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The Covid-19 pandemic hit the world hard. Ensnared by a large-scale emergency unprecedented in recent history, mobilization, the classic issue of emergency management, is under stress and test. Yet Taiwan stands out in its rather limited cases of infections despite its frequent contact with mainland China and high population density. Could its mobilization have made the difference? This article traces the steps and strategies that Taiwan took to implement a coordinated mobilization. Three strategies were highlighted: awareness mobilization by declaring emergency early on, resource mobilization by preemptively controlling, boldly incentivizing and surgically distributing resources, and agility mobilization via big data and technology to optimize the response system.

Aims Myocardial infarction (MI) accelerates atherosclerosis and greatly increases the risk of recurrent cardiovascular events for many years, in particular, strokes and MIs. Because B cell-derived autoantibodies produced in response to MI also persist for years, we investigated the role of B cells in adaptive immune responses to MI. Methods and results We used an apolipoprotein-E-deficient (ApoE−/−) mouse model of MI-accelerated atherosclerosis to assess the importance of B cells. One week after inducing MI in atherosclerotic mice, we depleted B cells using an anti-CD20 antibody. This treatment prevented subsequent immunoglobulin G accumulation in plaques and MI-induced accelerated atherosclerosis. In gain of function experiments, we purified spleen B cells from mice 1 week after inducing MI and transferred these cells into atherosclerotic ApoE−/− mice, which greatly increased immunoglobulin G (IgG) accumulation in plaque and accelerated atherosclerosis. These B cells expressed many cytokines that promote humoural immunity and in addition, they formed germinal centres within the spleen where they differentiated into antibody-producing plasma cells. Specifically deleting Blimp-1 in B cells, the transcriptional regulator that drives their terminal differentiation into antibody-producing plasma cells prevented MI-accelerated atherosclerosis. Alarmins released from infarcted hearts were responsible for activating B cells via toll-like receptors and deleting MyD88, the canonical adaptor protein for inflammatory signalling downstream of toll-like receptors, prevented B-cell activation and MI-accelerated atherosclerosis. Conclusion Our data implicate early B-cell activation and autoantibodies as a central cause for accelerated atherosclerosis post-MI and identifies novel therapeutic strategies towards preventing recurrent cardiovascular events such as MI and stroke.

The treatment of severe symptomatic aortic stenosis has undergone a paradigm shift over the last decade, paralleling the publication of several landmark trials showing efficacy and safety of transc...

Aims To investigate the change in atherosclerotic plaque volume in patients with chronic kidney disease (CKD) and declining renal function, using coronary computed tomography angiography (CCTA). Methods and results In total, 891 participants with analysable serial CCTA and available glomerular filtration rate (GFR, derived using Cockcroft–Gault formulae) at baseline (CCTA 1) and follow-up (CCTA 2) were included. CKD was defined as GFR Conclusion Decline in renal function was associated with more rapid plaque progression, whereas the presence of CKD was not.

With increasing adoption of CT coronary angiography (CTA) there is increasing demand for cost-effective, small footprint, dedicated cardiac scanners. We compared a state-of-the-art, small footprint dedicated cardiac scanner (DCCT) to a standard multidetector scanner (MDCT).The study was a retrospective unblinded single centre study. A total of 800 patients were included, with 400 undergoing a DCCT and MDCT coronary CTA scanning, respectively. Image quality was assessed using a 4-point grading score. Image noise and artifact, signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR), and acceptance rate for CT-derived fractional flow reserve (FFRct) were recorded.Overall image quality was higher in the DCCT group (3.8 ± 0.55 vs 3.6 ± 0.69; p = 0.042). There was no difference in overall image noise (p = 0.131) or artifact (p = 0.295). SNR was superior in the DCCT group (14.2 ± 6.85 vs 11.4 ± 3.32; p 0.005) as was CNR (12.7 ± 6.77 vs 11.9 ± 3.29; p 0.005). The heart rate was lower in the DCCT group (56 ± 9.1 vs 59 ± 8.1; p 0.005). No difference in the dose length product (DLP median 244.53 (IQR 105.6) vs 237.63 (IQR 160.1); p = 0.313) or FFRA DCCT scanner is capable of image quality similar to modern current generation general purpose CT technology. Such technology appears to be a viable option to serve the increasing demand for CTCA imaging.

