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The use of valve-in-valve transcatheter aortic valve implantation (ViV-TAVI) is increasing, but studies evaluating clinical outcomes in these patients are scarce. Also, there are limited data to guide the choice of valve type in ViV-TAVI. Therefore, this CENTER-study evaluated clinical outcomes in patients with ViV-TAVI compared to patients with native valve TAVI (NV-TAVI). In addition, we compared outcomes in patients with ViV-TAVI treated with self-expandable versus balloon-expandable valves. A total of 256 patients with ViV-TAVI and 11333 patients with NV-TAVI were matched 1:2 using propensity score matching, resulting in 256 patients with ViV-TAVI and 512 patients with NV-TAVI. Mean age was 81 +/- 7 years, 58% were female, and the Society of Thoracic Surgeons Predicted Risk of Mortality was 6.3% (4.0% to 12.8%). Mortality rates were comparable between ViV-TAVI and NV-TAVI patients at 30 days (4.1% vs 5.9%, p = 0.30) and 1 year (14.2% vs 17.3%, p = 0.34). Stroke rates were also similar at 30 days (2.8% vs 1.8%, p = 0.38) and 1 year (4.9% vs 4.3%, p = 0.74). Permanent pacemakers were less frequently implanted in patients with ViV-TAVI (8.8% vs 15.0%, relative risk 0.59, 95% confidence interval [CI] 0.37 to 0.92, p = 0.02). Patients with ViV-TAVI were treated with self-expandable valves (n = 162) and balloon-expandable valves (n = 94). Thirty-day major bleeding was less frequent in patients with self-expandable valves (3% vs 13%, odds ratio 5.12, 95% CI 1.42 to 18.52, p = 0.01). Thirty-day mortality was numerically lower in patients with self-expandable valves (3% vs 7%, odds ratio 3.35, 95% CI 0.77 to 14.51, p = 0.11). In conclusion, ViV-TAVI seems a safe and effective treatment for failing bioprosthetic valves with low mortality and stroke rates comparable to NV-TAVI for both valve types. (C) 2022 The Author(s). Published by Elsevier Inc.

Background Diabetes Mellitus (DM) affects a third of patients with symptomatic severe aortic valve stenosis undergoing transcatheter aortic valve implantation (TAVI). DM is a well-known risk factor for cardiac surgery, but its prognostic impact in TAVI patients remains controversial. This study aimed to evaluate outcomes in diabetic patients undergoing TAVI. Methods This multicentre registry includes data of > 12,000 patients undergoing transfemoral TAVI. We assessed baseline patient characteristics and clinical outcomes in patients with DM and without DM. Clinical outcomes were defined by the second valve academic research consortium. Propensity score matching was applied to minimize potential confounding. Results Of the 11,440 patients included, 31% (n = 3550) had DM and 69% (n = 7890) did not have DM. Diabetic patients were younger but had an overall worse cardiovascular risk profile than non-diabetic patients. All-cause mortality rates were comparable at 30 days (4.5% vs. 4.9%, RR 0.9, 95%CI 0.8–1.1, p = 0.43) and at one year (17.5% vs. 17.4%, RR 1.0, 95%CI 0.9–1.1, p = 0.86) in the unmatched population. Propensity score matching obtained 3281 patient-pairs. Also in the matched population, mortality rates were comparable at 30 days (4.7% vs. 4.3%, RR 1.1, 95%CI 0.9–1.4, p = 0.38) and one year (17.3% vs. 16.2%, RR 1.1, 95%CI 0.9–1.2, p = 0.37). Other clinical outcomes including stroke, major bleeding, myocardial infarction and permanent pacemaker implantation, were comparable between patients with DM and without DM. Insulin treated diabetics (n = 314) showed a trend to higher mortality compared with non-insulin treated diabetics (n = 701, Hazard Ratio 1.5, 95%CI 0.9–2.3, p = 0.08). EuroSCORE II was the most accurate risk score and underestimated 30-day mortality with an observed-expected ratio of 1.15 in DM patients, STS-PROM overestimated actual mortality with a ratio of 0.77 and Logistic EuroSCORE with 0.35. Conclusion DM was not associated with mortality during the first year after TAVI. DM patients undergoing TAVI had low rates of mortality and other adverse clinical outcomes, comparable to non-DM TAVI patients. Our results underscore the safety of TAVI treatment in DM patients. Trial registration The study is registered at clinicaltrials.gov (NCT03588247).

