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The role of multidetector-row computed tomography (CT) in the diagnosis of pulmonary embolism remains to be determined. In this study, the combined use of multidetector-row CT and D-dimer assays allowed pulmonary embolism to be excluded without the need for lower-extremity ultrasonography. The combined use of multidetector-row CT and D-dimer assays allowed pulmonary embolism to be excluded without the need for lower-extremity ultrasonography. Computed tomography (CT) is increasingly being used as the main thoracic imaging technique in suspected pulmonary embolism. 1 – 4 First-generation single-detector–row helical CT scanners have a 90 percent specificity but only a 70 percent sensitivity for pulmonary embolism. 5 – 8 In series in which venous-compression ultrasonography of the lower limbs and single-detector–row helical CT were performed in all patients with clinically suspected pulmonary embolism, 7 , 9 the proportion of patients with deep venous thrombosis despite findings on CT that were negative for pulmonary embolism was 6 to 9 percent. The implication of this finding is that lower-limb ultrasonography must be combined with CT . . .

Recent findings indicate that apolipoprotein A-I (ApoA-I) may be a protective humoral mediator involved in remote ischemic preconditioning (RIPC). This study sought to determine if ApoA-I mediates its protective effects via the RISK and SAFE signaling pathways implicated in RIPC. Wistar rats were allocated to one of the following groups. rats were subjected to myocardial ischemia/reperfusion (I/R) without any further intervention; RIPC: four cycles of limb I/R were applied prior to myocardial ischemia; ApoA-I: 10 mg/Kg of ApoA-I were intravenously injected prior to myocardial ischemia; ApoA-I + inhibitor: pharmacological inhibitors of RISK/SAFE pro-survival kinase (Akt, ERK1/2 and STAT-3) were administered prior to ApoA-I injection. Infarct size was significantly reduced in the RIPC group compared to CONTROL. Similarly, ApoA-I injection efficiently protected the heart, recapitulating RIPC-induced cardioprotection. The ApoA-I protective effect was associated with Akt and GSK-3β phosphorylation and substantially inhibited by pretreatment with Akt and ERK1/2 inhibitors. Pretreatment with ApoA-I in a rat model of I/R recapitulates RIPC-induced cardioprotection and shares some similar molecular mechanisms with those of RIPC-involved protection of the heart.

Remote ischemic preconditioning (RIPC) has emerged as an attractive strategy in clinical settings. Despite convincing evidence of the critical role played by circulating humoral mediators, their actual identities remain unknown. In this study, we aimed to identify RIPC-induced humoral mediators using a proteomic approach. and Results Rats were exposed to 10-min limb ischemia followed by 5- (RIPC 5') or 10-min (RIPC 10') reperfusion prior to blood sampling. The control group only underwent blood sampling. Plasma samples were analyzed using surface-enhanced laser desorption and ionization - time of flight - mass spectrometry (SELDI-TOF-MS). Three protein peaks were selected for their significant increase in RIPC 10'. They were identified and confirmed as apolipoprotein A-I (ApoA-I). Additional rats were exposed to myocardial ischemia-reperfusion (I/R) and assigned to one of the following groups RIPC+myocardial infarction (MI) (10-min limb ischemia followed by 10-min reperfusion initiated 20 minutes prior to myocardial I/R), ApoA-I+MI (10 mg/kg ApoA-I injection 10 minutes before myocardial I/R), and MI (no further intervention). In comparison with untreated MI rats, RIPC reduced infarct size (52.2±3.7% in RIPC+MI vs. 64.9±2.6% in MI; p<0.05). Similarly, ApoA-I injection decreased infarct size (50.9±3.8%; p<0.05 vs. MI). RIPC was associated with a plasmatic increase in ApoA-I. Furthermore, ApoA-I injection before myocardial I/R recapitulated the cardioprotection offered by RIPC in rats. This data suggests that ApoA-I may be a protective blood-borne factor involved in the RIPC mechanism.

