Cardiac screening before returning to elite sport after SARS-CoV-2 infection.

BACKGROUND: SARS-CoV-2 infection can induce cardiac damage. Therefore, in the absence of clear data, a cardiac evaluation was recommended for athletes before returning to play after recent SARS-CoV-2 infection. AIM: To assess the proportion of anomalies detected by this cardiac screening. METHODS: We reviewed the medical files of elite athletes referred for cardiac evaluation before returning to play after a non-hospitalized SARS-CoV-2 infection (based on a positive polymerase chain reaction or antigen test) from March 2020 to July 2021 in 12 French centres. RESULTS: A total of 554 elite athletes (professional or national level) were included (median age 22 years, 72.0% male). An electrocardiogram (ECG), echocardiogram and exercise test were performed in 551 (99.5%), 497 (89.7%) and 293 (52.9%) athletes, respectively. We found anomalies with a potential link with SARS-CoV-2 infection in four ECGs (0.7%), three echocardiograms (0.6%) and three exercise tests (1.0%). Cardiac magnetic resonance imaging was performed in 34 athletes (6.1%), mostly due to abnormal first-line examinations, and was abnormal in one (2.9%). The rates of those abnormalities were not higher among athletes with cardiac symptoms or more severe forms of non-hospitalized SARS-CoV-2 infection. Only one athlete had a possible SARS-CoV-2 myocarditis and sport was temporally contraindicated. None had a major cardiac event declared during the follow-up. CONCLUSION: The proportion of cardiac involvement after non-hospitalized forms of SARS-CoV-2 infection in athletes are very low. Systematic cardiac screening before returning to play seems to be unnecessary.

Resuming Training in High-Level Athletes After Mild COVID-19 Infection: A Multicenter Prospective Study (ASCCOVID-19).

BACKGROUND: There is a paucity of data on cardiovascular sequelae of asymptomatic/mildly symptomatic SARS-Cov-2 infections (COVID). OBJECTIVES: The aim of this prospective study was to characterize the cardiovascular sequelae of asymptomatic/mildly symptomatic COVID-19 among high/elite-level athletes. METHODS: 950 athletes (779 professional French National Rugby League (F-NRL) players; 171 student athletes) were included. SARS-Cov-2 testing was performed at inclusion, and F-NRL athletes were intensely followed-up for incident COVID-19. Athletes underwent ECG and biomarker profiling (D-Dimer, troponin, C-reactive protein). COVID(+) athletes underwent additional exercise testing, echocardiography and cardiac magnetic resonance imaging (CMR). RESULTS: 285/950 athletes (30.0%) had mild/asymptomatic COVID-19 [79 (8.3%) at inclusion (COVID(+)prevalent); 206 (28.3%) during follow-up (COVID(+)incident)]. 2.6% COVID(+) athletes had abnormal ECGs, while 0.4% had an abnormal echocardiogram. During stress testing (following 7-day rest), COVID(+) athletes had a functional capacity of 12.8 ± 2.7 METS with only stress-induced premature ventricular ectopy in 10 (4.3%). Prevalence of CMR scar was comparable between COVID(+) athletes and controls [COVID(+) vs. COVID(-); 1/102 (1.0%) vs 1/28 (3.6%)]. During 289 ± 56 days follow-up, one athlete had ventricular tachycardia, with no obvious link with a SARS-CoV-2 infection. The proportion with troponin I and CRP values above the upper-limit threshold was comparable between pre- and post-infection (5.9% vs 5.9%, and 5.6% vs 8.7%, respectively). The proportion with D-Dimer values above the upper-limit threshold increased when comparing pre- and post-infection (7.9% vs 17.3%, P = 0.01). CONCLUSION: The absence of cardiac sequelae in pauci/asymptomatic COVID(+) athletes is reassuring and argues against the need for systematic cardiac assessment prior to resumption of training (clinicaltrials.gov; NCT04936503).

Occurrence of Incomplete Endothelialization Causing Residual Permeability After Left Atrial Appendage Closure.