Objectives The aim of this study was to determine clinical and echocardiographic characteristics, mechanisms of failure, and outcomes of mitral valve (MV) surgery after transcatheter edge-to-edge repair (TEER). Background Although >100,000 mitral TEER procedures have been performed worldwide, longitudinal data on MV surgery after TEER are lacking. Methods Data from the multicenter, international CUTTING-EDGE registry were retrospectively analyzed. Clinical and echocardiographic outcomes were evaluated. Median follow-up duration was 9.0 months (interquartile range [IQR]: 1.2-25.7 months) after MV surgery, and follow-up was 96.1% complete at 30 days and 81.1% complete at 1 year. Results From July 2009 to July 2020, 332 patients across 34 centers underwent MV surgery after TEER. The mean age was 73.8 ± 10.1 years, median Society of Thoracic Surgeons risk for MV repair at initial TEER was 4.0 (IQR: 2.3-7.3), and primary/mixed and secondary mitral regurgitation were present in 59.0% and 38.5%, respectively. The median interval from TEER to surgery was 3.5 months (IQR: 0.5-11.9 months), with overall median Society of Thoracic Surgeons risk of 4.8% for MV replacement (IQR: 2.8%-8.4%). The primary indication for surgery was recurrent mitral regurgitation (33.5%), and MV replacement and concomitant tricuspid surgery were performed in 92.5% and 42.2% of patients, respectively. The 30-day and 1-year mortality rates were 16.6% and 31.3%, respectively. On Kaplan-Meier analysis, the actuarial estimates of mortality were 24.1% at 1 year and 31.7% at 3 years after MV surgery. Conclusions In this first report of the CUTTING-EDGE registry, the mortality and morbidity risks of MV surgery after TEER were not negligible, and only

Multislice computed tomography (MSCT) is the most common sizing method for transcatheter aortic valve implantation (TAVI) in the bicuspid aortic valve (BAV). It is unclear whether annular and supra...

Objectives This study sought to test the superiority in terms of efficacy and safety of a dedicated plug-based vascular closure device (VCD) during transcatheter aortic valve replacement (TAVR) over a suture-based VCD. Background Vascular complications after TAVR are relevant and often associated with VCD failure. Methods The MASH (MANTA vs. Suture-based vascular closure after transcatHeter aortic valve replacement) trial is an international, 2-center pilot randomized controlled trial comparing the MANTA VCD (Teleflex, Wayne, Pennsylvania) versus 2 ProGlides (Abbott Vascular, Abbott Park, Illinois). The primary composite endpoint consisted of access site–related major or minor vascular complications at 30-days’ follow-up. Secondary endpoints included clinically relevant access site bleeding, time to hemostasis, and modified VCD failure (defined as failure to achieve hemostasis within 5 min or requiring additional endovascular maneuvers such as endovascular stenting, surgical techniques, or additional closure devices). Adverse events were adjudicated by an independent clinical events committee according to the VARC-2 definitions. Results A total of 210 TAVR patients were included between October 2018 and January 2020. Median age was 81 years, 54% were male, and the median STS score was 2.7%. There was no significant difference in the primary endpoint of access site–related vascular complications between MANTA and ProGlide (10% vs. 4%; p = 0.16). Clinically significant access site bleedings were similar with both closure techniques (9% vs. 6%; p = 0.57). Modified VCD failure occurred less frequently in MANTA versus ProGlide (20% vs. 40%; p Conclusions Plug-based large-bore arteriotomy closure was not superior to suture-based closure. Plug-based closure required fewer, but a different kind of bailout maneuvers.

