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Introduction It is purported that patients with peripheral arterial disease (PAD) may have impaired cognitive function due to concomitant cerebrovascular disease. Such disease may be clinically unrecognized but can impact on a patient's recovery and prognosis. The purpose of this systematic review was to interrogate the body of published evidence on undiagnosed cognitive impairment in PAD patients. Methods A search strategy encompassing MEDLINE, Scopus, and the Cochrane database was developed to identify peer-reviewed articles examining rates of undiagnosed cognitive impairment in patients with PAD. The following search terms were used: ‘PAD’; ‘PVD’; ‘dementia’; ‘peripheral arterial disease’; ‘peripheral vascular disease’; ‘cognitive impairment'; 'alzheimer's disease’ and ‘cogniti∗’. Our primary outcome was the incidence of previously undiagnosed cognitive impairment in patients with PAD. Results The initial search yielded 1492 titles. After removal of duplicates, 961 abstracts were screened to ascertain if they were eligible for inclusion. Abstract review yielded 62 full texts for further evaluation. Eight case–control studies consisting of 1161 patients were included. Analysis of these studies revealed that PAD patients performed significantly worse than controls on a variety of neuropsychological measures. Conclusion Our review indicated that PAD patients are more likely to suffer with undiagnosed cognitive impairment than healthy controls.

Acute oesophageal necrosis is a rare cause of haematemesis associated with high mortality and morbidity in elderly patients with multiple comorbidities. Acute oesophageal necrosis is thought to be caused by a combination of hypoperfusion, vascular disease and duodenal disease causing transient gastric outlet obstruction and therefore reflux of gastric contents. The subsequent necrosis is associated with significant morbidity and mortality. We present a case of an 83-year-old man presenting with sepsis secondary to gallstone cholangitis, who developed haematemesis 2 days post admission. Oesopho-gastro-duodenoscopy demonstrated necrosis to the oesophagus and duodenal ulceration. This was the first case of acute oesophageal necrosis observed within our hospital. We review the literature on the management of acute oesophageal necrosis and discuss the impact of acute oesophageal necrosis and its complications on the patient’s long-term outcome.

Pulmonary arterial hypertension (PAH) is a chronic pulmonary vascular disease characterized by increased pulmonary arterial pressure and pulmonary arterioles remodeling. Some studies have discovered the relationship between sympathetic nerves (SNs) and pathogenesis of PAH. This review is aimed to illustrate the location and components of SNs in the pulmonary artery, along with different methods and effects of pulmonary artery denervation (PADN). Studies have shown that the SNs distributed mainly around the main pulmonary artery (MPA) and pulmonary artery (PA) bifurcation. And the SNs could be destroyed by three ways: the chemical way, the surgical way and the catheter-based way. PADN can significantly decrease pulmonary arterial pressure rapidly, improve hemodynamic varieties, and then palliate PAH. PADN has been recognized as a prospective and effective therapy for PAH patients, especially for those with medication-refractory PAH. However, further enlarged clinical studies are needed to confirm accurate distribution of SNs in the pulmonary artery and the efficacy of PADN.

Platelets are multifunctional cells that ensure the integrity of the vascular wall and modulate the immune response at the blood/vascular interface. Their pathological activation results in both thrombosis and inflammation and implicates them in the pathogenesis of vascular disease. Vascular diseases are sexually dimorphic in terms of incidence, clinical presentation, outcome, and efficacy of anti-platelet therapy. We here provide an overview of what is known about the role of platelets in the initiation and progression of vascular diseases and summarize what is known about the sex differences in platelet reactivity and in the thromboinflammatory mechanisms that drive these diseases, with a particular focus on atherosclerosis, obstructive and non-obstructive coronary artery disease, and ischemic stroke. Understanding the sex differences at the platelet–vascular interface is clinically relevant as it will enable: (1) to design new therapeutic strategies that prevent the detrimental effects of the immune-modulatory function of platelets taking sex into account, and (2) to evaluate if sex-specific anti-platelet drug regimens should be used to reduce the risk not only of thrombosis but also of vascular disease progression.

Background We investigated the relationship of sex with clinical outcomes after proximal aortic (ascending and arch) operations, and whether sex-specific preoperative factors are associated with mortality. Methods Of 3745 patients who underwent elective, urgent, and emergency proximal aortic operations over a 20-year period, 1153 pairs of men and women were propensity-matched, and their early and long-term outcomes were compared. Kaplan-Meier survival analysis was used to estimate late survival. Results Women and men had similar operative mortality (9.1% vs 8.8%, P = .8), stroke (5.7% vs 5.6%, P = .9), and renal failure rates (7.0% vs 6.6%, P = .7). Thirty-day mortality was 7.5% vs 5.6% (P = .06), respectively. Results were less favorable for women than for men regarding respiratory failure (34.3% vs 29.2%, P=0.008) and intensive care unit length of stay (9.11 ± 11.9 vs 7.87 ± 12.48 days; P = .023). Long-term survival was not significantly different between women and men: 66.3% (95% confidence interval [CI] 62.8%-69.5%) vs 67.1% (95% CI 63.6%-70.4%) at 5 years, and 45.9% (95% CI 41.76%-50.0%) vs 46.2% (95% CI 41.7%-50.6%) at 10 years (P = .4). Preoperative factors including diabetes, prior stroke, prior renal insufficiency, and peripheral vascular disease were associated with operative mortality in men, whereas chronic obstructive pulmonary disease was the main risk factor in women. Conclusions No differences were seen between the sexes in life-changing adverse outcomes after ascending aortic and arch procedures, although specific preoperative variables were associated with specific adverse events. Recognizing differences in preoperative risk factors for mortality between the sexes may facilitate targeted preoperative assessment, preparation, and counseling.

Background aims Several studies have shown the efficacy of mesenchymal stem cell (MSC) therapy for lower extremity vascular disease (LEVD) in diabetic patients, but the results are not consistent. Therefore, the authors conducted a meta-analysis of randomized controlled trials (RCTs) to examine the safety and efficacy of MSC therapy in diabetic patients with LEVD. Methods Eight available databases were searched in both English and Chinese to identify RCTs comparing MSC therapy-based conventional treatment with conventional treatment alone in diabetic patients with LEVD. Three investigators independently screened the literature, extracted the data and assessed the risk bias. Meta-analysis was performed using RevMan 5.4.1 and Stata 14.0. Results A total of 10 studies involving 453 patients were included. Compared with conventional treatment only, patients receiving MSC therapy-based conventional treatment had a higher ulcer healing rate, greater number of reduced ulcers and shorter complete healing time. MSC therapy also increased ankle–brachial index and transcutaneous oxygen pressure. In addition, four of the included studies showed that MSC therapy significantly improved the number of new collateral vessels. Moreover, no more adverse events were recorded in the MSC group. Conclusions This meta-analysis suggests that MSC therapy promotes ulcer healing in diabetic LEVD patients with ulcers, improves blood supply and has a favorable safety profile. More large and well-designed RCTs with long-term follow-up are still needed to explore the safety and efficacy of MSC therapy in diabetic patients with LEVD.

Background The relationship between retrograde arterial perfusion and stroke in patients with peripheral vascular disease has been widely documented. Antegrade arterial perfusion has been favoured as an alternative approach in less invasive mitral valve (MV) operations. We aimed to analyse our experience in patients with peripheral arterial disease undergoing MV surgery through a right mini-thoracotomy adopting antegrade arterial perfusion. Method A single-institution retrospective study on prospectively collected data was performed on patients undergoing right mini-thoracotomy MV surgery with antegrade arterial perfusion. Since 2009, indication for the latter was dictated by the severity of atherosclerotic burden. Preoperative screening included computed tomography, angiography, or both for the evaluation of the aorta and ileo-femoral arteries. Results Consecutive patients (n=117) underwent MV surgery through a right mini-thoracotomy with antegrade arterial perfusion, established either by transthoracic central aortic cannulation in 65 (55.6%) cases or by axillary arterial cannulation in 52 (44.4%). Mean logistic EuroSCORE was 11%±2.3%. Twenty-five (25) (21.4%) patients had undergone one or more previous cardiac operations. Operative mortality was 4.3% (n=5). Nonfatal iatrogenic aortic dissection occurred in one case (0.8%). The incidence of stroke was zero. Conclusions Axillary or central aortic cannulation is a promising alternative route to provide excellent arterial perfusion in right mini-thoracotomy MV surgery, with a very low incidence of stroke and other major perioperative complications in patients with severe aortic or peripheral arterial disease.