Background: CT coronary angiography (CTA) with Fractional Flow Reserve as determined by CT (FFR CT) is a safe alternative to invasive coronary angiography. A negative FFR CT has been shown to have low cardiac event rates compared to those with a positive FFR CT. However, the clinical utility of FFR CT according to age is not known. Methods: Patients’ in the ADVANCE (Assessing Diagnostic Value of Non-invasive FFRCT in Coronary Care) registry, were stratified into those ≥65 or CT on clinical decision-making, as assessed by patient age, was determined by evaluating patient management using CTA results alone, followed by site investigators submitting a report on the treatment plan based upon the newly provided FFR CT data. Outcomes at 1-year post CTA were assessed, including major adverse cardiovascular events (myocardial infarction, all-cause mortality or unplanned hospitalization for ACS leading to revascularisation) and total revascularisation. Positive FFR CT was deemed to be ≤ 0.8. Results: FFR CT was calculated in 1849 (40.6%) subjects aged CT strata for subjects above and below the age of 65. MACE and revascularisation rates were not significantly different for those ≥ or CT positivity or stenosis severity CT result, and anatomical stenosis ≥50%, those ≥ and CT and treatment (CABG, PCI, medical therapy), indicated a statistically significant, but small increase in the odds of a MACE event with increasing age (OR 1.04, 95% CI 1.006–1.08, p = 0.02). Amongst patients with a FFR CT > 0.80, there was no effect of age on the odds of revascularisation. Conclusion: The findings of this study point to a low risk of MACE events or need for revascularisation in those aged ≥ or CT>0.80, despite the higher incidence of anatomic obstructive CAD in those ≥65 years. The findings show the clinical usefulness and outcomes of FFR CT are largely constant regardless of age.

BackgroundBalloon aortic valvuloplasty (BAV) has seen renewed interest since the advent of transcatheter aortic valve implantation (TAVI). The study aimed to characterise a contemporary BAV cohort and determinants of clinical outcomes.MethodsPatients undergoing BAV at a single tertiary centre were retrospectively reviewed over a 10-year period, and functional and mortality outcomes were reported with up to a 2-year follow-up.Results224 patients (aged 82.5±8.3 years; 48% female) underwent BAV over the study period. Indications were either destination treatment (39%) or bridge-to-valve replacement (61%)—including bridge-to-decision (29%), symptom relief while on the waitlist (27%), and temporary contraindications to TAVI/aortic valve replacement (AVR) (5%). The mean reduction of aortic mean pressure gradient was 38%. Procedural mortality occurred in 0.5%, stroke in 1.3%, and major bleeding in 0.9%. Twelve-month mortality was 36% overall, and 26% and 50% in the bridging and destination groups, respectively. New York HeartAssociation (NYHA) class improved by ≥1 at 30 days in 50%. Among the bridge-to-TAVI/AVR group, 40% proceeded to TAVI/AVR within 12 months following BAV. In multivariate analysis, active malignancy at baseline (OR: 4.4, 95% CI: 1.3 to 15.1, p=0.02), smoking history (OR: 3.3, 95% CI: 1.3 to 7.9, pConclusionsBAV remains a useful procedure with relatively low rates of complications, however, 1-year mortality rates are high. Contemporary indications for BAV include a bridge to definitive valve replacement or destination treatment.

Atrial fibrillation is common and management by pharmacotherapy is limited by modest efficacy and significant toxicities. Pulmonary vein isolation (PVI) is a safe and effective alternative in select patients with atrial fibrillation. However, prolonged procedure time raises concerns of health risks from radiation exposure. This study aims to determine the significance of radiation exposure from PVI.In this study, we retrospectively reviewed patient demographics, fluoroscopy time, entrance skin dose and dose area product in 80 cases of PVI, radiofrequency ablation for atrial flutter and diagnostic coronary angiogram performed in our institution.Compared to other procedures, patients who underwent PVI were younger (age, mean±standard error of mean, 59.4±1.1 years old, p0.0001) and were more likely to be male (82%, p0.001). Body mass index was similar between the three groups. The median (and interquartile range) fluoroscopy time was similar between PVI (20.8 and 13.1-30.7mins) and flutter ablation (17.6 and 11.1-26.1mins) but longer than diagnostic angiography (4.2 and 2.3-6.7mins, p0.0001). Entrance skin dose was similar between PVI and flutter ablation groups but significantly higher in the diagnostic angiography group, with median and IQR for PVI vs. flutter ablation vs. diagnostic angiography, 100.4 (52.8-179.9) vs. 73.2 (37.0-142.1) vs. 393.5 (276.1-555.6) mGy (p0.0001). Dose area product in PVI (1831.2 and 887.7-3460.8cGycmDespite prolonged procedure time, radiation exposure from PVI was comparable to, or lower than, other fluoroscopy-guided cardiac procedures.

