Search

Compared with metallic drug-eluting stents (DES), bioresorbable vascular scaffolds (BVS) may further improve long-term outcomes of percutaneous coronary intervention (PCI) in patients with coronary artery disease. We report our early experience with BVS in Korea.We evaluated 105 consecutive patients with BVS implanted at Asan Medical Center, Korea between October 21, 2015 and June 3, 2016. Angiographic results, and in-hospital and 6-month clinical outcomes were assessed.A total of 134 BVS were implanted to treat 115 lesions. The mean age was 62 ± 10.5 years; 85 patients (81%) were males, 26 patients (25%) were presented with acute coronary syndrome. Among 115 lesions treated with BVS, 76 (66.1%) were B2/C type, 27 (23.5%) were bifurcation lesions, and four (3.5%) were chronic total occlusion. Pre-dilation and post-dilation using high-pressure non-compliant balloon was performed in 104 lesions (90.4%) and 113 lesions (98.2%), respectively. During the procedure, intravascular imaging was used for all patients (100%; intravascular ultrasound 89 and optical coherence tomography 40 patients). Device success rate was 100%. In-segment and in-scaffold acute again were 1.1 ± 0.6 and 1.3 ± 0.5 mm, respectively. Periprocedural myocardial infraction occurred in four patients (3.8%). No deaths, stent thrombosis, or urgent revascularizations occurred either during hospitalization or the follow-up period.In this single-center experience, implantation of BVS with intravascular imaging support was feasible and early clinical outcomes were excellent. Evaluation of long-term efficacy and safety of BVS and its feasibility in clinical use for a broader range of lesions is warranted.

AIMS The aim of this study was to compare the performance of the Tiger-II with Judkins 3.5L/4R catheters in coronary angiography (CAG) via the transradial approach (TRA). METHODS AND RESULTS Consecutive patients undergoing non-urgent CAG via the right TRA were randomised to either the Tiger-II (Terumo) or Judkins (3.5L/4R; Medtronic) 5 Fr catheters; 320 patients in each group were randomised. Catheter or access site change was required in 57 (17.8%) vs. 68 (21.3%) patients allocated to the Tiger-II and Judkins group, respectively (p=0.3). The study's primary endpoint of contrast volume (ml) used until completion of CAG was lower for Tiger-II vs. Judkins group: 66.8 (54.0-82.0) vs. 73.4 (60.0-94.1), p

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.

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.

Heart failure (HF) is rapidly growing, conferring considerable mortality, morbidity, and costs. Dedicated HF clinics improve patient outcomes, and the development of a national HF clinics network aims at addressing this need at national level. Such a network should respect the existing health care infrastructures, and according to the capacities of hosting facilities, it can be organized into three levels. Establishing the continuous communication and interaction among the components of the network is crucial, while supportive actions that can enhance its efficiency include involvement of multidisciplinary health care professionals, use of structured HF‐specific documents, such as discharge notes, patient information leaflets, and patient booklets, and implementation of an HF‐specific electronic health care record and database platform.