We assessed the value of speckle tracking imaging performed early after a first ST-segment elevation myocardial infarction (STEMI) in order to predict infarct size and functional recovery at 3-month follow-up. 44 patients with STEMI who underwent revascularization within 12 h of symptom onset were prospectively enrolled. Echocardiography was performed 3.9 ± 1.2 days after myocardial reperfusion, assessing circumferential (CGS), radial (RGS), and longitudinal global (GLS) strains. Late gadolinium-enhanced cardiac magnetic imaging (CMR), for assessing cardiac function, infarct size, and microvascular obstruction (MVO), was conducted 5.6 ± 2.5 days and 99.4 ± 4.6 days after myocardial reperfusion. GLS was evaluable in 97% of the patients, while CGS and RGS could be assessed in 85%. Infarct size significantly correlated with GLS (R = 0.601, p<0.001), RGS (R = -0.405, p = 0.010), CGS (R = 0.526, p = 0.001), ejection fraction (R = -0.699, p<0.001), wall motion score index (WMSI) (R = 0.539, p = 0.001), and left atrial volume (R = 0.510, p<0.001). Baseline ejection fraction and GLS were independent predictors of 3-month infarct size. MVO mass significantly correlated with GLS (R = 0.376, p = 0.010), WMSI (R = 0.387, p = 0.011), and ejection fraction (R = -0.389, p = 0.011). In multivariate analysis, GLS was the only independent predictor of MVO mass (p = 0.015). Longitudinal strain >-6.0% within the infarcted area exhibited 96% specificity and 61% sensitivity for predicting the persistence of akinesia (≥ 3 segments) at 3-month follow-up. Speckle-tracking strain imaging performed early after a STEMI is easy-to-use as a marker for persistent akinetic territories at 3 months. In addition, GLS correlated significantly with MVO and final infarct size, both parameters being relevant post-MI prognostic factors, usually obtained via CMR.

According to the so-called obesity paradox, obesity might present a protective role in patients with myocardial infarction. We aimed to assess the influence of the epicardial adipose tissue (EAT) volume on cardiac healing and remodeling in patients with acute ST-elevation myocardial infarction. We prospectively included 193 consecutive patients presenting a first STEMI without known coronary artery disease. Cardiac magnetic resonance imaging was performed at baseline and after a 3-month follow-up. EAT volume was computed, and the population was divided into quartiles: the highest quartile of EAT defining the high EAT group (h-EAT). h-EAT was associated with increased body mass index, higher rate of history of hypertension, and smaller infarct size at initial CMR assessment (18.3 ± 11.9% vs 23 ± 13.7% of total left ventricular [LV] mass, p = 0.041). Moreover, microvascular obstruction was less frequent in the h-EAT group (36.2% vs 59.3%, p = 0.006). There were no differences in LV ejection fraction (LVEF), LV volumes, systolic wall stress, coronary artery burden, and clinical events during the index hospitalization between the EAT groups at baseline and at follow-up. Linear regression analysis showed h-EAT to be associated with smaller infarct size at baseline (β coefficient = −3.25 [95% CI −5.89 to −0.61], p = 0.016). h-EAT also modified positively the effect of infarct size on LV remodeling, as assessed by the change in LVEF (p = 0.046). In conclusion, h-EAT was paradoxically related to smaller infarct size and acted as an effect modifier in the relation between the extent of infarct size and LVEF changes. Patients with higher extent of EAT presented better cardiac healing.