AIMS: Percutaneous left atrial appendage (LAA) occlusion is occasionally incomplete, with residual permeability of the LAA on cardiac computed tomography. The cause for this is unclear. Our objective was to determine if residual permeability was related to incomplete endothelialization. METHODS: A total of 35 consecutive patients contraindicated for anticoagulant therapy admitted for LAA occlusion were included; 12 patients received a Watchman device (Boston Scientific) and 23 patients received an Amplatzer Cardiac Plug (St. Jude Medical). Incomplete endothelialization was defined as residual permeability on cardiac computed tomography without peridevice leak on transesophageal echocardiography at follow-up. RESULTS: Five patients did not receive cardiac computed tomography. After 10 ± 6 months of follow-up, residual permeability of the LAA (at least partial) was recorded on cardiac computed tomography in 21 of 30 patients (70%). Seven of 30 patients presented with a peridevice leak on transesophageal echocardiography. Among the remaining 23 patients, 14 (61%) presented with incomplete endothelialization and 9 (39%) presented with complete endothelialization. There was no statistical difference between the patients presenting with complete vs incomplete endothelialization. CONCLUSION: We found that incomplete endothelialization, defined as residual permeability on cardiac computed tomography without peridevice leak on transesophageal echocardiography, occurred in 61% of the patients after 10 ± 6 months of percutaneous LAA closure. Predisposing factors and appropriate monitoring of LAA patients remain to be determined in larger cohorts.

Area at risk can be assessed by iodine-123-meta-iodobenzylguanidine single-photon emission computed tomography after myocardial infarction: a prospective study.

BACKGROUND: Myocardial salvage is an important surrogate endpoint to estimate the impact of treatments in patients with ST-segment elevation myocardial infarction (STEMI). AIM: The aim of this study was to evaluate the correlation between cardiac sympathetic denervation area assessed by single-photon emission computed tomography (SPECT) using iodine-123-meta-iodobenzylguanidine (I-MIBG) and myocardial area at risk (AAR) assessed by cardiac magnetic resonance (CMR) (gold standard). PATIENTS AND METHODS: A total of 35 postprimary reperfusion STEMI patients were enrolled prospectively to undergo SPECT using I-MIBG (evaluates cardiac sympathetic denervation) and thallium-201 (evaluates myocardial necrosis), and to undergo CMR imaging using T2-weighted spin-echo turbo inversion recovery for AAR and postgadolinium T1-weighted phase sensitive inversion recovery for scar assessment. RESULTS: I-MIBG imaging showed a wider denervated area (51.1±16.0% of left ventricular area) in comparison with the necrosis area on thallium-201 imaging (16.1±14.4% of left ventricular area, P<0.0001). CMR and SPECT provided similar evaluation of the transmural necrosis (P=0.10) with a good correlation (R=0.86, P<0.0001). AAR on CMR was not different compared with the denervated area (P=0.23) and was adequately correlated (R=0.56, P=0.0002). Myocardial salvage evaluated by SPECT imaging (mismatch denervated but viable myocardium) was significantly higher than by CMR (P=0.02). CONCLUSION: In patients with STEMI, I-MIBG SPECT, assessing cardiac sympathetic denervation may precisely evaluate the AAR, providing an alternative to CMR for AAR assessment.

COLIN trial: Value of colchicine in the treatment of patients with acute myocardial infarction and inflammatory response.

BACKGROUND: Inflammation is involved during acute myocardial infarction, and could be an interesting target to prevent ischaemia-reperfusion injuries. Colchicine, known for its pleiotropic anti-inflammatory effects, could decrease systemic inflammation in this context. AIMS: To evaluate the impact of colchicine on inflammation in patients admitted for ST-segment elevation myocardial infarction (STEMI). METHODS: All patients admitted for STEMI with one of the main coronary arteries occluded, and successfully treated with percutaneous coronary intervention, were included consecutively. Patients were randomized to receive either 1mg colchicine once daily for 1 month plus optimal medical treatment or optimal medical treatment only. C-reactive protein (CRP) was assessed at admission and daily until hospital discharge. The primary endpoint was CRP peak value during the index hospitalization. RESULTS: Forty-four patients were included: 23 were treated with colchicine; 21 received conventional treatment only. At baseline, both groups were well balanced regarding age, sex, risk factors, thrombolysis in myocardial infarction flow and reperfusion delay. The culprit artery was more often the left anterior descending artery in the colchicine group (P=0.07), reflecting a more severe group. There was no significant difference in mean CRP peak value between the colchicine and control groups (29.03mg/L vs 21.86mg/L, respectively; P=0.36), even after adjustment for type of culprit artery (26.99 vs 24.99mg/L, respectively; P=0.79). CONCLUSION: In our study, the effect of colchicine on inflammation in the context of STEMI could not be demonstrated. Further larger studies may clarify the impact of colchicine in acute myocardial infarction.

