COVID-19 from a cardiovascular perspective / COVID-19 desde una perspectiva cardiovascular

Currently, myocardial injury has been reported in patients hospitalized with coronavirus disease 2019 (COVID-19). The studies also show a correlation between cardiac events and severe forms of the disease. COVID-19 begins with an early infection phase in which the virus infiltrates the lung parenchyma and proliferates. It then progresses to the pulmonary phase, where the initial inflammatory process, characterized by vasodilation, vascular permeability, and leukocyte recruitment, leads to lung damage, hypoxemia, and cardiovascular stress. The renin angiotensin aldosterone system is important in the pathophysiology of severe acute respiratory syndrome coronavirus 2 infection and in the propagation of systemic inflammation. Within this system, the pathway mediated by angiotensin-converting enzyme 2 (ACE2) produces vasodilation, cardioprotection, anti-oxidation, and anti-inflammation. Furthermore, the free form of ECA2 prevents binding of the virus to host cells and reduces its damage to the lung.

Actualmente, se ha reportado injuria miocárdica en pacientes hospitalizados por enfermedad por coronavirus 2019 (COVID-19). Los estudios, además, demuestran una correlación entre los eventos cardiacos y formas severas de la enfermedad. La COVID-19 comienza con una fase de infección temprana en la que el virus infiltra el parénquima pulmonar y prolifera. Luego progresa a la fase pulmonar, donde el proceso inflamatorio inicial, caracterizado por vasodilatación, permeabilidad vascular y reclutamiento de leucocitos, lleva a daño pulmonar, hipoxemia y estrés cardiovascular. El sistema renina angiotensina aldosterona es importante en la fisiopatología de la infección por el coronavirus 2 del síndrome respiratorio agudo grave y en la propagación de la inflamación sistémica. Dentro de este sistema, la vía mediada por la enzima convertidora de angiotensina 2 (ECA2) produce vasodilatación, cardioprotección, antioxidación y antiinflamación. Además, la forma libre de la ECA2 previene la unión del virus a las células huésped y reduce su daño al pulmón.

Human cardiac organoids to model COVID-19 cytokine storm induced cardiac injuries.

Acute cardiac injuries occur in 20%-25% of hospitalized COVID-19 patients. Herein, we demonstrate that human cardiac organoids (hCOs) are a viable platform to model the cardiac injuries caused by COVID-19 hyperinflammation. As IL-1ß is an upstream cytokine and a core COVID-19 signature cytokine, it was used to stimulate hCOs to induce the release of a milieu of proinflammatory cytokines that mirror the profile of COVID-19 cytokine storm. The IL-1ß treated hCOs recapitulated transcriptomic, structural, and functional signatures of COVID-19 hearts. The comparison of IL-1ß treated hCOs with cardiac tissue from COVID-19 autopsies illustrated the critical roles of hyper-inflammation in COVID-19 cardiac insults and indicated the cardioprotective effects of endothelium. The IL-1ß treated hCOs thus provide a defined and robust model to assess the efficacy and potential side effects of immunomodulatory drugs, as well as the reversibility of COVID-19 cardiac injuries at baseline and simulated exercise conditions.

Evaluation of cardiac injury with biomarkers and echocardiography after COVID-19 infection.

Coronavirus disease 2019 (COVID-19) causes cardiovascular damage in the acute period. Knowledge regarding cardiovascular damage after COVID-19 infection and during longer-term follow-up is currently limited. In our study, we aimed to compare cardiac and inflammatory markers and echocardiographic parameters between patients who had recovered from COVID-19 and control group. A total of 224 individuals were included, comprising 126 patients with a history of COVID-19 and 98 healthy controls. The demographic characteristics of the two groups were similar. Complete blood count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), N-terminal pro-B type natriuretic peptide (NT-ProBNP), D-dimer, haemoglobin A1C, troponin T and creatine kinase myocardial band (CK-MB) levels were compared between both groups. The mean follow-up period of the COVID-19 group was 58.39 ± 39.1 days (range:10 - 180 days post-COVID-19). Red cell distribution width (RDW), ESR, CRP, NT-ProBNP, D-dimer and troponin T values were significantly higher in the COVID-19 group compared to the control group. Left ventricular ejection fraction (LVEF) was significantly lower in the COVID-19 group. Left ventricular diastolic diameter (LVDD) and incidence of pericardial effusion were higher in the COVID-19 group. For multivariate analysis, possible factors identified by univariate analysis were subjected to multivariate logistic regression analysis to determine independent predictors of COVID-19. Among these factors, RDW, CRP and LVEF were independently higher in the COVID-19 group than in the control group. We conclude that although the clinical and prognostic significance of cardiac and other inflammatory markers in the acute phase of COVID-19 is known, we found that these biomarkers and echocardiography parameters can also be used in the follow-up of cardiac injury for a mid-term period post-infection.

