The aim of the present clinical consensus statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases is to review the current knowledge on the epidemiology, pathogenesis, diagnosis, therapy, and outcomes of myocardial and pericardial complications of coronavirus disease 2019 (COVID-19) and vaccination in order to improve the awareness and clinical confidence on the management of patients with these complications. The risk of myopericardial complications is especially higher within 1 month of COVID-19 disease and vaccination. Forms related to the disease are generally more common and severe than those related to vaccination. Even if vaccination against COVID-19 increases myocarditis risk, this risk is lower in vaccinated than non-vaccinated COVID-19 individuals, supporting the vaccine use. Overall, COVID-19 related complications, especially myocarditis, are relatively rare.

Background: The association between Coronavirus Disease-2019 (COVID-19) and new-onset cardiomyopathy (NOC) is unclear. Objectives: We aim to assess the incidence of NOC in hospitalized COVID-19 patients and its impact on short- and long-term survival. Methods: We retrospectively studied 2219 COVID-19 patients hospitalized between March 2020 and February 2022 who underwent an in-hospital echocardiogram. NOC was defined as a left-ventricular ejection fraction (LVEF) reduction of >10%, resulting in an LVEF of <54% for females and <52% for males. The 30-day and 1-year survival outcomes in patients without and with NOC were studied. Results: Among 25,943 hospitalized COVID-19 patients, 2219 met our inclusion criteria, with 209 (9.4%) having NOC. NOC patients were more likely to be male (56.1% vs. 68.4%, p = 0.001) and have chronic kidney disease (51.4% vs. 60.3%, p = 0.018). They had a higher 30-day mortality rate (29.1% vs. 32%, p = 0.033), but the 1-year survival rate was similar between the patients without and with NOC (36.9% vs. 41.6%, p = 0.12). Multivariable regression revealed that advanced age, admission to intensive care unit, mechanical ventilation, treatment with glucocorticoids, and treatment with vasopressors were associated with higher odds of 30-day mortality in NOC patients. Only 74 (35.4%) NOC patients had follow-up echocardiograms after discharge, of which 47 showed persistent cardiomyopathy. Conclusions: NOC can affect around 1 out of 10 hospitalized COVID-19 patients undergoing echocardiography. While NOC was associated with worse short-term survival, it did not impact the long-term mortality of these patients. Persistent LVEF deficits in some patients emphasize the need for improved outpatient follow-up to identify at-risk individuals and optimize treatment.

COronaVIrus Disease-2019 (COVID-19) is associated with a hypercoagulable state. Intracardiac thrombosis is a potentially serious complication but has seldom been evaluated in COVID-19 patients. We assessed the incidence, associated factors, and outcomes of COVID-19 patients with intracardiac thrombosis. In 2020, COVID-19 inpatients were identified from the National Inpatient Sample (NIS) database. Data on clinical characteristics, intracardiac thrombosis, and adverse outcomes were collected. Multivariable logistic regression was used to identify factors associated with intracardiac thrombosis, in-hospital mortality, and morbidities. In 2020, 1,683,785 COVID-19 inpatients (mean age 63.8 years, 32.2% females) were studied. Intracardiac thrombosis occurred in 0.10% (1830) of cases. In-hospital outcomes included 13.2% all-cause mortality, 3.5% cardiovascular mortality, 2.6% cardiac arrest, 4.4% acute coronary syndrome (ACS), 16.1% heart failure, 1.3% stroke, and 28.3% acute kidney injury (AKI). Key factors for intracardiac thrombosis were congestive heart failure history and coagulopathy. Intracardiac thrombosis independently linked to higher risks of all-cause mortality (odds ratio [OR]: 3.32 (2.42-4.54)), cardiovascular mortality (OR: 2.95 (1.96-4.44)), cardiac arrest (OR: 2.04 (1.22-3.43)), ACS (OR: 1.62 (1.17-2.22)), stroke (OR: 3.10 (2.11-4.56)), and AKI (OR: 2.13 (1.68-2.69)), but not heart failure. While rare, intracardiac thrombosis in COVID-19 patients independently raised in-hospital mortality and morbidity risks.

Long COVID syndrome has had a major impact on million patients' lives worldwide. The cardiovascular system is an important aspect of this multifaceted disease that may manifest in many ways. We have hereby performed a narrative review in order to identify the extent of the cardiovascular manifestations of the Long COVID syndrome.

An in-depth systematic search of the literature has been conducted for this narrative review. The systematic search of PubMed and Cochrane databases yielded 3993 articles, of which 629 underwent full-text screening. A total of 78 studies were included in the final qualitative synthesis and data evaluation. The pathophysiology of the cardiovascular sequelae of Long COVID syndrome and the cardiac manifestations and complications of Long COVID syndrome are critically evaluated. In addition, potential cardiovascular risk factors are assessed, and preventive methods and treatment options are examined in this review.

This systematic review poignantly summarizes the evidence from the available literature regarding the cardiovascular manifestations of Long COVID syndrome and reviews potential mechanistic pathways, diagnostic approaches, preventive measures, and treatment options.

Background/Objectives: The clinical impact of neutrophil-to-lymphocyte ratio (NLR) and right ventricular (RV) dysfunction on clinical outcomes in COVID-19 remains understudied in the Indonesian population. This study aims to investigate their prognostic value in hospitalized Indonesian adults with COVID-19. Methods: A retrospective cohort study was conducted at a COVID-19 referral hospital in Indonesia. We included all consecutive adults hospitalized between April 2020 and April 2021 who underwent transthoracic echocardiography (TTE) during admission. Clinical information was extracted from electronic medical records. TTE variables were defined according to the American Society of Echocardiography criteria. Statistical analyses were performed using SPSS. Ethical approval was obtained from the Institutional Review Board of Universitas Indonesia (#2022-01-135). Results: A total of 488 patients were included in this study-29 with and 459 without RV dysfunction. The mean age of the population was 54.8, with 42% being female. An NLR >4.793 was considered elevated. Elevated NLR was independently associated with RV dysfunction (OR: 3.38, p = 0.02). Older age (HR: 1.02, p = 0.01), obesity (HR: 1.85, p < 0.01), chronic kidney disease (HR: 1.69, p = 0.01), high NLR (HR: 2.75, p < 0.001), and RV dysfunction (HR: 2.07, p = 0.02) independently increased the risk of 30-day mortality by multivariate Cox regression analysis. Conclusions: In adult Indonesian patients hospitalized with COVID-19, an elevated NLR was associated with RV dysfunction, and both of these parameters increased the risk of 30-day mortality. This retrospective cohort study highlights the prognostic importance of NLR and RV dysfunction in hospitalized COVID-19 patients, providing physicians with tools to identify high-risk patients.

