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Background/Introduction: The impact of COVID-19 goes beyond its acute form, and can lead to the persistence of symptoms and the emergence of systemic disorders, defined as Post-Covid or Long-Covid. Purpose(s): Assess the late impact on the cardiorespiratory system of patients recovered from severe Covid. Method(s): We performed cross-sectional study that included patients over 18 years of age who recovered from the severe form of COVID-19 after at least 60 days of their discharge. Patients and healthy controls were enrolled to perform transthoracic echocardiography (TTE) and cardiopulmonary exercise testing (CPET). Result(s): A total of 52 patients and 24 controls were enrolled. The standard TTE parameters (end diastolic diameters, left ventricular ejection fraction, diastolic function and right ventricular systolic function) showed no difference when compared to the control group. When analyzing the myocardial work, there was a higher Wasted MW (GWW): 135 mmHg% vs 84.5 mmHg% (p=0.002), with lower MW Efficiency (GWE): 94 vs. 96 (p=0.003);as well as lower values of global strain: Cases = 18.6% vs. 20.1% (p=0.009). No differences were found in the Constructive MW (GWC) and MW Global Index (GWI). In the CPET data we found lower peak values for the VO2: 24 ml/kg/min vs. 32.75 ml/kg/min (p<0.001);for the Heart Rate: 162 bpm vs. 175 bpm (p<0.001);for the Ventilation: 79.3 L/min vs. 109.85 L/min (p<0.001) and Respiratory Exchange Ratio: 1.12 vs. 1.19 (p=0.004). There was no difference in the maximum load reached, neither in the oxygen pulse values and in the Ve/CO2 slope. In relation to the oxygen kinetics, there was a significant reduction in OUES%: 85% vs. 98% (p=0.03);as well as an extended T1/4: 112 s vs. 88.5 s (p<0.001);and a slowing of the fall in heart rate in recovery time, as measured by the Heart Rate decay: -17.32 bpm vs. -22.08 bpm (p=0.005). Conclusion(s): Patients recovered from the severe form of COVID-19 had higherGWWwith lower efficiency (GWE). Such findings, added to changes in oxygen kinetics during exercise, may point to a possible cardiocirculatory mechanism associated with decreased aerobic capacity.
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Background: Long COVID emerged as a new condition, following the acute episode of coronavirus disease 2019 (COVID-19),exerting a significant impact on patients' quality of life [1]. Several studies involving COVID- 19 survivors emphasized the presence of cardiac abnormalities following the acute infection. However, data on possible mechanisms associated to long COVID remain limited. Clinical applications of myocardial work (MW) analysis, assessed by transthoracic echocardiography (TTE) have expended recently, showing an additional value in detecting cardiac dysfunction compared to standard parameters such as left ventricle ejection fraction (LVEF) or global longitudinal strain (GLS) in various pathologies, including COVID-19 [2]. Nevertheless, its potential role in detecting subclinical cardiac dysfunction in long COVID remained unexplored. Purpose(s): We assessed the association between subclinical cardiac dysfunction evaluated by global work index (GWI) and global constructive work (GCW) and long COVID. Method(s): We included 310 COVID-19 patients hospitalized between March and April 2020. All patients were invited to a systematic one-year follow-up, including clinical evaluation, TTE with MW assessment, chestcomputed tomography and spirometry. 140 patients completed the followup. Normal values for GWI and GCW were defined as 1926+/-247 mmHg% and 2224+/-229 mmHg% [3]. The primary endpoint was long COVID, characterized by a cluster of symptoms such as fatigue or dyspnea more than 3 months after the acute infection, without any other explanation. Result(s): 140 patients (57.1+/-13.9 years, 90 (64.3%) males) had a mean follow-up of 337.1+/-34.5 days.The mean values of LVEF, GWI and GCW were 55.2+/-3.2%, 2105.9+/-403.3 mmHg% and 2377.8+/-446.2 mmHg%. 83 (61%) patients had long COVID. No significant differences in terms of comorbidities, clinical evaluation and COVID-19 severity were found between patients with and without long COVID. GCW (2276.7+/-410.3 vs 2516.5+/-458.6, p=0.006) and GWI (2008.5+/-358.9 vs 2242.2+/-427.0, p=0.003) were the only TTE parameters different between patients with and without long COVID. Multivariable regression analysis showed that GWI <1926 mmHg% (OR 6.095;CI: 2.024-18.355, p=0.001) and GCW <2224 mmHg% (OR 3.205;CI: 1.181-8.694, p=0.022) were the only MW parameters independently associated with long COVID, irrespective of age or the severity of the acute infection, at one year. In a subgroup analysis of 77 patients without previous cardiovascular diseases, long COVID was diagnosed in 45 (58.4%)patients. GWI <1926 mmHg% (OR 8.015;CI: 2.149-29.887, p=0.002) remained independently associated with long COVID at 1 year follow-up. Conclusion(s): Long COVID, frequently observed in recovered COVID-19 patients may indicate the presence of subclinical cardiac dysfunction, reflected by a decrease of the left ventricle performance, assessed by GWI and GCW.Long-term follow-up including cardiac screening should be performed in order to identify patients at risk who would benefit from cardiac rehabilitation programs.
