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Sepsis-associated encephalopathy (SAE) is the term used to define brain dysfunction related to infections that are principally located outside the central nervous system (CNS). A number of published studies report that electroencephalography (EEG) has been used in the evaluation of patients with sepsis, alone or usually in combination, to evoked potentials and neuroimaging. This was in an effort to assess if EEG can be a tool in the diagnosis and monitoring of the neurological status in sepsis patients. Although there is no specific test for the diagnosis and prognosis of sepsis related encephalopathy, our literature review suggests that EEG has a role in the assessment of this clinical entity. Due to its low cost and simplicity in its performance, EEG could be a potential aid in the assessment of sepsis neurological complications even in the early, subclinical stages of the syndrome. The aim of this review is to summarize the published literature regarding the application and utility of electroencephalography in adult patients with sepsis.

This review summarizes the published literature referring to the use and validity of the biomarker soluble urokinase plasminogen activator receptor (suPAR) when used for the assessment of patients with cardiac diseases. It is measured by enzyme-linked immunosorbent assay (ELISA) in plasma samples. In cardiology a cut-off value range of 3.5 - 4.5 ng/mL has been commonly utilized. Different cut-off values may be applied based on the measuring kit used, the patient population and the clinical setting. A PubMed/Medline search was conducted aiming to identify all publications relevant to the use of suPAR in patients with cardiac diseases. A total of 39 studies were included in this review. suPAR as a marker of inflammation has been used more extensively in recent years, alone or in combination with other biomarkers of inflammation and cardiac pathology in the assessment of patients with acute and chronic cardiac diseases. suPAR is closely related to the pathophysiology of cardiac disease, and a number of publications encourages its use as a valuable biomarker in the assessment of patients presenting to the cardiology service. It may be most valuable in the risk assessment of patients with acute coronary syndromes and congestive heart failure, as suPAR elevation may be an independent predictor of mortality in these conditions. In conclusion, among several biomarkers used for clinical entities with underlying inflammatory pathophysiology including cardiac diseases, suPAR is a novel attractive index for the prognostic risk stratification of cardiac patients. More research is warranted to confirm its diagnostic and prognostic validity, alone or combined with other cardiac and inflammatory biomarkers.

A 12-year-old male patient suffering from congenital glaucoma developed bradycardia, left ventricular failure, and hypotension after induction of anesthesia. Electrocardiography and echocardiography revealed a complete normalization of ECG and a complete spontaneous recovery in the cardiac function 72 hours from the beginning of the clinical manifestations, while cardiac Magnetic Resonance Imaging was performed, and coronary Computed Tomography scan revealed a myocardial bridge of a tract of the left anterior descendent coronary artery. Diagnosis of Kounis syndrome (KS) was made, a relatively novel, under-recognized clinical condition, defined as the manifestation of an acute coronary syndrome accompanied by mast cell activation and platelet aggregation involving interrelated and interacting inflammatory cells in the setting of allergic, hypersensitivity, anaphylactic or anaphylactoid insults. We described one of the first pediatric cases of KS related to anesthetic medications. In children, this syndrome has been only described in isolated case reports or small case series. Thus, it appears critical to report new cases of KS in children to increase the awareness of this disease in pediatric healthcare workers so as to enhance its early recognition and optimal therapeutic strategy. Furthermore, it appears of paramount importance the implementation of universal guidelines accepted by allergology and cardiology societies, in order to standardize the management of pediatric and adult patients with KS. Finally, a close collaboration between pediatric allergists and cardiologists seems fundamental for an optimal multidisciplinary patient care.

BACKGROUND Scombroid syndrome constitutes a toxic illness caused by ingestion of improperly stored fish, usually contaminated by Gram-negative bacteria producing histamine and other toxins. Scombroid currently accounts for approximately 5% of food toxicities in the United States. Though cardiovascular complications are infrequent, some patients experienced acute coronary syndrome (ACS) on admission to hospital. This article focuses on the main pathophysiology, clinical features, therapy, and outcomes in scombroid-related ACS. METHODS Starting from the consolidated knowledge on histaminergic syndromes, we performed a literature search for studies describing patient series and single cases presenting at emergency department with scombroid toxicity complicated by myocardial ischemia. RESULTS After a pathophysiological overview on histaminergic syndromes, we carefully analyzed a dataset of 19 patients from 13 studies, published from 1997 to December 2020. Electrocardiographic, echocardiographic, angiographic features, clinical course, hospital complications, and therapeutic approach were described. Shared and differential aspects of scombroid ACS with typical atherosclerotic ischemia, Kounis, MINOCA and Takotsubo syndromes are also discussed. CONCLUSION An ischemic heart scombroid syndrome may occur in some patients after the eating of improperly stored fish food. Currently available studies indicate this as a benign condition, except for patients with history of coronary artery disease, previous ACS, or anaphylaxis. Of clinical concern, there is a potential of hemodynamic failure in the acute stage, even in apparently healthy people.

