Trajectory of cardiac troponin T following moderate-to-severe COVID-19 and the association with cardiac abnormalities.

BACKGROUND: COVID-19 has been associated with cardiac troponin T (cTnT) elevations and changes in cardiac structure and function, but the link between cardiac dysfunction and high-sensitive cardiac troponin T (hs-cTnT) in the acute and convalescent phase is unclear. OBJECTIVE: To assess whether hs-cTnT concentrations are associated with cardiac dysfunction and structural abnormalities after hospitalization for COVID-19, and to evaluate the performance of hs-cTnT to rule out cardiac pathology. METHODS: Patients hospitalized with COVID-19 had hs-cTnT measured during the index hospitalization and after 3-and 12 months, when they also underwent an echocardiographic study. A subset also underwent cardiovascular magnetic resonance imaging (CMR) after 6 months. Cardiac abnormalities were defined as left ventricular hypertrophy or dysfunction, right ventricular dysfunction, or CMR late gadolinium. RESULTS: We included 189 patients with hs-cTnT concentrations measured during hospitalization for COVID-19, and after 3-and 12 months: Geometric mean (95%CI) 13 (11-15) ng/L, 7 (6-8) ng/L and 7 (6-8) ng/L, respectively. Cardiac abnormalities after 3 months were present in 45 (30%) and 3 (8%) of patients with hs-cTnT ≥ and < 5 ng/L at 3 months, respectively (negative predictive value 92.3% [95%CI 88.5-96.1%]). The performance was similar in patients with and without dyspnea. Hs-cTnT decreased from hospitalization to 3 months (more pronounced in intensive care unit-treated patients) and remained unchanged from 3 to 12 months, regardless of the presence of cardiac abnormalities. CONCLUSION: Higher hs-cTnT concentrations in the convalescent phase of COVID-19 are associated with the presence of cardiac pathology and low concentrations (< 5 ng/L) may support in ruling out cardiac pathology following the infection.

Lung Ultrasound to Assess Pulmonary Congestion in Patients with Acute Exacerbation of COPD.

Purpose: Heart failure (HF) often coexists with chronic obstructive pulmonary disease (COPD) and is associated with worse outcomes. We aimed to assess the feasibility of detecting vertical artifacts (B-lines) on lung ultrasound (LUS) to identify concurrent HF in patients hospitalized with acute exacerbation of COPD (AECOPD). Second, we wanted to assess the association between B-lines and the risk of rehospitalization for AECOPD or death. Patients and Methods: In a prospective cohort study, 123 patients with AECOPD underwent 8-zone bedside LUS within 24h after admission. A positive LUS was defined by ≥3 B-lines in ≥2 zones bilaterally. The ability to detect concurrent HF (adjudicated by a cardiologist committee) and association with events were evaluated by logistic- and Cox regression models. Results: Forty-eight of 123 patients with AECOPD (age 75±9 years, 57[46%] men) had concurrent HF. Sixteen (13%) patients had positive LUS, and the prevalence of positive LUS was similar between patients with and without concurrent HF (8[17%] vs 8[11%], respectively, p=0.34). The number of B-lines was higher in concurrent HF: median 10(IQR 6-16) vs 7(IQR 5-12), p=0.03. The sensitivity and specificity for a positive LUS to detect concurrent HF were 17% and 89%, respectively. Positive LUS was not associated with rehospitalization and mortality: Adjusted HR: 0.93(0.49-1.75), p=0.81. Conclusion: LUS did not detect concurrent HF or predict risk in patients with AECOPD.

Minor Myocardial Scars in Association with Cardiopulmonary Function after COVID-19.

BACKGROUND: Myocardial scars detected by cardiovascular magnetic resonance (CMR) imaging after COVID-19 have caused concerns regarding potential long-term cardiovascular consequences. OBJECTIVE: The objective of this study was to investigate cardiopulmonary functioning in patients with versus without COVID-19-related myocardial scars. METHODS: In this prospective cohort study, CMR was performed approximately 6 months after moderate-to-severe COVID-19. Before (∼3 months post-COVID-19) and after (∼12 months post-COVID-19) the CMR, patients underwent extensive cardiopulmonary testing with cardiopulmonary exercise tests, 24-h ECG, and echocardiography. We excluded participants with overt heart failure. RESULTS: Post-COVID-19 CMR was available in 49 patients with cardiopulmonary tests at 3 and 12 months after the index hospitalization. Nine (18%) patients had small late gadolinium enhancement-detected myocardial scars. Patients with myocardial scars were older (63.2 ± 13.2 vs. 56.2 ± 13.2 years) and more frequently men (89% vs. 55%) compared to those without scars. Cardiorespiratory fitness was similar in patients with and without scars, i.e., peak oxygen uptake: 82.1 ± 11.5% versus 76.3 ± 22.5% of predicted, respectively (p = 0.46). The prevalence of ventricular premature contractions and arrhythmias was low and not different by the presence of myocardial scar. Cardiac structure and function assessed by echocardiography were similar between the groups, except for a tendency of greater left ventricular mass in those with scars (75 ± 20 vs. 62 ± 14, p = 0.02 and p = 0.08 after adjusting for age and sex). There were no significant associations between myocardial scar and longitudinal changes in cardiopulmonary function from 3 to 12 months. CONCLUSION: Our findings imply that the presence of minor myocardial scars has limited clinical significance with respect to cardiopulmonary function after COVID-19.

Changes in cardiac structure and function from 3 to 12 months after hospitalization for COVID-19.

BACKGROUND: Cardiac function may be impaired during and early after hospitalization for COVID-19, but little is known about the progression of cardiac dysfunction and the association with postacute COVID syndrome (PACS). METHODS: In a multicenter prospective cohort study, patients who had been hospitalized with COVID-19 were enrolled and comprehensive echocardiography was performed 3 and 12 months after discharge. Twenty-four-hour electrocardiogram (ECG) was performed at 3 and 12 months in patients with arrhythmias at 3 months. RESULTS: In total, 182 participants attended the 3 and 12 months visits (age 58 ± 14 years, 59% male, body mass index 28.2 ± 4.2 kg/m2 ). Of these, 35 (20%) had severe COVID-19 (treatment in the intensive care unit) and 74 (52%) had self-reported dyspnea at 3 months. From 3 to 12 months there were no significant overall changes in any measures of left or right ventricle (LV; RV) structure and function (p > .05 for all), including RV strain (from 26.2 ± 3.9% to 26.5 ± 3.1%, p = .29) and LV global longitudinal strain (from 19.2 ± 2.3% to 19.3 ± 2.3%, p = .64). Changes in echocardiographic parameters from 3 to 12 months did not differ by COVID-19 severity or by the presence of persistent dyspnea (p > .05 for all). Among patients with arrhythmia at 3 months, there was no significant change in arrhythmia burden to 12 months. CONCLUSION: Following COVID-19, cardiac structure and function remained unchanged from 3 to 12 months after the index hospitalization, irrespective of COVID-19 severity and presence of persistent dyspnea. These results suggest that progression of cardiac dysfunction after COVID-19 is rare and unlikely to play an important role in PACS.