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Introduction: COVID-19 infection has been associated with acute myocardial dysfunction. However, long-term effects of myocardial injury during COVID-19 infection are not well characterized. Novel speckle tracking echocardiography (STE) may lend further insights into COVID-19 myocardial dysfunction. Method(s): Patients hospitalized with acute COVID-19 infection from March 2020 to September 2021 who underwent STE and had evidence of myocardial dysfunction (defined as left ventricular ejection fraction (LVEF) less than 55% and/or global longitudinal strain (GLS) less negative than -18%) were enrolled in follow-up 3-12 months after hospitalization. Clinical and laboratory data were collected, and follow-up STE was performed, including LVEF, GLS, myocardial work index (MWI) and myocardial work efficiency (MWE) measurements. Statistical analysis was performed to determine risk factors for worsening myocardial dysfunction at follow-up. Result(s): Twenty-four patients were enrolled at an average 239+/-102 days after the initial hospitalization echocardiogram: 13 (54%) male, 14 (58%) Black, and average age 56+/-14 years. Average duration of initial admission was 24+/-25 days;14 patients (58%) were admitted to the intensive care unit. Ten (42%) patients had acute respiratory distress syndrome, 1 (4%) had ST-elevation myocardial infarction and 1 (4%) had cardiac arrest. Eleven (46%) patients required mechanical ventilation and 2 (8%) required extracorporeal membrane oxygenation. Five (21%) patients had elevated troponin on admission and average peak troponin was 1.35+/-3.83 ng/ml. Follow-up STE showed significant improvement in average GLS (-13.7+/-3.2% vs -16.0+/-3.7%, P=0.03). There were no significant changes in average LVEF (55.9+/-12.6% vs 55.5+/-8.8%, P=0.90), MWI (1519+/-425 vs 1681+/-412, P=0.24) and MWE (93+/-4 vs 92+/-4, P=0.65) at follow-up compared to during COVID-19 infection. Patients with lower LVEF at follow-up as compared to acute infection (n=11, 46%) were more likely to have had longer duration of symptoms prior to initial presentation (11+/-5 days vs 6+/-5 days, P=0.02) and higher peak erythrocyte sedimentation rate (94+/-30 mm/h vs 44+/-36 mm/h, P=0.007) compared to those with stable or improved LVEF. Conclusion(s): Approximately 8 months after COVID-19 infection, average GLS was significantly improved in patients with myocardial dysfunction during acute COVID-19 infection. Close follow-up is recommended for patients with evidence of myocardial injury during COVID-19 infection, especially those who present with prolonged symptoms and those with high inflammatory markers.Copyright © 2022
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Background/Introduction: Clinical applications of myocardial work(MW) analysis have expended recently, showing an additional value in detecting cardiac dysfunction compared to standard echocardiographic parameters such as left ventricle ejection fraction(LVEF) or global longitudinal strain(GLS). Nevertheless, its role in detecting subclinical cardiac dysfunction in long COVID remained unexplored. Purpose(s): We assessed the association between subclinical cardiac dysfunction evaluated by MW and long COVID. Method(s): All COVID-19 discharged patients were invited to a systematic one-year follow-up, including clinical evaluation, echocardiography, chest-computed tomography and spirometry. Normal values for global work index(GWI) and global constructive work(GCW) were defined as 1926 +/-247mmHg% and 2224+/-229mmHg%. The primary endpoint was long COVID, characterized by a cluster of symptoms (e.g. fatigue or dyspnea) more than 3 months after the acute infection, without any other explanation. Result(s): 140 patients(57.1 +/-13.9 years, 90(64.3%)males) had a mean follow-up of 337.1+/-34.5 days. The mean values of LVEF, GWI and GCW were 55.2+/-3.2%,2105.9+/-403.3mmHg% and 2377.8 +/-446.2mmHg%. 