Background Identification of reliable outcome predictors in Corona virus disease‐2019 (Covid‐19) is of paramount importance for improving patient’s management. Methods A systematic review of literature was conducted until April 24^th, 2020. From 6,843 articles, 49 studies were selected for a pooled assessment; cumulative statistics for age and sex were retrieved in 587,790 and 602,234 cases. Two endpoints were defined: 1) a composite outcome including death, severe presentation, hospitalization in intensive care unit (ICU) and/or mechanical ventilation; 2) in‐hospital mortality. We extracted numeric data on patients’ characteristics and cases with adverse outcomes and employed inverse variance random effects models to derive pooled estimates. Results We identified 18 and 12 factors associated with the composite endpoint and death, respectively. Among those, a history of CVD (odds ratio (OR)=3.15, 95% confidence intervals (CI) 2.26‐4.41), acute cardiac (OR=10.58, 5.00‐22.40) or kidney (OR=5.13, 1.78‐14.83) injury, increased procalcitonin (OR=4.8, 2.034‐11.31) or D‐dimer (OR=3.7, 1.74‐7.89), and thrombocytopenia (OR=6.23, 1.031‐37.67) conveyed the highest odds for the adverse composite endpoint. Advanced age, male sex, cardiovascular comorbidities, acute cardiac or kidney injury, lymphocytopenia and D‐dimer conferred an increased risk of in‐hospital death. With respect to the treatment of the acute phase, therapy with steroids was associated with the adverse composite endpoint (OR=3.61, 95% CI 1.934‐6.73), but not with mortality. Conclusions Advanced age, comorbidities, abnormal inflammatory and organ injury circulating biomarkers captured patients with an adverse clinical outcome. Clinical history and laboratory profile may then help identify patients with a higher risk of in‐hospital mortality.

Background: Patients with acute myocarditis (AM) are at increased risk of adverse cardiac events after the index episode. Late gadolinium enhancement (LGE) detected by cardiovascular magnetic resonance in patients with AM plays an important diagnostic role, but its prognostic significance remains unresolved. This systematic review and meta-analysis sought to assess the prognostic implications of cardiovascular magnetic resonance-derived LGE in patients with AM. Methods: Data search was conducted from inception through February 28, 2020, using the following Medical Subject Heading terms: Myocarditis, CMR, Magnetic Resonance Imaging, Magnetic Resonance . From 2422 articles retrieved, we selected 11 studies reporting baseline cardiovascular magnetic resonance assessment and long-term clinical follow-up in patients with AM. Hazard ratios and CIs for a combined clinical end point were recorded for LGE presence, extent (>2 segments or >10% of left ventricular [LV] mass or >17g) and location (anteroseptal versus non-anteroseptal). A combined end point comprised all-cause mortality, cardiac mortality, and major adverse cardiovascular events. Hartung and Knapp correction improved robustness of the results. Prespecified sensitivity analyses explored potential sources of heterogeneity. The meta-analysis was conducted according to the Meta-analysis of Observational Studies in Epidemiology guidelines. Results: LGE presence (pooled hazard ratios, 3.28 [95% CIs, 1.69–6.39], P <0.001 [95% CIs, 1.33–8.11] after Hartung and Knapp correction) and anteroseptal LGE (pooled-hazard ratios, 2.58 [95% CIs, 1.87–3.55], P <0.001 [95% CIs, 1.64–4.06] after Hartung and Knapp correction) were associated with an increased risk of the combined end point. Extensive LGE was associated with worse outcomes (pooled-hazard ratios, 1.96 [95% CIs, 1.08–3.56], P =0.027), but this association was not confirmed after Hartung and Knapp correction (95% CIs, 0.843–4.57). Conclusions: LGE presence and anteroseptal location at baseline cardiovascular magnetic resonance are important independent prognostic markers that herald an increased risk of adverse cardiac outcomes in patients with AM. Registration: https://www.crd.york.ac.uk/PROSPERO/ Unique identifier: CRD42019146619.

In mitral valve prolapse, myocardial fibrosis at cardiac MRI was associated with an increased risk of unexplained syncope, sustained ventricular tachycardia, or sudden cardiac death. Background Patients with mitral valve prolapse (MVP) may develop adverse outcomes even in the absence of mitral regurgitation or left ventricular (LV) dysfunction. Purpose To investigate the progno...