Kinetics of high-sensitivity cardiac troponin T and I differ in patients with ST-segment elevation myocardial infarction treated by primary coronary intervention.

PURPOSE: Cardiac biomarkers including troponins are the cornerstone of the biological definition of acute myocardial infarction. New high-sensitivity cardiac assays determining troponin T (hs-cTnT) as well as I ((hs-cTnI) from Abbott and s-cTnI from Siemens) raise concerns because of their unclear kinetics following the peak. AIMS: This study aims to compare kinetics of creatine kinases, hs-cTnT, hs-cTnI and s-cTnI in patients with ST-segment elevation myocardial infarction (STEMI) treated by percutaneous coronary intervention. METHODS: We prospectively studied 106 consecutive patients admitted in our institution for STEMI and treated by percutaneous coronary intervention. We evaluated for all the patients simultaneously kinetics of creatine kinases, hs-cTnT (Roche) and two different cTnIs (hs-cTnI from Abbott and s-cTnI from Siemens). Modelling of kinetics was realized using mixed effects with cubic splines. RESULTS: Kinetics of markers showed a first peak at 10.7h (8.0-12.0) for creatine kinases, 11.8h (10.4-13.3) for hs-cTnT (Roche); 11.8h (10.7-11.8) for hs-cTnI from Abbott and 10.2h (8.7-11.6) for s-cTnI from Siemens, respectively. This peak was followed by a nearly log linear decrease for hs-cTnI/s-cTnI and creatine kinases in contrast to hs-cTnT, which appeared with a biphasic shape curve marked by a second peak at 76.9h (69.5-82.8). The analysis of the decrease in percentage of the peak value at 77h showed that hs-cTnT follows a twice lower decrease than other markers. CONCLUSION: Kinetics of hs-cTnT, hs-cTnI and s-cTnI differ significantly with a linear decrease regarding both cTnI assays contrasting with a biphasic shape curve for hs-cTnT. This is of importance for clinical management of patients in routine settings especially in follow-up after STEMI including the suspicion of reinfarction.

Kinetics of high-sensitivity cardiac troponin T or troponin I compared to creatine kinase in patients with revascularized acute myocardial infarction.

BACKGROUND: Cardiac biomarkers are the cornerstone of the biological definition of acute myocardial infarction (AMI). The key role of troponins in diagnosis of AMI is well established. Moreover, kinetics of troponin I (cTnI) and creatine kinase (CK) after AMI are correlated to the prognosis. New technical assessment like high-sensitivity cardiac troponin T (hs-cTnT) raises concerns because of its unclear kinetic following the peak. This study aims to compare kinetics of cTnI and hs-cTnT to CK in patients with large AMI successfully treated by percutaneous coronary intervention (PCI). METHODS: We prospectively studied 62 patients with anterior AMI successfully reperfused with primary angioplasty. We evaluated two consecutive groups: the first one regularly assessed by both CK and cTnI methods and the second group by CK and hs-cTnT. Modeling of kinetics was realized using mixed effects with cubic splines. RESULTS: Kinetics of markers showed a peak at 7.9 h for CK, at 10.9 h (6.9-12.75) for cTnI and at 12 h for hs-cTnT. This peak was followed by a nearly log linear decrease for cTnI and CK by contrast to hs-cTnT which appeared with a biphasic shape curve marked by a second peak at 82 h. There was no significant difference between the decrease of cTnI and CK (p=0.63). CK fell by 79.5% (76.1-99.9) vs. cTnI by 86.8% (76.6-92.7). In the hs-cTnT group there was a significant difference in the decrease by 26.5% (9-42.9) when compared with CK that fell by 79.5% (64.3-90.7). CONCLUSIONS: Kinetic of hs-cTnT and not cTnI differs from CK. The role of hs-cTnT in prognosis has to be investigated.

Intracoronary administration of darbepoetin-alpha at onset of reperfusion in acute myocardial infarction: results of the randomized Intra-Co-EpoMI trial.