Coronary computed tomography angiography (CCTA) has emerged as the preferred modality in the diagnosis of coronary artery disease, but it is limited by modest specificity. By applying principles of computational fluid dynamics, flow fraction reserve, a measure of lesion-specific ischemia that is used to guide revascularization, can be noninvasively derived from CCTA, the so-called computed tomography-derived flow fractional reserve (FFR

Introduction Family history of premature coronary artery disease (CAD) is known to predispose individuals to adverse CAD events, often at a younger age. Current risk stratification strategy is suboptimal, as up to 50% of individuals were considered “low-risk” prior to their first presentation of myocardial infarction. Coronary artery calcium score (CACS) is a marker of atherosclerosis and provides incremental value in risk stratification. However, the utility of CACS may be limited in younger patients as they often have non-calcified atherosclerotic plaques. In this study, we evaluate the sensitivity of CACS in detecting subclinical atherosclerosis in different age groups. Method From 310 referrals to a specialized unit in the management of early atherosclerosis, 222 individuals with a family history of premature CAD (defined as CAD events in first-degree family members, male Results Of the 141 (59% male, mean age 45.9±6.0 year) individuals that completed clinical evaluation, 65 (73% male, mean age 47.4±6.9 years) have subclinical atherosclerosis (defined by the presence of atherosclerotic plaques in any of the coronary artery segments in cardiac CT). Of them, 52 have CACS>0, giving an overall sensitivity of 80%. The breakdown by age group is shown in table 1. The sensitivity of CACS in detecting subclinical atherosclerosis is quite modest in younger individuals (60% in individuals 85% in >45 years). Table 1. Sensitivity of CACS in different age groups Age group True Positive Fast Negative Sensitivity N (CAC+ CTCA+) (CAC+ CTCA−) (%) Conclusion In younger individuals (

Introduction Patients with family history of premature coronary artery disease (CAD) are at increased risk of CAD events at a younger age. Risk factor based approaches and clinical evaluation are most commonly used to assess these individuals. However, it has been recently shown that up to 50% of individual presenting with their first myocardial infarction (MI) were considered to be “low risk” prior to that event. MI is often a result of plaque rupture preceded by progression of subclinical atherosclerosis. Detection of subclinical atherosclerosis may therefore help target prevention of plaque progression. We assessed the value of clinical risk factor, biomarkers and Framingham Risk Score (FRS) in predicting subclinical atherosclerosis in individuals with a family history of premature CAD. Methods From 310 referrals, 222 individuals between the ages of 35 and 55 with a family history of premature CAD (CAD events in first-degree family members (male Results In this pilot, 141 individuals (59% male, mean age 45.9±6.0 years) completed evaluation, and 65 (46%) had evidence of subclinical atherosclerosis on CT coronary angiography or CT calcium score with a mean segment involvement score (SIS) of 2.8 and mean CS of 152, putting them above the 80th percentile for their age and sex. Aside from male sex, age, and smoking history, other traditional risk factors and biomarkers including diabetes mellitus, hypertension, total cholesterol, LDL-C, HDL-C and Cholesterol/HDL-C were not significantly different between those with or without subclinical atherosclerosis (Table 1). Table 1 Conclusion In young individuals with a family history of premature CAD, risk factors, biomarkers, and FRS failed to identify individuals with premature, subclinical atherosclerosis in this pilot study. Detection of subclinical atherosclerosis and early implementation of treatment with the aim of stabilizing plaques and stopping progression might prove vital in reducing events in these individuals. Further studies are warranted.