Background: Both balloon-expandable (BE) and self-expandable (SE) valves for transcatheter aortic valve implantation (TAVI) are broadly used in clinical practice. However, adequately powered randomized controlled trials comparing these two valve designs are lacking. Methods: The CENTER-study included 12,381 patients undergoing transfemoral TAVI. Patients undergoing TAVI with a BE-valve (n = 4096) were compared to patients undergoing TAVI with an SE-valve (n = 4096) after propensity score matching. Clinical outcomes including one-year mortality and stroke rates were assessed. Results: In the matched population of n = 5410 patients, the mean age was 81 ± 3 years, 60% was female, and the STS-PROM predicted 30-day mortality was 6.2% (IQR 4.0–12.4). One-year mortality was not different between patients treated with BE- or SE-valves (BE: 16.4% vs. SE: 17.0%, Relative Risk 1.04, 95%CI 0.02–1.21, p = 0.57). One-year stroke rates were also comparable (BE: 4.9% vs. SE: 5.3%, RR 1.09, 95%CI 0.86–1.37, p = 0.48). Conclusion: This study suggests that one-year mortality and stroke rates were comparable in patients with severe aortic valve stenosis undergoing TAVI with either BE or SE-valves.

Objective: This study sought to investigate the effect of body mass index on outcomes in patients with severe aortic valve stenosis undergoing transcatheter aortic valve implantation. Methods: A total of 12,381 patients undergoing transfemoral transcatheter aortic valve implantation were divided into body mass index categories: underweight (30 kg/m2). Primary endpoints were differences in 30-day and 1-year all-cause mortality. Secondary endpoints included all other clinical endpoints such as stroke. Univariate and multivariate odds ratios were calculated using logistic and cox regression analyses. Results: Two percent (n = 205) of patients were underweight, 29% (n = 3564) were normal weight, 44% (n = 5460) were overweight, and 25% (n = 3152) were obese. Thirty-day mortality was lower in overweight (5.3%, odds ratio, 0.73; 95% confidence interval, 0.61-0.88; P =.001) and obese patients (5.2%, odds ratio, 0.74; 95% confidence interval, 0.60-0.92; P =.006), but higher in underweight (9.8%, odds ratio, 1.51; 95% confidence interval, 0.92-2.47; P =.010) as compared to normal weight patients (6.9%). After multivariate adjustment, 30-day mortality was not significantly different across body mass index categories. However, 1-year mortality was higher in underweight patients (hazard ratio, 1.52; 95% confidence interval, 1.10-2.09; P =.011). Stroke rates were comparable between body mass index groups. Conclusions: For overweight and obese patients with severe aortic valve stenosis undergoing transcatheter aortic valve implantation, there was no 30-day difference in mortality compared with patients with normal weight. However, underweight patients showed higher rates of 1-year mortality after transcatheter aortic valve implantation.

Background Transcatheter aortic valve implantation (TAVI) is a well-established treatment for symptomatic aortic valve stenosis. The majority of patients treated are overweight or obese. Obesity has traditionally been linked to reduced survival and worse cardiovascular outcomes. However, an “obesity paradox” has been described in some diseases, with improved survival of obese patients after invasive and surgical procedures. Methods The CENTER-collaboration included data from 10 registries or clinical trials of patients undergoing transfemoral TAVI from 2007 to 2018. Patients were divided in four groups according to body mass index (BMI): underweight: BMI Results Of the 12,381 patients analysed, 2% (n=205) were underweight, 29% (n=3552) had normal weight, 44% (n=5460) were overweight and 25% (n=3140) obese. Older patients had lower BMI (median of 84 years for underweight and 81 years for obese patients, p Conclusions In this global analysis of more than 12 000 patients undergoing transfemoral TAVI, overweight and obese patients had better in-hospital and 30-day survival than normal weight patients, confirming the obesity paradox. There was an inverted J-shaped relationship of body mass index with prognosis, with higher mortality rates for underweight and extremely obese patients. Mortality and stroke per BMI category Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): The Dutch Heart Foundation; Netherlands Organisation for Health Research and Development

Advances in stent design and technology have made stent loss during percutaneous coronary intervention rare. When stent loss occurs, the risk of life-threatening procedural complications is high. We describe the use of an endovascular snare system to retrieve a dislodged stent from the proximal right coronary artery of a 54-year-old man during percutaneous coronary intervention after other conventional retrieval techniques had failed.