Aims: Quantitative echocardiography parameters are seldom used to grade tricuspid regurgitation (TR) severity due to relative paucity of validation studies and lack of prognostic data. To assess the relationship between TR severity and the composite endpoint of death and hospitalization for congestive heart failure (CHF); and to identify the threshold values of vena contracta width (VCavg), effective regurgitant orifice area (EROA), regurgitant volume (RegVol), and regurgitant fraction (RegFr) to define low, intermediate, and high-risk TR based on patients’ outcome data. Methods and results: A cohort of 296 patients with at least mild TR underwent 2D, 3D, and Doppler echocardiography. We built statistical models (adjusted for age, NYHA class, left ventricular ejection fraction, and pulmonary artery systolic pressure) for VCavg, EROA, RegVol, and RegFr to study their relationships with the hazard of outcome. The tertiles of the derived hazard values defined the threshold values of the quantitative parameters for TR severity grading. During 47-month follow-up, 32 deaths and 72 CHF occurred. Event-free rate was 14%, 48%, and 93% in patients with severe, moderate, and mild TR, respectively. Severe TR was graded as VCavg > 6 mm, EROA > 0.30 cm2, RegVol > 30 mL, and RegF > 45%. Conclusion: This outcome study demonstrates the prognostic value of quantitative parameters of TR severity and provides prognostically meaningful threshold values to grade TR severity in low, intermediate, and high risk.

Chronic inflammation is a pivotal driver in the progression of atherosclerosis, significantly contributing to the burden of cardiovascular disease (CVD). Patients with chronic inflammatory diseases, such as inflammatory bowel diseases (IBDs) (e.g., ulcerative colitis and Crohn’s disease), rheumatological disorders, as well as individuals with auto-immune diseases (such as systemic lupus erythematosus), present a higher risk of major adverse cardiac events (MACEs). Despite their elevated CVD risk, these populations remain underrepresented in cardiovascular research, leading to a critical underestimation of their cardiovascular risk (CVR) in clinical practice. Furthermore, even recent CVR scores poorly predict the risk of events in these specific populations. This narrative review examines the physiopathological mechanisms linking chronic inflammation, immunomodulation, atherosclerosis, thrombosis and cardiovascular events. We review data from epidemiological studies and clinical trials to explore the potential cardiovascular benefits of anti-inflammatory and immunomodulatory therapies. Despite existing evidence, significant gaps in knowledge remain. Future research is mandatory, focusing on innovative strategies for risk stratification and optimization, including lipidomics, proteomics, advanced inflammatory markers, microbiota profiling, and cardiovascular imaging. Addressing these unmet needs will enhance understanding of cardiovascular risk in chronic inflammatory diseases, enabling tailored interventions and better outcomes.

Background—: Radiofrequency ablation of atrial fibrillation has been associated with some risk of thromboembolic events. Previous studies showed that preventive short episodes of forearm ischemia (remote ischemic preconditioning [IPC]) reduce exercise-induced platelet reactivity. In this study, we assessed whether remote IPC has any effect on platelet activation induced by radiofrequency ablation of atrial fibrillation. Methods and Results—: We randomized 19 patients (age, 54.7±11 years; 17 male) undergoing radiofrequency catheter ablation of paroxysmal atrial fibrillation to receive remote IPC or sham intermittent forearm ischemia (control subjects) before the procedure. Blood venous samples were collected before and after remote IPC/sham ischemia, at the end of the ablation procedure, and 24 hours later. Platelet activation and reactivity were assessed by flow cytometry by measuring monocyte-platelet aggregate formation, platelet CD41 in the monocyte-platelet aggregate gate, and platelet CD41 and CD62 in the platelet gate in the absence and presence of ADP stimulation. At baseline, there were no differences between groups in platelet variables. Radiofrequency ablation induced platelet activation in both groups, which persisted after 24 hours. However, compared with control subjects, remote IPC patients showed a lower increase in all platelet variables, including monocyte-platelet aggregate formation ( P <0.0001), CD41 in the monocyte-platelet aggregate gate ( P =0.002), and CD41 ( P <0.0001) and CD62 ( P =0.002) in the platelet gate. Compared with control subjects, remote IPC was also associated with a significantly lower ADP-induced increase in all platelet markers. Conclusions—: Our data show that remote IPC before radiofrequency catheter ablation for paroxysmal atrial fibrillation significantly reduces the increased platelet activation and reactivity associated with the procedure.