Acute Myocardial Injury Assessed by High-Sensitive Cardiac Troponin Predicting Severe Outcomes and Death in Hospitalized Patients with COVID-19 Infection.

BACKGROUND: Cardiac injury has been linked to a poor prognosis during COVID-19 disease. Nevertheless, the risk factors associated are yet to be thoroughly investigated. OBJECTIVES: We sought to compare demographical characteristics and in-hospital outcomes in patients infected by the SARS-CoV-2 with and without cardiac injury, to further investigate the prevalence of acute cardiac injury as well as its impact on their outcomes in COVID-19-patients. METHODS: We included in a retrospective analysis, all COVID-19 patients admitted between October first and December first, 2020, at the University Hospital Center of Oujda (Morocco) who underwent a troponin assay which was systematically measured on admission. The study population was divided into two groups: cardiac-injured patients and those without cardiac injury. Clinical, biological data and in-hospital outcomes were compared between the two groups. RESULTS: 298 confirmed COVID-19 cases were included. Our study found that compared to non-cardiac-injured, cardiac-injured patients are older, with higher possibilities of existing comorbidities including hypertension (68 [42.2%] vs 40 [29.2%], P = 0.02), diabetes (81 [50.3%] vs 53 [38.7%] P = 0.044), the need for mechanical ventilation, ICU admission and mortality. A Cox proportional hazards regression analysis shows a significantly increased risk of death among cardiac-injured COVID-19-patients as compared to non-cardiac injured. (HR, 1.620 [CI 95%: 2.562-1.024]). CONCLUSION: Our retrospective cohort found that old age, comorbidities, a previous history of CAD, were significantly associated with acute cardiac injury. COVID-19 patients with acute cardiac injury are at a higher risk of ICU admission, and death.

De-novo development of fragmented QRS during a six-month follow-up period in patients with COVID-19 disease and its cardiac effects.

OBJECTIVE: The aim of this study is to examine the probability of de-novo fQRS in patients with mild COVID-19 disease, as an indicator of cardiac injury. METHODS: Data of 256 patients with normal admission electrocardiography and no comorbidities between 1.12.2020-31.12.2021, were examined retrospectively 6-month after mild COVID-19 disease. Patients were divided into two groups: fQRS+ group (n = 102) and non-fQRS group (n = 154). Relation between fQRS and other electrocardiography, echocardiographic and laboratory findings were investigated. RESULTS: No significant difference was found between the groups among age and gender. Troponin-I and creatine kinase myocardial band values (retrospectively 9.10 ± 1.76 vs 0.74 ± 1.43, 34.05 ± 82.20 vs. 14.68 ± 4.42), COVID-19 IgG levels (45.78 ± 14.82 vs. 36.49 ± 17.68), diastolic dysfunction (39.21% vs. 15.07%), EF value (58.02 ± 1.95 vs. 64.27 ± 3.07), dyspnea (41.17% vs. 6.84%), post-COVID-19 tachycardia syndrome (19.6% vs. 2.74) were more frequent in fQRS+ group compared to non-fQRS group. The EF value was lower in the presence of fQRS in the high lateral leads (57.12 ± 1.99, 58.47 ± 1.79, p:0.018). There was a positive correlation between IgG value and endsystolic diameter, septum thickness and left atrium diameter. In multivariate analysis de-novo fQRS, dyspnea, high troponin and IgG values, diastolic dysfunction, low EF value and left atrial diameter were determined as independent risk factors for post-COVID-19 tachycardia syndrome in follow-up. CONCLUSION: In COVID-19 disease de-novo fQRS, dyspnea, high IgG and troponin value, left atrial diameter, lower EF value, diastolic dysfunction were associated with post-COVID-19 tachycardia syndrome. The de-novo fQRS in SARS-COV-2 may be a predictor of future more important adverse cardiovascular outcomes and this should alert clinicians.

Role of a lower cutoff of high sensitivity troponin I in identification of early cardiac damage in non-severe patients with COVID-19.