Background/Objectives: Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has caused post-acute sequelae, especially for people with pre-existing conditions, including chronic kidney disease (CKD), which may impact the cardiovascular system. Yet, despite the preliminary description of the general population's long-COVID-19 consequences, data on CKD patients is scarce. The aim of this study was to investigate the longitudinal effects of COVID-19 on echocardiographic parameters of cardiac function and on cardiac biomarkers in patients with CKD. Methods: A total of 163 patients were included in this observational prospective trial (listed under NCT05125913 code): 88 in the COVID-19 group and 75 in the control group. The serial echocardiographic characteristics in patients who survived beyond one year, focused on left and right ventricular systolic function, together with cardiac biomarkers evolution, were compared between the two groups. Results: At baseline, there were no significant differences in left ventricular (LV) function parameters, except for a higher Tei Index in the COVID-19 group (p < 0.01). Right ventricular (RV) systolic dysfunction was more frequent in the COVID-19 group, with worse fractional area change (FAC) (p = 0.01), RV free wall longitudinal strain (RVFWLS) (p = 0.01), and RV Tei Index (p = 0.01). Over time, the control group showed a decline in LV ejection fraction (EF), while the COVID-19 group slightly improved. RV global systolic function was better preserved in the COVID-19 group. To the best of our knowledge, this is the first study that demonstrates a statistically significant increase in LAVi in patients with COVID-19. Conclusions: Prior COVID-19 infection influenced the trajectory of LV and RV function in CKD patients over 12 months, suggesting potential transient myocardial adaptations. While overall cardiac function did not differ significantly between groups, COVID-19 survivors exhibited better preservation of some ventricular function parameters.

Background: SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection may be associated with impaired cardiac function, especially in severe cases requiring hospitalization. Impedance cardiography (ICG) is a noninvasive method for assessing cardiac function. It could be useful for the early detection of hemodynamic dysfunction, particularly in patients with a severe course of COVID-19. Aim: This study aimed to analyze and compare the hemodynamic profiles of patients hospitalized with SARS-CoV-2-induced pneumonia to those of a control group. Methods: This prospective, observational, clinical study included 30 hospitalized patients (both men and women, mean age: 48 years) diagnosed with COVID-19 pneumonia (COVID group). Their data were compared to those of a retrospective control group (CG). The study participants were propensity score-matched based on clinical characteristics, including age, blood pressure (BP), and body mass index (BMI). ICG measurements of hemodynamic profiles were performed using a Niccomo device and included heart rate (HR), stroke volume index (SI), cardiac index (CI), velocity index (VI), acceleration index (ACI), Heather index (HI), systemic vascular resistance index (SVRI), and thoracic fluid content (TFC). Results: Patients with COVID-19 showed significantly higher HR (p < 0.0001) and SVRI (p = 0.0003) and lower values for several cardiac function parameters, including SI (p < 0.0001), VI (p < 0.0001), ACI (p = 0.004), and HI (p < 0.0001). Additionally, 11 patients (37%) in the COVID group had a low SI (<35 mL/m2), compared to only 1 patient (3%) in the control group (p < 0.0001). A statistically significant difference in left ventricular ejection fraction (LVEF) was also observed (p < 0.0001), although absolute values remained within the normal range. Conclusions: SARS-CoV-2 infection negatively affects the cardiovascular system, leading to impaired heart function even in low-risk patients. Impedance cardiography may serve as a simple, noninvasive tool for identifying individuals with cardiac dysfunction following COVID-19 pneumonia.

Impaired left and right ventricular (LV/RV) function during acute SARS-CoV-2 infection has been predominantly reported in hospitalized patients, but long-term cardiac sequelae in large, well-characterized cohorts remain inconclusive. This study evaluated cardiac structure and function in individuals with post-Coronavirus disease (COVID) syndrome (PCS) compared to recovered controls (CON), focusing on associations with cardiopulmonary symptoms and rapid physical exhaustion (RPE).

This multicenter, population-based study included 1154 participants (679 PCS, 475 age- and sex matched CON; mean age 49 ± 12 years; 760 women) 1.5 years post-infection. Transthoracic echocardiography assessed LV global longitudinal strain (GLS), RV GLS and RV free wall strain (FWS), and other measures. Cardiopulmonary exercise testing (CPET) measured maximum respiratory oxygen uptake (VO2max) as a marker of cardiopulmonary fitness.

PCS participants exhibited significantly lower LV GLS (-20.25% [-21.28 - -19.22] vs. -20.73% [-21.74 - -19.72], p = 0.003), reduced diastolic function (E/A 1.16 [1.04-1.27] vs. 1.21 [1.1-1.32], p = 0.022) and decreased TAPSE (24.45 mm [22.14-26.77] vs. 25.05 mm [22.78-27.32], p = 0.022) compared to CON, even after adjusting for confounders. RV strain values were similar between groups. LV GLS correlated inversely with VO2max (p = 0.004) and positively with RPE (p = 0.050), though no associations were observed with other cardiopulmonary symptoms.

This study demonstrates subtle yet consistent reductions in LV function, specifically LV GLS and diastolic function, and exercise capacity in PCS compared to CON. While these changes are within reference ranges, their potential impact on clinical outcomes warrants further investigation. These findings highlight the need for cardiac assessments and long-term follow-up in symptomatic PCS patients.

Coronavirus disease 2019 (COVID-19) was declared a global pandemic in 2019. It remains uncertain to what extent COVID-19 effects the heart in heathy individuals. To evaluate the effect of the COVID-19 on cardiac structure and function in middle-aged and older individuals.

A single-centre prospective observational study enroled a total of 124 participants (84 with history of COVID-19 [COVID-19 group] and 40 without a history of COVID-19 [non-COVID group]). All participants underwent echocardiography with speckle tracking to assess cardiac structure and function at rest and during peak exercise.

There were no differences in left and right ventricular diastolic function (p ≥ 0.05) between the COVID-19 and non-COVID-19 groups. Participants in COVID-19 group demonstrated higher left ventricular mass (130 ± 39.8 vs. 113 ± 27.2 g, p = 0.008) and relative wall thickness (0.38 ± 0.07 vs. 0.36 ± 0.13, p = 0.049). Left ventricular global longitudinal strain was reduced in the COVID-19 group at rest and at peak-exercise (rest: 18.3 ± 2.01 vs. 19.3 ± 1.53%, p = 0.004; peak exercise: 19.1 ± 2.20 vs. 21.0 ± 1.58%, p ≤ 0.001). However, no difference was seen in resting left ventricular ejection fraction (58 ± 2.89 vs. 59 ± 2.51%, p = 0.565) between groups. Right ventricular fractional area change was reduced in the COVID-19 group (p = 0.012).