Key Points Question Is the receipt of colchicine among patients hospitalized with symptomatic coronavirus disease 2019 associated with clinical benefit? Findings In this randomized clinical trial of 105 patients, the rate of the primary clinical end point (clinical deterioration) was higher in the control group than in the colchicine group, and the time to clinical deterioration was shorter in the control group than in the colchicine arm. No difference was observed in the primary biochemical end point (high-sensitivity troponin concentration), but patients in the colchicine group had a smaller increase in dimerized plasma fragment D compared with patients in the control group. Meaning The hypothesis-generating findings of this study suggest a role for colchicine in the treatment of patients with coronavirus disease 2019., This randomized clinical trial evaluates the effect of treatment with colchicine on cardiac and inflammatory biomarkers and clinical outcomes in patients hospitalized with coronavirus disease 2019 (COVID-19)., Importance Severe acute respiratory syndrome coronavirus 2 infection has evolved into a global pandemic. Low-dose colchicine combines anti-inflammatory action with a favorable safety profile. Objective To evaluate the effect of treatment with colchicine on cardiac and inflammatory biomarkers and clinical outcomes in patients hospitalized with coronavirus disease 2019 (COVID-19). Design, Setting, and Participants In this prospective, open-label, randomized clinical trial (the Greek Study in the Effects of Colchicine in COVID-19 Complications Prevention), 105 patients hospitalized with COVID-19 were randomized in a 1:1 allocation from April 3 to April 27, 2020, to either standard medical treatment or colchicine with standard medical treatment. The study took place in 16 tertiary hospitals in Greece. Intervention Colchicine administration (1.5-mg loading dose followed by 0.5 mg after 60 min and maintenance doses of 0.5 mg twice daily) with standard medical treatment for as long as 3 weeks. Main Outcomes and Measures Primary end points were (1) maximum high-sensitivity cardiac troponin level; (2) time for C-reactive protein to reach more than 3 times the upper reference limit; and (3) time to deterioration by 2 points on a 7-grade clinical status scale, ranging from able to resume normal activities to death. Secondary end points were (1) the percentage of participants requiring mechanical ventilation, (2) all-cause mortality, and (3) number, type, severity, and seriousness of adverse events. The primary efficacy analysis was performed on an intention-to-treat basis. Results A total of 105 patients were evaluated (61 [58.1%] men; median [interquartile range] age, 64 [54-76] years) with 50 (47.6%) randomized to the control group and 55 (52.4%) to the colchicine group. Median (interquartile range) peak high-sensitivity cardiac troponin values were 0.0112 (0.0043-0.0093) ng/mL in the control group and 0.008 (0.004-0.0135) ng/mL in the colchicine group (P = .34). Median (interquartile range) maximum C-reactive protein levels were 4.5 (1.4-8.9) mg/dL vs 3.1 (0.8-9.8) mg/dL (P = .73), respectively. The clinical primary end point rate was 14.0% in the control group (7 of 50 patients) and 1.8% in the colchicine group (1 of 55 patients) (odds ratio, 0.11; 95% CI, 0.01-0.96; P = .02). Mean (SD) event-free survival time was 18.6 (0.83) days the in the control group vs 20.7 (0.31) in the colchicine group (log rank P = .03). Adverse events were similar in the 2 groups, except for diarrhea, which was more frequent with colchicine group than the control group (25 patients [45.5%] vs 9 patients [18.0%]; P = .003). Conclusions and Relevance In this randomized clinical trial, participants who received colchicine had statistically significantly improved time to clinical deterioration. There were no significant differences in high-sensitivity cardiac troponin or C-reactive protein levels. These findings should be interpreted with caution. Trial Registration ClinicalTrials.gov Identifier: NCT04326790

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.

Patients with inflammatory bowel disease (IBD) have a higher incidence of coronary artery disease (CAD) compared with the general population. Left main coronary artery (LMCA) thrombosis constitutes a very rare but catastrophic manifestation of acute coronary syndrome. Case reports describing young patients with IBD and LMCA thrombosis are scarce. Most importantly, patients with a positive family history of thrombotic events and those with significant genetic or acquired risk factors such as the antiphospholipid antibody syndrome, advanced age, immobilization, pregnancy, oral contraceptive use, obesity, diabetes, and cigarette smoking may have a higher risk of thrombosis among those with active IBD. We describe a 28-year-old man who was admitted for coronary angiography (CA) due to ST-segment elevation myocardial infarction. He had a recent exacerbation of ulcerative colitis. The patient was a smoker without a family history of CAD. Proximal total occlusion of the left anterior descending (LAD) artery and left circumflex (LCX) artery with massive thrombus was shown on CA, whereas a normal dominant right coronary artery delivered collaterals to the LAD artery.

