In patients with DCM and presence of inflammatory cells in the myocardium, myocardial T2 relaxation times may help to non-invasively detect myocardial inflammation. Although there is an overlap of T2 values between patients and healthy controls, T2 mapping may facilitate the identification of patients who may benefit from EMB for therapeutic decision-making.

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Background: Several studies have revealed the link between Coronavirus Disease 2019 (COVID-19) and endothelial dysfunction. To better understand the global pattern of this relationship, we conducted a meta-analysis on endothelial biomarkers related to COVID-19 severity. Methods: We systematically searched the literature up to March 10, 2021, for studies investigating the association between COVID-19 severity and the following endothelial biomarkers: Intercellular Adhesion Molecule 1 (ICAM-1), Vascular Cell Adhesion Molecule 1 (VCAM-1), E-selectin, P-selectin, Von Willebrand Factor Antigen (VWF-Ag), soluble Thrombomodulin (sTM), Mid-regional pro-adrenomedullin (MR-proADM), and Angiopoietin-2 (Ang-2). Pooled estimates and mean differences (PMD) for each biomarker were reported. Results: A total of 27 studies (n=2213 patients) were included. Critically ill patients presented with higher levels of MR-proADM (PMD: 0.71 nmol/L, 95% CI: 0.22 to 1.20 nmol/L, p=0.02), E-selectin (PMD: 13,32 pg/ml, 95% CI: 4,89 to 21,75 pg/ml, p=0.008), VCAM-1 (PMD: 479 ng/ml, 95% CI: 64 to 896 ng/ml, p=0.03), VWF-Ag (PMD: 110.5 IU/dl, 95% CI: 44.8 to 176.1 IU/dl, p=0.04) and Ang-2 (PMD: 2388 pg/ml, 95% CI: 1121 to 3655 pg/ml, p=0.003), as compared to non-critically ill ones. ICAM-1, P-selectin and thrombomodulin did not differ between the two groups (p>0.05). Conclusion: Endothelial biomarkers display significant heterogeneity in COVID-19 patients, with higher MR-proADM, E-selectin, VCAM-1, VWF-Ag, and Ang-2 levels being associated with increased severity. These findings strengthen the evidence on the key role of endothelial dysfunction in disease progress.

The term “vulnerable plaque” is commonly used to refer to an atherosclerotic plaque that is prone to rupture and the formation of thrombosis, which can lead to several cardiovascular and cerebrovascular events. Coronary artery atherosclerosis has a wide variety of different phenotypes among patients who may have a substantially variable risk for plaque rupture and cardiovascular events. Mounting evidence has proposed three distinctive histopathological mechanisms: plaque rupture, plaque erosion and calcified nodules. Studies have demonstrated the characteristics of plaques with high vulnerability such as the presence of a thin fibrous cap, a necrotic lipid-rich core, abundant infiltrating macrophages and neovascularization. However, traditional coronary angiographic imaging fails to determine plaque vulnerability features, and its ability to individualize treatment strategies is limited. In recent decades, catheter-based intravascular ultrasound imaging (IVUS) modalities have been developed to identify vulnerable plaques and ultimately vulnerable patients. The aim is to individualize prediction, prevention and treatment of acute coronary events based on the identification of specific features of high-risk atherosclerotic plaques, and to identify the most appropriate interventional procedures for their treatment. In this context, the aim of this review is to discuss how personalized assessment of coronary atherosclerotic arteries can be achieved by intravascular ultrasound imaging focusing on vulnerable plaque detection.

SummaryPulmonary vein isolation (PVI) is a cornerstone therapy in patients with atrial fibrillation (AF). With increasing numbers of PVI procedures, demand arises to reduce the cumulative fluoroscopic radiation exposure for both the physician and the patient. New technologies are emerging to address this issue. Here, we report our first experiences with a new fluoroscopy integrating technology in addition to a current 3D-mapping system. The new fluoroscopy integrating system (FIS) with 3D-mapping was used prospectively in 15 patients with AF. Control PVI cases (n = 37) were collected retrospectively as a complete series. Total procedure time (skin to skin), fluoroscopic time, and dose-area-product (DAP) data were analyzed. All PVI procedures were performed by one experienced physician using a commercially available circular multipolar irrigated ablation catheter. All PVI procedures were successfully undertaken without major complications. Baseline characteristics of the two groups showed no significant differences. In the group using the FIS, the fluoroscopic time and DAP were significantly reduced from 571 ± 187 seconds versus 1011 ± 527 seconds (P = 0.0029) and 4342 ± 2073 cGycm 2 versus 6208 ± 3314 cGycm 2 (P = 0.049), respectively. Mean procedure time was not significantly affected and was 114 ± 31 minutes versus 104 ± 24 minutes (P = 0.23) by the FIS.The use of the new FIS with the current 3D-mapping system enables a significant reduction of the total fluoroscopy time and DAP compared to the previous combination of 3D-mapping system plus normal fluoroscopy during PVI utilizing a circular multipolar irrigated ablation catheter. However, the concomitant total procedure time is not affected. Thus, the new system reduces the radiation exposure for both the physicians and patients. (Int Heart J 2016; 57: 299-303)