Background & Aims Porto-sinusoidal vascular disease (PSVD) was recently proposed as novel clinical entity characterized by typical histological changes with or without portal hypertension (PH) in the absence of cirrhosis. Thus, we aimed to describe clinical characteristics and the outcome of PSVD patients and to compare these to patients meeting traditional idiopathic non-cirrhotic portal hypertension (INCPH) criteria. Methods Patients undergoing liver biopsy (baseline) ±hepatic venous pressure gradient (HVPG) measurement at the Vienna General Hospital between 2000-2019 were screened for PSVD and INCPH criteria. Results 91 patients were diagnosed with PSVD of which 28 (30.8%) also fulfilled INCPH criteria (INCPH+/PSVD+). Specific histological and specific clinical PH signs were found in 72 (79.1%) and 54 (59.3%) patients, respectively. INCPH+/PSVD+ showed higher Child-Pugh-scores (7±2 vs 6±1 points; P = .002) and a higher prevalence of decompensation (57.1% vs 28.6%; P = .009) than INCPH-/PSVD+ patients. Importantly, hepatic decompensation after three years (3Y) occurred in 11.2% of PSVD patients with specific clinical signs of PH, while no decompensation occurred in patients with only specific histological or with unspecific clinical/histological signs (P = .002). When categorizing by INCPH definition, 3Y decompensation was 13.4% in INCPH+/PSVD+ and 3.8% in INCPH-/PSVD+ (P = .120). While overall mortality was similar in INCPH+/PSVD+ (n = 6; 21.4%) and INCPH-/PSVD+ (n = 10; 15.9%) patients (P = .558), liver-related mortality tended to be higher in INCPH+/PSVD+ (6.9%) than in INCPH-/PSVD+ (0%; P = .078). Conclusion Novel PSVD criteria facilitate diagnosis. Compared to INCPH, clinical course of PSVD patients is more favorable. Importantly, specific signs of PH including varices and collaterals are associated with hepatic decompensation and mortality.

Background. Ankylosing spondylitis is a risk factor for severe vascular disease, which is characterized by a violation of vascular endothelial function, but clinical and pathogenetic role of these changes is not sufficiently studied. The purpose and objectives of the study: to evaluate the nature of endothelial dysfunction and vascular adsorption-rheological properties of the blood in patients with ankylosing spondylitis, to determine its characteristics in the presence of angiopathy, to establish correlation with the cli-nical and instrumental parameters of vascular disease and the state of immunity. Materials and methods. The study included 79 patients aged 15 to 66 years (mean 38 years), among whom there were 95 % of men and 5 % of women. The duration of the disease from its first manifestations was 11 years, I degree of activity occurred in 32 % of cases, II — in 39 % and III — in 29 %, and the ratio of slow progressive and rapidly progressive course of the pathological process was 4 : 1. Peripheral monooligoarthritis was detected in 47 % of patients, polyarthritis — in 53 %. Levels of vascular endothelial growth factor, endothelin-1, thromboxane A2, homocysteine, prostacyclin, cyclic guanosine monophosphate, E- and P-selectin were examined by immune-enzyme analysis in the blood serum, and surface parameters of viscosity, elasticity, tension, relaxation and modulus of viscoelasticity — by the method of interphase tensiometry. Results. Endothelial vascular dysfunction occurs in every second patient with ankylosing spondylitis, which in the presence of clinical and instrumental vascular pathology is accompanied by an increase in serum concentration of cyclic guanosine monophosphate and even greater reduction in prostacyclinemia parameters. The severity of disorders of vascular endothelial function in these patients is associated with disease duration, activity of the pathological process, the defeat of the peripheral nervous system, the severity of spondylopathies and sacroiliitis, at the same time there are correlations between certain immune parameters and vascular-rheological properties of the blood. The latest in ankylosing spondylitis are involved in the pathogenesis constructions of enthesopathies, tendovaginitis, uveitis and scleritis, determine the rate of progression of articular syndrome and integrated severity of angiopathy, and the content of cyclic guanosine monophosphate in the blood has prognostic significance.

Fibromuscular dysplasia (FMD) is a non-atherosclerotic vascular disease that may involve medium-sized muscular arteries throughout the body. The majority of FMD patients are women. Although a variety of genetic, mechanical, and hormonal factors play a role in the pathogenesis of FMD, overall, its cause remains poorly understood. It is probable that the pathogenesis of FMD is linked to a combination of genetic and environmental factors. Extensive studies have correlated the arterial lesions of FMD to histopathological findings of arterial fibrosis, cellular hyperplasia, and distortion of the abnormal architecture of the arterial wall. More recently, the vascular phenotype of lesions associated with FMD has been expanded to include arterial aneurysms, dissections, and tortuosity. However, in the absence of a string-of-beads or focal stenosis, these lesions do not suffice to establish the diagnosis. While FMD most commonly involves renal and cerebrovascular arteries, involvement of most arteries throughout the body has been reported. Increasing evidence highlights that FMD is a systemic arterial disease and that subclinical alterations can be found in non-affected arterial segments. Recent significant progress in FMD-related research has led to improve our understanding of the disease’s clinical manifestations, natural history, epidemiology, and genetics. Ongoing work continues to focus on FMD genetics and proteomics, physiological effects of FMD on cardiovascular structure and function, and novel imaging modalities and blood-based biomarkers that can be used to identify subclinical FMD. It is also hoped that the next decade will bring the development of multi-centred and potentially international clinical trials to provide comparative effectiveness data to inform the optimal management of patients with FMD.

Background: HIV is associated with accelerated decline in lung function and increased risk for chronic obstructive pulmonary disease (COPD). Recently, there has been growing attention toward the impairment in the diffusing capacity of the lungs for carbon monoxide (DLCO), a marker of pulmonary gas exchange, observed among persons living with HIV. Although increased emphysema can contribute to the DLCO impairment observed, other factors may drive this association. Methods: Using cross-sectional data from the Study of HIV in the Etiology of Lung Disease, we studied the association between HIV and DLCO independent of emphysema. We also analyzed the joint influence of HIV and COPD on DLCO impairment. An analysis was conducted among 339 participants (229 with HIV) with lung function and chest CT imaging data. Multivariable regression models were generated with percent predicted DLCO and odds of DLCO impairment as outcomes. Results: After adjusting for confounders, including emphysema severity, HIV was associated with lower DLCO (β −4.02%; P = 0.020) and higher odds of DLCO impairment (odds ratio 1.93; P = 0.017). Even among those without COPD, HIV was independently associated with lower DLCO (β −3.89%; P = 0.049). Compared with HIV-uninfected participants without COPD, those with both HIV and COPD experienced the greatest impairment in DLCO (β −14.81; P < 0.001). Conclusions: HIV is associated with impaired pulmonary gas exchange independent of emphysema severity. Our data also suggest a potentially additive influence between HIV and COPD on DLCO impairment. Further studies should investigate the other factors, including pulmonary vascular disease, which may contribute to DLCO impairment among persons living with HIV.

It is well known that post-stroke depression might be a negative factor for stroke recovery, however there is limited evidence to establish the link between pre-stroke depression and stroke outcome such motor recovery. The objective is to determine clinical risk factors in ischemic stroke patients with pre-stroke depression that are associated functional ambulatory outcome.Data from acute ischemic patients from a regional stroke registry were collected for consecutive recombinant tissue plasminogen activator(rtPA)-treated acute ischemic stroke patients between January 2010 and June 2016. Logistic regression model was used to predict risk factors that served as predictive variables, while the increase or reduce odds of improvement in ambulatory outcome was considered as the primary outcome. Multicollinearity and possible interactions among the independent variables were analyzed using the variance inflation factor.A total of 1446 patients were eligible for recombinant tissue plasminogen activator (rtPA) and 596 of these patients received rtPA. Of the 596 ischemic stroke patients, 286 patients presented with recent pre-stroke depression, 310 had no pre-stroke depression. Carotid artery stenosis (OR = 11.577, 95% CI, 1.281-104.636, P = 0.029) and peripheral vascular disease (OR = 18.040, 95% CI, 2.956-110.086, P = 0.002) were more likely to be associated with increase odds of improvement in ambulation in patients with no pre-stroke depression treated with rtPA, while antihypertensive medications (OR = 0.192, 95% CI, 0.035-1.067, P = 0.050),previous TIA (OR = 0.177, 95% CI, 0.038-0.818, P = 0.027), and congestive heart failure (OR = 0. 0.160, 95% CI, 0.030-0.846, P = 0.031) were associated with reduced odds of improvement in ambulation. In addition, carotid artery stenosis (OR = 0.078, 95% CI, 0.10-0.614, P = 0.015, congestive heart failure (OR = 0.217, 95% CI, 0.318-0.402, P = 0.030), previous TIA (OR = 0.444, 95% CI, 0.517-0.971, P = 0.012), higher NIHSS scores ((OR = 0.887, 95% CI, 0.830-0.948, P 0.001), and antihypertensive medications (OR = 0.810, 95% CI, 0.401-0.529, P = 0.019) were associated with the reduced odd of improvement in ambulation in an ischemic stroke population with pre-stroke depression treated with rtPA.Our findings indicate that more risk factors were associated with the decreased odds of an improvement in ambulation following thrombolytic therapy in an ischemic stroke population with pre-stroke depression when compared with those without pre-stroke depression. This finding maybe helpful in the development of management strategies to increase the use of thrombolytic therapy for pre-stroke depressed ischemic stroke to increased their eligibility for rtPA.