Cardiac structural and functional remodelling was observed in middle-aged and older otherwise healthy individuals with a history of COVID-19.

Coronavirus Disease 2019 causes significant morbidity, and different variants of concern (VOCs) can impact organ systems differently. We conducted a single-center retrospective cohort analysis comparing biomarkers and clinical outcomes in hospitalized patients infected with the wild-type or Alpha (wt/Alpha) VOC against patients infected with the Omicron VOC. We included 428 patients infected with the wt/Alpha VOC and 117 patients infected with the Omicron VOC. The Omicron cohort had higher maximal median high-sensitivity Troponin-T (hs-TnT) levels (wt/Alpha: 12.8 ng/L, IQR 6.6-29.5 vs. Omicron: 27.8 ng/L, IQR 13.7-54.0; p < 0.001) and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) (wt/Alpha: 256 ng/L, IQR 74.5-913.5 vs. Omicron: 825 ng/L, IQR 168-2759; p < 0.001) levels. This remained true for patients under 65 years of age and without pre-existing cardiovascular disease (hs-TnT (wt/Alpha: 6.1 ng/L, IQR 2.5-10.25 vs. Omicron: 8.6 ng/L, IQR 6.2-15.7; p = 0.007) and NT-proBNP (wt/Alpha: 63 ng/L, IQR 25-223.75 vs. Omicron: 158 ng/L, IQR 75.5-299.5; p = 0.006)). In-hospital mortality was similar between the two groups (wt/Alpha: 53 or 12.7% vs. Omicron: 9 or 7.7%; p = 0.132) and more patients infected with wt/Alpha VOC required intensive care admission (wt/Alpha: 93 or 22.2% vs. Omicron: 14 or 12%; p = 0.014). Increased cardiac biomarkers were correlated with a higher risk of mortality and ICU admission in both groups. Herein, we detected higher levels of cardiac biomarkers in hospitalized patients infected with the Omicron VOC when compared to wt/Alpha, being indicative of higher cardiac involvement. Although hs-TnT and NT-proBNP levels were higher in the Omicron cohort and both markers were linked to in hospital mortality in both groups, the mortality rates were similar.

To describe echocardiographic findings among mechanically ventilated patients with COVID-19 acute respiratory distress syndrome, comparing those with and without venovenous extracorporeal membrane oxygenation (VV ECMO) support.

Single-center, retrospective cohort study.

Intensive care unit (ICU) of a quaternary academic center.

Patients with COVID-19 admitted between March 2020 and June 2021 receiving mechanical ventilation, with an echocardiogram within 72 hours of admission.

Admission and follow-up echocardiograms during ICU stay.

Patient characteristics and echocardiographic findings were analyzed. Mortality odds ratio (OR) for right ventricular (RV) systolic dysfunction and acute cor pulmonale (ACP) was calculated.

Among 242 patients, 145 (60%) received VV ECMO. Median (IQR) PaO2/FiO2 was 76 (65-95) and 98 (85-140) in ECMO and non-ECMO patients, respectively (p ≤ 0.001). Initial echocardiograms showed no significant differences in left ventricular systolic dysfunction (10% v 15 %, p = 0.31) and RV systolic dysfunction (38% v. 27%, p = 0.27) between ECMO and non-ECMO patients. ACP was more frequent in the ECMO group at baseline (41% v. 26 %, p = 0.02). During the ICU stay, patients on ECMO exhibited a higher prevalence of RV systolic dysfunction (55% v 34%, p = 0.001) and ACP (51% v 26%, p = 0.002). RV systolic dysfunction (OR 1.99; 95% CI 1.09-3.63) and ACP (OR 2.95; 95% CI 1.55-5.62) on the follow-up echocardiograms were associated with higher odds of ICU mortality.

The prevalence of echocardiographic abnormalities, in particular RV dysfunction, was frequent among patients with COVID-19 receiving VV ECMO support and was associated with worse clinical outcomes.

Background/Objectives: Smoking and hypertension are major contributors to cardiovascular diseases, with smoker hypertensives typically presenting with exacerbated health risks. These factors are associated with COVID-19 aggravation, but their cumulative impact in the context of this disease remains understudied. Our hypothesis was that hypertensive smokers display a more vulnerable health profile (versus non-smokers) upon hospital admission for COVID-19. Methods: This exploratory observational study compared the clinical profiles of hypertensive COVID-19 patients depending on their smoking status. Focusing on key cardiometabolic, blood, renal, hepatic, and inflammatory markers, this investigation included 100 hypertensive COVID-19 patients (50 smokers and 50 non-smokers) aged 50 and above. Logistic regression and Spearman's correlations were used to identify significant predictors and relationships among variables. Results: Hypertensive smokers with COVID-19 were significantly more likely to exhibit higher heart rate (p = 0.047), left atrial size (p = 0.013) and diameter (p = 0.040), left ventricular end-systolic volume (p = 0.036), and interventricular septal thickness (p ≤ 0.001). These patients were also much more prone to display elevated CRP (p = 0.035) and hemoglobin (p = 0.011). The renal profiles of the smokers and non-smokers differed, with the smokers showing a significantly greater likelihood to have high serum urea (p = 0.036), but normal-to-low serum potassium (p = 0.011) and sodium (p ≤ 0.001). Their lipid profile was less favorable, with higher triglycerides (p ≤ 0.001), but lower HDL (p = 0.008). The strongest predictors of smoking status were interventricular septal thickness, triglycerides, and serum sodium. Conclusions: Hypertensive smokers admitted to the hospital with COVID-19 tend to exhibit a more adverse clinical profile, particularly in terms of cardiovascular remodeling, lipid imbalances, renal profile, and inflammation. These findings suggest that smoking exacerbates the effects of hypertension in the context of COVID-19, highlighting the need for more aggressive monitoring and management in this patient group.

While acute cardiovascular complications of coronavirus disease 2019 (COVID-19) are well described, less is known about longer-term cardiac sequelae. For many individuals with cardiac signs or symptoms arising after COVID-19 infection, the aetiology remains unclear. We examined immune profiles associated with magnetic resonance imaging (MRI) abnormalities in patients with unexplained cardiac injury after COVID-19.

