Facteurs influençant les index de perfusion myocardique en tomoscintigraphie influence des polluants atmosphériques : résultats intermédiaires de l’étude Evaperf pollution

Air pollution leads to cardiovascular morbidity and mortality, in part through alteration of endothelial function from epicardial arteries to coronary microvascular. Our team has developed a finer analysis technique of myocardial perfusion exploring the entire coronary tree by myocardial scintigraphy. The objective was to specify determinants of perfusion indices whose PM2.5 fine particles influence. Any outpatient who came to perform myocardial scintigraphy at University Hospital of Grenoble was included from July, 2017 to March, 2019. Perfusion analysis was done by calculating Summed Stress Score (SSS), Summed Rest Stress (SRS) and Myocardial perfusion entropy to stress (MPE stress) in blind clinical data. Exposure to PM2.5 was estimated via Atmo Aura sensors. This work focuses on the first 270 patients. The correlation was negative between MPE stress and SSS (p <10-4), SRS (p <10-4). Predictors of elevating SSS were diabetes (p = 0.03), myocardial infarction (p <10-4). MPE stress increased with a BMI ≥ 35 kg/m2 (p = 0.04), and was lower among women (p <10-4), patients under ICE / ARB II (p = 0.03), or diabetic patients (p = 0.007). Chronic PM2.5 exposure was associated with elevation of SSS (p = 0.02) and SRS (p = 0.008) in the adjusted model but was not associated with MPE (p = 0,13). These associations diminished after adjusting with other clinical factors. MPE Stress was negatively correlated with SSS and SRS. The analysis at the end of the study may confirm the suggested associations.La pollution de l’air entraîne une sur morbimortalité cardiovasculaire, s’expliquant en partie par altération endothéliale des troncs épicardiques à la microcirculation coronaire. Notre équipe a développé une technique d’analyse de la perfusion myocardique explorant l’ensemble de l’arbre coronaire en tomoscintigraphie myocardique. L’objectif était de préciser les déterminants des index de perfusion, dont un rôle éventuel des particules fines (PM2,5).Tout patient ambulatoire venu réaliser une scintigraphie myocardique au centre hospitalier universitaire de Grenoble entre 07/2017 et 03/2019 était inclus. La perfusion était caractérisée par les Summed Stress Score (SSS), Summed Rest Stress (SRS) et l’entropie de perfusion myocardique au stress (MPE stress) en aveugle des données cliniques. L’exposition aux PM2,5 était estimée via les modèles d’Atmo Aura. Ce travail portait sur les 270 premiers patients. La MPE stress était négativement corrélée avec le SSS (p <10-4) et le SRS (p <10-4). Les facteurs prédictifs d’un SSS accru étaient le diabète (p = 0.03), l’infarctus du myocarde (p <10-4). La MPE stress augmentait avec un IMC ≥ 35 kg/m2 (p = 0,04) et était plus faible chez les femmes (p <10-4), les patients sous IEC/ARA II (p = 0,03), ou diabétiques (p = 0,007). L’exposition annuelle aux PM2,5 était associée à une élévation du SSS (p = 0,02) et du SRS (p = 0,008) après ajustement mais pas à la MPE (p = 0,13) ; ces associations s’atténuaient après ajustement sur d’autres facteurs cliniques. La MPE Stress était corrélée négativement au SSS et au SRS. L’analyse au terme de l’étude pourra permettre de confirmer les associations suggérées

Clinical significance of energy loss index in patients with low-gradient severe aortic stenosis and preserved ejection fraction

We hypothesized that among patients with low-gradient severe aortic stenosis (AS) and preserved left ventricular ejection fraction (LVEF), reclassification of AS severity as moderate by pressure recovery adjusted indexed aortic valve area (AVAi) = energy loss index (ELI), may identify a subgroup of patients with a better outcome.; Three hundred and seventy-nine patients with low-gradient AS (defined by AVAi ≤ 0.6 cm2/m2 and mean aortic pressure gradient 0.6 cm2/m2. Cardiac events [cardiac mortality and/or need for aortic valve replacement (AVR)] during follow-up were studied. One hundred and forty-eight patients (39%) were reclassified as moderate AS by ELI. Reclassification as moderate AS was independently associated with decreased body surface area, normal flow status, decreased left ventricular mass index, and left atrial volume index (all P < 0.05). After adjustment for variables of prognostic interest, reclassification as moderate AS by ELI was associated with a considerable reduction of risk of cardiac events {adjusted hazard ratio (HR) 0.49 [95% confidence interval (CI) 0.33-0.72]; P < 0.001}, need for AVR [adjusted HR 0.52 (95% CI 0.34-0.81); P = 0.004], and cardiac mortality [adjusted HR 0.46 (95% CI 0.22-0.98); P = 0.044].; In patients with low-gradient severe AS and preserved LVEF, calculation of ELI permits to reclassify almost 40% of patients as having moderate AS. These reclassified patients have a considerable reduction of the risk of cardiac events during follow-up. Calculation of ELI is useful for decision-making in patients with low-gradient severe AS and preserved ejection fraction

