperemia in 27 human subjects (15 missing one or two α-globin genes and 12 healthy controls). Flow-mediated dilation was significantly higher in subjects with α-trait after controlling for age (P = .0357), but microvascular perfusion was not different between groups. As none of the subjects had anemia or hemolysis, the improvement in vascular function could be attributed to the difference in α-globin gene status. This may explain the beneficial effect of α-globin gene loss in sickle cell disease and suggests that α-globin gene status may play a role in other vascular diseases.

Natural Killer T Cells Are Involved in Atherosclerotic Plaque Instability in Apolipoprotein-E Knockout Mice.

The infiltration and activation of macrophages as well as lymphocytes within atherosclerotic lesion contribute to the pathogenesis of plaque rupture. We have demonstrated that invariant natural killer T (iNKT) cells, a unique subset of T lymphocytes that recognize glycolipid antigens, play a crucial role in atherogenesis. However, it remained unclear whether iNKT cells are also involved in plaque instability. Apolipoprotein E (apoE) knockout mice were fed a standard diet (SD) or a high-fat diet (HFD) for 8 weeks. Moreover, the SD- and the HFD-fed mice were divided into two groups according to the intraperitoneal injection of α-galactosylceramide (αGC) that specifically activates iNKT cells or phosphate-buffered saline alone (PBS). ApoE/Jα18 double knockout mice, which lack iNKT cells, were also fed an SD or HFD. Plaque instability was assessed at the brachiocephalic artery by the histological analysis. In the HFD group, αGC significantly enhanced iNKT cell infiltration and exacerbated atherosclerotic plaque instability, whereas the depletion of iNKT cells attenuated plaque instability compared to PBS-treated mice. Real-time PCR analyses in the aortic tissues showed that αGC administration significantly increased expressional levels of inflammatory genes such as IFN-γ and MMP-2, while the depletion of iNKT cells attenuated these expression levels compared to those in the PBS-treated mice. Our findings suggested that iNKT cells are involved in the exacerbation of plaque instability via the activation of inflammatory cells and upregulation of MMP-2 in the vascular tissues.

Metabolomics reveals the impact of Type 2 diabetes on local muscle and vascular responses to ischemic stress.

OBJECTIVE: Type 2 diabetes mellitus (T2DM) reduces exercise capacity, but the mechanisms are incompletely understood. We probed the impact of ischemic stress on skeletal muscle metabolite signatures and T2DM-related vascular dysfunction. METHODS: we recruited 38 subjects (18 healthy, 20 T2DM), placed an antecubital intravenous catheter, and performed ipsilateral brachial artery reactivity testing. Blood samples for plasma metabolite profiling were obtained at baseline and immediately upon cuff release after 5 min of ischemia. Brachial artery diameter was measured at baseline and 1 min after cuff release. RESULTS: as expected, flow-mediated vasodilation was attenuated in subjects with T2DM (P<0.01). We confirmed known T2DM-associated baseline differences in plasma metabolites, including homocysteine, dimethylguanidino valeric acid and ß-alanine (all P<0.05). Ischemia-induced metabolite changes that differed between groups included 5-hydroxyindoleacetic acid (healthy: -27%; DM +14%), orotic acid (healthy: +5%; DM -7%), trimethylamine-N-oxide (healthy: -51%; DM +0.2%), and glyoxylic acid (healthy: +19%; DM -6%) (all P<0.05). Levels of serine, betaine, ß-aminoisobutyric acid and anthranilic acid were associated with vessel diameter at baseline, but only in T2DM (all P<0.05). Metabolite responses to ischemia were significantly associated with vasodilation extent, but primarily observed in T2DM, and included enrichment in phospholipid metabolism (P<0.05). CONCLUSIONS: our study highlights impairments in muscle and vascular signaling at rest and during ischemic stress in T2DM. While metabolites change in both healthy and T2DM subjects in response to ischemia, the relationship between muscle metabolism and vascular function is modified in T2DM, suggesting that dysregulated muscle metabolism in T2DM may have direct effects on vascular function.

Distal Arterial Embolization from an Abandoned Native Brachio-Cephalic Fistula: A Case Report.

Abandoned thrombosed arterivenous fistulas are usually left in place with very rare complications. We describe a case of distal embolization from a thrombosed aneurismatic arteriovenous brachiocephalic fistula in a patient who vigorously used the affected arm for pushing his wheelchair. Vigorous physical activity with the hand bearing arteriovenous fistula (AVF) should probably be discouraged even after AVF thrombosis and especially, if the initial part of fistula vein is aneurysmatic. Antiagregation therapy should be considered in such cases.