This study sought to test the superiority in terms of efficacy and safety of a dedicated plug-based vascular closure device (VCD) during transcatheter aortic valve replacement (TAVR) over a suture-based VCD.Vascular complications after TAVR are relevant and often associated with VCD failure.The MASH (MANTA vs. Suture-based vascular closure after transcatHeter aortic valve replacement) trial is an international, 2-center pilot randomized controlled trial comparing the MANTA VCD (Teleflex, Wayne, Pennsylvania) versus 2 ProGlides (Abbott Vascular, Abbott Park, Illinois). The primary composite endpoint consisted of access site-related major or minor vascular complications at 30-days' follow-up. Secondary endpoints included clinically relevant access site bleeding, time to hemostasis, and modified VCD failure (defined as failure to achieve hemostasis within 5 min or requiring additional endovascular maneuvers such as endovascular stenting, surgical techniques, or additional closure devices). Adverse events were adjudicated by an independent clinical events committee according to the VARC-2 definitions.A total of 210 TAVR patients were included between October 2018 and January 2020. Median age was 81 years, 54% were male, and the median STS score was 2.7%. There was no significant difference in the primary endpoint of access site-related vascular complications between MANTA and ProGlide (10% vs. 4%; p = 0.16). Clinically significant access site bleedings were similar with both closure techniques (9% vs. 6%; p = 0.57). Modified VCD failure occurred less frequently in MANTA versus ProGlide (20% vs. 40%; p 0.01). Suture-based closure required more often additional closure devices, whereas MANTA numerically needed more covered stents and surgical bailouts.Plug-based large-bore arteriotomy closure was not superior to suture-based closure. Plug-based closure required fewer, but a different kind of bailout maneuvers.

Despite improvements in interventional and pharmacological therapy of atherosclerotic disease,it is still the leading cause of death in the developed world. Hence there is a need for further development of effective therapeutic approaches. This requires better understanding of the molecular mechanisms and pathophysiology of the disease. Atherosclerosis has long been identified as having an inflammatory component contributing to its pathogenesis, whilst the available therapy primarily targets hyperlipidaemia and prevention of thrombosis. Acknowledging a pleotropic anti-inflammatory effect to some therapies, such as acetyl salicylic acid and the statins, none of the currently approved medicines for management of either stable or complicated atherosclerosis has inflammation as a primary target. Monocytes, as representatives of the innate immune system, play a major role in the initiation, propagation and progression of atherosclerosis from a stable to an unstable state. Animal study data support a role of monocytes in acute coronary syndromes and in outcome post infarction; however, limited research has been done in humans. In this thesis I describe for the first time in a large cohort of ST elevation myocardial infarction(STEMI) patients followed up for three years that total monocyte count, monocyte subset 1(Mon 1), and monocyte subset 2 (Mon 2) are predictive of major adverse cardiac events (MACE)post STEMI (including death, new diagnosis of heart failure, recurrent acute coronary syndrome). Both the inflammatory function of monocyte subsets (via assessment and quantification of IKK as a surrogate for the NFB inflammatory pathway activation) as well as the phagocytic activity of monocytes were studied in order to describe the mechanism through which monocytes affect their action. There was no significant difference in the NFB pathway activity between those patients who developed an adverse event and those who did not. Also NFB activity was not predictive of MACE. However the phagocytic activity of Mon 1 and Mon 2 were predictive of MACE suggesting that phagocytic activity of monocytes is the mechanism through which monocytes implement their action. Also this supports that the newly described monocytes subset 2 (Mon 2) is predominantly an inflammatory monocyte subset, not reparative as Mon 3. Major adverse cardiac events were driven mainly by heart failure diagnosis and echocardiographic findings. Hence the association between ventricular remodelling and phenotypic and functional characterisation of monocytes subsets was studied in this thesis. Total monocyte count, Mon 1 and Mon 2 were again predictive of negative ventricular remodelling with increase in end systolic indexed volume of >15% at 6 months follow up echocardiogram post infarction. Subclinical parameters of systolic dysfunction, namely global longitudinal strain and global circumferential strain were also significantly correlated with total monocyte count as well as Mon 1 levels. Given the above, I studied the effect of incorporating total monocyte count in Thrombolysis in Myocardial Infarction (TIMI) STEMI score to predict patient outcome at 30 days post infraction.C- statistics indicated improved prognostication of the TIMI STEMI model after incorporation of the total monocyte count into the model with improved area under the curve from 0.67 (for TIMI STEMI score), to area under the curve of 0.77 (TIMIMon score). This allows individual tailoring of secondary preventative therapy in order to improve patient outcome post infarction.Having described a potential mechanism through which the innate immune system affects outcome in STEMI patients, namely Mon1 and Mon2 through their phagocytic activity, the results from this thesis could be a stepping stone into targeted anti-inflammatory therapy in management of myocardial infarction.