Cardiac damage in non-severe patients with coronavirus disease 2019 (COVID-19) is poorly explored. This study aimed to explore the manifestations of cardiac damage at presentation in non-severe patients with COVID-19. In this study, 113 non-severe patients with COVID-19 were grouped according to the duration from symptoms onset to hospital admission: group 1 (≤ 1 week, n = 27), group 2 (> 1 to 2 weeks, n = 28), group 3 (> 2 to 3 weeks, n = 27), group 4 (> 3 weeks, n = 31). Clinical, cardiovascular, and radiological data on hospital admission were compared across the four groups. The level of high sensitivity troponin I (hs-cTnI) in group 2 [10.25 (IQR 6.75-15.63) ng/L] was significantly higher than those in group 1 [1.90 (IQR 1.90-8.80) ng/L] and group 4 [1.90 (IQR 1.90-5.80) ng/L] (all Pbonferroni < 0.05). The proportion of patients who had a level of hs-cTnI ≥ 5 ng/L in group 2 (85.71%) was significantly higher than those in the other three groups (37.04%, 51.85%, and 25.81%, respectively) (all Pbonferroni < 0.05). Compared with patients with hs-cTnI under 5 ng/L, those with hs-cTnI ≥ 5 ng/L had lower lymphocyte count (P = 0.000) and SpO2 (P = 0.002) and higher CRP (P = 0.000). Patients with hs-cTnI ≥ 5 ng/L had a higher incidence of bilateral pneumonia (P = 0.000) and longer hospital length of stay (P = 0.000). In conclusion, non-severe patients with COVID-19 in the second week after symptoms onset were most likely to suffer cardiac damage. A detectable level of hs-cTnI ≥ 5 ng/L might be a manifestation of early cardiac damage in the patients.

Cardiac Dysfunction and Arrhythmias 3 Months After Hospitalization for COVID-19.

Background The extent of cardiac dysfunction post-COVID-19 varies, and there is a lack of data on arrhythmic burden. Methods and Results This was a combined multicenter prospective cohort study and cross-sectional case-control study. Cardiac function assessed by echocardiography in patients with COVID-19 3 to 4 months after hospital discharge was compared with matched controls. The 24-hour ECGs were recorded in patients with COVID-19. A total of 204 patients with COVID-19 consented to participate (mean age, 58.5 years; 44% women), and 204 controls were included (mean age, 58.4 years; 44% women). Patients with COVID-19 had worse right ventricle free wall longitudinal strain (adjusted estimated mean difference, 1.5 percentage points; 95% CI, -2.6 to -0.5; P=0.005) and lower tricuspid annular plane systolic excursion (-0.10 cm; 95% CI, -0.14 to -0.05; P<0.001) and cardiac index (-0.26 L/min per m2; 95% CI, -0.40 to -0.12; P<0.001), but slightly better left ventricle global strain (-0.8 percentage points; 95% CI, 0.2-1.3; P=0.008) compared with controls. Reduced diastolic function was twice as common compared with controls (60 [30%] versus 29 [15%], respectively; odds ratio, 2.4; P=0.001). Having dyspnea or fatigue were not associated with cardiac function. Right ventricle free wall longitudinal strain was worse after intensive care treatment. Arrhythmias were found in 27% of the patients, mainly premature ventricular contractions and nonsustained ventricular tachycardia (18% and 5%, respectively). Conclusions At 3 months after hospital discharge with COVID-19, right ventricular function was mildly impaired, and diastolic dysfunction was twice as common compared with controls. There was little evidence for an association between cardiac function and intensive care treatment, dyspnea, or fatigue. Ventricular arrhythmias were common, but the clinical importance is unknown. Registration URL: http://clinicaltrials.gov. Unique Identifier: NCT04535154.

ECG pathology and its association with death in critically ill COVID-19 patients, a cohort study.