The aim of this study is to investigate the impact of optimal antihypertensive medication on cognitive function. In this 6-month clinical trial, 248 adults were randomly selected by a registry of hypertensive-treated patients (based on a National Hypertension Treatment Program), followed health centers located in Rafsanjan County, Southeast, Iran. Blood pressure was measured 3 times in each appointment pre- and posttreatment. Mini-Mental State Examination was used for cognitive performance evaluation. Paired t test and multiple regression model showed significant correlation between “the differences of systolic and diastolic blood pressure levels” and “cognitive performance in treated patients more than 40 years old.” Cognitive performance was not significantly different in patients less than 40 years old post antihypertensive treatment. Cognitive performance scores demonstrated significant increase in responders more than 40 years old post antihypertensive treatment. Antihypertensive treatment in responders with age equal or more than 40 years improves the level of cognitive performance significantly.

Coronary symptoms associated with conditions related to mast cell activation and inflammatory cell interactions, such as those involving T-lymphocytes and macrophages, further inducing allergic, hypersensitivity, anaphylactic, or anaphylactic insults, are currently referred to as the Kounis syndrome. Kounis syndrome is caused by inflammatory mediators released during allergic insults, post-inflammatory cell activation, and interactions via multidirectional stimuli. A platelet subset of 20% with high- and low-affinity IgE surface receptors is also involved in this process. Kounis syndrome is not just a single-organ but also a complex multisystem and multi-organ arterial clinical condition; it affects the coronary, mesenteric, and cerebral arteries and is accompanied by allergy–hypersensitivity–anaphylaxis involving the skin, respiratory, and vascular systems in the context of anesthesia, surgery, radiology, oncology, or even dental and psychiatric medicine; further, it has significantly influences both morbidity and mortality. Kounis syndrome might be caused by numerous and continuously increasing causes, with broad clinical symptoms and signs, via multi-organ arterial system involvement, in patients of any age, thereby demonstrating predominant anaphylactic features in terms of a wide spectrum of mast cell-association disorders. Cardiac symptoms, such as chest pain, coronary vasospasm, angina pectoris, myocardial infarction, stent thrombosis, acute cardiac failure, and sudden cardiac death associated with subclinical, clinical, acute, or chronic allergic reactions, constitute the clinical manifestations of this syndrome. Since its first description, a common pathway between allergic and non-allergic coronary events has been demonstrated. The hypothesis is based on the existence of a much higher degree of mast cell degranulation at plaque erosion or rupture sites compared with at the adjacent areas or even more distant segments in post-acute myocardial infarction of non-allergic etiology. Although mast cell activation, differentiation, and mediator release takes days or weeks, the mast cell degranulation may occur just before any acute coronary event, further resulting in coronary artery vasoconstriction and atheromatous plaque rupture. It seems that medications and natural molecules stabilizing the mast cell membrane as well as monoclonal antibodies protecting the mast cell surface can emerge as novel therapeutic modalities for acute coronary and cerebrovascular event prevention.

In the very important meta-analysis published this month in Acta Cardiologica [1] that was performed to comprehensively evaluate the risk of major bleeding events, the authors found that non-vitami...