A 73-year old woman presented to our hospital with a few hours of chest pain. Her first troponin-I level was 705 ng/l. The electrocardiogram (ECG) showed normal sinus rhythm with a normal QRS axis and duration, and inverted T waves in leads V2 and V3. She was started on dual-antiplatelet

Despite improvements in interventional and pharmacological therapy of atherosclerotic disease, it is still the leading cause of death in the developed world. Hence, there is a need for further development of effective therapeutic approaches. This requires better understanding of the molecular mechanisms and pathophysiology of the disease. Atherosclerosis has long been identified as having an inflammatory component contributing to its pathogenesis, whereas the available therapy primarily targets hyperlipidemia and prevention of thrombosis. Notwithstanding a pleotropic anti-inflammatory effect to some therapies, such as acetyl salicylic acid and the statins, none of the currently approved medicines for management of either stable or complicated atherosclerosis has inflammation as a primary target. Monocytes, as representatives of the innate immune system, play a major role in the initiation, propagation, and progression of atherosclerosis from a stable to an unstable state. Experimental data support a role of monocytes in acute coronary syndromes and in outcome post-infarction; however, limited research has been done in humans. Analysis of expression of various cell surface receptors allows characterization of the different monocyte subsets phenotypically, whereas downstream assessment of inflammatory pathways provides an insight into their activity. In this review we discuss the functional role of monocytes and their different subpopulations in atherosclerosis, acute coronary syndromes, cardiac healing, and recovery with an aim of critical evaluation of potential future therapeutic targets in atherosclerosis and its complications. We will also discuss technical difficulties of delineating different monocyte subpopulations, understanding their differentiation potential and function.

Eur J Clin Invest 2012 Abstract Background Monocytes are important mediators in the pathophysiology of cardiovascular disease, but only scarce data are available on biological and methodological factors affecting their levels. Design Three monocyte subsets, CD14++ CD16− CCR2+ (Mon1), CD14++ CD16+ CCR2+ (Mon2), CD14+ CD16+ CCR2− (Mon3), and monocyte-platelet aggregates (MPAs) were analysed by flow cytometry. The effects of treadmill exercise were assessed on 12 healthy volunteers. Diurnal variation was evaluated in 16 healthy volunteers, and the effects of delayed blood processing were measured in 12 samples. Results Mon1 were increased when measured 15 min after exercise followed by a reduction at 1 h (P

Oral anticoagulation (OAC), usually with vitamin K antagonists (such as warfarin, target international normalized ratio [INR] 2 3, or higher with some prosthetic valves) is the proven therapy and recommended treatment for a wide range of patients at risk of thromboembolic events, including atrial fibrillation (AF), mechanical heart valves, deep vein thrombosis, pulmonary embolism and left ventricular thrombi. These conditions are common, and with an increasing average life expectancy, some of these conditions (especially AF) are increasing in prevalence [Lip and Lim, 2007; Kannel et al. 1998]. Furthermore, pathologies such as AF are commonly associated with coronary artery disease: approximately 20 30% of AF patients have concomitant coronary artery disease [Nieuwlaat et al. 2005]. Such patients may present with acute coronary syndrome (ACS) and/or undergo percutaneous coronary intervention (PCI), often with stenting (PCI-S).

Despite improvements in interventional and pharmacological therapy of atherosclerotic disease, it is still the leading cause of death in the developed world. Hence, there is a need for further development of effective therapeutic approaches. This requires better understanding of the molecular mechanisms and pathophysiology of the disease. Atherosclerosis has long been identified as having an inflammatory component contributing to its pathogenesis, whereas the available therapy primarily targets hyperlipidemia and prevention of thrombosis. Notwithstanding a pleotropic anti-inflammatory effect to some therapies, such as acetyl salicylic acid and the statins, none of the currently approved medicines for management of either stable or complicated atherosclerosis has inflammation as a primary target. Monocytes, as representatives of the innate immune system, play a major role in the initiation, propagation, and progression of atherosclerosis from a stable to an unstable state. Experimental data support a role of monocytes in acute coronary syndromes and in outcome post-infarction; however, limited research has been done in humans. Analysis of expression of various cell surface receptors allows characterization of the different monocyte subsets phenotypically, whereas downstream assessment of inflammatory pathways provides an insight into their activity. In this review we discuss the functional role of monocytes and their different subpopulations in atherosclerosis, acute coronary syndromes, cardiac healing, and recovery with an aim of critical evaluation of potential future therapeutic targets in atherosclerosis and its complications. We will also discuss technical difficulties of delineating different monocyte subpopulations, understanding their differentiation potential and function.

