Batric Popovic

Femoral pseudoaneurysms and current cardiac catheterization: evaluation of risk factors and treatment.

OBJECTIVES We sought to determine the incidence of femoral pseudoaneurysm (FPA) following cardiac catheterization, identify the risk factors for FPA and factors influencing therapeutic strategy. METHODS 11,992 consecutive patients who underwent cardiac catheterization via femoral artery were studied over a period of four years in one University Hospital. Our prospective case control group analysis registered patients who developed FPA after the procedure. Patient-related factors, procedure related factors and peri-procedure treatment were compared between the two groups. RESULTS 76 FPA were diagnosed over the study period accounting for a global incidence of 0.6% procedures. By univariate analysis, interventional procedure (p<0.01), rhythmologic procedure (p=0.03), sheath>or=6F (p=0.04) and left groin puncture (p<0.001) were FPA risk factors. By multivariate analysis, interventional procedure (adjusted odds ratio [OR]=1.99; 95% confidence interval [CI]1.14-3.44 p=0.01) and left groin puncture (OR=4.65; 95% CI, 1.78-12.1 p=0.001) are independent predictive factors of FPA. FPA thrombosis was obtained by ultrasound guided compression (UGC) in 71% of the cases. By univariate analysis, PFA diameter larger than 4 cm (p<0.001), the use of anticoagulation (p<0.01) or GPIIbIIIa inhibitors (p=0.001) and UGC under anticoagulation (p=0.01) are predictive factors of need for FPA surgical repair. By multivariate analysis, FPA diameter>4 cm and use of GPIIbIIIa inhibitors are independent predictive factors of FPAs surgical treatment. Superficial femoral puncture was predictive of successful UGC both by uni and multivariate analysis. CONCLUSIONS Our study shows that FPA occurrence is mainly due to by procedure-related factors. FPA size, level of puncture and the use of GPIIbIIIa inhibitors are independent predictive factors of need for surgical therapy.

Cardiac power index, mean arterial pressure, and Simplified Acute Physiology Score II are strong predictors of survival and response to revascularization in cardiogenic shock.

ABSTRACT Short-term prognostic factors in patients with cardiogenic shock (CS) have previously been established using only hemodynamic parameters without taking into account classic intensive care unit (ICU) severity score or organ failure/support. The aim of this study was to assess early predictors of in-hospital mortality of a monocentric cohort of patients with ST-elevation myocardial infarction complicated by early CS. We retrospectively studied 85 consecutive patients with CS complicating acute myocardial infarction and Thrombolysis in Myocardial Infarction flow grade 3 after percutaneous coronary revascularization. All patients were managed according to the following algorithm: initial resuscitation by a mobile medical unit or in-hospital critical care physician unit followed by percutaneous coronary revascularization and CS management in the ICU. Prehospital CS was diagnosed in 69% of cases, initially complicated by an out-of-hospital cardiac arrest in 64% of cases. All patients were treated with vasopressors, 82% were ventilated, and 22% underwent extrarenal epuration. The 28-day mortality rate was 39%. Under multivariate analysis, initial cardiac power index, mean arterial pressure of less than 75 mmHg at hour 6 of ICU management, and Simplified Acute Physiology Score II were independent predictive factors of in-hospital mortality. In conclusion, parameters directly related to cardiac performance and vascular response to vasopressors and admission Simplified Acute Physiology Score II are strong predictors of in-hospital mortality.

Pharmacological inhibition of the triggering receptor expressed on myeloid cells‐1 limits reperfusion injury in a porcine model of myocardial infarction

Limitation of ischemia/reperfusion injury is a major therapeutic target after acute myocardial infarction (AMI). Toll‐like receptors are implicated in the inflammatory response that occurs during reperfusion. The triggering receptor expressed on myeloid cells (TREM)‐1 acts as an amplifier of the immune response triggered by toll‐like receptor engagement. We hypothesized that administration of a TREM‐1 inhibitory peptide (LR12) could limit reperfusion injury in a porcine model of AMI.