BACKGROUND: We investigated the prevalence of ECG abnormalities and their association with mortality, organ dysfunction and cardiac biomarkers in a cohort of COVID-19 patients admitted to the intensive care unit (ICU). METHODS: This cohort study included patients with COVID-19 admitted to the ICU of a tertiary hospital in Sweden. ECG, clinical data and laboratory findings during ICU stay were extracted from medical records and ECGs obtained near ICU admission were reviewed by two independent physicians. RESULTS: Eighty patients had an acceptable ECG near ICU-admission. In the entire cohort 30-day mortality was 28%. Compared to patients with normal ECG, among whom 30-day mortality was 16%, patients with ECG fulfilling criteria for prior myocardial infarction had higher mortality, 63%, odds ratio (OR) 9.61 (95% confidence interval (CI) 2.02-55.6) adjusted for Simplified Acute Physiology Score 3 and patients with ST-T abnormalities had 50% mortality and OR 6.05 (95% CI 1.82-21.3) in univariable analysis. Both prior myocardial infarction pattern and ST-T pathology were associated with need for vasoactive treatment and higher peak plasma levels of troponin-I, NT-pro-BNP (N-terminal pro-Brain Natriuretic Peptide), and lactate during ICU stay compared to patients with normal ECG. CONCLUSION: ECG with prior myocardial infarction pattern or acute ST-T pathology at ICU admission is associated with death, need for vasoactive treatment and higher levels of biomarkers of cardiac damage and strain in severely ill COVID-19 patients, and should alert clinicians to a poor prognosis.

Myocardial injury in patients with SARS-CoV-2 pneumonia: Pivotal role of inflammation in COVID-19.

AIMS: Infection by SARS-CoV-2 may result in a systemic disease and a proportion of patients ranging 15%-44% experienced cardiac injury (CI) diagnosed by abnormal troponin levels. The aim of the present study was to analyse the clinical characteristics of a large series of hospitalized patients for COVID-19 in order to identify predisposing and/or protective factors of CI and the outcome. METHODS AND RESULTS: This is an observational, retrospective study on patients hospitalized in two Italian centres (San Raffaele Hospital and Cremona Hospital) for COVID-19 and at least one high-sensitivity cardiac troponin (hs-cTnt) measurement during hospitalization. CI was defined if at least one hs-cTnt value was above the 99th percentile. The primary end-point was the occurrence of CI during hospitalization. We included 750 patients (median age 67, IQR 56-77 years; 69% males), of whom 46.9% had history of hypertension, 14.7% of chronic coronary disease and 22.3% of chronic kidney disease (CKD). Abnormal troponin levels (median troponin 74, IQR 34-147 ng/l) were detected in 390 patients (52%) during the hospitalization. At multivariable analysis age, CKD, cancer, C-reactive protein (CRP) levels were independently associated with CI. Independent predictors of very high troponin levels were chronic kidney disease and CRP levels. Patients with CI showed higher rate of all-cause mortality (40.0% vs. 9.1%, p = 0.001) compared to those without CI. CONCLUSION: This large, multicentre Italian study confirmed the high prevalence of CI and its prognostic role in hospitalized patients with COVID-19, highlighting the leading role of systemic inflammation for the occurrence of CI.

Imaging Findings of COVID-19-Related Cardiovascular Complications.

Other than respiratory disease, patients with coronavirus disease 2019 (COVID-19) commonly have cardiovascular manifestations, which are recognized as significant risk factors for increased mortality. COVID-19 patients may present with a wide spectrum of clinical presentations ranging from asymptomatic heart disease detected incidentally by cardiac investigations (troponin, BNP, and imaging) to cardiogenic shock and sudden cardiac death. In this broad clinical course, advanced imaging plays an important role in the diagnosis of different patterns of myocardial injury, risk stratification of COVID-19 patients, and in detecting potential cardiac side effects of the current treatments and vaccines against the severe acute respiratory syndrome.

Cardiac manifestations of the coronavirus disease-19: a review of pathogenesis, clinical manifestations, diagnosis, and treatment.

The coronavirus disease-19 (COVID-19), first appearing in Wuhan, China, and later declared as a pandemic, has caused serious morbidity and mortality worldwide. Severe cases usually present with acute respiratory distress syndrome (ARDS), pneumonia, acute kidney injury (AKI), liver damage, or septic shock. However, with recent advances in severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) research, the virus´s effect on cardiac tissues has become evident. Reportedly, an increased number of COVID-19 patients manifested serious cardiac complications such as heart failure, increased troponin, and N-terminal pro-B-type natriuretic peptide levels (NT-proBNP), cardiomyopathies, and myocarditis. These cardiac complications initially present as chest tightness, chest pain, and heart palpitations. Diagnostic investigations such as telemetry, electrocardiogram (ECG), cardiac biomarkers (troponin, NT-proBNP), and inflammatory markers (D-dimer, fibrinogen, PT, PTT), must be performed according to the patient´s condition. The best available options for treatment are the provision of supportive care, anti-viral therapy, hemodynamic monitoring, IL-6 blockers, statins, thrombolytic, and anti-hypertensive drugs. Cardiovascular disease (CVD) healthcare workers should be well-informed about the evolving research regarding COVID-19 and approach as a multi-disciplinary team to devise effective strategies for challenging situations to reduce cardiac complications.