Twenty-one participants {mean age 47 [standard deviation (SD) 13] years, 71% female} with long COVID-19 (n = 17), raised troponin (n = 2), or unexplained new-onset heart failure (n = 2), who did not have pre-existing heart conditions or recent steroid/immunosuppression treatment, were enrolled a mean 346 (SD 191) days after COVID-19 infection in a prospective observational study. Cardiac MRI and blood sampling for deep immunophenotyping using mass cytometry by time of flight and measurement of proteomic inflammatory markers were performed. Nine of the 21 (43%) participants had MRI abnormalities (MRI(+)), including non-ischaemic patterns of late gadolinium enhancement and/or visually overt myocardial oedema in 8 people. One patient had mildly impaired biventricular function without fibrosis or oedema, and two had severe left ventricular (LV) impairment. MRI(+) individuals had higher blood CCL3, CCL7, FGF-23, and CD4 Th2 cells, and lower CD8 T effector memory (TEM) cells, than MRI(-). Cluster analysis revealed lower expression of inhibitory receptors PD1 and TIM3 in CD8 TEM cells from MRI(+) patients than MRI(-) patients, and functional studies of CD8 T αβ cells showed higher proportions of cytotoxic granzyme B+(GZB+)-secreting cells upon stimulation. CD8 TEM cells and CCL7 were the strongest predictors of MRI abnormalities in a least absolute shrinkage and selection operator regression model (composite area under the curve 0.96, 95% confidence interval 0.88-1.0). CCL7 was correlated with diffuse myocardial fibrosis/oedema detected by quantitative T1 mapping (r = 0.47, P = 0.04).

COVID-19-related cardiac injury in symptomatic patients with non-ischaemic myocarditis-like MRI abnormalities is associated with immune dysregulation, including decreased peripheral CD8 TEM cells and increased CCL7, persisting long after the initial infection.

SARS-CoV-2 infection may lead to myocardial and endothelial damage. The present study sought to characterize the cardiovascular sequel in a large group of consecutive patients admitted for out-patient cardiovascular follow-up after a symptomatic COVID-19 infection.

The aims of this study were as follows: to evaluate the presence of post-covid cardiovascular symptoms in an unselected population of outpatients referred to a post-COVID outpatient cardiology clinic and to characterize the long-term abnormalities associated with a more severe COVID-19 infection clinical course. A total of 914 patients were included in this single-center, observational, cross-sectional study, of which 163 were hospitalized and 149 required mechanical ventilation for COVID-19 pneumonia. Patients were analyzed at follow-up according to the care setting during the initial presentation.

The median time to follow-up was 126 days. At that time, only 3.5% of patients reported no persistent dyspnea, chest pain, or fatigue on exertion. In a follow-up echocardiographic assessment, patients who required hospitalization showed slight alterations in the pulmonary acceleration time and the tricuspid regurgitation pressure gradient, as well as reduced exercise tolerance during treadmill exercise testing when compared to patients with a benign clinical course. 24-hour Holter EKG monitoring or 24-hour blood pressure monitoring did not identify significant differences between the analyzed subgroups.

The current study reports on an association between COVID-19 severity and the presence of cardiovascular alterations at follow-up. A simple diagnostic protocol, comprising an exercise treadmill test and transthoracic echocardiography is useful in identifying patients who may benefit from regular, structured cardiovascular medical care.

The risk of cardiovascular complications due to SARS-CoV-2 are significantly increased within the first 6 months of the infection. Patients with COVID-19 have an increased risk of death, and there is evidence that many may experience a wide range of post-acute cardiovascular complications. Our work aims to provide an update on current clinical aspects of diagnosis and treatment of cardiovascular manifestations during acute and long-term COVID-19.

SARS-CoV-2 has been shown to be associated with increased incidence of cardiovascular complications such as myocardial injury, heart failure, and dysrhythmias, as well as coagulation abnormalities not only during the acute phase but also beyond the first 30 days of the infection, associated with high mortality and poor outcomes. Cardiovascular complications during long-COVID-19 were found regardless of comorbidities such as age, hypertension, and diabetes; nevertheless, these populations remain at high risk for the worst outcomes during post-acute COVID-19. Emphasis should be given to the management of these patients. Treatment with low-dose oral propranolol, a beta blocker, for heart rate management may be considered, since it was found to significantly attenuate tachycardia and improve symptoms in postural tachycardia syndrome, while for patients on ACE inhibitors or angiotensin-receptor blockers (ARBs), under no circumstances should these medications be withdrawn. In addition, in patients at high risk after hospitalization due to COVID-19, thromboprophylaxis with rivaroxaban 10 mg/day for 35 days improved clinical outcomes compared with no extended thromboprophylaxis. In this work we provide a comprehensive review on acute and post-acute COVID-19 cardiovascular complications, symptomatology, and pathophysiology mechanisms. We also discuss therapeutic strategies for these patients during acute and long-term care and highlight populations at risk. Our findings suggest that older patients with risk factors such as hypertension, diabetes, and medical history of vascular disease have worse outcomes during acute SARS-CoV-2 infection and are more likely to develop cardiovascular complications during long-COVID-19.

Coronavirus disease-2019 (COVID-19) affects the cardiovascular system even after the acute phase of the disease. Cardiopulmonary rehabilitation may improve post-COVID-19 symptoms. This study aims to evaluate the impact of a cardiopulmonary rehabilitation program after acute COVID-19 on arterial stiffness, left ventricular function, and ventriculoarterial coupling (VAC).

Forty-eight adults were examined 1 (T0) and 3-mo (T1) following recovery from COVID-19 and randomized 1:1 to participate or not in a 3-mo rehabilitation program. Matched subjects were enrolled as a non-COVID-19 group. Arterial stiffness was evaluated by carotid-femoral pulse wave velocity (PWV). Left ventricular (LV) systolic performance was evaluated with global longitudinal strain (GLS). The PWV/LV-GLS ratio was calculated as an index of VAC. High-sensitivity C reactive protein (hs-CRP) was measured.

At T0, convalescent patients with COVID-19 had impaired PWV ( P = .001) and reduced VAC ( P = .001) compared to non-COVID-19 subjects. PWV (8.15 ± 1.37 to 6.55 ± 0.98 m/sec, P < .001) and LV-GLS (-19.67 ± 1.98 to -21.3 ± 1.93%, P < .001) improved only in convalescent patients with COVID-19 undergoing rehabilitation. Similarly, VAC was only improved in the rehabilitation group (-0.42 ± 0.11 to -0.31 ± 0.06 m · sec -1  ·% -1 , P < .001). A significant improvement in VO 2max was noted after rehabilitation (15.70 [13.05, 21.45] to 18.30 [13.95, 23.75] ml · kg -1  · min -1 , P = .01). Finally, hs-CRP was improved in both groups with a significantly greater improvement in the rehabilitation group.

A 3-mo rehabilitation program in convalesced patients with COVID-19 enhances the recovery of arterial stiffness, left ventricular function, and VAC, highlighting the beneficial mechanisms of rehabilitation in this patient population.

SGLT-2i are increasingly recognized for their benefits in patients with cardiometabolic risk factors. Additionally, emerging evidence suggests potential applications in acute illnesses, including COVID-19. This systematic review aims to evaluate the effects of SGLT-2i in patients facing acute illness, particularly focusing on SARS-CoV-2 infection.