Progress in pharmaceutical development is highly-dependent on preclinical in vivo animal studies. Small animal imaging is invaluable for the identification of new disease markers and the evaluation of drug efficacy. Here, we report for the first time the use of a three-dimensional fluorescence bioimager called FLuorescence Emission Computed Tomography (FLECT) for the detection of a novel recombinant fluoroprobe that is safe, easily prepared on a large scale and stably stored prior to scan. This novel fluoroprobe (Targ-Cy7) comprises a single-chain antibody-fragment (scFvTarg), which binds exclusively to activated-platelets, conjugated to a near-infrared (NIR) dye, Cy7, for detection. Upon mouse carotid artery injury, the injected fluoroprobe circulates and binds within the platelet-rich thrombus. This specific in vivo binding of the fluoroprobe to the thrombus, compared to its non-targeting control-fluoroprobe, is detected by the FLECT imager. The analyzed FLECT image quantifies the NIR signal and localizes it to the site of vascular injury. The detected fluorescence is further verified using a two-dimensional IVIS® Lumina scanner, where significant NIR fluorescence is detected in vivo at the thrombotic site, and ex vivo, at the injured carotid artery. Furthermore, fluorescence levels in various organs have also been quantified for biodistribution, with the highest fluoroprobe uptake shown to be in the injured artery. Subsequently, this live animal imaging technique is successfully employed to monitor the response of the induced thrombus to treatment over time. This demonstrates the potential of using longitudinal FLECT scanning to examine the efficacy of candidate drugs in preclinical settings. Besides intravascular thrombosis, we have shown that this non-invasive FLECT-imaging can also detect in vivo pulmonary embolism. Overall, this report describes a novel fluorescence-based preclinical imaging modality that uses an easy-to-prepare and non-radioactive recombinant fluoroprobe. This represents a unique tool to study mechanisms of thromboembolic diseases and it will strongly facilitate the in vivo testing of antithrombotic drugs. Furthermore, the non-radiation nature, low-cost, high sensitivity, and the rapid advancement of optical scanning technologies make this fluorescence imaging an attractive development for future clinical applications.

Venous thromboembolism (VTE), encompassing deep vein thrombosis and pulmonary embolism, is a major clinical problem, and its pharmacological prevention incurs a high cost to healthcare systems. With an annual incidence of 1 to 2 per 1000 person-years, it affects ≤600 000 individuals per year in the United States alone and carries a substantial case fatality of 10% to 30% at 1 month.1 Despite well-documented risk factors, the pathogenesis of VTE remains incompletely understood. Historically, it is thought to result from a combination of Virchow’s triad, namely, vascular wall injury, flow stasis, and hypercoagulability. Although this serves as a useful conceptual framework and led to the development of preventative strategies and therapeutics, significant side effects (bleeding rate of ≤8%)2 remain a major clinical problem and call for a better understanding of the pathophysiology of VTE. Ponomaryov et al3 now report on a potential new cellular player of this disease. Article, see p 941 Over the last decade, the importance of inflammation in venous thrombosis has been increasingly appreciated. It was found that neutrophils release neutrophil extracellular traps, a lattice of DNA, histone, and proteins (eg, elastase, myeloperoxidase, and cathepsin G), that function as a scaffold to facilitate the interactions between platelets, von Willebrand factor, and coagulation factors (Figure).4 Individual components of neutrophil extracellular traps can also promote thrombosis. For example, serine proteases including neutrophil elastase inactivate tissue factor pathway inhibitor and extracellular histones promote the generation of thrombin (Figure).5 Importantly, these experimental studies were corroborated with clinical data. Indeed, neutrophil extracellular traps were found in the organizing phase of human venous thrombi,6 and elevated levels of circulating nucleosomes and markers of neutrophil activation were associated with an increased risk of deep vein thrombosis.7 Similarly, experimental studies have shown that …

Objectives Assess the effect of aspiration thrombectomy on diagnosis and management of embolic acute myocardial infarction. Background Discrimination of embolic acute myocardial infarction from atherosclerotic plaque rupture/erosion prompts oral anticoagulation treatment of source of embolus, as well as avoiding unnecessary stenting and dual antiplatelet therapy. However, detection is difficult without aspiration. Methods We compared rates of diagnosis of embolic infarction for 2.5 years prior to (pre-RAT) and 2.5 years post routine aspiration thrombectomy (post-RAT). Baseline demographics, outcomes, and treatment strategies were also compared between the embolic infarction and atherosclerotic infarction. Results Diagnosed embolic infarction rose from 1.2% in the pre-RAT era to 2.8% in the post-RAT period (P

The mitral valve is a complex structure with a three-dimensional saddle shape annulus. Mitral regurgitation occurs from leaflet coaptation failure that is either primary (a problem with the leaflets) or secondary (chamber dilatation in the setting of cardiomyopathy). There has been an increase in focus on transcatheter mitral valve interventions, for both mitral repair and replacement. These technologies have rapidly developed to provide treatment for a substantial number of patients with severe symptomatic mitral regurgitation who are at too high of a risk to undergo open heart surgery. CT assessment of the mitral valve has developed with equal rapidity, with regard to preprocedural planning for transcatheter therapies. This review will provide an overview of mitral valve anatomy, an update on the current transcatheter repair and replacement therapies, as well as a focused overview of the role of multislice CT in mitral assessment prior to intervention. © RSNA, 2020.