Infrared Thermography as a Diagnostic Tool for Peripheral Artery Disease.

OBJECTIVE: The prevalence of peripheral arterial disease (PAD) is increasing worldwide. The ankle-brachial index (ABI) is considered the criterion standard of noninvasive screening, but it does have limitations. The present study aimed to clarify the clinical diagnostic potential of infrared thermography (IRT) compared with conventional noninvasive measurements for PAD. METHODS: Patients were divided into two groups: the healthy control group (n = 93) and the PAD group (n = 164). Control participants had an ABI 0.9 to 1.4 and no former PAD diagnosis. The PAD group was divided into three subgroups based on ABI classifications and two subgroups based on toe pressure measurements. Investigators performed IRT using a standardized protocol with temperature measurements at five different foot sites. MAIN RESULTS: Differences in skin temperatures between feet were greater (P < .001) in the PAD group than in healthy controls. In general, mean foot temperatures were lower in the PAD group than in controls but did not differ significantly among PAD subgroups based on ABI classifications or toe pressure measurements. CONCLUSIONS: Infrared thermography effectively distinguished temperature differences between feet and thus might be diagnostically useful. However, because normal skin surface temperature varies among individuals, IRT alone cannot be recommended for evaluating PAD. However, it does have potential to provide additional information about circulation, subclinical infections, and the severity of vascular disease.

The peripheral atherosclerotic profile in patients with type 1 diabetes warrants a thorough vascular assessment of asymptomatic patients.

AIMS: Epidemiological data on subclinical atherosclerotic disease in type 1 diabetes mellitus (DM1) are scarce. We aimed to estimate the subclinical atherosclerosis profile of asymptomatic patients with DM1 and an abnormal ankle-brachial index (ABI). MATERIAL AND METHODS: In a cross-sectional design (ClinicalTrials.gov Identifier: NCT02910271), we estimated ABI in 289 consecutive asymptomatic patients with DM1. An abnormal ABI led to measurements of toe-brachial index (TBI) and peripheral doppler ultrasound (DUS) to diagnose peripheral artery disease (PAD) and/or atherosclerotic carotid plaques (ACP). RESULTS: A reduced (≤0.9) or increased (>1.2) ABI was detected in 17 (6%) and 75 (26%) patients, respectively. PAD was confirmed by TBI and DUS in 9 (53%) patients with a reduced ABI and 28 (37%) patients with an increased ABI, resulting in a 12.8% (9.4-17.2) prevalence of asymptomatic PAD. Fourteen patients with an abnormal ABI also exhibited ACP [4.8% (2.9-7.9)], with 64% of these patients showing bilateral disease. Artery stenosis was mild or moderate in 21% and 29% of patients, respectively. Thus, 46 [16% (12-21)] patients showed asymptomatic PAD, ACP, or both. According to our data, we would have to explore three asymptomatic patients with DM1 and normal pulses to unmask one case of PAD, and seven asymptomatic patients showing abnormal ABI values to detect one carotid disease. CONCLUSIONS: Peripheral artery disease is often undiagnosed in asymptomatic patients with DM1. However, its presence may change medical management in a substantial percentage of cases, highlighting the potential benefit of a thorough vascular assessment on these patients.

Fatal Rupture of Brachial Pseudoaneurysm in a Drug Abuser: Case Report and Review of the Literature.

The injection of drugs of abuse causes many millions of deaths each year; deaths are mostly due to fatal overdose and the trauma and infection caused by repeated injections. The scientific literature widely reports cases of infected pseudoaneurysm in injecting drug abusers; however, most of these autopsy cases deal with the rupture of pseudoaneurysm of the femoral artery. We present fatal hemorrhagic shock in a heroin-cocaine abuser subsequent to rupture of pseudoaneurysm of the brachial artery; the man collapsed just before injecting himself with a dose of heroin-cocaine (speedball).

Brachial Artery Wall Stiffness Assessment by Shear Wave Elastography: A Promising New Diagnostic Tool for Endothelial Dysfunction Detection.