Following PRISMA guidelines, a systematic search of PubMed, Scopus, medRxiv, Research Square, and Google Scholar identified 22 studies meeting inclusion criteria, including randomized controlled trials and observational studies. Data extraction and quality assessment were conducted independently.

Out of the 22 studies included in the review, six reported reduced mortality in DM-2 patients taking SGLT-2i, while two found a decreased risk of hospitalization. Moreover, one study demonstrated a lower in-hospital mortality rate in DM-2 patients under combined therapy of metformin plus SGLT-2i. However, three studies showed a neutral effect on the risk of hospitalization. No increased risk of developing COVID-19 was associated with SGLT-2i use in DM-2 patients. Prior use of SGLT-2i was not associated with ICU admission and need for MV. The risk of acute kidney injury showed variability, with inconsistent evidence regarding diabetic ketoacidosis.

Our systematic review reveals mixed findings on the efficacy of SGLT-2i use in COVID-19 patients with cardiometabolic risk factors. While some studies suggest potential benefits in reducing mortality and hospitalizations, others report inconclusive results. Further research is needed to clarify optimal usage and mitigate associated risks, emphasizing caution in clinical interpretation.

Takotsubo Syndrome (TS) is a heart disease caused by extreme exposure of the body to physical or psychological stress. In the context of COVID-19, the virus can be a significant source of stress, with particular attention being paid to the cytokine storm as a cause of damage to the body. New research shows that the production of specific cytokines is linked to the activation of immune checkpoint proteins such as PD-1, PD-L1, and CTLA-4 on T cells. Although initially beneficial in combating infections, it can suppress defense and aid in disease progression. Therefore, checkpoint inhibitor therapy has been highlighted beyond oncological therapies, given its effectiveness in strengthening the immune system. However, this treatment can lead to excessive immune responses, inflammation, and stress on the heart, which can cause Takotsubo Syndrome in patients. Several studies investigate the direct link between this therapy and cardiac injuries in these patients, which can trigger TS. From this perspective, we must delve deeper into this treatment and consider its effects on the prognosis against SARS-CoV-2 infection.

The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has led to a diverse pattern of myocardial injuries, including myocarditis, which is linked to adverse outcomes in patients. Research indicates that myocardial injury is associated with higher mortality in hospitalized severe COVID-19 patients (75.8% vs 9.7%). Cardiovascular Magnetic Resonance (CMR) has emerged as a crucial tool in diagnosing both ischaemic and non-ischaemic myocardial injuries, providing detailed insights into the impact of COVID-19 on myocardial tissue and function. This review synthesizes existing studies on the histopathological findings and CMR imaging patterns of myocardial injuries in COVID-19 patients. CMR imaging has revealed a complex pattern of cardiac damage in these patients, including myocardial inflammation, oedema, fibrosis, and ischaemic injury, due to coronary microthrombi. This review also highlights the role of LLC criteria in diagnosis of COVID-related myocarditis and the importance of CMR in detecting cardiac complications of COVID-19 in specific groups, such as children, manifesting multisystem inflammatory syndrome in children (MIS-C) and athletes, as well as myocardial injuries post-COVID-19 infection or following COVID-19 vaccination. By summarizing existing studies on CMR in COVID-19 patients and highlighting ongoing research, this review contributes to a deeper understanding of the cardiac impacts of COVID-19. It emphasizes the effectiveness of CMR in assessing a broad spectrum of myocardial injuries, thereby enhancing the management and prognosis of patients with COVID-19 related cardiac complications.

A growing proportion of people experience incomplete recovery months after contracting coronavirus disease 2019 (COVID-19). These COVID-19 survivors develop a condition known as post-COVID syndrome (PCS), where COVID-19 symptoms persist for > 12 weeks after acute infection. Limited studies have investigated PCS risk factors that notably include pre-existing cardiovascular diseases (CVD), which should be examined considering the most recent PCS data. This review aims to identify CVD as a risk factor for PCS development in COVID-19 survivors.

Following the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) checklist, systematic literature searches were performed in the PubMed, Scopus, and Web of Science databases from the earliest date available to June 2023. Data from observational studies in English that described the association between CVD and PCS in adults (≥ 18 years old) were included. A minimum of two authors independently performed the screening, study selection, data extraction, data synthesis, and quality assessment (Newcastle-Ottawa Scale). The protocol of this review was registered under PROSPERO (ID: CRD42023440834).

In total, 594 studies were screened after duplicates and non-original articles had been removed. Of the 11 included studies, CVD including hypertension (six studies), heart failure (three studies), and others (two studies) were significantly associated with PCS development with different factors considered. The included studies were of moderate to high methodological quality.

Our review highlighted that COVID-19 survivors with pre-existing CVD have a significantly greater risk of developing PCS symptomology than survivors without pre-existing CVD. As heart failure, hypertension and other CVD are associated with a higher risk of developing PCS, comprehensive screening and thorough examinations are essential to minimise the impact of PCS and improve patients' disease progression.

Takotsubo syndrome (TTS) is a rare complication of vaccination. In this study, we sought to provide insight into the characteristics of reported TTS induced by vaccination.

We did a systematic review, searching PubMed, Embase, Web of Science, Ovid MEDLINE, Journals@Ovid, and Scopus databases up to 26 April 2023 to identify case reports or case series of vaccine-induced TTS. We then extracted and summarized the data from these reports. Eighteen reports were identified, with a total of 19 patients with TTS associated with vaccinations. Of the 19 included patients, the majority were female (n = 13, 68.4%) with a mean age of 56.6 ± 21.9 years. Seventeen patients developed TTS after coronavirus disease 2019 vaccination, 14 of whom received an mRNA vaccination. Two cases of TTS occurred after influenza vaccination. Among the 19 patients, 17 (89.5%) completed transthoracic echocardiography and 16 (84.2%) underwent angiography procedures. Seven patients (36.8%) completed cardiac magnetic resonance imaging. The median time to symptom onset was 2 (inter-quartile range, 1-4) days. The most common symptoms were chest pain (68.4%), dyspnoea (57.9%), and digestive symptoms (31.6%). A total of 57.9% of patients developed nonspecific symptoms such as fatigue, myalgia, diaphoresis, and fever. Among the 16 reported cases of TTS, 15 patients (93.8%) exhibited elevated cardiac troponin levels, while among the nine reported cases, eight patients (88.9%) had elevated natriuretic peptide levels. All patients had electrocardiographic changes: ST-segment change (47.1%), T-wave inversion (58.8%), and prolonged corrected QT interval (35.3%). The most common TTS type was apical ballooning (88.2%). Treatment during hospitalization typically included beta-blockers (44.4%), angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (33.3%), and diuretics (22.2%). After treatment, 81.3% of patients were discharged with improved symptoms. Among this group, nine patients (56.3%) were reported to have recovered ventricular wall motion during follow-up. Two patients (12.5%) died following vaccination without resuscitation attempts.