Non-coronary vascular disease (NCVD) is associated with adverse cardiovascular events. Little is known about physician risk assessment, prevalence of coronary artery disease (CAD), cardiac catheterization, and the performance of the atherosclerotic cardiovascular disease (ASCVD) risk score in patients with NCVD.Retrospective analysis of outpatients with angina and no known CAD from the PROMISE trial. NCVD included carotid artery stenosis ≥50%, or history of stroke or peripheral artery disease. Multivariable models of physician estimates of the probability of obstructive CAD, prevalence of non-obstructive and obstructive CAD, referral to cardiac catheterization, and all-cause death/myocardial infarction/unstable angina were performed.Among 10,001 patients in the PROMISE trial, 379 (3.8%) patients had NCVD. Only 8.5% of participants with NCVD were categorized as high-risk for obstructive CAD by physicians, though 15.5% (25/161) had obstructive CAD in those randomized to coronary computed tomography (CTA). NCVD was independently associated with non-obstructive (aOR = 1.58; 95% CI 1.18-2.61; P = .006) but not obstructive CAD by CTA. Adjusted referral to cardiac catheterization was similar with and without NCVD (aOR 1.04; 95% CI 0.88-1.94, P = .19). NCVD was associated with an increased risk of all-cause death/MI/UA (aOR 2.03; 95% CI 1.37-3.01, P.001). There was no interaction between NCVD status and ASCVD risk score.Among patients with NCVD and angina, NCVD had increased adjusted risks of CAD and adverse outcomes which were not well described by ASCVD risk score and were underrecognized by physicians. Increased awareness and better risk stratification tools for patients with NCVD may be necessary to recognize the associated CV risk and optimize diagnostic testing and therapies.

Objective The aim of this study was to examine whether there were independent associations between abdominal aortic diameter, size index, and height index and the risk of major adverse events in patients referred for treatment of various types of aortic and peripheral occlusive and aneurysmal disease (APOAD). Methods In total, 1 752 participants with a variety of APOADs were prospectively recruited between 2002 and 2020 and had a maximum abdominal aortic diameter, aortic size index (aortic diameter relative to body surface area), and aortic height index (aortic diameter relative to height) measured by ultrasound at recruitment. Participants were followed for a median of 4.6 years (interquartile range 2.0 – 8.0 years) to record outcome events, including major adverse cardiovascular events (MACE), peripheral artery surgery, abdominal aortic aneurysm (AAA) events (rupture or repair), and all cause mortality. The association between aortic size and events was assessed using Cox proportional hazard analysis. The ability of aortic size to improve risk of events classification was assessed using the net reclassification index (NRI). Results After adjusting for other risk factors, larger aortic diameter was associated with an increased risk of MACE (hazard ratio [HR] 1.17, 95% confidence interval [CI] 1.05 – 1.31), requirement for peripheral artery surgery (HR 2.05, 95% CI 1.90 – 2.22), AAA events (HR 3.01, 95% CI 2.77 – 3.26), and all cause mortality (HR 1.20, 95% CI 1.08 – 1.32). Findings were similar for aortic size and aortic height indices. According to the NRI, all three aortic size measures significantly improved classification of risk of peripheral artery surgery and AAA events but not MACE. Aortic size index, but not aortic diameter or aortic height index, significantly improved the classification of all cause mortality risk. Conclusion Larger abdominal aortic diameter, size index, and height index are all independently associated with an increased risk of major adverse events in patients with established vascular disease.

Background Leukoaraiosis is a type of lesion characterized by tissue rarefaction or myelin pallor resulting from axons loss and gliosis. Synthetic magnetic resonance imaging (MRI) could yield quantitative T1, T2, proton density (PD) values of leukoaraiosis in addition to information on the volume of the lesion. Purpose To investigate the feasibility of quantifying leukoaraiosis using synthetic MRI and to explore the association between leukoaraiosis and cerebral small vascular diseases and cerebral atherosclerosis. Material and Methods Patients with acute ischemic stroke were enrolled in this study. All participants underwent a conventional T2-weighted image, brain volume, CUBE fluid attenuated inversion recovery, and synthetic MRI acquisition using a 3.0-T MR system. A time-of-flight magnetic resonance angiography was also obtained. We evaluated the T1, T2, PD values and leukoaraiosis volume. Results Analysis of the leukoaraiosis volume ratios demonstrated a positive association with T2 values, a negative association with T1 values, and no association with PD values. Leukoaraiosis volume ratios were independently correlated with age ( P < 0.001), lacunes ( P = 0.022), and cerebral microbleeds ( P = 0.010). A statistical association was found between both age ( P < 0.001) and lacunes ( P = 0.047) and leukoaraiosis T2 values. Conclusion Synthetic MRI may enhance the evaluation of leukoaraiosis, in addition to providing information on its volume. Leukoaraiosis may represent a type of cerebral small vascular disease rather than cerebral atherosclerosis and may share the same pathological mechanism as lacunes and cerebral microbleeds.

Objective To study coronary interventions and mortality among patients with ST-elevated myocardial infarction (STEMI) who were admitted with septic shock. Methods Data from the national emergency department sample (NEDS) that constitutes 20% sample of hospital-owned emergency departments in the United States was analyzed for the septic shock related visits from 2016 to 2018. Septic shock was defined by the ICD codes. Results Out of 1 375 507 adult septic shock patients, 521 300 had a primary diagnosis of septic shock (mean age 67.41±15.67 years, 51.1% females) in the national emergency database for the years 2016 to 2018. Of these patients, 2768 (0.53%) had STEMI recorded during the hospitalization. Mortality rates for STEMI patients were higher than patients without STEMI (52.3% vs 23.5%). Mortality rates improved with PCI among STEMI patients (43.8% vs 56.2%). Coronary angiography was performed among 16% of patients of which percutaneous coronary intervention (PCI) rates were 7.7% among patients with STEMI septic shock. PCI numerically improved mortality, however, had no significant difference than patients without PCI on multivariate logistic regression and univariate logistic regression post coarsened exact matching of baseline characteristics among STEMI patients. Among the predictors, STEMI was a significant predictor of mortality in septic shock patients (OR 2.87, 95% CI 2.37-3.49; PConclusion STEMI complicating septic shock worsens mortality. PCI and coronary angiography numerically improved mortality, however, had no significant difference from patients without PCI. More research will be needed to improve mortality in such a critically ill subgroup of patients.

BACKGROUND The purpose of this document is to provide clinicians with guidance, using expert consensus, to help summarize evidence and offer practical recommendations. METHODS Expert Consensus Documents are intended to provide guidance for clinicians in areas in which there are no clinical practice guidelines, especially for new and evolving tests such as arterial stiffness measurements, until any formal guidelines are released. RESULTS This expert consensus document is intended as a source of information for decision-making and to guide clinician–patient discussions in various clinical scenarios. CONCLUSIONS The goal is to help clinicians and patients make a more informed decision together.

INTRODUCTION In three phase III randomized controlled trials, ceftaroline fosamil was shown to be non-inferior to vancomycin plus aztreonam for the treatment of complicated skin and soft tissue infections (cSSTIs). This exploratory analysis evaluated the impact of underlying comorbidities on clinical outcomes in patients with cSSTI pooled from these three studies. METHODS CANVAS 1 and 2 and COVERS evaluated ceftaroline fosamil (600 mg every 12 h [q12h]; 600 mg every 8 h [q8h; COVERS]) versus vancomycin plus aztreonam (1 g q12h each [CANVAS 1 and 2]; vancomycin 15 mg/kg q12h and aztreonam 1 g q8h [COVERS]) in hospitalized adults with cSSTI. The primary efficacy variable in each trial was clinical response at the test-of-cure (TOC) visit. Subgroup analyses were performed on the pooled clinically evaluable (CE) population, exploring the impact of age and various baseline comorbidities. RESULTS Overall, 1808 patients were included in the CE population (1005 ceftaroline fosamil; 803 vancomycin plus aztreonam). Clinical cure rates at TOC were 89.7% (ceftaroline fosamil) and 90.8% (vancomycin plus aztreonam) (difference [95% confidence interval] - 1.13 [- 3.87, 1.67]). Clinical response rates were similar between treatment groups, regardless of age (≤ 65 years or > 65 years), and in subgroups of patients with and without diabetes mellitus, peripheral vascular disease, cancer/malignancy, renal impairment, and obesity; within these subgroups, efficacy and safety results were generally consistent with those of the overall cSSTI population. CONCLUSIONS This analysis provides supportive evidence of the efficacy of ceftaroline fosamil in patients with cSSTI and underlying comorbidities. TRIAL REGISTRATION CANVAS 1, NCT00424190 and CANVAS 2, NCT00423657 (both trials first posted on ClinicalTrials.gov 18/01/2007); COVERS, NCT01499277 (first posted on ClinicalTrials.gov 26/12/2011).