The idiom “the straw that breaks the camel’s back” describes scenarios where seemingly minor incidents eventuate in a sudden, unexpected, and often detrimental downfall. In the case of atherosclerosis, over time multiple subclinical cellular events result in the development of unstable, vulnerable atherosclerotic lesions, which leads to the rupture of atherosclerotic plaques, culminating in the often catastrophic clinical manifestation of myocardial infarction or ischemic stroke. In this review, we first summarize lessons learned from autopsy studies, clinical investigations, and animal models mainly published in ATVB . We then present recent experimental studies published in ATVB that shed light on the underlying pathophysiological development of plaque instability and disruption, and how differential and sometimes maladaptive responses at cellular levels contribute to this complex process. These many publications in ATVB are a testament to the journal’s leading role in research on atherosclerotic plaque instability, an area of research with utmost translational relevance. Our understanding of the pathology of unstable, vulnerable atherosclerotic plaques is mainly based on a limited number of postmortem examinations of human coronary arteries and the analysis of resected surgical specimens from patients who underwent carotid endarterectomy and performed for primary/secondary prevention of transient ischemia attack or stroke.1–3 The histopathologic definition of unstable plaques includes, as the most central features, thin fibrous caps (thickness 40% of the total lesion volume).4–7 Importantly, repeated subclinical plaque ruptures, histologically and potentially macroscopically visible as intraplaque hemorrhage, are described as an additional cause of plaque instability.8 From an autopsy series of 800 cases of sudden coronary …

Objectives— Sedentary lifestyle increases the risk of cardiovascular disease and diabetes. Vascular dysfunction contributes to atherogenesis and has been linked to insulin resistance. Methods and Results— We measured insulin sensitivity by glucose tolerance test and vascular function by ultrasound and venous occlusion plethysmography in 20 healthy subjects (14 men, 6 women) at baseline and during 5 days of bed rest. Bed rest led to a 67% increase in the insulin response to glucose loading ( P P =0.01) and the calf (28.5±7.0 to 22.2±8.7 mL/min/dL, P =0.003) indicating impaired microvascular function. Bed rest decreased brachial artery diameter and increased systolic blood pressure suggesting increased basal arterial tone. There were no changes in circulating inflammatory markers arguing against systemic inflammation as a mechanism for vascular dysfunction in this setting. Conclusions— Physical inactivity was associated with the development of insulin resistance, dyslipidemia, increased blood pressure, and impaired microvascular function in healthy volunteers. Our findings may provide insight into the pathogenesis of vascular disease in sedentary individuals and emphasize that even short-term physical inactivity may have adverse metabolic and vascular consequences.

Objective— Reactive hyperemia is the compensatory increase in blood flow that occurs after a period of tissue ischemia, and this response is blunted in patients with cardiovascular risk factors. The predictive value of reactive hyperemia for cardiovascular events in patients with atherosclerosis and the relative importance of reactive hyperemia compared with other measures of vascular function have not been previously studied. Methods and Results— We prospectively measured reactive hyperemia and brachial artery flow-mediated dilation by ultrasound in 267 patients with peripheral arterial disease referred for vascular surgery (age 66±11 years, 26% female). Median follow-up was 309 days (range 1 to 730 days). Fifty patients (19%) had an event, including cardiac death (15), myocardial infarction (18), unstable angina (8), congestive heart failure (6), and nonhemorrhagic stroke (3). Patients with an event were older and had lower hyperemic flow velocity (75±39 versus 95±50 cm/s, P =0.009). Patients with an event also had lower flow-mediated dilation (4.5±3.0 versus 6.9±4.6%, P P =0.018) and lower flow-mediated dilation (OR 4.2, 95% CI: 1.8 to 9.8, P =0.001) both predicted cardiovascular events while adjusting for other risk factors. Conclusions— Thus, lower reactive hyperemia is associated with increased cardiovascular risk in patients with peripheral arterial disease. Furthermore, flow-mediated dilation and reactive hyperemia incrementally relate to cardiovascular risk, although impaired flow-mediated dilation was the stronger predictor in this population. These findings further support the clinical relevance of vascular function measured in the microvasculature and conduit arteries in the upper extremity.