TTS is a rare but potentially life-threatening complication of vaccination. Typical TTS symptoms such as chest pain and dyspnoea should be considered alarming symptoms, though nonspecific symptoms are common. The risks of such rare adverse events should be balanced against the risks of infection.

This study aims to explore the predictive roles of echocardiographic parameters and biomarkers in determining outcomes among hospitalized COVID-19 patients experiencing cardiovascular events.

A retrospective cohort study was conducted involving 49 COVID-19 patients who encountered cardiovascular events during hospitalization and underwent echocardiography. Our findings revealed notable associations between echocardiographic parameters and survival time.

A decrease in left ventricular ejection fraction (LVEF) of 10% was linked to a 20% reduction in survival time (TR: 0.80, 95% CI: 0.67 - 0.96, p = .017). Similarly, an increase in left ventricular (LV) volume by 10 mL was associated with a 9% decrease in survival time (TR: 0.91, 95% CI: 0.84 - 0.98, p = .011). Moreover, an increase in left atrial (LA) volume by 10 mL corresponded to an 8% decrease in survival time (TR: 0.92, 95% CI: 0.86 - 0.99, p = .026). Additionally, each 1 cm increase in right ventricular (RV) diameter was linked to a 22% reduction in survival time (TR: 0.78, 95% CI: 0.61 - 0.99, p = .043). Furthermore, a 10 mL increase in right atrial (RA) volume was associated with a 12% decrease in survival time (TR: 0.88, 95% CI: 0.78 - 0.98, p = .017). Notably, a tenfold rise in troponin levels was linked to a 33% decrease in survival time (TR: 0.67, 95% CI: 0.48 - 0.93, p = .014).

Our study emphasizes the significant associations between various echocardiographic parameters and troponin levels with reduced survival time among COVID-19 patients experiencing cardiovascular events. These findings highlight the potential utility of echocardiography and troponin assessment in predicting outcomes and guiding management strategies in this patient population.

Long COVID affects both children and adults, including subjects who experienced severe, mild, or even asymptomatic SARS-CoV-2 infection. We have provided a comprehensive overview of the incidence, clinical characteristics, risk factors, and outcomes of persistent COVID-19 symptoms in both children and adults, encompassing vulnerable populations, such as pregnant women and oncological patients. Our objective is to emphasize the critical significance of adopting an integrated approach for the early detection and appropriate management of long COVID. The incidence and severity of long COVID symptoms can have a significant impact on the quality of life of patients and the course of disease in the case of pre-existing pathologies. Particularly, in fragile and vulnerable patients, the presence of PASC is related to significantly worse survival, independent from pre-existing vulnerabilities and treatment. It is important try to achieve an early recognition and management. Various mechanisms are implicated, resulting in a wide range of clinical presentations. Understanding the specific mechanisms and risk factors involved in long COVID is crucial for tailoring effective interventions and support strategies. Management approaches involve comprehensive biopsychosocial assessments and treatment of symptoms and comorbidities, such as autonomic dysfunction, as well as multidisciplinary rehabilitation. The overall course of long COVID is one of gradual improvement, with recovery observed in the majority, though not all, of patients. As the research on long-COVID continues to evolve, ongoing studies are likely to shed more light on the intricate relationship between chronic diseases, such as oncological status, cardiovascular diseases, psychiatric disorders, and the persistent effects of SARS-CoV-2 infection. This information could guide healthcare providers, researchers, and policymakers in developing targeted interventions.

Coronavirus disease 2019 (COVID-19) has been a major global health concern since its emergence in 2019, with over 680 million confirmed cases as of April 2023. While COVID-19 has been strongly associated with the development of cardiovascular complications, the specific mechanisms by which viral infection induces myocardial dysfunction remain largely controversial as studies have shown that the severe acute respiratory syndrome coronavirus-2 can lead to heart failure both directly, by causing damage to the heart cells, and indirectly, by triggering an inflammatory response throughout the body. In this review, we summarize the current understanding of potential mechanisms that drive heart failure based on in vitro studies. We also discuss the significance of three-dimensional heart-on-a-chip technology in the context of the current and future pandemics.

SARS-CoV-2 has spread rapidly worldwide and infected hundreds of millions of people worldwide. With the increasing number of COVID-19 patients discharged from hospitals, the emergence of its associated complications, sequelae, has become a new global health crisis secondary to acute infection. For the time being, such complications and sequelae are collectively called "Post-acute sequelae after SARS-CoV-2 infection (PASC)", also referred to as "long COVID" syndrome. Similar to the acute infection period of COVID-19, there is also heterogeneity in PASC. This article reviews the various long-term complications and sequelae observed in multiple organ systems caused by COVID-19, pathophysiological mechanisms, diagnosis, and treatment of PASC, aiming to raise awareness of PASC and optimize management strategies.

Coronavirus disease 2019 (COVID-19) has been revealed as a severe illness with a wide-ranging cardiac manifestation and has a worldwide burden on the health-care system.

Our aim in this study is to assess the impact of mild COVID-19 infection on cardiac function in patients without previous structural heart disease.

We evaluated 100 outpatients with a history of mild COVID-19 infection without needing hospitalization within 3 weeks to 3 months after recovery from the acute phase of the illness between August 2020 and July 2021.

The patients were compared with 105 healthy participants without a history of COVID-19 as the control group. All participants underwent comprehensive transthoracic echocardiography.

Data were analyzed using IBM SPSS statistics 23. For all tests, P < 0.05 was defined as statistically significant.

COVID-19 patients had higher global longitudinal strain (P = 0.001), systolic pulmonary artery pressure (P = 0.008), RV E' (P = 0.049), and RV A' (P = 0.003), while had lower septal tissue velocities (P = 0.01) and left ventricular ejection fraction (EF) (LVEF) (P = 0.03). Abnormal EF (LVEF <55%) was noted in 19% of the COVID-19 patients and 8.6% of the control group (P = 0.03). Moderate or more diastolic dysfunction was noted in 10 COVID-19 patients but only in one participant in the control group (P = 0.005).

Mild COVID-19 infection can result in cardiac functional and structural changes, even in patients without known previous structural heart disease. Echocardiography can be a useful modality for risk assessment and follow-up in patients with COVID-19.

Covid-19 patients can have both regional and global ventricular dysfunction. We aim to study the spectrum of myocardial involvement in Covid-19 patients on echocardiography.

This is a single center, observational study where wall motion abnormality patterns were studied in Covid-19 patients along with global and regional longitudinal strain analysis (GLS).