Background: Ticagrelor may exert pleiotropic actions, beyond platelet inhibition, which are possibly adenosine-mediated. It has been suggested that in patients with coronary artery disease (CAD) ticagrelor may influence endothelial function. Objective: We aimed to assess the possibility of endothelial function deterioration following ticagrelor treatment cessation. Methods: This was a prospective, observational study, in stable CAD patients with prior percutaneous coronary intervention (PCI) for acute coronary syndrome manifested 1 year earlier, under ticagrelor maintenance dose (90 mg bid) and due to discontinue ticagrelor. Endothelial function was assessed by Peripheral Arterial Tonometry (EndoPat 2000 system, Itamar Medical, Caesarea, Israel) immediately after receiving the last tablet of ticagrelor (Day 0) and at Day 2 and Day 5 post-ticagrelor cessation. Reactive hyperaemia index (RHI) was calculated by automated software and endothelial dysfunction (ED) was defined as a RHI

To explore the effect of early-onset preeclampsia on the blood pressure of offspring during the first month of life.This prospective case-control study included 106 neonates of mothers with early-onset preeclampsia (developing at34 weeks of gestation) and 106 infants of normotensive mothers, matched 1-to-1 for sex and gestational age. Serial blood pressure measurements were obtained on admission, daily for the first postnatal week, and then weekly up to the fourth week of life.There were no differences in blood pressure values on admission and the first day of life between cases and controls. Conversely, infants exposed to preeclampsia had significantly higher systolic (SBP), diastolic (DBP), and mean blood pressure (MBP) on the subsequent days up to the fourth postnatal week (P .001-.033). Multiple regression analyses with adjustment for sex, gestational age, antenatal corticosteroid use, and maternal antihypertensive medication use confirmed the foregoing findings (P .001-.048). Repeated-measures ANOVA also identified preeclampsia as a significant determinant of trends in SBP, DBP, and MBP during the first month of life (F = 16.2, P .001; F = 16.4, P .001; and F = 17.7, P .001, respectively).Infants of mothers with early-onset preeclampsia have elevated blood pressure values throughout the neonatal period compared with infants born to normotensive mothers.

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, FCεRI and FCεRII, 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.

Background Kounis syndrome is a systemic complication following an allergic reaction, presenting with coronary artery spasm or thrombosis and occasionally with stent thrombosis that can have fatal outcome. Objectives Heparins can induce allergic reactions via tissue antigenicity, heparin induced thrombocytopenia and contact system-activating effects of contaminants but allergy bivalirudin has not been reported so far. Methods Herein, we describe a patient with fatal acute coronary in-stent thrombosis following an allergic reaction soon after an intra-arterial heparin dose and intravenous administration of bivalirudin during angioplasty. Results The patient received intense myocardial infarction protocol treatment including angioplasty and defibillation together with antiallergic therapy but despite all of these efforts and measures, he succumbed 2 h later. Conclusions Significant suspicion should be raised that life saving drugs such as heparin and bivalirudin could join forces with concurrent medication acting as antigens and induce fulminant and fatal stent thrombosis as a manifestation of Kounis syndrome

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 Delay in the onset of antiplatelet action occurs in patients with ST-elevation myocardial infarction (STEMI) and is likely due to disturbed absorption. We hypothesized that patients presenting relatively late after the onset of symptoms would have faster antiplatelet action. METHODS AND RESULTS We analyzed patient-level data from 5 studies of 207 P2Y12 receptor antagonist-naive patients with STEMI undergoing primary percutaneous coronary intervention (PCI). All patients had available platelet reactivity (PR) assessment with the VerifyNow assay (in P2Y12 reaction units; PRU) prior to and 2 h after loading. High PR (HPR) was defined as ≥ 208 PRU. Pain-to-antiplatelet loading time independently predicted PR at 2 h after loading: every 1-h increase in pain-to-antiplatelet loading time produced a 7% decrease in PR (P=0.001). Pretreatment PR, body mass index, morphine and novel P2Y12 receptor antagonist also affected PR 2 h after loading. Novel P2Y12 receptor antagonist use and per hour increase in pain-to-antiplatelet loading time were independently associated with lower probability for HPR with an OR (95% CI) of 0.145 (0.095-0.220) and 0.776 (0.689-0.873), P