OBJECTIVES: This study was designed to measure the changes in brachial artery wall stiffness by shear wave elastography (SWE) and evaluate the accuracy of SWE changes for detection of endothelial dysfunction. METHODS: Sixty-five consecutive participants (19 patients with atherosclerosis proven by coronary angiography, 16 healthy young adults, 15 patients with cardiovascular risk factors, and 15 healthy older adults between 50 and 60 years) were prospectively included in this study. They were examined in the same week by SWE, and flow-mediated dilatation was evaluated for each patient. RESULTS: The mean flow-mediated dilatation values ± 2 SDs after forearm occlusion were 8.54% ± 1.4% in healthy young adults, 7.61% ± 1.4% in healthy older adults, 5.83% ± 0.7% in patients with risk factors (P < .001), and 3.81% ± 2.4% in patients with atherosclerosis (P < .001, with respect to the risk factor group). There was a significant decrease in stiffness measurements in parallel with the increase in flow-mediated dilatation: 19.9% ± 6.3% in healthy young adults, 16.3% ± 5.1% in healthy older adults, 9.8% ± 5.4% in patients with risk factors (P < .05 with respect to the group with no risk factors), and 7.8% ± 6.4% in patients with atherosclerosis (P < .001 with respect to the healthy older adults). CONCLUSIONS: Shear wave elastography in combination with flow-mediated dilatation could be a promising, widely available noninvasive diagnostic tool for detecting endothelial dysfunction.

[Characteristics and clinical associations of arterial stiffness and subclinical atherosclerosis in patients with rheumatoid arthritis].

Te aim of the study was to evaluate parameters of arterial stiffness (AS) (carotid-femoral pulse wave velocity (cf PWV), central pulse pressure (PP), cardio-ankle vascular index (CAVI) and stiffness gradient between aorta and brachial artery) and subclinical atherosclerosis (carotid intima-media thickness (CIMT) and ankle-brachial index (ABI)) according to inflammatory activity in patients with R. MATERIALS AND METHODS: 85 patients with R (EULAR/ACR 2010) were examined (age 59,7±14,3 years, 64,7% with arterial hypertension (AH). Median duration of R was 7 years. PWV and central pulse wave were assessed by applanation tonometry. Arterial stiffness gradient was calculated as a ratio between carotid-femoral and carotid-radial PWV: its elevation ≥1 was considered as arterial stiffness mismatch. ABI and CAVI were measured by sphygmometry. CIMT was assessed according to the standard protocol, CIMT≥0,9 mm was considered as a subclinical marker of atherosclerosis. p.

[Cytomegalovirus Infection and Endothelial Function in Patients With Acute Myocardial Infarction].

PURPOSE: to study elucidate association of active cytomegalovirus (CMV) infection with endothelial dysfunction in patients with acute myocardial infarction (AMI). MATERIALS AND METHODS: The study included 42 volunteers without ischemic heart disease (IHD) and 63 patients with AMI. Blood samples for analysis of the deoxyribonucleic acid (DNA) of CMV in plasma by real-time polymerase chain reaction were taken in patients - before coronary angiography, in volunteers - at admission. In addition, in patients with AMI and volunteers without IHD, endothelial function was analyzed using endothelium-dependent vasodilatation (EDVD) test of the brachial artery. RESULTS: We showed that in patients with AMI, the concentration of CMV DNA in plasma was statistically significantly increased when compared with that in volunteers without IHD, which reflects active CMV infection - 1185.7 (0; 3003.0) vs. 0 (0; 910.8) copies of DNA / ml plasma (p=0.011). In comparison with volunteers without IHD, patients with AMI also more often had endothelial dysfunction - 11.5 (7.5, 15.2) % vs. 4.4 (0; 9.6) % of cases (p.

Congenital Bilateral Absence of the Radial Artery: A Very Rare Variation in Humans - Phylogenetic and Ontogenetic Aspects.

In an 80-year-old Caucasian woman, both radial arteries were found to be replaced by an enlarged anterior interosseous artery. Additionally, the right forearm revealed a persistent median artery which formed the superficial palmar arch together with the ulnar artery. In both hands, the replaced radial artery was connected only to the deep but not the superficial palmar arch. In clinical practice, lack of an arterial pulse on the radial aspect of the wrist joint may indicate the presence of this anatomic variation. In this case, arterial blood sample collections, application of contrast media, invasive measurements of blood pressure, and several angiographic interventions cannot be performed via the radial artery. As this is the fourth reported case since 1830, bilateral aplasia of the radial artery appears to be an exceptional variation in humans. Thus, the phylo- and ontogenetic aspects of this anomaly are discussed.