Sepsis is a condition characterized by high morbidity and mortality which is commonly encountered in an emergency and critical care setting. Despite a substantial body of research, the ideal biomarker for the diagnosis and prognostic stratification of septic patients remains unknown. This review aimed to summarize the publications referring to the validity of the biomarker presepsin when used for the detection, monitoring and prognosis in patients suffering with sepsis. This work is a narrative review based on a PubMed/Medline search conducted in order to identify all relevant publications referring to the use of presepsin in sepsis. Search was not limited by year of publication so all articles archived in the database would be retrieved. No article from before 2010 was identified. A total of 57 publications of the last decade were included, all of which support the use of presepsin as a biomarker for the assessment of septic patients. It has been used alone or in combination with commonly used biomarkers in the evaluation of patients with sepsis in settings such as the emergency department and the intensive care unit. It is useful in the initial workup of patients with suspected sepsis in the emergency setting and may be a predictive factor of mortality and the most severe complication of sepsis. Presepsin seems to be a valuable tool for the laboratory workup of sepsis, especially when used in conjunction with other biomarkers and clinical rating scores with an established role in this population. Further research is needed to evaluate the clinical implications of utilizing presepsin measurements in the workup of sepsis.

Kounis Syndrome is defined as a hypersensitivity coronary disorder constituted by the association of an acute coronary syndrome with a hypersensitivity, allergic, anaphylactic or anaphylactoid reaction, in a pathophysiologic context involving mast-cells, platelets, eosinophils and various interacting inflammatory cells. Currently, Kounis Syndrome is established in the literature, as accompanied by a plethora of clinical case reports that further elucidate its aspects. To the best of our knowledge, a specific analysis regarding the pediatric data of Kounis Syndrome has never been performed. The aim of this review was to reveal all the pediatric Kounis Syndrome cases in the literature, in an attempt to define its clinical implications in children. Moreover, based on the data of this analysis, a new classification for Kounis Syndrome is proposed, focusing mainly in the presence or the absence of allergic myocardial infarction, as the central clinical feature for the stratification of the patients' clinical manifestations.

Objectives The aim of this study was to test the hypothesis that more intensive over standard anticoagulation administered during coronary angiography would significantly reduce rates of radial artery occlusion (RAO). Background RAO, although silent, remains a frequent and therefore worrisome complication following transradial coronary angiography. Anticoagulation is effective in reducing RAO, but the optimal heparin dose remains ill defined. Methods In this multicenter, randomized superiority trial, a high dose (100 IU/kg body weight administered in divided doses) and a standard dose (50 IU/kg body weight) of heparin during 5- or 6-F coronary angiography were compared. A total of 3,102 patients were randomized, of whom 1,836 patients not proceeding to percutaneous coronary intervention and without need for arterial access crossover entered the trial. Post-catheterization hemostasis did not follow a rigid protocol. Results A total of 102 early RAOs were found on ultrasonography (incidence 5.6%). In the high-dose heparin group, the rate of RAO was significantly lower compared with the standard-dose heparin group (27 [3.0%] vs. 75 [8.1%]; odds ratio: 0.35; 95% confidence interval: 0.22 to 0.55; p Conclusions High compared with standard heparin dose significantly reduced the rate of RAO in patients undergoing coronary angiography. High-intensity anticoagulation should be considered in transradial diagnostic procedures. (High [100IU/Kg] Versus Standard [50IU/Kg] Heparin Dose for Prevention of Forearm Artery Occlusion; NCT02570243 )

Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are a major complication in COPD patients which can be triggered by bacterial or viral infections, environmental pollutants and other causes. Procalcitonin (PCT), a peptide that markedly increases in cases of bacterial infection, has been extensively investigated as a biomarker in the diagnosis, prognosis and treatment in patients with AECOPD. A number of studies published in the last decade, tried to investigate whether PCT levels can differentiate between bacterial and other causes of exacerbations, if they can be used as a guide for optimal antibiotic therapy and if they can be a tool in the assessment of the severity and the need for further interventions in the management of those patients. This review aims to gather, summarize and critically present all the available data to date.

Transcatheter aortic valve implantation (TAVI) or transcatheter aortic valve replacement (TAVR) has been established as a vital alternative to surgical aortic valve replacement (AVR) for intermediate and high surgical risk patients.

Chronic inflammation is a well-established background process in many age-related diseases. Many recent studies investigate the use of various inflammatory biomarkers such as C-reactive protein (CRP), interleukin-6, and interleukin-1 as predictors of physical and cognitive performance among elders. The phenotype of frailty has also been associated with underlying inflammatory mechanisms. The aim of this article was to review the literature referring to the correlation of CRP serum levels and frailty in older individuals. We tried to identify all relevant publications regarding the relation of CRP as an index of frailty in the elderly and its potential use. Although many studies in the recent medical literature positively associate serum CRP levels and frailty in older individuals, some do not, and some raise some interesting questions and set the basis for future studies. The association of CRP and frailty in elder patients should be considered when clinicians interpret inflammatory biomarkers in various clinical settings in such patients. Well-designed, prospective clinical trials are warranted to better assess the role and pathophysiology of frailty in the elderly and its mechanisms as also the exact role of CRP as an inflammatory marker and as a prognostic index in this syndrome.