Monocytes are important mediators in the pathophysiology of cardiovascular disease, but only scarce data are available on biological and methodological factors affecting their levels.Three monocyte subsets, CD14(++) CD16(-) CCR2+ (Mon1), CD14(++) CD16(+) CCR2(+) (Mon2), CD14(+) CD16(+) CCR2(-) (Mon3), and monocyte-platelet aggregates (MPAs) were analysed by flow cytometry. The effects of treadmill exercise were assessed on 12 healthy volunteers. Diurnal variation was evaluated in 16 healthy volunteers, and the effects of delayed blood processing were measured in 12 samples.Mon1 were increased when measured 15 min after exercise followed by a reduction at 1 h (P0·05 for both). MPAs were significantly reduced at 15 min and 1 h (P0·05 for both). There was significant diurnal variation in the numbers of Mon2, which were highest at 6 pm and lowest at 6 am. There were also significant diurnal variations in phagocytic activity of Mon1 and Mon2, which were highest at 12 pm and lowest at 12 am. Monocyte counts remained stable up to 2 h after venipuncture. MPAs were significantly increased at 2 h and increased further by 4 h after sampling.Monocyte subset Mon2 and monocyte phagocytic activity undergo significant diurnal variation. A single bout of exercise causes a temporal increase in monocytes and a reduction in MPAs. Monocyte subset counts should be analysed within 2 h of blood sampling, whereas measurement of MPAs and monocyte CD14 and CD16 expression should be performed within 1 h.

Sudden cardiac death can be the presenting feature of coronary disease. Limited epidemiological studies from the US suggest an increased prevalence of sudden death in the African–American community. There are no reports in UK minority communities. We present sudden death data from an area with a high density of underprivileged ethnic minority groups. Methods Ambulance data forms and accident and emergency records of all sudden unexpected deaths bought to City Hospital Birmingham in 2002 were extracted by retrospective review. The clinical characteristics and timing of the events were defined and analysed on the basis of the ethnic origins of the victims. Results The prevalence of sudden death amongst Caucasians was substantially greater than among minorities. Both Indo-Asians and Afro-Caribbean groups had a lower than expected sudden death rate. Caucasian patients more commonly demonstrated a ventricular fibrillation (VF) rhythm at presentation while Indo-Asians and Afro-Caribbean's demonstrated a non-VF rhythm (asystole and pulseless electrical activity (PEA). Collapse with syncope was more common in Afro-Caribbean subjects while Indo-Asian subjects more often arrested in transit. There were no differences in call or transfer times. Conclusions Despite a well-described pattern of more aggressive coronary disease, particularly noted in South Asian communities in the UK, the sudden death rate are not increased and may be decreased. This implies a potentially separate mechanism or a confounding cultural influence in these events.

Introduction - Monocytes, with 3 different subsets, are implicated in the initiation and progression of the atherosclerotic plaque contributing to plaque instability and rupture. Mon1 are the “classical” monocytes with inflammatory action, whilst Mon3 are considered reparative with fibroblast deposition ability. The function of the newly described Mon2 subset is yet to be fully described. In PCI era, fewer patients have globally reduced left ventricular ejection fraction post infarction, hence the importance of studying regional wall motion abnormalities and deformation at segmental levels using longitudinal strain. Little is known of the role for the 3 monocyte subpopulations in determining global strain in ST elevation myocardial infarction patients (STEMI). Conclusion In patients with normal or mildly impaired EF post infarction, higher counts of Mon1 and Mon2 are correlated with GLS within 7 days and at 6 months of remodelling post infarction. Adverse clinical outcomes in patients with reduced convalescent GLS were predicted with Mon1 and Mon2 suggestive of an inflammatory role for the newly identified Mon2 subpopulation. These results imply an important role for monocytes in myocardial healing when assessed by subclinical ventricular function indices. Methodology - STEMI patients (n = 101, mean age 64 ± 13 years; 69% male) treated with percutaneous revascularisation were recruited within 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2) and CD14+CD16++CCR2- (Mon3). Phagocytic activity of monocytes was measured using flow cytometry and Ecoli commercial kit. Transthoracic 2D echocardiography was performed within 7 days and at 6 months post infarct to assess global longitudinal strain (GLS) via speckle tracking. MACE was defined as recurrent acute coronary syndrome and death. Results - STEMI patients with EF ≥50% by Simpson’s biplane (n = 52) had GLS assessed. Using multivariate regression analysis higher counts of Mon1 and Mon 2 and phagocytic activity of Mon2 were significantly associated with GLS (after adjusting for age, time to hospital presentation, and peak troponin levels) (Table 1). At 6 months, the convalescent GLS remained associated with higher counts of Mon1, Mon 2. At one year follow up, using multivariate Cox regression analysis, Mon1 and Mon2 counts were an independent predictor of MACE in patients with a reduced GLS (n = 21)