83(61%)patients had long COVID. No significant differences in terms of comorbidities or COVID-19 severity were found between groups.GCW(2276.7 +/-410.3 vs 2516.5+/-458.6, p=0.006) and GWI(2008.5+/-358.9 vs 2242.2+/-427.0, p=0.003) were significantly different between patients with and without long COVID. Additionally, GWI <1926mmHg%(OR 6.095 CI2.024-18.355, p=0.001) and GCW <2224mmHg%(OR 3.205, CI 1.181-8.694, p=0.022) were the only MW parameters associated with long COVID, irrespective of age or the disease severity, at one-year. In a subgroup analysis of 77 patients without cardiovascular diseases, long COVID was diagnosed in 45(58.4%)patients. GWI <1926mmHg%(OR 8.015, CI 2.149-29.887, p=0.002)remained independently associated with the primary endpoint. Conclusion(s): Long COVID may indicate the presence of subclinical cardiac dysfunction, reflected by a decrease of the cardiac performance, assessed by MW. Long-term follow-up including cardiac screening should be performed in order to identify patients at risk who would benefit from cardiac rehabilitation programs.
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Aims: SARS-CoV-2 infection may lead to endothelial and vascular dysfunction. We investigated alterations of arterial stiffness, endothelial coronary and myocardial function markers four months after COVID-19 infection. Methods: In a case-control prospective study, we included 100 patients four months after COVID-19 infection, 50 age- and sex-matched healthy individuals. We measured a) pulse wave velocity (PWV), b) flow-mediated dilation (FMD) of brachial artery, c) coronary Flow Reserve (CFR) by Doppler echocardiography d) left ventricular (LV) global longitudinal strain (GLS), e) left ventricular myocardial work index, constructive work, wasted work and work efficiency and e) von-Willenbrand factor and thrombomodulin as endothelial biomarkers. Results: COVID-19 patients had lower CFR and FMD values than controls (2.39 ± 0.39 vs 3.31 ± 0.59, p = 0.0122, 5.12 ± 2.95% vs 8.12 ± 2.23%, p = 0.006 respectively). Compared to controls, COVID-19 patients had higher PWV (PWVc-f 12.32 ± 2.44 vs 10.11 ± 1.85 m/sec, p = 0.033) and impaired LV GLS (-19.11 ± 2.14% vs -20.41 ± 1.61%, p = 0.001). Compared to controls, COVID-19 patients had higher myocardial work index, and wasted work (2067.7 ± 325.9 mmHg% vs 1929.4 ± 312.7 mmHg%, p = 0.026, 104.6 ± 58.9 mmHg% vs 75.1 ± 52.6 mmHg%, p = 0.008, respectively), while myocardial efficiency was lower (94.8 ± 2.5% vs 96.06 ± 2.3%, p = 0.008). and thrombomodulin were higher in COVID-19 patients than controls (3716.63 ± 188.36 vs 2590.02 ± 156.51pg/ml, p < 0.001). MDA was higher in COVID-19 patients than controls (10.55 ± 2.45 vs 1.01 ± 0.50 nmole/L, p = 0.001). Residual cardiovascular symptoms at 4 months were associated with oxidative stress markers. Myocardial work efficiency was related with PWV (F=-0.309, p = 0.016) and vWillenbrand (F=-0.541, p = 0.037). Myocardial wasted work was related with PWV (F = 0.255, p = 0.047) and vWillenbrand (F = 0.610, p = 0.016). Conclusions: SARS-CoV-2 may cause vascular dysfunction, followed by a waste of cardiac work, in order to compensate for increased arterial stiffness 4 months after infection.