True Brachial Artery Aneurysm after Arteriovenous Fistula for Hemodialysis - Case Report.

INTRODUCTION: Brachial artery aneurysms are relatively uncommon and generally due to infectious, post-traumatic or iatrogenic etiology. They seem to affect 4.5% of arteriovenous fistula. The usual manifestation is an accidental finding of a pulsatile, painless, and asymptomatic mass. Complications include sac thrombosis, thromboembolic ischaemic events, and disruption with profuse bleeding. METHODS: The aim of this study is to present a case of true brachial artery aneurysm in end-stage renal disease patient after arteriovenous fistula creation. RESULTS: Sixty-six-year-old men with a past medical history of hypertension, dyslipidemia, smoking and poliquistic renal disease. He started a hemodialysis program in March 2006, using a brachiocephalic fistula on the left upper limb, built in February 2005. Submitted to kidney transplant in June 2010 and subsequent fistula ligation in December 2012. He goes to the emergency service in June 2016 with a pulsatile mass on the medial aspect of the left arm. Pain, redness and heat were present. Radial pulse was palpable. Inflammatory parameters were high and ultrasound revealed a fusiform aneurysm of the brachial artery with partial thrombosis and triphasic flow. An MRI was performed, documenting a brachial artery aneurysm, with 44mm greatest diameter and an extension of 17.5cm. Patient was hospitalized under antibiotic therapy and submitted to a reversed great saphenous vein interposition graft. Discharge from hospital occurred on the 7th postoperative day, with no sensitive or motor deficits and a present radial pulse. CONCLUSION: Arterial aneurysm is a rare, but significant complication long after the creation of a hemodialysis access. High flow, immunosuppression and increased resistance following ligation of the AV fistula may accelerate this process.

True Brachial Artery Aneurysm in a Patient with Vascular Access for Haemodialysis and Kidney Graft.

INTRODUCTION: True brachial artery aneurysms are rare and some of them have been described as a late complication in patients with vascular access for haemodialysis and kidney graft. The purpose of this paper is to present a clinical case of a patient with a true brachial artery aneurysm and its following treatment. METHODS: This case concerns a caucasian male patient with 43 years old who had vesicoureteral reflux at 7 years old, and subsequent end-stage renal disease, and started on haemodialysis at the age of twelve. The patient had homolateral radial and brachiocephalic arteriovenous fistulas (AVF), two sequential kidney grafts and was under immunosuppressant therapy for several years. As part of the medical history he also had bilateral amaurosis, Hepatitis B and C and was submitted to total parathyroidectomy and a following auto-transplant. In the latest years the patient presented with several aneurysms related to the vascular access. After the finding of an anastomotic false aneurysm and venous aneurysms complicating the AVF, the patient had removal of the aneurysms and ligation of the AVF. Later, he was diagnosed, in different times, with two true brachial artery aneurysms. At the time of the diagnosis of the first true aneurysm, the patient presented with local pain and occasional paraesthesias relative to compression symptoms. At physical examination the patient had a brachial pulsatile mass and a palpable radial pulse. The Doppler ultrasound exam revealed a true brachial artery aneurysm with 4,5 cm diameter. After two years, the patient was once again diagnosed with a true brachial artery aneurysm with 3,1 cm diameter. At this time the patient was asymptomatic and had palpable brachial mass and radial pulse. RESULTS: At the time of the diagnosis of the first true brachial aneurysm the patient was submitted to partial aneurysmectomy and brachiobrachial graft with PTFE 8. The patency of the graft persisted until the diagnosis of the second aneurysm. After two years, the patient was submitted to partial aneurysmectomy and axilobrachial graft with PTFE 8. During the follow-up period, the patient remained asymptomatic, had palpable radial pulse and the Doppler ultrasound exam confirmed the patency of the graft. CONCLUSION: The surveillance of patients with long duration AVF and kidney grafts might be advantageous in the early detection of arterial aneurysms. The surgical treatment in this group of patients is a first treatment option that is associated to a low morbidity.

Microvascular oxygen consumption during sickle cell pain crisis.