Cardiac biomarkers alterations in patients with SARS-CoV-2 infection.

Reliable biomarkers are necessary for the risk stratification of patients infected with SARS-CoV-2. This novel coronavirus is now established to affect several organs in addition to the lungs, most prominently the heart. This is achieved through direct damage to the myocardium and indirect immune-associated effects during the cytokine storm. We performed a literature review aiming to identify the prognostic value of alterations of cardiac biomarkers in SARS-CoV-2 infection. Cardiac biomarkers are significantly elevated in patients with severe COVID-19 and are independent predictors of mortality. High-sensitivity troponin I and T are correlated with multiple inflammatory indexes and poor outcomes. Although cut-off values have been established for most of cardiac biomarkers, lower limits for troponins may have better prognostic values and longitudinal monitoring of cardiac biomarkers can help the clinician assess the patient's course. Additional measurements of NT-proBNP, can detect the subgroup of patients with poor prognosis.

COVID-19 Severity: Lung-Heart Interplay.

In December 2019, a novel COVID-19 infection caused by SARS-CoV-2 has emerged as a global emergency. In a few months, the pathogen has infected millions of people in the world. Primarily SARS-CoV-2 infects the pulmonary system which ultimately leads to ARDS and lung failure. The majority of patients develop milder symptoms but the infection turns severe in a huge number of people, which ultimately results in enhanced mortality in COVID-19 patients. Co-morbid conditions, primarily cardiovascular complications and diabetes, have been reported to show a strong correlation with COVID-19 severity. Further, the onset of myocardial injury secondary to pulmonary damage has been observed in critically ill patients who have never reported heart-related ailments before. Due to drastic health risks associated with virus infection, the unprecedented disruption in normal business throughout the world has caused economic misery. Apparently, newer treatments are urgently needed to combat the virus particularly to reduce the severity burden. Therefore, understanding the crosstalk between lung and heart during COVID-19 might give us better clarity for early diagnosis followed by appropriate treatment in patients with the likelihood of developing severe symptoms. Accordingly, the present review highlights the potential mechanisms that may explain the crosstalk between lung and heart so that effective treatment/management strategies can be evolved swiftly in this direction.

Clinical outcomes in patients infected with different SARS-CoV-2 variants at one hospital during three phases of the COVID-19 epidemic in Marseille, France.

OBJECTIVES: To compare the demographics, clinical characteristics and severity of patients infected with nine different SARS-CoV-2 variants, during three phases of the COVID-19 epidemic in Marseille. METHODS: A single centre retrospective cohort study was conducted in 1760 patients infected with SARS-CoV-2 of Nextstrain clades 20A, 20B, and 20C (first phase, February-May 2020), Pangolin lineages B.1.177 (we named Marseille-2) and B.1.160 (Marseille-4) variants (second phase, June-December 2020), and B.1.1.7 (alpha), B.1.351 (beta), P.1 (gamma) and A.27 (Marseille-501) variants (third phase, January 2021-today). Outcomes were the occurrence of clinical failures, including hospitalisation, transfer to the intensive-care unit, and death. RESULTS: During each phase, no major differences were observed with regards to age and gender distribution, the prevalence of chronic diseases, and clinical symptoms between variants circulating in a given phase. The B.1.177 and B.1.160 variants were associated with more severe outcomes. Infections occurring during the second phase were associated with a higher rate of death as compared to infections during the first and third phases. Patients in the second phase were more likely to be hospitalised than those in the third phase. Patients infected during the third phase were more frequently obese than others. CONCLUSION: A large cohort study is recommended to evaluate the transmissibility and to better characterise the clinical severity of emerging variants.

Imaging of COVID-19: An update of current evidences.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been reported as a global emergency. As respiratory dysfunction is a major clinical presentation of COVID-19, chest computed tomography (CT) plays a central role in the diagnosis and management of patients with COVID-19. Recent advances in imaging approaches using artificial intelligence have been essential as a quantification and diagnostic tool to differentiate COVID-19 from other respiratory infectious diseases. Furthermore, cardiovascular involvement in patients with COVID-19 is not negligible and may result in rapid worsening of the disease and sudden death. Cardiac magnetic resonance imaging can accurately depict myocardial involvement in SARS-CoV-2 infection. This review summarizes the role of the radiology department in the management and the diagnosis of COVID-19, with a special emphasis on ultra-high-resolution CT findings, cardiovascular complications and the potential of artificial intelligence.