The objective of this study was to assess the pharmacokinetic and pharmacodynamic behavior of ticagrelor administered either as crushed (in the semi-upright sitting position) or as integral (in the supine position) tablets in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PCI). We randomized 20 patients to ticagrelor 180 mg either as 2 integral tablets administered in the supine position (standard administration) or as 2 tablets crushed and dispersed, administered in the semi-upright sitting position. Blood samples were drawn for pharmacokinetic and pharmacodynamic assessment at randomization (0 h) and at 0.5, 1, 2, and 4 h. At 1 h, ticagrelor plasma exposure and area under the plasma concentration–time curve from time zero to 1 h (AUC1) (co-primary endpoints) were higher in the crushed versus integral tablets group (median 586 vs. 70.1 ng/mL and 234 vs. 24.4 ng·h/mL, respectively), with a ratio of adjusted geometric means (95 % confidence interval [CI]) of 12.67 (2.34–68.51) [p = 0.005] and 19.28 (3.51–106.06) [p = 0.002], respectively. Time to maximum plasma concentration was shorter in the crushed versus integral tablets group (median 2 vs. 4 h), with a ratio of adjusted geometric means (95 % CI) of 0.69 (0.49–0.97) [p = 0.035]. Parallel findings were observed with AR-C124910XX (active metabolite). Platelet reactivity (VerifyNow®) at 1 h was lower with crushed versus standard administration with least squares estimates mean difference (95 % CI) of 92 (−158.4 to 26.6) P2Y12 reaction units (p = 0.009). In patients with STEMI undergoing primary PCI, ticagrelor crushed tablets administered in the semi-upright sitting position seems to lead to a faster—compared with standard administration—absorption, with stronger antiplatelet activity within the first hour. Trial registration: ClinicalTrials.gov identifier: NCT02046486.

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 development and progression of atherosclerosis and its predisposition for unstable angina, myocardial infarction and stroke is associated with traditional risk factors such as family history, cigarette smoking, hypertension, dyslipidemia, diabetes mellitus, obesity, imbalance of the hemostatic/fibrinolytic system and sedentary lifestyle. However, much of the variability in atherosclerosis and its manifestations still remains unexplained. Nowadays, there is increasing evidence that immunologic mechanisms play a major role in etiology, prediction of coronary plaque instability and foreseeing severe reaction leading to an actual coronary event. Cells of the immune system such as macrophages, mast cells and T-lymphocytes are major components of human atheromatous plaque. These cells participate in a vicious immune cycle and activate each others via bidirectional stimuli. For example, mast cells can activate macrophages and may enhance T-cell activation. Inducible macrophage protein 1a may activate mast cells, while CD169+ macrophages activate CD8 T cells. T cells may mediate mast-cell activation and proliferation and regulate macrophage activity. Mediators secreted by these cells, including histamine, neutral proteases, arachidonic acid products, platelet activating factor and a variety of cytokines and chemokines, can induce coronary artery spasm and atheromatous plaque erosion and rupture, culminating in the development of acute coronary syndromes.

Transcatheter aortic valve implantation (TAVR) has emerged as an alternative, rapidly evolving treatment option for patients with severe aortic stenosis and high surgical risk. Stroke is a devastating complication being confined mainly in the periprocedural and 30-day period following TAVR, with a lower and relatively constant frequency thereafter. Early stroke is mainly due to debris embolization during the procedure, whereas later events are associated with patient specific factors. Despite the fact that the rate of clinical stroke has been constantly decreasing compared to initial TAVR experience, modern neuro-imaging with MRI suggests that new ischemic lesions post-TAVR are almost universal. The impact of the latter is largely unknown. However, they seem to correlate with a reduction in neurocognitive function. Because TAVR is set to expand its indication to lower surgical-risk patients, stroke prophylaxis during and after TAVR becomes of paramount importance. Based on clinical and pathophysiological evidence, three lines of research are actively employed towards this direction: improvement in valve and delivery system technology with an aim to reduce manipulations and contact with the calcified aortic arch and native valve, antithrombotic therapy, and embolic protection devices. Careful patient selection, design of the procedure, and tailored antithrombotic strategies respecting the bleeding risks of this fragile population constitute the main defense against stroke following TAVR.