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Introduction: Coronavirus disease 2019 (COVID-19) impacted healthcare systems worldwide, evolving into a global pandemic(1,2). Recent studies showed the presence of persistent exertional dyspnea or fatigue at one- to three-months follow-up after COVID-19(1,2). However, little is known regarding the mechanisms behind the possible cardiac-related symptoms post COVID-19 at mid- and long- term follow-up. Purpose: We investigated the presence of persistent dyspnea one year after the acute phase of COVID-19 in patients without previous cardiovascular or pulmonary disease. Secondly, we analyzed the potential subclinical cardiac dysfunction in these patients, assessed by echocardiography. Methods: 310 COVID-19 patients were prospectively included between March and April 2020. 143 patients continued the follow-up at 6 months and one year.Patients with a previous history of cardiovascular or respiratory disease were excluded from the analysis.The follow-up consisted in clinical evaluation, and spirometry at 6 and 12 months, chest computed tomography and comprehensive transthoracic echocardiography (TTE) including speckle tracking and myocardial work analysis at one-year follow-up. Results: 66 patients (mean age 49.64 ± 10.66 years, 37 (67.3%) males)were included in the final analysis.In these patients, TTE parameters were in the normal range, with a mean left ventricle ejection fraction of 56.98 ± 4.64%, mean global longitudinal strain (GLS) of -20.90 ± 2.37%, global constructive work (GCW) of 2381.45 ±463.68mmHg% and global work index (GWI) of 2132.49 ±419.22.Type 1 diastolic dysfunction was observed in 11(16.7%) patients.One (1.5%) patient had type 2 diastolic dysfunction. A normal respiratory pattern was reported in 31(47%) patients at 6 months spirometry evaluation, while 19(28.8%) patients presented pulmonary restriction patterns.23 (34.8%) patients reported exertional dyspnea at one year follow-up. No significant differences regarding clinical, laboratory or imaging findings at baseline were found between patients with and without dyspnea. TTE showed that GLS, GCW and GWI were different between symptomatic and asymptomatic patients (-19.97 ± 2.14 vs. -20.90 ± 2.37, p = 0.039;2183.14 ± 2483.14 ± 422.42, p = 0.024;1960.06 ± 396.21 vs 2221.17 ± 407.99, p = 0.030).(Figure 1) Multivariable analysis showed that GCW, GWI and normal respiratory pattern at 6 months were inversely associated with persistent dyspnea (p = 0.038, OR 0.998, 95% CI 0.996-1.000;p = 0.042, OR 0.998, 95% CI 0.996-1.000;p = 0.020, OR 0.195, 95% CI 0.049-0.773, respectively).(Figure.2) Conclusion: Persistent exertional dyspnea one year after COVID-19 infection was present in more than a third of apparently healthy patients. GCW and GWI were independently associated with symptoms, suggesting a decrease in myocardial performance in this population. Further studies should focus on the long-term evolution of COVID-19 patients and the occurrence of possible cardiac consequences.
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Background: Multisystem inflammatory syndrome in children (MIS-C) is a hyperinflammatory syndrome after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Cardiovascular complications include left ventricular dysfunction and coronary artery abnormalities (CAA). Little is known, however, about the interaction between LV function and CAA. We aimed to assess the hypothesis that increased coronary artery size is inversely correlated with LV function utilizing left ventricular ejection fraction (LVEF) and indices of myocardial work. Methods: Two-dimensional and speckle-tracking echocardiograms were performed in 34 MIS-C patients at admission. Biplane LVEF and coronary artery Z scores were measured, and pressurestrain loops were used to calculate indices of myocardial work: global work index (GWI), global work efficiency (GWE), global wasted work (GWW), global constructive work (GCW), and global longitudinal strain (GS). Treating coronary artery Z-scores as a continuous variable, correlation analysis was performed. Results: LVEF and left anterior descending artery (LAD) Z-scores were inversely correlated (Spearman coefficient of -0.47;P=0.005). Both GWI and GCW demonstrated an inverse relationship with increasing LAD Z-scores, but both were not statistically significant (Spearman coefficient -0.21;P=0.239 and Spearman coefficient -0.21;P=0.235). GS also exhibited a trend of worsening (less negative scores) with increasing LAD Z-scores but was not statistically significant (Spearman coefficient 0.29;P=0.095). GWE and GWW did not correlate with any coronary artery Z-scores and left main coronary or right coronary artery Z-scores did not correlate with any markers of function. Conclusion: Increasing LAD Z-score showed a statistically significant association with decreased LVEF. Additionally, while not statistically significant, GWI, GCW, and GS all demonstrated a trend of decreased indices of myocardial work as LAD Z-score increases. In conclusion, this data suggests that patients with higher coronary artery Z-scores at admission are at increased risk of myocardial dysfunction.