Percutaneous transluminal coronary angioplasty with coronary stent implantation is a life-saving medical procedure that has become, nowadays, the most frequent performed therapeutic procedure in medicine. Plain balloon angioplasty, bare metal stents, first and second generation drug-eluting stents, bioresorbable and bioabsorbable scaffolds have offered diachronically a great advance against coronary artery disease and have enriched our medical armamentarium. Stented areas constitute vulnerable sites for endothelial damage, endothelial dysfunction, flow turbulence, hemorheologic changes, platelet dysfunction, coagulation changes and fibrinolytic disturbances. Implant surface attracts several proteins such as albumin, fibronectin, fibrinogen, and complement that lead to complement system activation. Macrophages recognize the implant as foreign substance due to protein adsorption and its continuous presence results in macrophage differentiation and fusion into foreign body giant cells. Polymer coating, stent metallic platforms and the released drugs can act as strong antigenic complex that apply continuous, repetitive, persistent and chronic hypersensitivity irritation to the coronary intima. The concomitant administration of oral antiplatelet drugs and environmental exposures can induce hypersensitivity inflammation. A class of platelets, activated via high-affinity and low-affinity IgE hypersensitivity receptors FCγRI, FCγRII, FCeRI and FCeRII, can induce Kounis hypersensitivity-associated thrombotic syndrome inside the stented coronaries. Type III variant of this syndrome is diagnosed when coronary artery stent thrombosis is associated with thrombus infiltrated by eosinophils or mast cells and/or when coronary intima, media and adventitia adjacent to stent, is infiltrated by eosinophils or mast cells. Careful history of hypersensitivity reactions to all implanted materials and concomitant drugs with monitoring of inflammatory mediators as well as lymphocyte transformation studies to detect hypersensitivity must be undertaken in order to avoid disastrous consequences. Food and Drug Administration recommendations for coronary stent implantation should be applied also to bioresorbable scaffolds. Further studies with inert and non-allergenic implants are necessary.

Kounis syndrome is the concurrence of coronary spasm, acute myocardial infarction or stent thrombosis, with allergic reactions in the setting of mast-cell and platelet activation. In this report Kounis syndrome manifesting as stent thrombosis with left ventricular thrombus formation was triggered by a food-induced allergic reaction. The allergic reaction to food was confirmed by oral rice pudding ingredients challenge test while skin tests were inconclusive. To our knowledge, this is first report of early stent thrombosis secondary to food allergic reaction in a 70-year-old man patient who was found to have left ventricular thrombus and undiagnosed hypertrophic cardiomyopathy.

Objective To conduct a systematic review evaluating the utility of brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) as biomarkers in adult patients with septic shock. Materials and methods Pubmed/Medline databases were searched from inception to November 2018 using the search terms: (septic[Title/Abstract] AND shock[Title/Abstract]) AND bnp[Title/Abstract]) and (septic[Title/Abstract]) AND shock[Title/Abstract]) AND natriuretic[Title/Abstract]). No restriction was applied regarding date of publication. Comparative observational studies evaluating BNP and NT-proBNP in patients with septic shock aged ≥18 years were eligible for inclusion. Bibliographies from the extracted articles were also reviewed to identify additional relevant publications. Results In total, 46 studies met all eligibility criteria and were included. A strong body of literature has demonstrated that in patients with septic shock, increased values of BNP and NT-proBNP are associated with increased mortality. An increase from baseline BNP values has also been associated with increased mortality, whereas decreases from baseline values are not related to worse outcome. Brain natriuretic peptides have also been associated with cardiac dysfunction in patients with sepsis. Moreover, BNP values have been found to be significantly elevated in septic shock, regardless of cardiac dysfunction, and have been used to distinguish between septic and cardiogenic shock. Furthermore, BNP and NT-proBNP are significantly increased in patients with septic shock, compared to patients with sepsis and severe sepsis. Conclusions BNP and NT-proBNP appear to be reliable predictors of outcome in septic shock.