30 Covid-19 patients were included in the study, with a mean age of 35.3±6.4 years. Echocardiography revealed characteristic wall motion abnormality involving hypokinesia of anterolateral and apical segments, which produced an operculum like appearance in all patients. Strain derived ejection fraction(EF) was lower in 4 chamber as compared to 2 chamber indicating regional myocardial dysfunction. Reduced GLS values in presence of normal EF indicates global systolic function impairment. Endocardial effacement was also noted in these segments along with stretching of interventricular septum.

Specific myocardial involvement pattern can be detected on echocardiography, thus helping in diagnosis of Covid myocarditis.

To investigate intraindividual cardiac structural and functional changes before and after COVID-19 infection in a previously healthy population with a 3T cardiac magnetic resonance (CMR).

A total of 39 unhospitalized patients with COVID-19 were recruited. They participated in our previous study as non-COVID-19 healthy volunteers undergoing baseline CMR examination and were recruited to perform a repeated CMR examination after confirmed COVID-19 infection in December 2022. The CMR parameters were measured and compared between before and after COVID-19 infection with paired t tests. The laboratory measures including myocardial enzymes and inflammatory indicators were also collected when performing repeated CMR.

The median duration was 393 days from the first to second CMR and 26 days from clinical symptoms onset to the second CMR. Four patients (10.3%, 4/39) had the same late gadolinium enhancement pattern at baseline and repeated CMR and 5 female patients (12.8%, 5/39) had myocardial T2 ratio >2 (2.07 to 2.27) but with normal T2 value in post-COVID-19 CMR. All other CMR parameters were in normal ranges before and after COVID-19 infection. Between before and after the COVID-19 infection, there were no significant differences in cardiac structure, function, and tissue characterization, no matter with or without symptoms (fatigue, chest discomfort, palpitations, shortness of breath, and insomnia/sleep disorders) (all P >0.05). The laboratory measures at repeated CMR were in normal ranges in all participants.

These intraindividual CMR studies showed unhospitalized patients with COVID-19 with normal myocardial enzymes had no measurable CMR abnormalities, which can help alleviate wide social concerns about COVID-19-related myocarditis.

Cardiac injury is frequently reported in COVID-19 patients, the right ventricle (RV) is mostly affected. We systematically evaluated the cardiac function and longitudinal changes in severe COVID-19 acute respiratory distress syndrome (ARDS) admitted to the intensive care unit (ICU) and assessed the impact on survival.

We prospectively performed comprehensive echocardiographic analysis on mechanically ventilated COVID-19 ARDS patients, using 2D/3D echocardiography. We defined left ventricular (LV) systolic dysfunction as ejection fraction (EF) < 40%, or longitudinal strain (LS) > - 18% and right ventricular (RV) dysfunction if two indices among fractional area change (FAC) < 35%, tricuspid annulus systolic plane excursion (TAPSE) < 1.6 cm, RV EF < 44%, RV-LS > - 20% were present. RV afterload was assessed from pulmonary artery systolic pressure (PASP), PASP/Velocity Time Integral in the right ventricular outflow tract (VTIRVOT) and pulmonary acceleration time (PAcT). TAPSE/PASP assessed the right ventriculoarterial coupling (VACR).

Among 176 patients included, RV dysfunction was common (69%) (RV-EF 41.1 ± 1.3%; RV-FAC 36.6 ± 0.9%, TAPSE 20.4 ± 0.4mm, RV-LS:- 14.4 ± 0.4%), usually accompanied by RV dilatation (RVEDA/LVEDA 0.82 ± 0.02). RV afterload was increased in most of the patients (PASP 33 ± 1.1 mmHg, PAcT 65.3 ± 1.5 ms, PASP/VTIRVOT, 2.29 ± 0.1 mmHg/cm). VACR was 0.8 ± 0.06 mm/mmHg. LV-EF < 40% was present in 21/176 (11.9%); mean LV-EF 57.8 ± 1.1%. LV-LS (- 13.3 ± 0.3%) revealed a silent LV impairment in 87.5%. A mild pericardial effusion was present in 70(38%) patients, more frequently in non-survivors (p < 0.05). Survivors presented significant improvements in respiratory physiology during the 10th ICU-day (PaO2/FiO2, 231.2 ± 11.9 vs 120.2 ± 6.7 mmHg; PaCO2, 43.1 ± 1.2 vs 53.9 ± 1.5 mmHg; respiratory system compliance-CRS, 42.6 ± 2.2 vs 27.8 ± 0.9 ml/cmH2O, all p < 0.0001). Moreover, survivors presented significant decreases in RV afterload (PASP: 36.1 ± 2.4 to 20.1 ± 3 mmHg, p < 0.0001, PASP/VTIRVOT: 2.5 ± 1.4 to 1.1 ± 0.7, p < 0.0001 PAcT: 61 ± 2.5 to 84.7 ± 2.4 ms, p < 0.0001), associated with RV systolic function improvement (RVEF: 36.5 ± 2.9% to 46.6 ± 2.1%, p = 0.001 and RV-LS: - 13.6 ± 0.7% to - 16.7 ± 0.8%, p = 0.001). In addition, RV dilation subsided in survivors (RVEDA/LVEDA: 0.8 ± 0.05 to 0.6 ± 0.03, p = 0.001). Day-10 CRS correlated with RV afterload (PASP/VTIRVOT, r: 0.535, p < 0.0001) and systolic function (RV-LS, 0.345, p = 0.001). LV-LS during the 10th ICU-day, while ΔRV-LS and ΔPASP/RVOTVTI were associated with survival.

COVID-19 improvements in RV function, RV afterload and RV-PA coupling at day 10 were associated with respiratory function and survival.

Aim      Prospective assessment of the nature of cardiac injury in patients with post-COVID syndrome according to contrast-enhanced MRI in routine clinical practice.Material and methods  106 previously unvaccinated patients were evaluated. 62 (58.5%) of them were women with complaints that persisted after COVID-19 (median age, 57.5 [49; 64] years). In addition to standard indexes, markers of inflammation and myocardial injury were determined, and cardiac contrast-enhanced MRI was performed in each patient.Results The median time from the onset of COVID-19 to cardiac MRI was 112.5 [75; 151] days. The nature of cardiac injury according to MRI in patients with post-COVID syndrome was complex and included a decrease in left ventricular (LV) and right ventricular ejection fraction, pericardial effusion, and pathological foci of late and early contrast enhancement at various locations. In 29 (27.4%) cases, there was a combination of any two signs of heart injury. In 28 (26.4%) patients with focal myocardial injury during the acute phase of COVID-19, hydroxychloroquine and tocilizumab were administered significantly more frequently, but antiviral drugs were administered less frequently. The presence of focal myocardial injury was associated with pathological LV remodeling.Conclusion      According to contrast-enhanced cardiac MRI, at least 27.4% of patients with post-COVID syndrome may have signs of cardiac injury in various combinations, and in 26.4% of cases, foci of myocardial injury accompanied by LV remodeling are detected. The nature of heart injury after COVID-19 depends on the premorbid background, characteristics of the course of the infectious process, and the type of prescribed therapy. An algorithm for evaluating patients with post-COVID syndrome is proposed.