PRÉCIS: Multiple systemic vascular-associated conditions including systemic hypertension and hypotension, diabetes mellitus, migraine headache, peripheral vascular disease, Raynaud syndrome, and anemia were associated with low-tension glaucoma. PURPOSE: The purpose of this study was to identify systemic risk factors associated with low-tension glaucoma. PATIENTS AND METHODS: A retrospective case-control study design was employed to identify patients seen at the Mayo Clinic Department of Ophthalmology between 2005 and 2015 with low-tension glaucoma and an age-matched and sex-matched control group, each containing 277 patients. RESULTS: The low-tension glaucoma group had more myopic refractive errors (−1.6 vs. −1.0 D, P < 0.001), lower intraocular pressure (14.2 vs. 15.2 mm Hg, P < 0.001), and a higher cup-to-disc ratio (0.7 vs. 0.3, P < 0.001). The low-tension glaucoma group was significantly less likely to be obese (body mass index > 30, P = 0.03). This group had a significantly higher prevalence of systemic hypertension [odds ratio (OR): 1.64, P = 0.004], diabetes mellitus (OR: 3.01, P < 0.001), peripheral vascular disease (OR: 2.61, P = 0.009), migraine headache (OR: 2.12, P = 0.02), anemia (OR: 2.18, P = 0.003), systemic hypotension (OR: 4.43, P < 0.001), Raynaud syndrome (OR: 3.09, P = 0.05), and angiotensin-converting enzyme inhibitor (OR: 1.64, P = 0.01) or calcium channel blocker use (OR: 1.98, P = 0.004). After adjusting for systemic hypertension, calcium channel blocker use remained significant (OR: 1.70, P = 0.03). No significant difference was found between groups with respect to hyperlipidemia, obstructive sleep apnea, coronary artery disease, carotid stenosis, stroke, or statin, angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, beta-blocker, or metformin use. CONCLUSIONS: Multiple vascular-associated conditions were associated with low-tension glaucoma including systemic hypertension, diabetes mellitus, peripheral vascular disease, migraine headache, Raynaud syndrome, anemia, systemic hypotension, and calcium channel blocker use. This study strengthens the evidence for the vascular hypothesis of low-tension glaucoma.

Previous studies showed that postmenopausal women are more likely to have poorly controlled hypertension than men of the same age. Whether this is caused by inadequate treatment or poor response to antihypertensive agents remains unknown. The aim of this study is to analyze treatment response to the most potent renin angiotensin aldosterone system (RAAS) inhibitor perindopril in different age categories in women and men. Individual patient data were used from the combined European Trial on Reduction of Cardiac Events With Perindopril (EUROPA), Perindopril Protection Against Recurrent Stroke Study (PROGRESS), and Action in Diabetes and Vascular disease: Preterax and Diamicron-MR Controlled Evaluation (ADVANCE) trials, which include patients with vascular disease (n = 29,463). We studied the relative and absolute changes in systolic blood pressure (SBP) and diastolic blood pressure (DBP) during a 4-week run-in phase in which all patients were treated with the perindopril-based treatment in different age categories. In total, 8366 women and 21,097 men were included in the analysis. Women greater than 65 years of age showed a significantly smaller blood pressure reduction after perindopril treatment (2.8 mmHg [95% confidence interval {CI} = 0.1–5.5] less reduction compared to women ≤45 years, p = 0.039). In men, the SBP reduction after perindopril in patients greater than 55–65 and greater than 65 years was lower compared to the age category less than or equal to 45 years (adjusted mean difference >55–65: 2.8 mmHg [95% CI = 1.8–3.7], p 65: 3.7 mmHg [95% CI = 2.7–4.7], p

Renal artery stenosis is caused by atherosclerosis and fibromuscular dysplasia and is associated with ischemic nephropathy, renovascular hypertension, and accelerated cardiovascular disease. Routine screening for renal artery stenosis is not recommended but is reasonable in patients who have rapid onset of hypertension, resistant hypertension, progressive renal insufficiency, recurrent pulmonary edema, or repeat admissions for heart failure. Acute mesenteric ischemia is caused by arterial embolism or thrombosis, mesenteric venous thrombosis, or nonocclusive mesenteric ischemia, whereas chronic mesenteric ischemia is most often caused by arterial obstruction. This article reviews the epidemiology, pathophysiology, diagnosis, and management of these two conditions.

Objectives: Alpha-1-Antitrypsin (AAT) is one of the major plasmatic protease inhibitors. In the last decade, an association between Alpha-1-Antitrypsin Deficiency (AATD) and Abdominal Aortic Aneurysms (AAA) has been hypothesized. Multiple factors may be involved in AAA's etiopathogenesis, and an underlying structural defect of the extracellular matrix (ECM) is always present. AATD could be a reasonable risk factor for AAA because it is related to protease/antiprotease imbalance and enhanced ECM degradation of the vessel wall. Methods: We performed genotyping of 138 patients hospitalized in the Vascular Surgery Division of the ASST-Spedali Civili di Brescia, Italy, for non-traumatic rupture of AAA. The second purpose was to observe the distribution of main non-genetic risk factors for AAA between patients with and without AATD. Results: Out of 138 patients, 22 were found with AATD: 16 MS, 1 SS, 3 MZ, and 2 with a new rare AAT variant. When compared to the general Italian population, our cohort's frequency of deficient S allele was significantly higher (7.8 vs 2.2% respectively, P0.05). Although we found no differences in age, gender, hypertension, diabetes, and smoke habits between AAA patients with and without AATD, hyperlipidemia was significantly less frequent in patients with AATD (46.4 vs 12.5% respectively, P

Background Prior US studies have shown increasing rotator cuff repair rates through 2009. We hypothesize that rotator cuff repair rates are continuing to increase and the comorbidity profiles of patients are becoming more complex over time. Methods We identified rotator cuff repairs in a large US cohort of people 18-64 years of age with ≥1 year of commercial insurance coverage. Repair rate trends across time were standardized by age, sex, and geographic region. Procedures were categorized as inpatient vs. outpatient and as arthroscopic vs. open. Prevalent comorbidities were defined as 1 inpatient diagnosis claim or 2 outpatient diagnosis claims during the year before rotator cuff repair. General population comorbidity prevalence was determined based on a random 5% sample of the commercially insured population and compared with patients with rotator cuff repair using standardized morbidity ratios. Results From 2007 to 2016, 314,239 rotator cuff repairs were identified (165 repairs per 100,000 person-years). Rotator cuff repairs were performed more frequently in men, older people, and in the Midwest. Across time, cuff repair rates increased by 1.6% per year (95% confidence interval [CI] = +1.4%-1.7%) adjusting for demographics. The highest increases in repair rates were observed among patients aged 50-64 years (+2.0%, 95% CI = +1.8%-2.2%). Rotator cuff repairs were more frequently performed using an arthroscopic approach and in an outpatient setting in later calendar years. In 2016, 83% of rotator cuff repairs were arthroscopic procedures and 99% were performed as outpatient procedures. Comorbidity prevalence in rotator cuff repair patients increased across calendar time by 4.5% per year for hypertension (95% CI = +4.2%-4.7%), 2.3% per year for diabetes (+1.9%-2.7%), 0.9% per year for hypercholesterolemia (+0.3%-1.5%), 2.9% for congestive heart failure (+0.8%-4.9%), 4.2% for peripheral vascular disease (+2.4%-6.0%), and 4.2% for chronic pulmonary disease (+3.6%-4.8%). Comorbidity prevalence in repair patients was higher than prevalence in the general population, and prevalence relative to the general population was most heightened during later calendar years. For example, hypertension prevalence was 1.58 times higher in repair patients than the general population in 2007 (95% CI = 1.53-1.62), and 2.06 times higher in 2016 (95% CI = 2.02-2.11). Conclusion Rotator cuff repair is becoming more frequent in the US commercially insured population, particularly in those 50-64 years of age. More rotator cuff repairs are being performed using an arthroscopic approach and in an outpatient setting. Over time, the comorbidity profile of patients undergoing rotator cuff repair is becoming more complex with greater prevalence of numerous conditions, including hypertension, peripheral vascular disease, and chronic pulmonary disease.

Background Type 2 diabetes is a condition associated with a state of low-grade inflammation caused by adipose tissue dysfunction and insulin resistance. High sensitive-CRP (hs-CRP) is a marker for systemic low-grade inflammation and higher plasma levels have been associated with cardiovascular events in various populations. The aim of the current study is to evaluate the relation between hs-CRP and incident cardiovascular events and all-cause mortality in high-risk type 2 diabetes patients. Methods Prospective cohort study of 1679 type 2 diabetes patients included in the Second Manifestations of ARTerial disease (SMART). Cox proportional hazard models were used to evaluate the risk of hs-CRP on cardiovascular events (composite of myocardial infarction, stroke and vascular mortality) and all-cause mortality. Hs-CRP was log-transformed for continuous analyses. Findings were adjusted for age, sex, BMI, current smoking and alcohol use, non-HDL-cholesterol and micro-albuminuria. Results 307 new cardiovascular events and 343 deaths occurred during a median follow-up of 7.8 years (IQR 4.2–11.1). A one unit increase in log(hs-CRP) was related to an increased vascular- and all-cause mortality risk (HR 1.21, 95% CI 1.01–1.46 and HR 1.26, 95% CI 1.10–1.45 respectively). No relation was found between log(hs-CRP) and myocardial infarction or stroke. The relations were similar in patients with and without previous vascular disease. Conclusion Low grade inflammation, as measured by hs-CRP, is an independent risk factor for vascular- and all-cause mortality but not for cardiovascular events in high-risk type 2 diabetes patients. Chronic low-grade inflammation may be a treatment target to lower residual cardiovascular risk in type 2 diabetes patients.