Sir, Chronic periaortitis has a wide range of causes [1]. Obstructive uropathy associated with chronic periaortitis complicating abdominal aortic aneurysm (AAA) repair is well recognized and tends to occur early within 12 months of AAA repair. It is unusual for this to occur many years after surgery. A 71-year-old male was referred to the renal team after an emergency hospital admission by the medical team with acute kidney injury. Serum creatinine was 774 µmol/L (eGFR 7 mL/min/L), having been 140 µmol/L (eGFR 47 mL/min/L) 4 months previously. There was history of an atherosclerotic AAA open repair with an aortic graft in 1990. In 1994, the patient had a surgical exploration and evacuation for retroperitoneal haematoma. In 1995, the patient underwent surgical repair for leaking AAA. The proximal half of the graft was resected and replaced with a second Gelsoft graft (rifampicin soaked). In September 2008, the patient was admitted to our hospital with malaise, anorexia and oliguria. On examination, there was a pulsatile abdominal mass just lateral (left) to his midline laparotomy scar. An abdominal CT scan showed a large infrarenal AAA measuring 9.2 cm. The right kidney was of normal size but severely hydronephrotic with a hydroureter extending down to the level of the aortic bifurcation. The left kidney was small and also hydronephrotic (Figure 1). There was extensive fibrosis noted at the level of the aortic bifurcation associated with obstructive uropathy (Figure 2). Fig. 1 Bilateral hydronephrotic kidneys. Fig. 2 A large infrarenal abdominal aortic aneurysm with extensive fibrosis. The patient remained hypotensive with a poor urine output. He subsequently deteriorated and died 4 days after admission. Early hydronephrosis developing within the first year occurs in 10–20% of patients following surgical graft repair of AAA. The most probable cause for this is mechanical due to the compression of the ureter against the native iliac artery from the anteriorly placed graft [2]. In a prospective study of 101 patients who underwent aortofemoral and aortoiliac reconstructive surgery, 12% of patients developed mild to moderate hydronephrosis. All patients were asymptomatic, and the obstruction resolved spontaneously in 10 of 11 patients within 3 months of onset. The incidence of delayed hydronephrosis occurring 1 year or more post surgical repair is unknown. This complication may be relatively common after reconstructive vascular surgery as in our patient, especially in association with infected grafts [3]. The mechanism for the development is not fully understood. The most widely held view is that this complication develops secondary to an inflammatory process causing fibrosis [4]. The long time interval is unusual and suggests perhaps a different mode of inflammatory pathways compared to what is commonly seen in early obstructive uropathy associated with surgical graft repair of AAA. More research is needed to elucidate the mechanisms underlying chronic periaortitis [5]. Conflict of interest statement. None declared.