Triggering Receptor Expressed on Myeloid cells-1: a new player in platelet aggregation

Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) is an immunoreceptor initially known to be expressed on neutrophils and monocytes/macrophages. TREM-1 acts as an amplifier of the inflammatory response during both infectious and aseptic inflammatory diseases. Another member of the TREM family, The Triggering receptor expressed on myeloid cells Like Transcript-1 (TLT-1) is exclusively expressed in platelets and promotes platelet aggregation. As the gene that encodes for TLT-1 is located in the TREM-1 gene cluster, this prompted us to investigate the expression of TREM-1 on platelets. Here we show that TREM-1 is constitutively expressed in α-granules and mobilised at the membrane upon platelet activation. Pharmacologic inhibition of TREM-1 reduces platelet activation as well as platelet aggregation induced by collagen, ADP, and thrombin in human platelets. Aggregation is similarly impaired in platelets from Trem-1-/- mice. In vivo, TREM-1 inhibition decreases thrombus formation in a carotid artery model of thrombosis and protects mice during pulmonary embolism without excessive bleeding. These findings suggest that TREM-1 inhibition could be useful adducts in antiplatelet therapies.

Epinephrine and short-term survival in cardiogenic shock: an individual data meta-analysis of 2583 patients

AbstractObjectiveCatecholamines have been the mainstay of pharmacological treatment of cardiogenic shock (CS). Recently, use of epinephrine has been associated with detrimental outcomes. In the present study we aimed to evaluate the association between epinephrine use and short-term mortality in all-cause CS patients. DesignWe performed a meta-analysis of individual data with prespecified inclusion criteria: (1) patients in non-surgical CS treated with inotropes and/or vasopressors and (2) at least 15% of patients treated with epinephrine administrated alone or in association with other inotropes/vasopressors. The primary outcome was short-term mortality.Measurements and resultsFourteen published cohorts and two unpublished data sets were included. We studied 2583 patients. Across all cohorts of patients, the incidence of epinephrine use was 37% (17–76%) and short-term mortality rate was 49% (21–69%). A positive correlation was found between percentages of epinephrine use and short-term mortality in the CS cohort. The risk of death was higher in epinephrine-treated CS patients (OR [CI] = 3.3 [2.8–3.9]) compared to patients treated with other drug regimens. Adjusted mortality risk remained striking in epinephrine-treated patients (n = 1227) (adjusted OR = 4.7 [3.4–6.4]). After propensity score matching, two sets of 338 matched patients were identified and epinephrine use remained associated with a strong detrimental impact on short-term mortality (OR = 4.2 [3.0–6.0]).ConclusionsIn this very large cohort, epinephrine use for hemodynamic management of CS patients is associated with a threefold increase of risk of death.

Incidence, indications and predicting factors of permanent pacemaker implantation after transcatheter aortic valve implantation: A retrospective study

BACKGROUND As the number of transcatheter aortic valve implantation (TAVI) procedures is constantly increasing, it is important to consider common complications, such as pacemaker (PM) implantation, and their specific risk factors. AIMS Echocardiographic, computed tomography and electrocardiographic data were analysed to determine the predicting factors, if any, associated with PM implantation. METHODS This retrospective study included patients referred to Nancy University Hospital for a TAVI procedure from January 2013 to December 2015. Both Medtronic CoreValve and Edwards SAPIEN valves were implanted. Patients with preprocedurally implanted PMs and/or referred from another institution were excluded. RESULTS Of 208 TAVI patients, 23 had a pre-existing PM and were excluded. A new PM was required in 38 patients (20.5%). Pre-existing right bundle branch block (RBBB), the use of the Medtronic CoreValve and large prostheses were identified as predictors of PM implantation (P=0.0361, P=0.0004 and P=0.0019, respectively). Using logistic regression, predictors of PM implantation included first-degree atrioventricular block (odds ratio 3.7, 95% confidence interval 1.5-9.1; P=0.0054) and large aortic annulus diameter in echocardiography (odds ratio 1.2, 95% confidence interval 1-1.4; P=0.0447), with a threshold of 24.1mm. For the combination of preTAVI PR duration >220ms and QRS duration >120ms, the positive predictive value for PM implantation reached 80%. CONCLUSION Use of the Medtronic CoreValve, RBBB and first-degree atrioventricular block are major risk factors for post-TAVI PM implantation. In addition, large aortic annulus and large valvular prosthesis are independent risk factors for PM implantation. The combination of preTAVI prolonged PR interval and increased QRS duration could be used as a marker for periprocedural PM implantation.