Background Chest radiographs can identify important abnormalities in patients undergoing diagnostic evaluation for cardiovascular diseases. Cardiomegaly often reflects cardiac chamber dilation, or cardiac muscle hypertrophy, or both conditions. The clinical implications of cardiomegaly depend on the underlying clinical disorder. Does cardiomegaly have any clinical, laboratory, echocardiographic, and right heart catheterization associations in patients undergoing evaluation for pulmonary hypertension? Methods Patients referred to a pulmonary vascular disease clinic for possible pulmonary hypertension underwent a comprehensive evaluation that included right heart catheterization. These patients also had chest radiographs, laboratory studies, and echocardiograms. The patients were divided into two groups based on the presence or absence of cardiomegaly. Results This study included 102 patients (63.7% female) with a mean age of 62.3 ± 15.0 years. Patients with cardiomegaly (n = 64) had elevated BNP, BUN, and creatinine levels. They had elevated right atrial pressures, right ventricular pressures, and pulmonary artery pressures and reduced cardiac indices and reduced mixed venous oxygen saturations. There were no differences in echocardiographic parameters between the two groups. Conclusions This study demonstrates that the presence of cardiomegaly on chest radiographs has important clinical implications, including increased BNP levels and increased right heart pressures, in patients undergoing evaluation for pulmonary hypertension. Consequently, the presence of cardiomegaly supports the need for additional evaluation, including right heart catheterization, and provides useful information for primary care physicians and specialists.

Background: Thromboangiitis obliterans (TAO) is a chronic, non-atherosclerotic, progressive inflammatory vascular disease affecting the small- and medium-size arteries and veins of the extremities. Objective: To evaluate whether long-term anticoagulation with low-molecular-weight heparin (LMWH) and warfarin is beneficial for treating the inflammation and symptoms associated with TAO. Methods: Patients with TAO who underwent anticoagulation as the mainstay of treatment were included in this prospective study. Rest pain relief and healing of trophic lesions (as the primary and secondary endpoint) were investigated at Day 14 and after 6 months of follow-up. High sensitivity C-reactive protein (hsCRP), monocyte count, and ankle-brachial index (ABI) were recorded, and the difference was compared before and after 2-week anticoagulation. The Chi-square test was used to compare the difference between anticoagulant and aspirin groups (based on the literature). Results: From 2014 to 2019, 18 patients were included. Only 1 patient with wet gangrene received endo-therapy for a failing stent at the start of treatment. After ~14 days, 12 of 13 (92%) patients showed complete ulcer healing, and 17 of 18 (94%) patients showed complete relief from rest pain. Monocyte-counts and hsCRP levels decreased significantly (p Conclusion: Anticoagulant therapy may alleviate the inflammation and symptoms of TAO.

Background Arteriovenous fistula (AVF) stenosis leading to its failure is a major cause of morbidity in hemodialysis patients; however, detailed pathogenesis of AVF stenosis is still under investigation. To date, monocytes/macrophages have been considered pivotal players in chronic inflammation of vascular disease including atherosclerosis and AVF stenosis. However, recent evidence strongly suggests that neutrophils and neutrophil granule proteins are important contributors to vascular disease. The aim of the present study was to evaluate the relationship between AVF stenosis and neutrophil activation by measuring circulating levels of neutrophil elastase (NE) and lactoferrin, enzymes released on neutrophil activation, as well as other inflammation markers including neutrophil counts. Methods This was a single-center, prospective observational study conducted on 83 prevalent hemodialysis patients with AVF. Blood levels of biomarkers and sonography (US) measurement were assessed at baseline and 1 year after enrollment. Clinical follow-up continued for one more year (a total of 2 years for each patient) to observe any AVF events. Results Circulating levels of both NE and lactoferrin positively correlated with the degree of AVF stenosis. Patients with significant AVF stenosis had older AVFs, higher neutrophil-to-lymphocyte ratio (NLR), and higher circulating levels of NE and lactoferrin. On multivariate logistic regression analysis, both circulating levels of NE and NLR remained independent predictors of significant AVF stenosis. Conclusions Circulating levels of NE and the NLR were identified as independent predictors of at-risk AVF with significant stenosis. Our data suggest the potential role of neutrophil and innate immunity activation on the development of AVF stenosis.

Objectives The purpose of this study was to detect cardiovascular changes after mild severe acute respiratory syndrome coronavirus 2 infection. Background Concern exists that mild coronavirus disease 2019 may cause myocardial and vascular disease. Methods Participants were recruited from COVIDsortium, a 3-hospital prospective study of 731 health care workers who underwent first-wave weekly symptom, polymerase chain reaction, and serology assessment over 4 months, with seroconversion in 21.5% (n = 157). At 6 months post-infection, 74 seropositive and 75 age-, sex-, and ethnicity-matched seronegative control subjects were recruited for cardiovascular phenotyping (comprehensive phantom-calibrated cardiovascular magnetic resonance and blood biomarkers). Analysis was blinded, using objective artificial intelligence analytics where available. Results A total of 149 subjects (mean age 37 years, range 18 to 63 years, 58% women) were recruited. Seropositive infections had been mild with case definition, noncase definition, and asymptomatic disease in 45 (61%), 18 (24%), and 11 (15%), respectively, with 1 person hospitalized (for 2 days). Between seropositive and seronegative groups, there were no differences in cardiac structure (left ventricular volumes, mass, atrial area), function (ejection fraction, global longitudinal shortening, aortic distensibility), tissue characterization (T1, T2, extracellular volume fraction mapping, late gadolinium enhancement) or biomarkers (troponin, N-terminal pro–B-type natriuretic peptide). With abnormal defined by the 75 seronegatives (2 SDs from mean, e.g., ejection fraction 1,072 ms, septal T2 >52.4 ms), individuals had abnormalities including reduced ejection fraction (n = 2, minimum 50%), T1 elevation (n = 6), T2 elevation (n = 9), late gadolinium enhancement (n = 13, median 1%, max 5% of myocardium), biomarker elevation (borderline troponin elevation in 4; all N-terminal pro–B-type natriuretic peptide normal). These were distributed equally between seropositive and seronegative individuals. Conclusions Cardiovascular abnormalities are no more common in seropositive versus seronegative otherwise healthy, workforce representative individuals 6 months post–mild severe acute respiratory syndrome coronavirus 2 infection., Central Illustration

PURPOSE To evaluate the association between severity of hepatic steatosis/fibrosis with clinical, laboratory, and echocardiographic characteristics, including visceral obesity and type 2 diabetes mellitus (T2DM)-related micro- and macrovascular complications in diabetic patients with non-alcoholic fatty liver disease (NAFLD). METHODS We studied 60 consecutive NAFLD outpatients with T2DM, recording several demographic and clinical characteristics, trunk and visceral fat, cardiac ultrasound, and micro- and macrovascular complications of diabetes mellitus including microalbuminuria, diabetic peripheral neuropathy, peripheral vascular disease, and cardiac autonomic function. Severity of steatosis and fibrosis was evaluated with abdominal ultrasound and liver stiffness measurements, respectively. RESULTS Twenty-three (41%) of the patients had grade 1 steatosis and mean liver stiffness was 7.5 ± 3 kPa. After applying Bonferroni correction for multiple comparisons, ferritin concentration was the only factor significantly different between patients with mild (grade 1) compared to those with moderate/severe (grade 2/3) steatosis and showed good discriminative ability for the presence of moderate/severe steatosis (AUC: 0.74, sensitivity 88%, specificity 48%, PPV 74%, and NPV 72%). In addition, waist circumference was the only factor associated with the presence of significant fibrosis (≥ F2) with very good discriminative ability (AUC: 0.77, sensitivity 89%, specificity 45%, PPV 75%, and NPV 70%). CONCLUSION Specific clinical and laboratory characteristics, which may be determined via widely accessible and noninvasive techniques, were associated with severity of diabetics NAFLD, taking into account echocardiographic characteristics, visceral obesity, and T2DM-related systemic complications.