Limited data are available on high platelet reactivity (HPR) rate early post fibrinolysis, while no effective way to overcome it has been proposed. In this context, we aimed to compare ticagrelor versus high dose clopidogrel in patients with ST-segment elevation myocardial infarction (STEMI) who exhibit HPR post fibrinolysis. In a prospective, randomized, parallel design, 3-center study, 56 STEMI patients, out of 83 (67.5 %) screened, who presented with HPR (PRU ≥ 208 by VerifyNow) 3–48 h post fibrinolysis and prior to coronary angiography were allocated to ticagrelor 180 mg loading dose (LD)/90 mg bid maintenance dose (MD) or clopidogrel 600 mg LD/150 mg MD. Platelet reactivity was assessed at randomization (Hour 0), at Hour 2, Hour 24 and pre-discharge. The primary endpoint of platelet reactivity (in PRU) at Hour 2 was significantly lower for ticagrelor compared to clopidogrel with a least square mean difference (95 % confidence interval) of −141.7 (−173.4 to −109.9), p

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.

We suggest that before implanting bioresorbable vascular scaffolds, further improvements in technical procedures and technology are warranted.

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 …

Background Obstructive Sleep Apnea (OSA) is an independent risk factor for cardiovascular disease and has been linked to the development of atherosclerosis. However, the underlying role of metabolic derangements in the development of atherosclerosis in OSA patients is not well-defined yet. Objective The aim of this study was to test whether patients with newly diagnosed OSA have an increased probability to develop carotid atherosclerosis as compared to healthy individuals. Methods A total of 40 subjects without a previous history of cardiovascular disease that underwent full night polysomnography were included in the study. Subjects with an apnea/hypopnea index (AHI) ≥15/h) were classified as moderate/severe OSA. Ultrasound was used to measure the carotid mean intima media thickness (cIMT) and the presence of atheromatic plaques on both carotid arteries of the subjects. Results All participants were well matched and had a similar cardiovascular risk profile (Framingham risk factors). Moderate to severe OSA was diagnosed in 21 subjects. The two groups had similar measurements of cIMT (0.66±0.17 vs 0.75±0.20 p= 0.33) and presence of atheromatic plaque (50% vs 45%, p=1.00). Conclusion Our study suggests that in patients with a similar cardiovascular risk profile and without history of cardiovascular disease, the severity of newly diagnosed OSA is not correlated to carotid atherosclerosis.

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.

Red blood cell and platelet microparticles (RBCm and PLTm, respectively) have drawn research attention as to their potential prothrombotic and vasoconstrictive effects in experimental settings. However, the relevance of circulating microparticles in clinical settings is largely undetermined.Circulating microparticles were quantified with a flow cytometric method in blood samples from consecutive STEMI patients after primary PCI. A matched cohort of healthy volunteers was used to derive reference values for comparison. STEMI patients were followed for 6 months for a composite clinical endpoint.Fifty-one STEMI patients (age 59.8 ± 8.8 years) and 50 controls (age 56.2 ± 9.2 years; p=0.155) were enrolled. RBCm concentration was 18,198 ± 6062/μl in the reference cohort versus 33,740 ± 21,169/μl in STEMI patients (p0.001). RBCm count was not correlated to total RBCs (standardized beta 0.018; p=0.861). PLTm did not differ between groups (17,529 ± 16,292/μl in STEMI patients versus 14,372 ± 6211/μl in controls; p=0.203). RBCm c-statistic was 0.832 (95% confidence interval 0.720 to 0.944), while PLTm prognostic value was not statistically significant (c-statistic 0.614, 95% confidence interval 0.444 to 0.784). In the multivariate analysis, RBCm concentration was independently associated with the occurrence of the clinical endpoint, after adjustment for age, ejection fraction, serum creatinine and presence of diabetes (adjusted p=0.034).The present study demonstrates for the first time that erythrocyte microparticles are elevated in patients with STEMI treated with primary PCI, with levels approximately double those measured in a reference population of healthy volunteers, and their concentrations appear to be positively associated with adverse clinical events.