Introduction:Despite suffering a severe aortic stenosis, some patients are denied either surgical or transcatheter aortic valve implantation (TAVI) therapy because of a frail condition. We aimed to identify whether a comprehensive geriatric assessment (CGA) might be useful to predict the prognosis of presumably frail patients with severe aortic stenosis.Material and methods:Between March 2011 and July 2016, 818 patients were consecutively and prospectively enrolled. 161 had a CGA and were considered for analysis. Considering combined CGA and heart team recommendations, 102 TAVI procedures were performed (TAVI group) and 59 patients constituted the no-TAVI group. The primary endpoint was all-cause mortality at 1 year.Results:There was no difference between the TAVI and the no-TAVI groups considering morphometric data, cardiovascular risk factors or symptoms. The no-TAVI group had higher surgical risk (logistic EuroSCORE1 33.4 ±17.8 vs. 22.7 ±14.9; p < 0.001) and more moderate renal insufficiency (82% vs. 57%; p = 0.001). One-year mortality was 16% in the TAVI group and 46% in the no-TAVI group (p < 0.001). Multivariate analysis revealed that history of pulmonary edema, moderate renal failure, and not having a TAVI were associated with 1-year mortality. There was an interaction between the Five-Times-Sit-to-Stand-Test (FTSST) and the effect of TAVI on mortality (p = 0.049), as FTSST was the only predictor for 1-year mortality in the no-TAVI group (HR = 0.18, 95% CI: 0.04–0.76; p = 0.019).Conclusions:One-year mortality was higher in geriatric-assessed frail patients who did not undergo TAVI. FTSST, which assesses patients’ mobility, was the only prognostic marker for 1-year mortality, on top of the usual medical parameters.

Background: Amoxicillin (AMX)-induced crystal nephropathy (AICN) is considered as a rare complication of high dose intravenous (IV) AMX administration. However, recently, its incidence seems to be increasing based on French pharmacovigilance centers. Occurrence of AICN has been observed mainly with IV administration of AMX and mostly under doses over 8 g/day. Given that pharmacovigilance data are based on declaration, the real incidence of AICN may be underestimated. Thus, the primary objective of the present study was to determine the incidence of AICN in the current practice. Materials and Methods: We conducted a retrospective study between 1 January 2015 and 31 December 2017 in Angers University Hospital. Inclusion criteria were age over 18 years-old and IV AMX administration of at least 8 g/day for more than 24 h. Patients admitted directly into the intensive care units were excluded. Medical records of patients that developed Kidney Disease:Improving Global Outcome (KDIGO) stage 2–3 acute kidney injury (AKI) were reviewed by a nephrologist and a specialist in pharmacovigilance. AICN was retained if temporality analysis was conclusive, after exclusion of other causes of AKI, in absence of other nephrotoxic drug administration. Results: A total of 1303 patients received IV AMX for at least 24 h. Among them, 358 (27.5%) were exposed to AMX doses of at least 8 g/day and were included. Patients were predominantly males (68.2%) with a mean age of 69.1 years-old. AMX was administered for a medical reason in 78.5% of cases. Patients received a median dose of AMX of 12 g/day (152.0 mg/kg/day). Seventy-three patients (20.4%) developed AKI, 42 (56.8%) of which were KDIGO stage 2 or 3. Among the latter, AICN diagnosis was retained in 16 (38.1%) patients, representing an incidence of 4.47% of total patients exposed to high IV AMX doses. Only female gender was associated with an increased risk of AICN. AMX dose was not significantly associated with AICN development. Conclusion: This study suggests a high incidence of AICN in patients receiving high IV AMX doses, representing one third of AKI causes in our study. Female gender appeared as the sole risk factor for AICN in this study.

Introduction : Despite of suffering a severe aortic stenosis, some patients are denied from either surgical or Transcatheter Aortic Valve Implantation (TAVI) therapy because of a frail condition. We aim to identify whether a comprehensive geriatric assessment (CGA) might be useful to predict prognosis of presumably frail patients with severe aortic stenosis. Material and methods : Between March 2011 and July 2016, 818 patients were consecutively and prospectively enrolled. 161 had a CGA and were considered for analysis. Considering combined CGA and Heart team recommendations, 102 TAVI were performed (TAVI group) and 59 patients constituted the no TAVI group. Primary endpoint was all-cause mortality at one year. Results : There was no difference between the TAVI and the no TAVI groups considering morphometric data, cardiovascular risk factors or symptoms. The no TAVI group had higher surgical risk (logistic EuroSCORE1 33.4±17.8 vs. 22.7±14.9; p<0.001) and more moderate renal insufficiency (82% vs. 57%; p=0.001). One-year mortality was 16% in the TAVI group and 46% in the no TAVI group (p<0.001). Multivariate analysis revealed history of pulmonary edema, moderate renal failure, and not having a TAVI, to relate to 1-year mortality. There was an interaction of the Five-Times-Sit-to-Stand-Test (FTSST) upon the effect of TAVI on mortality (p=0.049), as FTSST was the only predictor for 1-year mortality in the no TAVI group (HR=0.18 95%CI :0.04–0.76; p=0.019). Conclusions : One-year mortality was higher in geriatric-assessed frail patient who did not undergo TAVI. FTSST, which assesses patients’ mobility, was the only prognostic marker for 1-year mortality, on top of usual medical parameters.