Summary Objective Epidemiological data suggest that moderate habitual coffee consumption associates with lower cardiovascular disease (CVD) risk; however scarce data exist regarding the association of coffee with subclinical vascular disease (SVD). We aimed at investigating the above association with habitual instant coffee consumption - a widely consumed coffee in Greece–in high CVD risk but free of established CVD adults. Research methods & procedures In a cross-sectional design study we measured: (i) two 24 h dietary recalls to assess coffee consumption, (ii) arterial stiffness, by carotid to femoral pulse wave velocity - (PWV) and carotid compliance, arterial remodeling by carotid intima-media thickness (IMT), pressure wave reflection by augmentation index (AIx) and atheromatosis by carotid plaques. Results In 1041 participants (55.6% females, 53.6 ± 14.0 years), 30% habitually consumed instant coffee (0.53 ± 1.15 cups/day). Consumption of instant coffee was inversely associated with systolic blood pressure (β = −1.19, p = 0.007), AIx (β = −0.71, p = 0.043), PWV (β = −0.22, p = 0.000) and IMT (β = −0.01, p = 0.025), but these associations lost their significance after multiple adjustments for confounders. Instant coffee consumption was positively associated with carotid compliance independent from all possible confounders (β = 0.005, p = 0.003). Conclusion Habitual moderate instant coffee consumption is inversely associated with arterial stiffening and potential with arterial remodeling. These favorable vascular associations offer a potential pathophysiological link between habitual coffee consumption and lower incidence of CVD. Future studies are needed to examine the long-term effects of habitual instant coffee consumption on vascular structure and function.

Pulmonary arterial hypertension is a kind of heart and lung vascular disease with low incidence and poor prognosis. Genetic variants are the important factors of pulmonary arterial hypertension. The mutations of activin receptor-like kinase-1 (ACVRL1) could cause pulmonary arteriole obstruction and occlusion in pulmonary arterial hypertension patients. The ACVRL1 gene mutation and clinical characteristics of Chinese idiopathic or hereditary pulmonary hypertension (IPAH/HPAH) patients are still unclear. This study aimed to retrospectively study the mutation characteristics of ACVRL1 gene in Chinese IPAH/HPAH patients and its effect on clinical prognosis. We analyzed the clinical, functional, hemodynamic and mutation characteristics of 12 IPAH/HPAH patients with ACVRL1 mutations and compared with 94 IPAH/HPAH patients (27 patients carried bone morphogenetic protein receptor type 2 (BMPR2) mutations and 67 without mutations). All ACVRL1 mutations of 12 patients were single nucleotide missense mutations. The ratio of male to female in 12 patients was 1:1. The diagnosis age of ACVRL1 mutation patients was younger than that of BMPR2 mutation patients (13.6 ± 11.3 years vs. 16.0 ± 12.9 years) but higher than that of patients without mutations (13.6 ± 11.3 years vs. 8.8 ± 8.5 years, p = 0.006). IPAH/HPAH patients with ACVRL1 mutation have rapid disease progresses, high overall mortality rate (approximately 50%) and no response to the acute pulmonary vasodilation test. In conclusion, this is the first study to analyze the ACVRL1 gene mutation and clinical characteristics of Chinese IPAH/HPAH patients. It is beneficial to screen ACVRL1 gene mutation for IPAH/HPAH patients to facilitate genetic counseling and early prevention and treatment.

Meccanismi vascolari nella vestibolopatia periferica acuta unilaterale: una revisione sistematica.La vestibolopatia periferica unilaterale acuta (AUPVP) è causa frequente di perdita della funzione vestibolare. Sono state proposte diverse eziologie, ma il meccanismo esatto rimane sconosciuto. Lo scopo di questo studio è condurre un’analisi sistematica della letteratura per valutare l’eziologia vascolare dell’AUPVP. Una ricerca sistematica della letteratura è stata eseguita mediante PubMed, Cochrane Library ed Embase, includendo articoli pubblicati dal 1 gennaio 2010 al 30 novembre 2020. Due revisori hanno selezionato in modo indipendente articoli che studiano un collegamento tra AUPVP e malattie vascolari. Sono state estratte le seguenti informazioni: anno di pubblicazione, paese, livello di evidenza, fattori di rischio vascolare valutati e numero di pazienti. In totale sono stati identificati 450 articoli. Tra questi sono stati considerati gli undici su cui vi era completo accordo fra i due revisori. In una popolazione aggregata di 805 pazienti, i risultati principali sono stati il più alto rapporto tra neutrofili e linfociti e la maggiore prevalenza di fattori di rischio vascolare tra i pazienti con AUPVP. Non è stata eseguita una meta-analisi perché gli studi erano troppo eterogenei per quanto riguarda la metodologia. Sono stati trovati argomenti indiretti per i meccanismi vascolari in AUPVP. Questi risultati indicano che sono necessari studi prospettici più ampi e ben controllati per chiarire l’eziologia vascolare in AUPVP.Acute unilateral peripheral vestibulopathy (AUPVP) is a frequent cause of vestibular loss. Several aetiologies have been proposed, but the exact mechanism remains unknown. The aim of this study is a systematic analysis of the literature evaluating the vascular aetiology of AUPVP. A systematic literature search was performed in PubMed, Cochrane Library and Embase, including articles published from January 1

Pulmonary hypertension is associated with increased morbidity and mortality, and growing evidence suggests that even mild elevations in pulmonary artery pressure estimated with echocardiography are linked to increased mortality. In healthy individuals who undergo right heart catheterisation, the average pulmonary artery systolic pressure ranges from 17 mm Hg to 25 mm Hg; on echocardiography, estimated pulmonary artery systolic pressure of more than 30 mm Hg is outside the normal range for most healthy individuals. Increased pulmonary artery systolic pressure (>30 mm Hg) is reported on more than 40% of clinically indicated echocardiograms, often in the presence of metabolic and cardiopulmonary comorbidities, and is associated with a 5-year mortality of 25-40%. However, current guidelines do not sufficiently highlight risk and risk-reduction approaches for the sizable patient population with elevated pulmonary artery pressure who do not have underlying severe pulmonary vascular disease such as pulmonary arterial hypertension. Increased awareness of this frequently reported high-risk echocardiographic finding, and multidisciplinary risk-reduction approaches for patients with metabolic and cardiopulmonary comorbidities and elevated pulmonary artery pressure, are urgently needed.

Background The soluble receptor for advanced glycation end product (sRAGE) and endogenous secretory RAGE (esRAGE) are novel biomarkers that are associated with vascular disease. We carried out a systematic review to provide a more complete picture of sRAGE, esRAGE, carotid atherosclerosis and cardiovascular disease (CVD) in patients with diabetes. Methods We searched the Cochrane Library, PubMed and Embase databases. Systematic review best practices were followed, and study quality was assessed. Results Ultimately, 11 studies met all the inclusion criteria. Meta-analysis indicated that esRAGE was not significantly lower in patients with type 1 diabetes (T1D) (standardized mean difference [SMD], −0.76; 95% confidence interval [CI], −1.57 to 0.05; I2=90%; p=0.002), whereas it was significantly lower in patients with type 2 diabetes (T2D) (SMD, −1.08; 95% CI, −1.53 to −0.62; I2=80%; p=0.006). Meta-analysis suggested that sRAGE levels were not significantly lower or higher in T1D (SMD, 0.06; 95% CI, −0.14 to 0.26; I2=38%; p=0.20) or T2D (SMD, 0.00; 95% CI, −0.26 to 0.26; I2=0.00%; p=1.00) patients. The level of esRAGE was inversely correlated with carotid intima-media thickness (IMT) in T2D patients, whereas there was a contrasting relationship between sRAGE and carotid IMT in T1D patients. Higher sRAGE was associated with cardiovascular events. Conclusion Our meta-analysis showed that circulating esRAGE was lower and inversely correlated with IMT in T2D patients.

Penetrating aortic ulcers typically occur in severely diseased vessels. We present the case of a 46-year-old woman, without extensive atherosclerosis, who had sudden cardiac arrest related to ischemia from a mobile intraluminal aortic thrombus adherent to a penetrating ulcer in the ascending aorta. (Level of Difficulty: Intermediate.), Central Illustration

Diabetic foot is a serious infection of the lower limbs. It is caused by diabetic neuropathy and vascular disease. It is also the primary cause of disability and death in patients with severe diabetes, so prompt treatment is essential for positive outcomes. The clinical use of nano-silver dressings can be considered to further optimize the treatment process and improve the treatment efficacy in diabetic foot patients. Nano-silver dressings have a larger contact surface and a stronger bactericidal effect when compared to ordinary silver dressings. Besides, it can be disinfected repeatedly to better wound infection control and promote wound healing. The current article discusses the pathogenesis of diabetic foot, diabetic foot dressing treatment, the application of nanotechnology in diabetic foot treatment, the efficacy evaluation of different dressings, and the practical prospects of adopting nanotechnology in the treatment of diabetic foot.

The incidence of new cardiovascular events in patients with chronic coronary syndrome remains high, particularly in the presence of concomitant high thrombotic risk factors (diabetes mellitus, renal failure, multivessel coronary artery disease, multiple district atherosclerosis, recurrent events, heart failure). The risk of such recurrent events can be reduced by implementing various strategies, which include careful individual stratification of ischaemic and haemorrhagic risk and the choice of the most appropriate antithrombotic therapy for the individual patient, also by combining aspirin with a second antiplatelet agent/a low-dose anticoagulant, in order to achieve the maximum net clinical benefit.