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Background and objectives: Despite myocardial injury being related to excess mortality in acute COVID-19 infection, its impact on imaging findings remains unclear. This study aimed to characterize transthoracic echocardiographic (TTE) findings in patients admitted with COVID-19 infections and its impact on management and prognosis. Methods: A prospective observational cohort study was performed among 66 COVID-19 patients who were admitted to a tertiary center between March 1 and May 25, 2020 and underwent TTE. High-sensitivity troponin I (hs-cTnI) data, echocardiographic assessment of right and left ventricular (LV) functional parameters, strain, and myocardial work analysis were obtained. Results: 2025 patients were admitted with COVID-19 and in 200 a complete TTE study was performed. Due to poor image quality, only 66 studies were included in the final analysis. The median age was 62 years (IQR, 55-70) and 59.1% of patients were males. The most common comorbidity was hypertension (47%), followed by smoking history (30.3%), atrial fibrillation (9.1%), and chronic obstructive pulmonary disease (7.9%). More than half of the patients (39, 59%) were admitted to the ICU, and half of them (33, 50%) required invasive mechanical ventilation. TTE was mainly indicated because of concerns for systemic conditions (50%) and evaluation of hemodynamic assessment (30%). Thirty-six patients (54.5%) had an abnormal TTE result and 57% had elevated hs-cTnI levels. The most common cardiac abnormality was LV diastolic dysfunction in 33% of the patients, followed by right ventricular dysfunction (12%) and LV dysfunction (6%) (Figure 1). LV GLS was reduced in 48.5% of the cases. Myocardial work performance indices were all reduced in patients with an abnormal TTE (GWI 30%, GCW 30%, GWW 40%, and GWE 40%), although differences were not significant (P>0.2 for all parameters). Patients with an abnormal TTE were older and presented a higher cardiovascular risk profile. There were no significant differences in the levels of D-dimer, NTproBNP, and hs-cTnI between patients with and without diastolic dysfunction, RV, or LV dysfunction (P>0.3 for all parameters). Using Spearman rank correlation, there was an inverse relationship between hs-cTnI and LV strain and myocardial work analysis. TTE results impacted clinical management in 60 patients, mainly de-escalation of medical treatment (Figure 2). Abnormal TTE results did not impact in-hospital outcomes. Conclusions: Severe echocardiographic abnormalities are uncommon in hospitalized patients with COVID-19 infections, presenting mostly with subclinical myocardial changes, such as diastolic dysfunction, reduced LV GLS, and myocardial work indices, both associated with high-sensitivity troponin I elevation. An echocardiographic study should be limited to rule out long-term ICU complications or to evaluate hemodynamic instability. Although TTE was a valuable tool for guiding management, it had no significant impact on prognosis. (Figure Presented).
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The proceedings contain 3127 papers. The topics discussed include: automated left ventricular dimension assessment using artificial intelligence;fully automated global longitudinal strain assessment using artificial intelligence developed and validated by a UK-wide echocardiography expert collaborative;pocket-size ultrasound devices may improve the prompt assessment of Covid-19 patients;left atrial appendage velocity as an instrument of predicting atrial fibrillation recurrence after successful catheter ablation a useful tool?;RV free wall longitudinal strain as an independent predictor of survival in wtATTR-CA patients;global longitudinal strain as a predictor of cardiovascular events and mortality in patients with ischemic heart disease and heart failure with preserved/mid-range ejection fraction;myocardial work and long-term prognosis in patients after ST-segment elevation acute myocardial infarction;left atrial appendage function by strain predicts subclinical atrial fibrillation in patients with cryptogenic stroke/TIA;a comprehensive model to estimate underlying atrial fibrillation in cryptogenic stroke: the decrypting score;and exploration of electrocardiographic and echocardiographic findings to screen transthyretin amyloid cardiomyopathy in patients with mild left ventricular hypertrophy.