Preclinical studies and pilot clinical trials have shown that high-dose erythropoietin (EPO) reduces infarct size in acute myocardial infarction. We investigated whether a single high-dose of EPO administered immediately after reperfusion in patients with ST-segment elevation myocardial infarction (STEMI) would limit infarct size. A total of 110 patients undergoing successful primary coronary intervention for a first STEMI was randomized to receive standard care either alone (n = 57) or combined with intravenous administration of 1,000 U/kg of epoetin β immediately after reperfusion (n = 53). The primary end point was infarct size assessed by gadolinium-enhanced cardiac magnetic resonance after 3 months. Secondary end points included left ventricular (LV) volume and function at 5-day and 3-month follow-up, incidence of microvascular obstruction (MVO), and safety. Erythropoietin significantly decreased the incidence of MVO (43.4% vs 65.3% in the control group, P = .03) and reduced LV volume, mass, and function impairment at 5-day follow-up (all P < .05). After 3 months, median infarct size (interquartile range) was 17.5 g (7.6-26.1 g) in the EPO group and 16.0 g (9.4-28.2 g) in the control group (P = .64); LV mass, volume, and function were not significantly different between the 2 groups. The same number of major adverse cardiac events occurred in both groups. Single high-dose EPO administered immediately after successful reperfusion in patients with STEMI did not reduce infarct size at 3-month follow-up. However, this regimen decreased the incidence of MVO and was associated with transient favorable effects on LV volume and function.

The aim of the study was to identify the determinants of pericardial effusion (PE) after a first myocardial infarction (MI). Cardiac magnetic resonance enables early analysis of multiple post-MI parameters; 193 patients with a first ST-elevation MI admitted to the Angers University Hospital (France) were enrolled prospectively. Cardiac magnetic resonance was performed at baseline (median of 5 days [4 to 7]) and repeated at a 3-month follow-up to investigate left ventricular (LV) volumes, LV ejection fraction, infarct size, microvascular obstruction (MVO), systolic wall stress (SWS), and PE presence and extent. A 1-year follow-up was also performed. Overall, 113 patients (58.5%) showed a PE with a median size of 31.6 ± 24.0 ml in the event that a PE was present. Patients with PE typically presented larger initial infarct sizes and LV volumes, and higher SWS, with more depressed LV ejection fraction and more frequent MVO and pleural effusions. Patients with PE exhibited higher rates of heart failure during hospitalization. At follow-up, there was no relevant PE, with no pericardiocentesis required. The multivariate analysis revealed SWS (odds ratio [OR] 1.092 [95% CI 1.007 to 1.184], p = 0.042), infarct size (OR 1.048 [95% CI 1.014 to 1.083], p = 0.003), and MVO extent (OR 1.274 [95% CI 1.028 to 1.579], p = 0.018) to be independent predictors for PE presence and volume. One patient died of LV free wall rupture during initial hospitalization, with only “small” PE found. In conclusion, infarct size, MVO, and SWS were independently related to PE presence and volume. Post-MI PE was found in 58.5% of cases, being regressive at follow-up. Among these patients with early reperfusion and optimal medical therapy, PE volume did not seem to be related to future clinical events.