INTRODUCTION The Alzheimer's Disease Neuroimaging Initiative (ADNI) has accumulated 15 years of clinical, neuroimaging, cognitive, biofluid biomarker and genetic data, and biofluid samples available to researchers, resulting in more than 3500 publications. This review covers studies from 2018 to 2020. METHODS We identified 1442 publications using ADNI data by conventional search methods and selected impactful studies for inclusion. RESULTS Disease progression studies supported pivotal roles for regional amyloid beta (Aβ) and tau deposition, and identified underlying genetic contributions to Alzheimer's disease (AD). Vascular disease, immune response, inflammation, resilience, and sex modulated disease course. Biologically coherent subgroups were identified at all clinical stages. Practical algorithms and methodological changes improved determination of Aβ status. Plasma Aβ, phosphorylated tau181, and neurofilament light were promising noninvasive biomarkers. Prognostic and diagnostic models were externally validated in ADNI but studies are limited by lack of ethnocultural cohort diversity. DISCUSSION ADNI has had a profound impact in improving clinical trials for AD.

Актуальність. Анкілозуючий спондиліт є хронічним прогресуючим системним автоімунним ревматичним захворюванням хребта, периферичних суглобів, крижово-клубових зчленувань, ентезисів, зв’язкового апарату й внутрішніх органів, належить до факторів ризику тяжкої судинної патології. Мета дослідження: вивчити при анкілозуючому спондиліті клініко-інструментальний перебіг ангіопатії, з’ясувати патогенетичні зв’язки з імунними показниками. Матеріали та методи. Під наглядом перебували 79 хворих віком від 15 до 66 років (в середньому 38 років), серед яких чоловіки становили 95 %, жінки — 5 %. Тривалість хвороби від перших її проявів дорівнювала 11 рокам, І ступінь активності відмічався в 32 % спостережень, ІІ — у 39 % і ІІІ — у 29 %, а співвідношення повільнопрогресуючого та швидкопрогресуючого перебігу патологічного процесу становило 4 : 1. Периферичний моноолігоартрит констатовано в 47 % від числа хворих, поліартрит — у 53 %. Пацієнтам виконували ехокардіографію, ультра­звукову допплерографію судин й біомікроскопію судин кон’юнктиви. Результати. Ангіопатія спостерігається у 85 % від числа хворих на анкілозуючий спондиліт, розвиток якої прямо пов’язаний зі ступенем активності патологічного процесу й обернено — із серопозитивністю за ревматоїдним фактором. Шкірний васкуліт залежить від віку пацієнтів, увеїт, склерит, синдром Рейно, ураження центральної та периферичної нервової системи — від особливостей перебігу суглобового синдрому. Інтегральні клінічні й інструментальні судинні показники вірогідно співвідносяться з імунними параметрами — рівнями ревматоїдного фактора, С-реактивного протеїну, циркулюючих імунних комплексів, значеннями імуноглобулінемії, а ураження судин перебігає з підвищенням значень легеневого артеріального тиску та судинного опору, у генезі яких бере участь C-реактивний протеїн, що має прогностичну значущість.

Concept of No-Reflow (NR) phenomenon is largely studied in cardiological intervention characterised by the failure of myocardial reperfusion despite the absence of mechanical obstruction of large and medium sized vessels. NR negatively affects outcome of procedure, so there is great importance of prediction and management. The objective was to introduce concept of NR in neuro-intervention and have an idea of incidence and independent predictors of NR in patients with post intervention no-reflow in large and medium sized brain arteries.This was a single-centre prospective case– control study between march 2017-march 2021 in the department of Neurosurgery, Dr. R.M.L.I.M.S., Lucknow, India. Cases were subjects who suffered NR, and the control comparators were those who did not. Clinical outcomes were documented. Salient variables relating to the patients and their presentation, history and angiographical findings were documented.Of 153 consecutive patients, 11(7.2%) suffered from NR, with all cases occurring post intervention in the form of coiling with or without stent/balloon support or flow diverter placement with or without coiling. Patients with NR had increased risk of in-hospital death and disability (1 patient/9.1% death, 8 patients/72.72% with one or multiple neurological dysfunction with varying severity) in comparison to patients without NR (4 patients/2.8% deaths and 12 patients/8.5% disabilities, out of 142 patients). From baseline variables available prior to neuro-endovascular surgery, the independent predictors of NR were increased complexity of pathology, admission systolic hypertension, weight of more than 75 kg and history of hypertension, history of DM, history of ischaemic vascular disease/dissection/aneurysm in the brain or elsewhere, history of systemic arteritis, history of autoimmune disease and atherosclerosis, history of smoking, female gender, elderly. Patients with NR have a higher rate of morbidity and mortality following ischaemia and embolism. Predictors of NR include lesion complexity, systolic hypertension and high body weight, female gender, elderly, dyslipidaemia and preexisting arterial disease. Further validation of this risk model is required with lager number of patients and multicenter studies.

Purpose To assess the prevalence of the neuroradiological indices of cerebral small vessel disease (CSVD) in patients with severe aortic valve stenosis (AS) in magnetic resonance imaging (MRI). Material and methods 34 patients (age 60-90 years, 17 women and 17 men) with severe AS and 50 healthy controls (age 61-85 years, 29 women and 21 men) underwent MRI brain examinations, which were analysed for the neuroradiological indices of CSVD: hyperintensities in periventricular white matter (PVWM) and deep white matter (DWM), enlarged perivascular spaces (ePVS), lacunar strokes, and cerebral microbleeds (CMBs). Results PVWM hyperintensities were found in 46% of volunteers and was significantly lower (p = 0.027), corresponding to AS patients (80%), the density of lesions was higher in the AS group than in controls (p = 0.019). DWM hyperintensities were found more often in AS patients (76%) than in controls (66%) (p = 0.303), but the densities were similar in both groups. Lacunar strokes were found in 35% of AS patients and 16% of controls (p = 0.042). The average number of lacunar strokes per person was 0.9 in the AS group and 0.3 in the controls (p = 0.035). The AS group showed higher variance in the number of strokes: SD = 1.96 vs. SD = 1.06 in controls. Both prevalence and density of the ePVS and CMBs did not differ significantly between the groups. Conclusions Neuroradiological indices of the vascular disease do not provide an unequivocal clue to the pathogenesis of CSVD in patients with severe AS. Most observations imply that CSVD is primarily a consequence of cerebral hypoperfusion caused by AS.

Fibrinogen increases in the acute inflammatory response since it is an acute-phase reactant. Fibrinogen was defined as an independent risk factor for cardiovascular diseases. We aimed to assess the alterations in plasma fibrinogen levels in patients with obstructive sleep apnea syndrome (OSAS) by comparing them with the control cases and determine their relationship with polysomnography (PSG) parameters. The study included 125 newly diagnosed patients with moderate to severe OSAS (defined as apnea-hypopnea index [AHI] ≥ 15) and 82 non-apneic control subjects (AHI [Med-Science 2021; 10(3.000): 770-4]

This study aimed at analysing the causes and predictors of acute hospitalization and mortality in a cohort of SSc. Retrospective analysis of all acute hospital admissions of SSc patients fulfilling the 2013 EULAR/ACR Classification Criteria, from a single-centre cohort of 95 patients, between 2010 and 2020. The total number of SSc patients registered in our hospital, in this period, was 123. Clinical data were collected from medical files of our institution and from the National Healthcare Registry platform. 53 patients needed acute hospitalization, in a total of 164 admissions. The most frequent causes for admission were: infectious diseases [27%; 70% due to pneumoniae, of which 74% had SSc-associated interstitial lung disease (ILD)], cardiac disease (16.5%), peripheral vascular disease [12.8%; all due to digital ulcers], pulmonary hypertension (PH) (9.8%) and ILD (9.1%). There was an increase in admissions due to cardiac disease over the 10 years of follow-up, and a decrease of ILD over the last 5 years. Fourteen patients died (in-hospital mortality of 9%) mainly due to pneumoniae (36%), heart failure (21%), neoplastic diseases (21%), PH (14%) and ILD (7%). From all the admissions due to infection 70.5% were under immunosuppression at the time of the hospitalization. The frequency of acute admissions superior to 1 was associated with infection (OR 2.29, 95%CI 1.11–4.71). There were several factors associated with both acute admissions and mortality, including: gender, race, digital ulcers, cardiac dysfunction, ILD and PH. Infection was the principal cause of acute hospitalization and mortality, mainly due to pneumoniae. Although a high percentage of those had ILD, it has been decreasing in the last years in our cohort, as a direct cause of hospital admission and mortality, possibly reflecting the advances in its management.