Assess the effect of aspiration thrombectomy on diagnosis and management of embolic acute myocardial infarction.Discrimination of embolic acute myocardial infarction from atherosclerotic plaque rupture/erosion prompts oral anticoagulation treatment of source of embolus, as well as avoiding unnecessary stenting and dual antiplatelet therapy. However, detection is difficult without aspiration.We compared rates of diagnosis of embolic infarction for 2.5 years prior to (pre-RAT) and 2.5 years post routine aspiration thrombectomy (post-RAT). Baseline demographics, outcomes, and treatment strategies were also compared between the embolic infarction and atherosclerotic infarction.Diagnosed embolic infarction rose from 1.2% in the pre-RAT era to 2.8% in the post-RAT period (P 0.05). In addition, more successful removal of thrombus by aspiration led to less stenting (20% vs. 55% P 0.05) in the post-RAT period thus avoiding the hazards of "triple therapy." Embolic infarction was more frequently associated with atrial fibrillation (55% vs. 8%), had higher mortality (17% vs. 4%), and had higher rates of embolic stroke (13% vs. 0.3%) when compared with atherosclerotic MI (all P 0.05).Routine aspiration thrombectomy more readily identifies embolic infarction allowing more specific therapy and avoidance of stenting and triple anticoagulant therapy.

A 68-year-old woman underwent successful emergency repair of a type A aortic dissection ( Panel A ). Post-operative course was complicated by persistent fever. An ECG-gated CT aortic angiogram confirmed the clinical suspicion of intra-thoracic collection, but also identified a left ventricular apical pseudoaneurysm or …

In response: We thank Calderaro et al for their interest in our work. They provide interesting data from their unpublished study that examined the relation between measures of vascular function and adverse events in a cohort of …

Mitochondria produce reactive oxygen species that may contribute to vascular dysfunction. alpha-Lipoic acid and acetyl-L-carnitine reduce oxidative stress and improve mitochondrial function. In a double-blind crossover study, the authors examined the effects of combined alpha-lipoic acid/acetyl-L-carnitine treatment and placebo (8 weeks per treatment) on vasodilator function and blood pressure in 36 subjects with coronary artery disease. Active treatment increased brachial artery diameter by 2.3% (P=.008), consistent with reduced arterial tone. Active treatment tended to decrease systolic blood pressure for the whole group (P=.07) and had a significant effect in the subgroup with blood pressure above the median (151+/-20 to 142+/-18 mm Hg; P=.03) and in the subgroup with the metabolic syndrome (139+/-21 to 130+/-18 mm Hg; P=.03). Thus, mitochondrial dysfunction may contribute to the regulation of blood pressure and vascular tone. Further studies are needed to confirm these findings and determine the clinical utility of alpha-lipoic acid/acetyl-L-carnitine as antihypertensive therapy.

The importance of inflammation in the pathogenesis of atherosclerosis is well established. The vascular endothelium contributes to and is affected by the inflammatory process. For example, a variety of cytokines have the ability to “activate” the endothelium and thereby promote expression of adhesion molecules and chemotactic factors that accelerate the inflammatory process and direct accumulation of leukocytes to specific sites in the arterial tree. In experimental systems, activation of endothelial cells is also associated with a loss of the biologic activity of endothelium-derived nitric oxide, an effect that accelerates the inflammatory process and also promotes local thrombosis and impairs local control of vasomotor tone. Consistent with these experimental studies, recent studies have provided evidence that inflammation is associated with an impairment of nitric oxide-dependent responses in human subjects. This article will review the experimental and clinical studies that support the relevance of inflammation to nitric oxide bioactivity in human atherosclerosis.

R A L A B ST R who discontinued on the day of surgery. Fifty-one percent of current smokers resumed smoking in the year after surgery, with 80% of these resuming within 2 weeks. Conclusion: The timing of smoking cessation prior to surgery does not impact on cardiovascular, major medical outcomes or death in the perioperative period. Therefore, physicians seeing a patient even within 8 weeks of surgery should have no reservations about encouraging abstinence. Resumption of smoking after surgery is common and indicates that there are opportunities to encourage more sustained abstinence. Disclosure of Interest: None Declared A C T S O063