In the interesting report of Pradhan, Christ and Trapper (1) published in the Journal of Cardiovascular Diagnosis and Therapy , a 22-year-old man developed acute retrosternal pain and chest tightness with ischemic changes in inferolateral wall (ST elevation =0.2 mV) and positive troponin following a single dose of amoxicillin administered for acute tonsillitis treatment. Urgent coronary angiography demonstrated normal coronary arteries. The initial diagnosis of acute ST elevation myocardial infarction (STEMI) was attributed to coronary artery spasm, whereas acute myocarditis considered as a differential diagnosis.

Extracorporeal circulation has led to a great development in cardiovascular surgery during the last five decades. Its time-proven efficacy and safety have made on-pump coronary artery bypass grafting (CABG) the gold standard method of surgical revascularization. However, coronary revascularization on cardiopulmonary bypass and the accompanying aortic manipulation are related to plenty of deleterious complications. Therefore, off-pump CABG surgery was established to avoid complications. Nevertheless, despite the initial enthusiasm on this technique, only 20% of myocardial revascularization procedures worldwide are performed off-pump. Not only are off-pump cardiac procedures more technically difficult but also they do not provide better results in terms of graft patency, completeness of revascularization, repeat revascularization requirement, cost, and quality of life. Completeness of revascularization and anastomotic quality should not be compromised to avoid cardiopulmonary bypass.

The aim of the review was to summarize the literature over the last 25 years regarding bicarbonate administration in out-of-hospital cardiac arrest. A PubMed search was conducted using the terms “bicarbonates” and “cardiac arrest”, limited to human studies and reviews published in English (or at least with a meaningful abstract in English) in the last 25 years. Clinical and experimental data raised questions regarding the safety and effectiveness of sodium bicarbonate (SB) administration during cardiac arrest. Earlier advanced cardiac life support (ACLS) guidelines recommended routine bicarbonate administration as part of the ACLS algorithm, but recent guidelines no longer recommend its use. The debate in the literature is ongoing, but at the present time, SB administration is only recommended for cardiac arrest related to hypokalemia or overdose of tricyclic antidepressants. Several studies challenge the assumption that bicarbonate administration is beneficial for treatment of acidosis in cardiac arrest. At the present time, there is a trend against using bicarbonates in cardiac arrest, and this trend is supported by guidelines published by professional societies and organizations. J Clin Med Res. 2016;8(4):277-283 doi: http://dx.doi.org/10.14740/jocmr2456w

The first reported human anaphylactic death is considered to be the Pharaoh Menes death, caused by a wasp sting. Currently, anaphylactic cardiovascular events represent one of most frequent medical emergencies. Rapid diagnosis, prompt and appropriate treatment can be life saving. The main concept beyond anaphylaxis lies to myocardial damage and ventricular dysfunction, thus resulting in cardiovascular collapse. Cardiac output depression due to coronary hypoperfusion from systemic vasodilation, leakage of plasma and volume loss due to increased vascular permeability, as well as reduced venous return, are regarded as the main causes of cardiovascular collapse. Clinical reports and experiments indicate that the human heart, in general, and the coronary arteries, in particular, could be the primary target of the released anaphylactic mediators. Coronary vasoconstriction and thrombosis induced by the released mediators namely histamine, chymase, tryptase, cathepsin D, leukotrienes, thromboxane and platelet activating factor (PAF) can result to further myocardial damage and anaphylaxis associated acute coronary syndrome, the so-called Kounis syndrome. Kounis syndrome with increase of cardiac troponin and other cardiac biomarkers, can progress to heart failure and cardiovascular collapse. In experimental anaphylaxis, cardiac reactions caused by the intracardiac histamine and release of other anaphylactic mediators are followed by secondary cardiovascular reactions, such as cardiac arrhythmias, atrioventricular block, acute myocardial ischemia, decrease in coronary blood flow and cardiac output, cerebral blood flow, left ventricular developed pressure (LVdp/dtmax) as well as increase in portal venous and coronary vascular resistance denoting vascular spasm. Clinically, some patients with anaphylactic myocardial infarction respond satisfactorily to appropriate interventional and medical therapy, while anti-allergic treatment with antihistamines, corticosteroids and fluid replacement might be ineffective. Therefore, differentiating the decrease of cardiac output due to myocardial tissue hypoperfusion from systemic vasodilation and leakage of plasma, from myocardial tissue due to coronary vasoconstriction and thrombosis might be challenging during anaphylactic cardiac collapse. Combined antiallergic, anti-ischemic and antithrombotic treatment seems currently beneficial. Simultaneous measurements of peripheral arterial resistance and coronary blood flow with newer diagnostic techniques including cardiac magnetic resonance imaging (MRI) and myocardial scintigraphy may help elucidating the pathophysiology of anaphylactic cardiovascular collapse, thus rendering treatment more rapid and effective.