BACKGROUND We explored the associations between serum leptin concentration and cardiovascular prognosis in maintenance hemodialysis patients. METHODS In our prospective study with no intervention, demographics data at baseline were collected from electronic medical records. Serum leptin concentration was determined by ELISA. Patients underwent body composition assessment and echocardiographic measurements after hemodialysis. The primary endpoints were defined as cardiovascular events (CVEs), cardiovascular death (CVD) and all-cause death. RESULTS A total of 165 eligible patients aged 51(43-65) y were enrolled and the mean serum leptin concentration was 35.49 (29.98) ng/ml. During a median follow-up of 18 (12-22) months, CVEs occurred in 37 (22.42%) patients and the cardiovascular and all-cause mortality was 10.91% and 21.82%. Serum leptin concentration was associated with CVEs (HR = 0.982, p = 0.003), CVD (HR = 0.934, p = 0.002) and all-cause death (HR = 0.943, p

Stroke is one of the manifestations of COVID-19-associated coagulopathy. Arterial infarcts are the most common presentation; however involvement of both arterial and venous irrigation is possible but rare. We report, what is, to our knowledge, the second case of concomitant arterial and venous brain thrombosis evidenced in magnetic resonance. A 62-year-old man presented with acute weakness of the left hand and lack of coordination in the left arm. Nine days earlier, he was positive for SARS-CoV-2 RT-PCR. The brain images revealed two subacute infarcts, one corresponding to the territory of the right middle cerebral artery, and the other in the right frontal cortical vein. The existence of both venous and arterial brain infarcts due to COVID-19 infection, has been previously reported once. Most of the cases of stroke are due to only arterial thrombosis; therefore, this could be the starting point to start collecting data about simultaneous compromise in order to assess and compare outcomes, severity of the disease, among other variables.

Introduction: Ankle peak systolic flow velocity can measure peripheral arterial blood flow which can predict extent of peripheral arterial disease. Atherosclerosis is more common in patients with diabetes mellitus and can affect simultaneously coronary circulation and peripheral circulation. Aims and Objectives: The primary objective of the study was to determine the occurrence of peripheral vascular disease by ankle Peak Systolic Velocity (PSV) in patients admitted for coronary artery disease with diabetes mellitus .The secondary objective was to see the association between the ankle Peak Systolic Flow Velocity (PSV) with the extent of abnormality of coronary angiogram in diabetic patients. Materials and Methods: All patients admitted in the hospital with coronary artery disease with diabetes mellitus in whom coronary angiogram was done were included in the study over a period of one year Presence of significant vessel disease CAD was defined as at least >70 % stenosis at one or more major coronary arteries (left anterior descending, left circumflex and right coronary artery). Ankle Peak Systolic Velocity (PSV) was measured in all patients by the Duplex method. The peak systolic velocities in the distal posterior tibial artery and the distal anterior tibial artery was measured and the average peak systolic velocities within three cardiac cycles6 was recorded by the radiologist. The ankle peak systolic flow above 40cm/s was considered as good flow in the lower limb extremity [7]. The data was analysed using SPSS version 17.0 software and mean and standard deviation was used . Results: Out of the cases studied 24 patients (80%) were males and 6 patients (20%) were females. All the Coronary angiograms was classified to single 13(43.3%), double 8(26.7%) and triple 9 (30%) vessel disease by the cardiologist. Out of the 13 patients with single vessel disease 3 patients had < 40 cm/s flow in the right anterior tibial artery and 10 patients had >40 cm/s flow in the right tibial artery indicating good perfusion.Out of the 8 patients with double vessel disease 4 patients had flow 40 cm/s. In triple vessel disease category 5 patients had flow 40cm/s. The p value was 0.2 was not significant and the chi square was 2.79 Similar results were obtained while compared with left ankle peak systolic flow velocity. Conclusion: In this study patients with single vessel disease have higher ankle peak systolic velocity though statistically not significant. Lower ankle peak systolic flow velocity corroborates with peripheral arterial disease [12] and is seen in patients with coronary artery disease [13].

Systemic sclerosis is an autoimmune disease characterized by vascular disease, fibrosis of the skin, and internal organ dysfunction. Gastrointestinal involvement is the most frequent complication of internal organs, impacting up to 90% of patients. Gastrointestinal involvement can affect any region of the gastrointestinal tract from the mouth to the anus, with a predominance of disorders being observed at the level of the upper digestive tract. The gastrointestinal involvement primarily involves the esophagus, small bowel, and rectum. The severity of gastrointestinal involvement affects quality of life and is a marker of worse prognosis and mortality in these patients. In this review, we describe the current findings regarding gastrointestinal involvement by this entity.

INTRODUCTION Gender-based differences in atrial fibrillation have been identified, but limited data exist for patients undergoing left atrial appendage occluder (LAAO) implantation. This study reports gender-related periprocedural and 1-year outcomes of the prospective, multicenter German left atrial appendage occlusion registry (LAARGE). METHODS LAARGE enrolled 641 patients who were scheduled for LAAO implantation from July 2014 to January 2016 in 38 hospitals in Germany. The data collected included demographics, clinical characteristics, details of implantation, and outcome. Efficacy and safety at 1-year follow-up were assessed by the occurrence of thrombembolic and bleeding events, as well as mortality. RESULTS Of 638 patients undergoing LAAO implantation 38.9% were female and 61.1% male. Females were older (76.4 ± 8.2 [females] vs. 75.6 ± 7.7 [males], p = .042) and had a higher stroke risk (CHA2 DS2 -VASc score: 4.9 ± 1.5 vs. 4.3 ± 1.5, p

Eisenmenger syndrome (ES) develops in association with unrepaired, non-restrictive cardiac shunt lesions at the atrial, ventricular or arterial level over time. In developed countries, cardiac defects are being operated on in a timely manner, before pulmonary vascular disease develops. However, with rising immigration from underserved countries, we increasingly see patients with shunt lesions, that are not amenable for repair as pulmonary vascular disease has already established. ES describes a symptom complex and patients present with heterogeneous problems involving many organ systems (multisystem disorder). Care in tertiary specialist cardiac centers with access to multidisciplinary subspecialities is required. Central cyanosis with secondary erythrocytosis is one of the key features of patients with ES. Clinical consequences of longstanding hypoxia can lead to other organ complications, that involve other organs than the heart alone. Although ES patients have a better prognosis compared to other patients with pulmonary arterial hypertension, ES grossly affects quality of life and morbidity is frequent. Follow-up and care at specialist congenital heart disease centers is highly recommended to prevent, to early diagnose and to timely manage complications of ES. This is necessary to maintain functional capacity, decrease morbidity and increase life expectancy for these vulnerable patients. The leading reasons for mortality are sudden cardiac death, progressive heart failure, and infectious diseases. Various factors have been shown to be associated with mortality like decreased arterial oxygen saturation, functional class, impaired exercise tolerance, syncopal events, iron deficiency, presence of pre-tricuspid shunts, arrhythmias, increased (NT-pro) brain natriuretic peptide, echocardiographic variables of right ventricular dysfunction and hospitalization for heart failure. Although to date there is no causal therapy to reverse pulmonary vascular disease, a greater armamentarium of targeted therapies is available, which have been shown to be beneficial in patients with ES.

The Fontan circulation is a palliative concept for patients with univentricular hearts. The central veins are connected directly to the pulmonary arteries (cavo-pulmonary connection) to separate the pulmonary and the systemic circulation. There is no sub-pulmonary ventricle that generates pressure to drive blood through the pulmonary arteries. Pulmonary blood flow is determined by central venous pressure (CVP) and pulmonary vascular resistance (PVR). The capability of the Fontan circulation to compensate for alterations in PVR is limited, as CVP can only be increased within narrow ranges without adverse clinical consequences. Consequently, systemic ventricular preload and cardiac output are dependent on a healthy lung with low PVR. Failure of the Fontan circulation is relatively common. In addition to ventricular dysfunction, maladaptive pulmonary vascular remodeling resulting in increased pulmonary resistance may play a key role. The pathophysiology of the maladaptive vascular processes remains largely unclear and diagnosis of an increased PVR is challenging in Fontan circulation as accurate measurement of pulmonary arterial blood flow is difficult. In the absence of a sub-pulmonary ventricle, pulmonary artery pressure will almost never reach the threshold conventionally used to define pulmonary arterial hypertension. There is a need for markers of pulmonary vascular disease complementary to invasive hemodynamic data in Fontan patients. In order to treat or prevent failure of the Fontan circulation, pathophysiological considerations support the use of pulmonary vasodilators to augment pulmonary blood flow and systemic ventricular preload and lower CVP. However, to date the available trial data have neither yielded enough evidence to support routine use of pulmonary vasodilators in every Fontan patient nor have they been helpful in defining subgroups of patients that might benefit from such therapies. This review discusses potential pathomechanisms of pulmonary vascular disease; it summarizes the current knowledge of the effects and efficacy of pulmonary vasodilator therapy in Fontan patients and tries to outline areas of potential future research on the diagnosis and treatment of pulmonary vascular disease and Fontan failure.