Sickle cell disease is an inherited blood disorder characterized by chronic hemolytic anemia and episodic vaso-occlusive pain crises. Vaso-occlusion occurs when deoxygenated hemoglobin S polymerizes and erythrocytes sickle and adhere in the microvasculature, a process dependent on the concentration of hemoglobin S and the rate of deoxygenation, among other factors. We measured oxygen consumption in the thenar eminence during brachial artery occlusion in sickle cell patients and healthy individuals. Microvascular oxygen consumption was greater in sickle cell patients than in healthy individuals (median [interquartile range]; sickle cell: 0.91 [0.75-1.07] vs healthy: 0.75 [0.62-0.94] -ΔHbO2/min, P < .05) and was elevated further during acute pain crisis (crisis: 1.10 [0.78-1.30] vs recovered: 0.88 [0.76-1.03] -ΔHbO2/min, P < .05). Increased microvascular oxygen consumption during pain crisis could affect the local oxygen saturation of hemoglobin when oxygen delivery is limiting. Identifying the mechanisms of elevated oxygen consumption during pain crisis might lead to the development of new therapeutic interventions. This trial was registered at www.clinicaltrials.gov as #NCT01568710.

Migraine and endothelial function: The HUNT3 Study.

BACKGROUND: Reduced endothelial function is associated with elevated risk of cardiovascular disease, but evidence on the association between migraine and endothelial function is conflicting. The aim of this population-based study was to examine the relationship between flow-mediated dilatation (FMD) and migraine with aura, migraine without aura and tension-type headache. METHODS: In the third Nord-Trøndelag Healthy Study (HUNT3) FMD was measured by ultrasound during reactive hyperaemia of the brachial artery in a sample of 4739 healthy adult participants, 3929 of whom answered headache questions. The cross-sectional association between different headache diagnoses and FMD was evaluated by logistic regression, using a categorical approach. RESULTS: Mean FMD did not differ between the headache groups and headache-free controls. In multi-adjusted analyses, no consistent association was found between FMD quintiles and headache groups. CONCLUSIONS: There was no relationship between FMD and migraine or other headache diagnoses in this large cross-sectional study of otherwise healthy respondents including freedom from pulmonary and cardiovascular diseases.

Effects of estradiol on measurements of conduit artery endothelial function after ischemia and reperfusion in premenopausal women.

In premenopausal women, ovarian steroids are felt to play a role in the prevention of cardiovascular disease. We aimed to assess whether menstrual cycle variations in estrogen can modify the response to ischemia-reperfusion (IR) injury in humans. In an investigator-blinded crossover study, 10 healthy premenopausal women with regular menstrual cycles were studied. They had flow-mediated dilatation (FMD) measured by ultrasound in the radial artery before and after IR (15 min of brachial artery ischemia, 15 min of reperfusion) during both the early and late follicular phases of the menstrual cycle. The order of these visits was not randomized. IR significantly blunted FMD in the early follicular phase (pre-IR: 7.1% ± 1.0%; post-IR: 3.6% ± 1.0%, P = 0.01) when estradiol levels were low (148.4 ± 19.8 pmol/L). Conversely, FMD was preserved after IR during the late follicular phase (pre-IR: 7.2% ± 0.9%; post-IR: 7.0% ± 0.8%, P = NS, P = 0.03 compared with early follicular) when estradiol levels were high (825.7 ± 85.8 pmol/L, P < 0.001 compared with early follicular). There was a significant inverse relationship between estradiol concentration and IR-induced endothelial dysfunction (i.e., change in FMD after IR) (r = 0.59, r2 = 0.36, P < 0.01). These findings demonstrate, for the first time in humans, a clear relationship between the cyclical changes in serum concentrations of estradiol and the endothelium's response to IR.

[The state of brachiocephalic artery endothelium in individuals with inflammatory periodontal disease and different cardiovascular risks].

The study included 35 patients (19 men and 16 women, aged 35 to 65 years) with chronic generalized severe periodontitis and atherosclerosis of the brachiocephalic artery (BCA). The changes of the BCA tone were evaluated by ultrasonic duplex scanning before and after transient limb ischemia created by endothelium-dependent vasodilation at baseline and at different laps after the anti-inflammatory and surgical treatment. The size of atherosclerotic plaques before and after the treatment was measured. In the early stages of treatment there were no changes of the tone of the brachial artery. The long-term results after conservative treatment also showed no changes but 6 months after surgical treatment in all patients the study showed the improved of the brachial artery tone on average 3-4% and a slight tendency to decrease of the atherosclerotic plaque.

Preoperative arterial microcalcification and clinical outcomes of arteriovenous fistulas for hemodialysis.