BACKGROUND: Several trials investigating erythropoietin as a novel cytoprotective agent in myocardial infarction (MI) failed to translate promising preclinical results into the clinical setting. These trials could have missed crucial events occurring in the first few minutes of reperfusion. Our study differs by earlier intracoronary administration of a longer-acting erythropoietin analogue at the onset of reperfusion. AIM: To evaluate the ability of intracoronary administration of darbepoetin-alpha (DA) at the very onset of the reperfusion, to decrease infarct size (IS). METHODS: We randomly assigned 56 patients with acute ST-segment elevation MI to receive an intracoronary bolus of DA 150 µg (DA group) or normal saline (control group) at the onset of reflow obtained by primary percutaneous coronary intervention (PCI). IS and area at risk (AAR) were evaluated by biomarkers, cardiac magnetic resonance (CMR) and validated angiographical scores. RESULTS: There was no difference between groups regarding duration of ischemia, Thrombolysis in Myocardial Infarction flow grade at admission and after PCI, AAR size and extent of the collateral circulation, which are the main determinants of IS. The release of creatine kinase was not significantly different between the two groups even when adjusted to AAR size. Between 3-7 days and at 3 months, the area of hyperenhancement on CMR expressed as a percentage of the left ventricular myocardium was not significantly reduced in the DA group even when adjusted to AAR size. CONCLUSION: Early intracoronary administration of a longer-acting erythropoietin analogue in patients with acute MI at the time of reperfusion does not significantly reduce IS.

Could heart rate play a role in pericardial inflammation?

UNLABELLED: PURPOSE AND MEDICAL HYPOTHESIS: Rest is usually recommended in acute pericarditis, as it could help to lower heart rate (HR) and contribute to limit "mechanical inflammation". Whether HR on admission could be correlated and perhaps participate to inflammation has not been reported. METHODS: Between March 2007 and February 2010, we conducted a retrospective study on all patients admitted to our center for acute pericarditis. Diagnosis criteria included two of the following ones: typical chest pain, friction rub, pericardial effusion on cardiac echography, or typical electrocardiogram (ECG) findings. Primary endpoint was biology: CRP on admission, on days 1, 2, 3, and especially peak. RESULTS: We included 73 patients. Median age was 38 years (interquartiles 28-51) and median hospitalization duration was 2.0 days (1.5-3.0). Median heart rate was 88.0 beats per minute (bpm) on admission (interquartiles 76.0-100.0) and 72.0 on discharge (65.0-80.0). Heart rate on admission was significantly correlated with CRP peak (p<0.001), independently of temperature on admission, hospitalization duration and age. Recurrences occurred within 1 month in 32% of patients. Heart rate on hospital discharge was correlated with recurrence, independently of age. CONCLUSION: In acute pericarditis, heart rate on admission is independently correlated with CRP levels and heart rate on discharge seems to be independently correlated to recurrence. This could suggest a link between heart rate and pericardial inflammation.

Exercise response in hypertrophic cardiomyopathy: blunted left ventricular deformational and twisting reserve with altered systolic-diastolic coupling.

BACKGROUND: Abnormal left ventricular (LV) deformational mechanics have been demonstrated in patients with hypertrophic cardiomyopathy (HCM) at rest, but there is a lack of information on their adaptation to exercise. The aim of this study was to assess the adaptability of LV strains and torsional mechanics during exercise in HCM patients. METHODS AND RESULTS: Twenty nonobstructive HCM patients (age, 48.3±12.3 years; 14 men) and 20 control subjects underwent speckle-tracking echocardiographic measurement of longitudinal, radial, and circumferential strains, systolic twist, and diastolic untwisting rate (UTR) at rest and submaximal exercise. HCM patients showed lower resting longitudinal (-15.7±5.0% versus -19.4±2.6%, P<0.001) and radial (38.1±11.3% versus 44.7±14.4%, P<0.05) strains but higher circumferential strain (-21.9±4.0% versus -18.8±2.3%, P<0.05) and twist (15.7±3.6° versus 9.3±2.6°, P<0.0001) than control subjects. Exercise induced an increase in all strains in control subjects but only a moderate increase in longitudinal strain (to -18.4±5.0%), without significant changes in radial and circumferential strains or twist in HCM patients. Exercise peak UTR was lower (-119.0±31.5°/s versus -137.3±41.1°/s) and occurred later (137±18% versus 125±11% systolic time, P<0.05) in HCM than in control subjects. A significant relationship between twist and UTR was obtained in control subjects (ß=-0.0807, P<0.001) but not in HCM patients (ß=-0.0051, P=0.68). CONCLUSIONS: HCM patients had severely limited strain adaptability and no LV twisting reserve at exercise. They had reduced and delayed UTR with reduced systolic-diastolic coupling efficiency by twist-untwist mechanics.