We sought to prospectively investigate the accuracy of an artificial intelligence (AI)-based tool for left ventricular ejection fraction (LVEF) assessment using a hand-held ultrasound device (HUD) in COVID-19 patients and to examine whether reduced LVEF predicts the composite endpoint of in-hospital death, advanced ventilatory support, shock, myocardial injury, and acute decompensated heart failure. COVID-19 patients were evaluated with a real-time LVEF assessment using an HUD equipped with an AI-based tool vs. assessment by a blinded fellowship-trained echocardiographer. Among 42 patients, those with LVEF < 50% were older with more comorbidities and unfavorable exam characteristics. An excellent correlation was demonstrated between the AI and the echocardiographer LVEF assessment (0.774, p < 0.001). Substantial agreement was demonstrated between the two assessments (kappa = 0.797, p < 0.001). The sensitivity, specificity, PPV, and NPV of the HUD for this threshold were 72.7% 100%, 100%, and 91.2%, respectively. AI-based LVEF < 50% was associated with worse composite endpoints; unadjusted OR = 11.11 (95% CI 2.25-54.94), p = 0.003; adjusted OR = 6.40 (95% CI 1.07-38.09, p = 0.041). An AI-based algorithm incorporated into an HUD can be utilized reliably as a decision support tool for automatic real-time LVEF assessment among COVID-19 patients and may identify patients at risk for unfavorable outcomes. Future larger cohorts should verify the association with outcomes.

Coronavirus disease 2019 (COVID-19) has been declared a new pandemic in March 2020. Although most patients are asymptomatic, those with underlying cardiovascular comorbidities may develop a more severe systemic infection which is often associated with fatal pneumonia. Nonetheless, neurological and cardiovascular manifestations could be present even without respiratory symptoms. To date, no COVID-19-specific drugs are able for preventing or treating the infection and generally, the symptoms are relieved with general anti-inflammatory drugs. Angiotensin-converting-enzyme 2 (ACE2) may function as the receptor for virus entry within the cells favoring the progression of infection in the organism. On the other hand, ACE2 is a relevant enzyme in renin angiotensin system (RAS) cascade fostering Ang1-7/Mas receptor activation which promotes protective effects in neurological and cardiovascular systems. It is known that RAS is composed by two functional countervailing axes the ACE/AngII/AT1 receptor and the ACE/AngII/AT2 receptor which counteracts the actions mediated by AngII/AT1 receptor by inducing anti-inflammatory, antioxidant and anti-growth functions. Subsequently an "alternative" ACE2/Ang1-7/Mas receptor axis has been described with functions similar to the latter protective arm. Here, we discuss the neurological and cardiovascular effects of COVID-19 highlighting the role of the stimulation of the RAS "alternative" protective arm in attenuating pulmonary, cerebral and cardiovascular damages. In conclusion, only two clinical trials are running for Mas receptor agonists but few other molecules are in preclinical phase and if successful these drugs might represent a successful strategy for the treatment of the acute phase of COVID-19 infection.

SARS-CoV-2 infection is associated with myocardial inflammation, new onset cardiomyopathy, and arrhythmias. Here, we describe the utilization of POCUS and management of concurrent new onset atrial tachycardia and heart failure with reduced ejection fraction (HfrEF) in a patient with SARS-CoV-2 infection.

An 80-year-old female with multiple medical problems presented with sudden onset of shortness of breath and cough. She tested positive for SARS-CoV-2. Initially, she was hypoxic on room air and her heart rhythm was sinus tachycardia. CT angiogram of the chest showed consolidation, pleural effusion, and absence of pulmonary embolism. Because of persistent tachycardia, repeat EKGs and POCUS were performed. Subsequent EKGs showed intermittent atrial tachycardia and sinus tachycardia. Initially, home beta blockers were continued on admission, and additional dosages were considered for rate control, but Cardiac POCUS revealed HfrEF and was subsequently confirmed by comprehensive cardiac echocardiogram, consistent with SARS-CoV-2 infection-related cardiomyopathy. Beta blockers were discontinued, and treatment with amiodarone and furosemide showed improvement in symptoms. The patient was discharged with oral amiodarone and supplemental oxygen. Additionally, once the patient's hemodynamics improved, oral carvedilol was also started as part of GDMT for HfrEF. Follow-up echocardiogram 4 months later showed recovery of systolic EF to 60%.

It is essential to consider new onset HFrEF in the evaluation and management of new onset tachyarrhythmias since IV fluids and AV nodal blocking agents can be harmful in decompensated HFrEF. With the advent of POCUS, HFrEF can be quickly identified, and therapy can be tailored to that diagnosis.

The COVID-19 pandemic has impacted the world that was not previously conceivable. In early 2020, hospitals on all continents were overwhelmed with patients afflicted with this novel virus, with unanticipated mortality worldwide. The virus has had a deleterious effect, particularly the respiratory and cardiovascular systems. Cardiovascular biomarkers demonstrated an array of cardiovascular insults from hypoxia to inflammatory and perfusion abnormalities of the myocardium to life-threatening arrhythmias and heart failure. Patients were at increased risk of a pro-thrombotic state early in the course of the disease. Cardiovascular imaging became a primary tool in diagnosing, prognosing and risk-stratifying patients. Transthoracic echocardiography became the initial imaging modality in management of cardiovascular implications. In addition to cardiac function, LV longitudinal strain (LVLS) and right ventricular free wall strain (RVFWS) were indicators of increased morbidly and mortality. Cardiac MRI has become the diagnostic cardiovascular imaging for myocardial injury and tissue evaluation in the age of COVID-19.

The COVID-19 pandemic has evolved since the publication of the initial American Society of Echocardiography (ASE) statements providing guidance to echocardiography laboratories. In light of new developments, the ASE convened a diverse, expert writing group to address the current state of the COVID-19 pandemic and to apply lessons learned to echocardiography laboratory operations in future pandemics. This statement addresses important areas specifically impacted by the current and future pandemics: (1) indications for echocardiography, (2) application of echocardiographic services in a pandemic, (3) infection/transmission mitigation strategies, (4) role of cardiac point-of-care ultrasound/critical care echocardiography, and (5) training in echocardiography.