Background: Monocytes are implicated in the initiation and progression of theatherosclerotic plaque contributing to plaque instability and rupture. Little is knownof the role played by the 3 phenotypically and functionally different monocytesubpopulations in determining ventricular remodeling following ST elevation my-ocardial infarction (STEMI). Mon1 are "classical" inflammatory monocytes, whilstMon3 are considered reparative with fibroblast deposition ability. The function ofthe newly described Mon2 is yet to be elucidated. Method: STEMI patients (n=196, mean age 62±13 years; 72% male) treatedwith percutaneous revascularization were recruited within the first 24 hours. Pe-ripheral blood monocyte subpopulations were enumerated and characterizedusing flow cytometry after staining for CD14, CD16 and CCR2. Phenotypi-cally, monocyte subpopulations are defined as: CD14+CD16-CCR2+ (Mon1),CD14+CD16+CCR+ (Mon2) and CD14lowCD16+CCR2- (Mon3) cells. Transtho-racic 2D echocardiography was performed within 7 days and 6 months post infarctto assess ventricular volumes, mass, systolic, and diastolic functions. Results: Using linear regression analysis higher counts for Mon1, and lowercounts for Mon2 and Mon3 were significantly associated with the baseline leftventricular ejection fraction (LVEF) within seven days post infarction. At 6 monthspost STEMI lower counts of Mon2 remained positively associated with decreasedLVEF (p value= 0.002).Monocyte subsets correlation with LVEFMonocytes mean florescence Baseline left ventricular Left ventricular ejectionintensity (cells/μl) ejection fraction (%) fraction (%) at 6 months post infarctβ-value P-valueβ-value P-valueTotal Mon0.31 P

Background: Monocytes are implicated in the initiation and progression of the atherosclerotic plaque contributing to plaque instability and rupture. Little is known about the role of the three phenotypically and functionally different monocyte subpopulations in determining ventricular remodelling following ST elevation myocardial infarction (STEMI). Mon1 are the ‘classical’ monocytes with inflammatory action, whilst Mon3 are considered reparative with fibroblast deposition ability. The function of the newly described Mon2 subset is yet to be fully described. Method: STEMI patients (n=196, mean age 62±13 years; 72% male) treated with percutaneous revascularization were recruited within the first 24 h post-infarction. Peripheral blood monocyte subpopulations were enumerated and characterised using flow cytometry after staining for CD14, CD16 and CCR2. Phenotypically, monocyte subpopulations are defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR2+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells. Transthoracic 2D echocardiography was performed within 7 days and at 6 months post infarct to assess ventricular volumes, mass, systolic, and diastolic functions as well as strain and strain rate. Results: Using linear regression analysis higher counts for Mon1, and lower counts for Mon2 and Mon3 were significantly associated with the baseline left ventricular ejection fraction (LVEF) within 7 days post infarct (table 1). At 6 months post STEMI lower counts of Mon2 remained positively associated with a decrease in LVEF at completion of remodelling (p=0.002). Conclusion: Peripheral monocytes of all three subsets correlate with LVEF after a myocardial infarction. High counts of the inflammatory Mon1 are associated with the reduced baseline ejection fraction post infarction. After remodelling, the convalescent ejection fraction was independently predicted by monocyte subpopulation 2. As lower counts depicted negative ventricular remodelling, this suggests a possible myofibroblast deposition and angiogenesis role for the newly described intermediate monocyte subpopulation Mon2 as opposed to the previously anticipated inflammatory role.

Background Monocytes are implicated in the initiation and progression of the atherosclerotic plaque contributing to its instability and rupture. Although peripheral monocytosis has been related to poor clinical outcome post ST elevation myocardial infarction (STEMI), only scarce information is available of mechanisms of this association. Tumour necrosis factor alpha (TNFα) is a key cytokine in the acute phase inflammatory response, and it is predominantly produced by inflammatory macrophages. Little is known about TNFα association with circulating monocyte subpopulations post STEMI. Method A total of 142 STEMI patients (mean age 62±13 years; 72% male) treated with percutaneous revascularization were recruited with blood samples obtained within first 24 hours from the onset and on day 10-14. Peripheral blood monocyte subpopulations were enumerated and characterized using flow cytometry after staining for CD14, CD16 and CCR2 and were defined as: CD14++CD16-CCR2+ (Mon1), CD14++CD16+CCR+ (Mon2) and CD14+CD16++CCR2- (Mon3) cells. Plasma levels of TNFα were measured by enzyme-linked immunosorbent assay (ELISA, Peprotec system, UK). Major adverse cardiac events (MACE), defined as recurrent STEMI, new diagnosis of heart failure and death were recorded at follow up, mean of 164±134 days. Results TNFα levels were significantly higher 24 hours post STEMI, compared to day 14 (paired t-test, p