Pulmonary embolism in COVID-19 patients: a French multicentre cohort study

International audienceAims: While pulmonary embolism (PE) appears to be a major issue in COVID-19, data remain sparse. We aimed to describe the risk factors and baseline characteristics of patients with PE in a cohort of COVID-19 patients.Methods and results: In a retrospective multicentre observational study, we included consecutive patients hospitalized for COVID-19. Patients without computed tomography pulmonary angiography (CTPA)-proven PE diagnosis and those who were directly admitted to an intensive care unit (ICU) were excluded. Among 1240 patients (58.1% men, mean age 64 ± 17 years), 103 (8.3%) patients had PE confirmed by CTPA. The ICU transfer and mechanical ventilation were significantly higher in the PE group (for both P 0.05), while patients under therapeutic dose anticoagulation before hospitalization or prophylactic dose anticoagulation introduced during hospitalization had lower PE occurrence [odds ratio (OR) 0.40, 95% confidence interval (CI) 0.14-0.91, P = 0.04; and OR 0.11, 95% CI 0.06-0.18, P < 0.001, respectively]. In a multivariable analysis, the following variables, also statistically significant in univariable analysis, were associated with PE: male gender (OR 1.03, 95% CI 1.003-1.069, P = 0.04), anticoagulation with a prophylactic dose (OR 0.83, 95% CI 0.79-0.85, P < 0.001) or a therapeutic dose (OR 0.87, 95% CI 0.82-0.92, P < 0.001), C-reactive protein (OR 1.03, 95% CI 1.01-1.04, P = 0.001), and time from symptom onset to hospitalization (OR 1.02, 95% CI 1.006-1.038, P = 0.002).Conclusion: PE risk factors in the COVID-19 context do not include traditional thrombo-embolic risk factors but rather independent clinical and biological findings at admission, including a major contribution to inflammation

NEXN gene in cardiomyopathies and sudden cardiac deaths: prevalence, phenotypic expression, and prognosis

International audienceBACKGROUND: Few clinical data are available on NEXN mutation carriers, and the gene’s involvement in cardiomyopathies or sudden death has not been fully established. Our objectives were to assess the prevalence of putative pathogenic variants in NEXN and to describe the phenotype and prognosis of patients carrying the variants. METHODS: DNA samples from consecutive patients with cardiomyopathy or sudden cardiac death/sudden infant death syndrome/idiopathic ventricular fibrillation were sequenced with a custom panel of genes. Index cases carrying at least one putative pathogenic variant in the NEXN gene were selected. RESULTS: Of the 9516 index patients sequenced, 31 were carriers of a putative pathogenic variant in NEXN only, including 2 with double variants and 29 with a single variant. Of the 29 unrelated probands with a single variant (16 males; median age at diagnosis, 32.0 [26.0–49.0] years), 21 presented with dilated cardiomyopathy (prevalence, 0.33%), and 3 presented with hypertrophic cardiomyopathy (prevalence, 0.14%). Three patients had idiopathic ventricular fibrillation, and there were 2 cases of sudden infant death syndrome (prevalence, 0.46%). For patients with dilated cardiomyopathy, the median left ventricle ejection fraction was 37.5% (26.25–50.0) at diagnosis and improved with treatment in 13 (61.9%). Over a median follow-up period of 6.0 years, we recorded 3 severe arrhythmic events and 2 severe hemodynamic events. CONCLUSIONS: Putative pathogenic NEXN variants were mainly associated with dilated cardiomyopathy; in these individuals, the prognosis appeared to be relatively good. However, severe and early onset phenotypes were also observed—especially in patients with double NEXN variants. We also detected NEXN variants in patients with hypertrophic cardiomyopathy and sudden infant death syndrome/idiopathic ventricular fibrillation, although a causal link could not be established

Carbon monoxide and prognosis in smokers hospitalised with acute cardiac events: a multicentre, prospective cohort studyResearch in context

Summary: Background: Smoking cigarettes produces carbon monoxide (CO), which can reduce the oxygen-carrying capacity of the blood. We aimed to determine whether elevated expiratory CO levels would be associated with a worse prognosis in smokers presenting with acute cardiac events. Methods: From 7 to 22 April 2021, expiratory CO levels were measured in a prospective registry including all consecutive patients admitted for acute cardiac event in 39 centres throughout France. The primary outcome was 1-year all-cause death. Initial in-hospital major adverse cardiac events (MAE; death, resuscitated cardiac arrest and cardiogenic shock) were also analysed. The study was registered at ClinicalTrials.gov (NCT05063097). Findings: Among 1379 patients (63 ± 15 years, 70% men), 368 (27%) were active smokers. Expiratory CO levels were significantly raised in active smokers compared to non-smokers. A CO level >11 parts per million (ppm) found in 94 (25.5%) smokers was associated with a significant increase in death (14.9% for CO > 11 ppm vs. 2.9% for CO ≤ 11 ppm; p  11 ppm was associated with a significant increase in MAE in smokers during initial hospitalisation after adjustment for comorbidities (odds ratio [OR] 15.75, 95% CI [5.56–44.60]) or parameters of in-hospital severity (OR 10.67, 95% CI [4.06–28.04]). In the overall population, CO > 11 ppm but not smoking was associated with an increased rate of all-cause death (HR 4.03, 95% CI [2.33–6.98] and 1.66 [0.96–2.85] respectively). Interpretation: Elevated CO level is independently associated with a 6-fold increase in 1-year death and 10-fold in-hospital MAE in smokers hospitalized for acute cardiac events. Funding: Grant from Fondation Coeur &amp; Recherche