Coronavirus disease (COVID-19) is a respiratory disease, although arterial function involvement has been documented. We assess the impact of a post-acute COVID-19 rehabilitation program on endothelium-dependent vasodilation and arterial wall properties. We enrolled 60 convalescent patients from COVID-19 and one-month post-acute disease, who were randomized at a 1:1 ratio in a 3-month cardiopulmonary rehabilitation program (study group) or not (control group). Endothelium-dependent vasodilation was evaluated by flow-mediated dilation (FMD), and arterial wall properties were evaluated by carotid–femoral pulse wave velocity (cf-PWV) and augmentation index (AIx) at 1 month and at 4 months post-acute disease. FMD was significantly improved in both the study (6.2 ± 1.8% vs. 8.6 ± 2.4%, p < 0.001) and control groups (5.9 ± 2.2% vs. 6.6 ± 1.8%, p = 0.009), but the improvement was significantly higher in the study group (rehabilitation) (p < 0.001). PWV was improved in the study group (8.2 ± 1.3 m/s vs. 6.6 ± 1.0 m/s, p < 0.001) but not in the control group (8.9 ± 1.8 m/s vs. 8.8 ± 1.9 m/s, p = 0.74). Similarly, AIx was improved in the study group (25.9 ± 9.8% vs. 21.1 ± 9.3%, p < 0.001) but not in the control group (27.6 ± 9.2% vs. 26.2 ± 9.8 m/s, p = 0.15). Convalescent COVID-19 subjects of the study group (rehabilitation) with increased serum levels of circulating IL-6 had a greater reduction in FMD. Conclusively, a 3-month cardiopulmonary post-acute COVID-19 rehabilitation program improves recovery of endothelium-dependent vasodilation and arteriosclerosis.

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Introduction Cardiovascular complications of Coronavirus disease (COVID-19), resulting from the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), have been documented. Endothelium-induced “cytokine storm” in critically ill COVID-19 patients is one of the leading causes of morbidity and mortality. Vascular endothelial damage caused by COVID-19 emphasizes the crucial role of endothelium in COVID-19 clinical impact. Purpose To examine the mid-term (1-month) impact of COVID-19 in endothelial function. Methods In this case control study, 20 consecutive patients who were hospitalized for COVID-19 either on Intensive Care Unit (ICU) or non-ICU were examined one month following hospital discharge. In the control group we recruited 12 consecutive subjects from the outpatient cardiology clinic. Demographic and clinical data were collected, and endothelial function was evaluated by brachial artery flow-mediated dilation (FMD). Results There was no difference in age between COVID-19 patients and control subjects (66±12 years vs. 71±5 years, p&lt;0.17), in male sex (63% vs. 54%, p=0.66) in history of diabetes mellitus (27% vs. 36%, p=0.64), hypertension (36% vs. 54%, p=0.39), cardiovascular disease (27% vs.18%, p=0.61). From the COVID-19 subjects 65% were overweight or obese. During their hospitalization [3 ICU (15%)/17 non-ICU (85%), mean days: 17±6.7], 4 (20%) of COVID-19 patients developed ARDS, while single cases of stress-induced cardiomyopathy, pulmonary embolism, and acute coronary syndrome were detected. One month post discharge D-dimers (0.71±0.55 μg/ml) levels were above upper reference limit. Importantly, FMD one month after hospital discharge date, was significantly impaired in the COVID-19 group (3.59±1.63% vs. 9.31±2.98%, p&lt;0.001) compared to control group. Conclusion Post COVID-19 subjects one month post discharge have significant impaired endothelial function compared to control subjects. These findings highlight the significant interaction of COVID-19 with arterial endothelium and merit further research to conclude on the exact impact of vascular endothelium in physical history of SARS-CoV-2 infection. FUNDunding Acknowledgement Type of funding sources: None.