Endothelial-driven increase in plasma thrombin generation characterising a new hypercoagulable phenotype in acute heart failure

BACKGROUND Subjects with heart failure (HF) are at higher risk of developing thrombosis. We investigated whether endothelium activation and inflammation induce a prothrombotic biological profile in patients with acute decompensated HF (ADHF) and sinus rhythm. METHODS Our prospective study included 34 ADHF patients, 30 patients with stable chronic HF (CHF) and 30 control inpatients without HF. In vitro thrombin generation and its downregulation by activated protein C (APC) was monitored by calibrated automated thrombography at hospital admission, at the day of discharge and after discharge, following at least six weeks of clinical stability. Circulating endothelium-derived extracellular vesicles (eEVs) were quantified by flow cytometry and nucleosomes by ELISA. RESULTS Thrombin generation is increased and APC sensitivity is decreased independently of platelets in ADHF at admission compared to controls (p < 0.01). Thrombin generation was also increased in CHF but only in the presence of platelets. Plasma markers of endothelium activation (von Willebrand factor, factor VIII, procoagulant eEVs and circulating nucleosomes) and the ability of plasmas to induce neutrophil extracellular trap formation in control neutrophils are elevated in ADHF at admission compared to controls (p < 0.001). In-hospital prothrombotic changes in ADHF improved significantly at the post-discharge time-point. Circulating nucleosomes were positively correlated with APC sensitivity (p = 0.013) and annexin-V-positive eEVs (p = 0.004). CONCLUSIONS This proof-of-concept study identified an endothelial-driven hypercoagulable phenotype at the acute phase of decompensated HF contrasting with the platelet-dependent prothrombotic state in CHF. These results highlighted a cross-talk between circulating eEVs and nucleosomes, procoagulant factors and impairment of the APC anticoagulant activity in ADHF.

Correction to: Epinephrine and short-term survival in cardiogenic shock: an individual data meta-analysis of 2583 patients

Because of a technical error, the code corresponding to the outcome for the Basir et al. cohort was mis-implemented in the original version of our article. Characteristics of the cohort are in fact the followings.

Myocardial reperfusion for acute myocardial infarction under an optimized antithrombotic medication: What can you expect in daily practice?

AIMS To assess both epicardiac macrovascular as well as microvascular and tissue reperfusion following different intravenous preadmission antithrombotic strategies prior primary PCI in STEMI patients. METHODS AND RESULTS Consecutive STEMI patients (n = 488) undergoing pPCI received prehospitally either bivalirudin (n = 179), bivalirudin and periprocedural GPIIb/IIIa inhibitors (GPI) (n = 109), heparin (n = 99) or heparin and periprocedural GPI (n = 101). Epicardial perfusion and microvascular perfusion were assessed by angiography (TIMI flow rate and corrected TIMI frame count [cTFC]) and by ECG (ST resolution [STR]). TIMI 3 flow was restored at the end of the procedure in 85.2% of the cases; cTFC of ≤23 was obtained in 37.2% of cases and STR >70% in 42.5% of the cases. The rates of STR >70% and cTFC ≤23 were not different between the three groups. Multivariate analysis did not identify a predictive antithrombotic treatment to obtain either post-procedural TIMI 3 flow rate or a STR rate >70%. TIMI 3 flow before procedure and delay first symptoms-balloon <6 h represented a positive predictive value of STR rate >70% and the LAD as infarct related artery a negative predictive value of STR rate of >70%. CONCLUSION The process of myocardial reperfusion by pPCI continues to be improved with earlier reperfusion but an optimal tissular reperfusion was present in only half of the cases.

Heart failure with preserved ejection fraction: A systemic disease linked to multiple comorbidities, targeting new therapeutic options

Heart failure is a pathology associated with severe morbidity and mortality. In this large field, heart failure with preserved ejection fraction (HFpEF) appears to be an increasing global health problem; it should be considered as a progressive syndrome, characterized by complex mechanisms of systemic and cardiac adaptation that vary over time, particularly with ageing. Multiple biological phenotypes contribute to the heterogeneous clinical syndrome. HFpEF emerges as a model with proinflammatory cardiovascular and non-cardiovascular coexisting comorbidities, leading to systemic inflammation and subsequent fibrosis and to diverse clinical HFpEF phenotypes. All of these aspects are often present in the elderly population, bordering on the emergence of a true geriatric syndrome. The therapeutic approach cannot be uniform, and must involve management of the different comorbidities according to a phenotype treatment strategy, respecting the pharmacological approaches to the biological pathways involved in the proinflammatory comorbidity-related status. Future studies should consider these multiple distinct HFpEF phenotypes in the development of large morbimortality trials adapted to comorbidities or specific risk factors.