Radial artery (RA) occlusion (RAO) remains the Achilles heel of transradial coronary procedures. Although of silent nature, RAO is relatively frequent, results in graft shortage for future coronary artery bypass surgery, and may occur even after short-lasting, 5F coronary angiography (CAG). The most frequent predictors of RAO are RA size, body size, female gender, and periprocedural anticoagulation intensity. Methods to detect RAO are variable, of which the Barbeau test and ultrasonography have similar diagnostic accuracy. Data indicate that late RAO recanalization may occur. Meticulous handling of RA and the use of appropriate hemostatic devices and techniques along with sufficient heparin dose appear important measures to reduce RAO rates. Recent contradictory studies indicate that the decreasing incidence of RAO overtime is not as uniform as previously thought. In 2 meta-analyses, the benefit of higher over lower anticoagulation intensity became evident. As “it may all be appropriate anticoagulation” for a simplified approach against RAO, the results of an ongoing trial comparing 100 with 50 IU/kg body weight in transradial CAG are eagerly awaited.

Background: Major, noncoronary complications are rarely encountered following transradial coronary procedures. Methods and Results: Among 1600 prospectively studied patients with complete follow-up, 7 patients experienced major complications following coronary forearm procedures corresponding to an incidence of 0.44%. We found inadvertent symptomatic intramyocardial contrast medium injection, 2 cases with compartment syndrome of which 1 was managed surgically, exertional hand ischemia due to radial artery occlusion, a large ulnar artery pseudoaneurysm, an ulnar arteriovenous fistula, and 1 critical hand ischemia due to late occlusion of the distal brachial artery. Conclusions: Although infrequent, surveillance for major complications should be encouraged after forearm coronary procedures.

Background Radial artery occlusion (RAO) remains the Achilles' heel of transradial coronary procedures. Standard over lower systemic anticoagulation levels are believed to reduce RAO rates but this is ill-supported by scientific evidence. We compared whether standard in comparison with less intensive anticoagulation was superior in preventing vessel closure. Methods and results The two arms of this analysis included 731 pooled patients with the same inclusion and exclusion criteria. We assessed forearm arterial access site occlusion rate by unfractionated heparin (UFH) dose in an individual participant data meta-analysis of this randomized study and of consecutive eligible patients from our previous trial. We randomized 308 consecutive patients undergoing transradial coronary angiography with 5 French (5Fr) catheters without need to crossover to receive 2500 or 5000UFH units. The primary end-point was the ultrasonographically determined vessel occlusion rate. Incident RAOs in the randomized arm were 15.9% vs. 14%, in the low and standard UFH dose, respectively (p=0.7). Corresponding figures for forearm arterial occlusion rates in the pooled population were 13.0% vs. 9.9% (relative risk: 1.3, 95% confidence interval — CI: 0.88–1.98; p=0.2). Procedural and fluoroscopy duration was less than 15 and 3min, respectively. The mean UFH dose difference was 3.52 (95% CI: −0.45 to 7.49) units per kilo body weight between occluded (n=84) and patent forearm arteries (n=647); (p=0.053). Conclusions Incident forearm arterial occlusions were high despite using 5Fr catheters for a short-lasting procedure. Systemic anticoagulation with standard over lower UFH dose did not reduce the frequency of RAOs after coronary angiography.

The bioresorbable scaffolds have been introduced recently in an effort to eliminated metals from the coronary arteries, to maintain vessel pulsatility and to diminish late and especially very late stent thrombosis.