BACKGROUND: Arteriovenous fistulas (AVFs) often fail to mature, but the mechanism of AVF nonmaturation is poorly understood. Arterial microcalcification is common in patients with chronic kidney disease (CKD) and may limit vascular dilatation, thereby contributing to early postoperative juxta-anastomotic AVF stenosis and impaired AVF maturation. This study evaluated whether preexisting arterial microcalcification adversely affects AVF outcomes. STUDY DESIGN: Prospective study. SETTING & PARTICIPANTS: 127 patients with CKD undergoing AVF surgery at a large academic medical center. PREDICTORS: Preexisting arterial microcalcification (≥1% of media area) assessed independently by von Kossa stains of arterial specimens obtained during AVF surgery and by preoperative ultrasound. OUTCOMES: Juxta-anastomotic AVF stenosis (ascertained by ultrasound obtained 4-6 weeks postoperatively), AVF nonmaturation (inability to cannulate with 2 needles with dialysis blood flow ≥ 300mL/min for ≥6 sessions in 1 month within 6 months of AVF creation), and duration of primary unassisted AVF survival after successful use (time to first intervention). RESULTS: Arterial microcalcification was present by histologic evaluation in 40% of patients undergoing AVF surgery. The frequency of a postoperative juxta-anastomotic AVF stenosis was similar in patients with or without preexisting arterial microcalcification (32% vs 42%; OR, 0.65; 95% CI, 0.28-1.52; P=0.3). AVF nonmaturation was observed in 29%, 33%, 33%, and 33% of patients with <1%, 1% to 4.9%, 5% to 9.9%, and ≥10% arterial microcalcification, respectively (P=0.9). Sonographic arterial microcalcification was found in 39% of patients and was associated with histologic calcification (P=0.001), but did not predict AVF nonmaturation. Finally, among AVFs that matured, unassisted AVF maturation (time to first intervention) was similar for patients with and without preexisting arterial microcalcification (HR, 0.64; 95% CI, 0.35-1.21; P=0.2). LIMITATIONS: Single-center study. CONCLUSIONS: Arterial microcalcification is common in patients with advanced CKD, but does not explain postoperative AVF stenosis, AVF nonmaturation, or AVF failure after successful cannulation.

Neointimal hyperplasia and calcification in medium sized arteries in adult patients with chronic kidney disease.

The nature of arterial changes resulting in cardiovascular events and dialysis vascular access failures in adult predialysis patients is not well known. This study examined intimal changes, calcium deposition, and consequent stiffness in brachial and radial arteries of adult CKD patients. Ten brachial-artery and seven radial-artery specimens were obtained during fistula creation from nine predialysis and eight dialysis-dependent, nondiabetic patients; and age-gender matched controls undergoing coronary bypass grafts (6 radial) or kidney donation (6 renal). Arterial stiffness was measured at baseline. Vessel histology, morphometric analysis of intima-media, and direct quantification of calcium load was performed using standard techniques. Both predialysis and dialysis patients demonstrated significant arterial intimal hyperplasia with intima:media ratio higher than controls (0.13 ± 0.12 vs. 0.02 ± 0.05, p = 0.01). Calcium deposition was demonstrated on histology and the calcium content in patients was higher than controls (34.68 ± 26.86 vs. 10.95 ± 9.18 µg/µg, p = 0.003). The blood vessel calcium content correlated with arterial stiffness (r = 0.64, p = 0.018). This study for the first time describes, and suggests mechanistic linkage between, intimal hyperplasia, pathological calcium deposition, and increased functional arterial stiffness in dialysis and predialysis patients. Our research could serve as a unique window into the in vivo status of the uremic vasculature impacting fistula maturation and cardiovascular disease.

Systematic review of anaemia and inflammatory markers in chronic obstructive pulmonary disease.

This systematic review synthesizes the relevant published articles on the prevalence of anaemia in patients with chronic obstructive pulmonary disease (COPD) and its relationship with inflammatory markers. The upregulation of erythropoietin in anaemia maintains homeostasis. However, anaemic COPD patients do not respond to increased levels of erythropoietin. The increased levels could be an indicator of the peripheral erythropoietin resistance in COPD. Anaemia and inflammation are associated with an increased risk of hospitalization and mortality in these patients. The understanding of anaemia in chronic inflammation is that anaemia is at least partially due to the excessive production of inflammatory cytokines, which can contribute to improvements in the management, prognosis, and survival of patients with COPD and anaemia.