Novel effects of acute COVID-19 on cardiac mechanical function: Two case studies.

The spread of the novel coronavirus 2019 (COVID-19) has caused a global pandemic. The disease has spread rapidly, and research shows that COVID-19 can induce long-lasting cardiac damage. COVID-19 can result in elevated cardiac biomarkers indicative of acute cardiac injury, and research utilizing echocardiography has shown that there is mechanical dysfunction in these patients as well, especially when observing the isovolumic, systolic, and diastolic portions of the cardiac cycle. The purpose of this study was to present two case studies on COVID-19 positive patients who had their cardiac mechanical function assessed every day during the acute period to show that cardiac function in these patients was altered, and the damage occurring can change from day-to-day. Participant 1 showed compromised cardiac function in the systolic time, diastolic time, isovolumic time, and the calculated heart performance index (HPI), and these impairments were sustained even 23 days post-symptom onset. Furthermore, Participant 1 showed prolonged systolic periods that lasted longer than the diastolic periods, indicative of elevated pulmonary artery pressure. Participant 2 showed decreases in systole and consequently, increases in HPI during the 3 days post-symptom onset, and these changes returned to normal after day 4. These results showed that daily observation of cardiac function can provide detailed information about the overall mechanism by which cardiac dysfunction is occurring and that COVID-19 can induce cardiac damage in unique patterns and thus can be studied on a case-by-case basis, day-to-day during infection. This could allow us to move toward more personalized cardiovascular medical treatment.

Echocardiography in suspected coronavirus infection: indications, limitations and impact on clinical management.

OBJECTIVES: To describe the use of echocardiography in patients hospitalised with suspected coronavirus infection and to assess its impact on clinical management. METHODS: We studied 79 adults from a prospective registry of inpatients with suspected coronavirus infection at a single academic centre. Echocardiographic indications included abnormal biomarkers, shock, cardiac symptoms, arrhythmia, worsening hypoxaemia or clinical deterioration. Study type (limited or complete) was assessed for each patient. The primary outcome measure was echocardiography-related change in clinical management, defined as intensive care transfer, medication changes, altered ventilation parameters or subsequent cardiac procedures within 24 hours of echocardiography. Coronavirus-positive versus coronavirus-negative patient groups were compared. The relationship between echocardiographic findings and coronavirus mortality was assessed. RESULTS: 56 patients were coronavirus-positive and 23 patients were coronavirus-negative with symptoms attributed to other diagnoses. Coronavirus-positive patients more often received limited echocardiograms (70% vs 26%, p=0.001). The echocardiographic indication for coronavirus-infected patients was frequently worsening hypoxaemia (43% vs 4%) versus chest pain, syncope or clinical heart failure (23% vs 44%). Echocardiography changed management less frequently in coronavirus-positive patients (18% vs 48%, p=0.01). Among coronavirus-positive patients, 14 of 56 (25.0%) died during hospitalisation. Those who died more often had echocardiography to evaluate clinical deterioration (71% vs 24%) and had elevated right ventricular systolic pressures (37 mm Hg vs 25 mm Hg), but other parameters were similar to survivors. CONCLUSIONS: Echocardiograms performed on hospitalised patients with coronavirus infection were often technically limited, and their findings altered patient management in a minority of patients.

Cardiac manifestations of COVID-19.

COVID-19 is a novel viral infection caused by severe acute respiratory syndrome (SARS) beta-coronavirus. Epidemiological status changes dynamically as the pandemy is far from ending. Several complications of presented virus may be similar to those observed in other viral infections. Despite lacking data, the heart involvement may be comparable to cardiac complications observed previously in those with SARS as well as Middle East Respiratory Syndrome (MERS). In COVID-19 we observe elevated levels of cardiac biomarkers, such as natriuretic peptides, troponins, myoglobin, C-reactive protein (CRP), interleukin-2 (IL-2), interleukin-6 (IL-6) and ferritin, which is likely the result of myocardial injury. The possible mechanisms of cardiovascular injury include direct toxicity through the viral invasion of cardiac myocytes, ACE-2 receptor-mediated CV (cardiac and endothelial) injury, microvascular dysfunction and thrombosis and cytokine release syndrome (mainly IL-6 mediated). Cardiac manifestations of COVID-19 are focal or global myocardial inflammation, necrosis, ventricular dysfunction, heart failure and arrhythmia.