Prospective cardiovascular events in patients with advanced thoracic cancer treated with immune checkpoint inhibitor.

INTRODUCTION: Myocarditis is the most lethal cardiovascular immune related adverse events with a low incidence, depending on the studies. We prospectively studied the potential interest of a systematic screening to early detect immune related myocarditis and confirm the incidence of immune-induced myocarditis in advanced lung cancer and the impact of troponin systematic screening in early detection of other major cardiovascular events (MACE). MATERIAL AND METHODS: This prospective bicentric study includes adults who received at least one dose of immune checkpoint inhibitor (ICI) for advanced lung cancer. Cardiac biomarkers dosage, ECG and transthoracic echography (TTE) were done at baseline. Diagnosis of myocarditis was based on European Society of Cardiology recommendations. MACEs were reported during the observation period. RESULTS: Among 298 patients, 5 (1.68 %) immune-induced myocarditis occurred, all being asymptomatic with at first troponin elevation, treated by corticosteroids and ICI's discontinuation. No attributable death occurred, and no specific clinical characteristics were identified with myocarditis onset. Three patients were rechallenged with ICI after troponin normalization in the absence of other therapeutic options. Recurrence occurred in 2 patients, with a re-increase of troponin and a de novo modification of the ECG. Systematic cardiovascular screening also led to 14 cardiovascular diseases detection and 11 MACEs during ICI. CONCLUSION: Systematic cardiovascular screening has uncovered slightly more immuno-induced myocarditis cases than reported previously, but without altering treatment strategies due to their subclinical nature. Additionally, it helps detecting other cardiovascular diseases in this comorbid population.

COCARDE Study-Cardiac Imaging Phenotype in Patients With COVID-19: Protocol for a Prospective Observational Study.

BACKGROUND: The effects of SARS-CoV-2 (COVID-19) on the myocardium and their role in the clinical course of infected patients are still unknown. The severity of SARS-CoV-2 is driven by hyperinflammation, and the effects of SARS-CoV-2 on the myocardium may be significant. This study proposes to use bedside observations and biomarkers to characterize the association of COVID-19 with myocardial injury. OBJECTIVE: The aim of the study is to describe the myocardial function and its evolution over time in patients infected with SARS-CoV-2 and to investigate the link between inflammation and cardiac injury. METHODS: This prospective, monocentric, observational study enrolled 150 patients with suspected or confirmed SARS-CoV-2 infection at Toulouse University Hospital, Toulouse, France. Patients admitted to the intensive care unit (ICU), regular cardiologic ward, and geriatric ward of our tertiary university hospital were included during the pandemic period. Blood sampling, electrocardiography, echocardiography, and morphometric and demographic data were prospectively collected. RESULTS: A total of 100 patients were included. The final enrolment day was March 31, 2020, with first report of results at the end of the first quarter of 2021. The first echocardiographic results at admission of 31 patients of the COCARDE-ICU substudy population show that biological myocardial injury in COVID-19 has low functional impact on left ventricular systolic function. CONCLUSIONS: A better understanding of the effects of COVID-19 on myocardial function and its link with inflammation would improve patient follow-up and care. TRIAL REGISTRATION: Clinicaltrials.gov NCT04358952; https://clinicaltrials.gov/ct2/show/NCT04358952. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/24931.

Cardiac imaging phenotype in patients with coronavirus disease 2019 (COVID-19): results of the cocarde study.

Biological cardiac injury related to the Severe Acute Respiratory Syndrome Coronavirus-2 infection has been associated with excess mortality. However, its functional impact remains unknown. The aim of our study was to explore the impact of biological cardiac injury on myocardial functions in patients with COVID-19. 31 patients with confirmed COVID-19 (CoV+) and 16 controls (CoV-) were prospectively included in this observational study. Demographic data, laboratory findings, comorbidities, treatments and myocardial function assessed by transthoracic echocardiography were collected and analysed in CoV+ with (TnT+) and without (TnT-) elevation of troponin T levels and compared with CoV-. Among CoV+, 13 (42%) exhibited myocardial injury. CoV+/TnT + patients were older, had lower diastolic arterial pressure and were more likely to have hypertension and chronic renal failure compared with CoV+/TnT-. The control group was comparable except for an absence of biological inflammatory syndrome. Left ventricular ejection fraction and global longitudinal strain were not different among the three groups. There was a trend of decreased myocardial work and increased peak systolic tricuspid annular velocity between the CoV- and CoV + patients, which became significant when comparing CoV- and CoV+/TnT+ (2167 ± 359 vs. 1774 ± 521%/mmHg, P = 0.047 and 14 ± 3 vs. 16 ± 3 cm/s, P = 0.037, respectively). There was a decrease of global work efficiency from CoV- (96 ± 2%) to CoV+/TnT- (94 ± 4%) and then CoV+/TnT+ (93 ± 3%, P = 0.042). In conclusion, biological myocardial injury in COVID 19 has low functional impact on left ventricular systolic function.

Prognostic value of residual vegetation after antibiotic treatment for infective endocarditis: A retrospective cohort study.

BACKGROUND: The prognostic impact of residual vegetation (RV) after medical treatment for endocarditis remains unknown. METHODS: 134 consecutive patients hospitalized for infective endocarditis, not surgically treated, with the presence of vegetation at diagnosis, were included retrospectively. The follow-up started at the end of antibiotic treatment when healing was complete. The presence or absence of RV was assessed at this time. The primary endpoint was a composite of the occurrence of embolic events, recurrence of endocarditis, or death from any cause. RESULTS: Eighty-five patients were men (63%), mean age was 69 ± 15 years, and median follow-up was 16.3 (IQR: 5-30) months. Sixty-six patients (49%) had RV, 15 (11%) had RV > 10 mm and nine (7%) had RV with an increase in size relative to that of the diagnosis. The primary endpoint occurred in 23 patients (35%) in the group with RV, and in 16 patients (24%) without RV, which was not statistically relevant (HR 1.70; 95% confidence interval (CI) 0.89-3.22; p = 0.10). Based on univariate Cox regression analysis, the occurrence of the primary endpoint was associated with RV that increased (HR 3.90 95% CI 1.61-9.43; p < 0.01), RV size (HR 1.05; 95% CI 1.01-1.09; p < 0.01) or RV > 10 mm (HR 3.35; 95% CI 1.51-7.39; p < 0.01). Only RV > 10 mm remained significant in multivariate Cox regression: HR3.29; 95% CI 1.20-8.96; p = 0.02. CONCLUSIONS: RV is frequent but has no clear prognostic impact in itself; however, its size, particularly in comparison with the start-of-treatment data, merits particular attention as being potentially associated with increased risk.