Background Incidence of radial artery occclusions (RAO) and ulnar artery occclusions (UAO) in coronary procedures, factors predisposing to forearm arteries occlusion, and the benefit of anticoaggulation vary significantly in existing literature. We sought to determine the incidence of RAO/UAO and the impact of anticoagulation intensity. Methods and Results Meta‐analysis of 112 studies assessing RAO and/or UAO (N=46 631) were included. Overall, there was no difference between crude RAO and UAO rates (5.2%; 95% confidence interval [CI], 4.4–6.0 versus 4.0%; 95% CI, 2.8–5.8; P =0.171). The early occlusion rate (in‐hospital or within 7 days after procedure) was higher than the late occlusion rate. The detection rate of occlusion was higher with vascular ultrasonography compared with clinical evaluation only. Low‐dose heparin was associated with a significantly higher RAO rate compared with high‐dose heparin (7.2%; 95% CI, 5.5–9.4 versus 4.3%; 95% CI, 3.5–5.3; Q=8.81; P =0.003). Early occlusions in low‐dose heparin cohorts mounted at 8.0% (95% CI, 6.1–10.6). The RAO rate was higher after diagnostic angiographies compared with coronary interventions, presumably attributed to the higher intensity of anticoagulation in the latter group. Hemostatic techniques (patent versus nonpatent hemostasis), geography (US versus non‐US cohorts) and sheath size did not impact on vessel patency. Conclusions RAO and UAO occur with similar frequency and in the order of 7% to 8% when evaluated early by vascular ultrasonography following coronary procedures. More‐intensive anticoagulation is protective. Late recanalization occurs in a substantial minority of patients.

This significant meta-analysis1 of 6 high-quality randomized trials reporting clinical outcomes beyond 1 year and comparing everolimus-eluting bioresorbable vascular scaffolds with everolimus-eluting metallic stents in 5392 patients demonstrated that the risk of definite or probable stent/scaffold thrombosis and very late stent/scaffold thrombosis was higher with bioresorbable vascular scaffolds. Specifically, the definite or probable stent/scaffold thrombosis was estimated in the range of 2.1% and 0.8% and very late stent/scaffold thrombosis between 0.8% and 0.2%, respectively, based on DerSimonian–Laird and Peto methods. The authors speculate that this difference could be attributed to the potential malposition, late discontinuity, peristrut low-intensity area, uncovered strut, underdeployment, incomplete lesion coverage, recoil, restenosis, strut …

Atrial fibrillation is the most common cardiac arrhythmia in western society affecting more than 35 million individuals worldwide annually. It is a common postoperative complication and may also occur spontaneously during general and local anesthesia administration. Aging, diabetes mellitus, hypertension, and cardiovascular diseases including cardiomyopathies, congenital cardiac anomalies, heart failure, myocardial ischemia, pericarditis, previous cardiac surgery, vascular disease, and valvular heart disease are some correlated factors. Beyond age, increased incidence of atrial fibrillation has been correlated to autoimmune system activation as it is the underlying mechanism of persistent atrial fibrillation development. Current research supports an association between the complement system activation and lymphocyte-pro-inflammatory cytokines release with the cardiac conduction system and atrial fibrosis. The loss of CD28 antigen from CD4+ CD28+ T lymphocytes seems to play a major role in atrial fibrillation development and prognosis. Except atrial fibrillation, a variety of additional electrocardiographic changes, resembling those with digitalis intoxication may accompany anaphylaxis and particularly Kounis syndrome. Histamine is one well-known mediator in allergic and inflammatory conditions as physiologically regulates several cardiovascular and endothelial functions with arrhythmogenic potential. The increased oxidative stress, measured by the redox potentials of glutathione, has been correlated with atrial fibrillation incidence and prevalence. The use of antazoline, a first-generation antihistamine agent used for rapid conversion of recent-onset atrial fibrillation in patients with preserved left ventricular function and for rapid atrial fibrillation termination during accessory pathway ablation denotes that anaphylaxis-induced histamine production could be the cause of atrial fibrillation at least in some instances. The anaphylaxis diagnosis in anesthesia can be challenging owing to the absence of cutaneous manifestetions such as flushing, urticaria, or angioedema. Anticoagulation for stroke prevention, rate and rhythm control medications, invasive methods such as radiofrequency ablation or cryoablation of pulmonary veins as well surgical ablation constitute the treatment basis of atrial fibrillation. Understanding the underlying mechanisms of atrial fibrillation by cardiologists, anesthesiologists and surgeons, as well as potential treatments, to optimize care is of paramount importance.