Low-flow, low-gradient severe aortic stenosis despite normal ejection fraction is associated with severe left ventricular dysfunction as assessed by speckle-tracking echocardiography: a multicenter study.

BACKGROUND: Low-flow low-gradient (LFLG) is sometimes observed in severe aortic stenosis (AS) despite normal ejection fraction, but its frequency and mechanisms are still debated. We aimed to describe the characteristics of patients with LFLG AS and assess the presence of longitudinal left ventricular dysfunction in these patients. METHODS AND RESULTS: In a multicenter prospective study, 340 consecutive patients with severe AS and normal ejection fraction were studied. Longitudinal left ventricular function was assessed by 2D-strain and global afterload by valvulo-arterial impedance. Patients were classified according to flow and gradient: low flow was defined as a stroke volume index ≤35 mL/m(2), low gradient as a mean gradient ≤40 mm Hg. Most patients (n=258, 75.9%) presented with high-gradient AS, and 82 patients (24.1%) with low-gradient AS. Among the latter, 52 (15.3%) presented with normal flow and low gradient and 30 (8.8%) with LFLG. As compared with normal flow and low gradient, patients with LFLG had more severe AS (aortic valve area=0.7±0.12 cm(2) versus 0.86±0.14 cm(2)), higher valvulo-arterial impedance (5.5±1.1 versus 4±0.8 mm Hg/mL/m(2)), and worse longitudinal left ventricular function (basal longitudinal strain=-11.6±3.4 versus -14.8±3%; P<0.001 for all). CONCLUSIONS: LFLG AS is observed in 9% of patients with severe AS and normal ejection fraction and is associated with high global afterload and reduced longitudinal systolic function. Patients with normal-flow low-gradient AS are more frequent and present with less severe AS, normal afterload, and less severe longitudinal dysfunction. Severe left ventricular longitudinal dysfunction is a new explanation to the concept of LFLG AS.

Mitral valve repair by Alfieri's technique does not limit exercise tolerance more than Carpentier's correction.

OBJECTIVE: The main goal of this study was to evaluate if the edge-to-edge mitral repair could be a limiting factor for exercise tolerance and to compare these results to those of classical techniques. METHODS: Between 2000 and 2002, 54 consecutive patients were operated on for mitral valve regurgitation (MR). Twenty-five patients were operated with Alfieri's technique (group A) and 29 patients with Carpentier's technique (group C). The mean age was 63.9 years in group A and 63.8 years in group C (p = 0.98). After a mean follow-up of 16.2+/-12 months, survivor patients were seen at the outpatient clinic, by the same physician for a clinical evaluation, an echocardiogram at rest and at peak exercise, and received a cardiorespiratory exercise testing with maximal oxygen uptake (VO2 max) recording. RESULTS: Clinical status improved with 0% of the patients in class NYHA III or IV in either group postoperatively versus 77% preoperatively. There was no significant MR in 80% of cases in group A versus 89.6% in group C (p = 0.54). The mean mitral valve area was 2.5 and 2.9 cm2 in groups A and C, respectively (p = 0.018). The mitral gradient at rest was 3.8 and 3.3 mmHg (p = 0.31) and the mitral gradient at peak exercise was 8.5 and 9.7 mmHg (p = 0.22) in groups A and C, respectively. Cardiorespiratory exercise testing showed a mean VO2 max of 73.7+/-15% of normal value in group A versus 79.6+/-13.1% in group C (p = 0.18). CONCLUSION: Alfieri's technique has the same efficiency on improvement of MR and clinical status than classical repair. Despite a higher restriction of mitral valve area at rest in group A, gradient and mean VO2 max at peak exercise were similar in both groups.

Prognostic value of cardiac troponin T in patients with both acute and chronic stable congestive heart failure: comparison with atrial natriuretic peptide, brain natriuretic peptide and plasma norepinephrine.

BACKGROUND: The prognostic value of cardiac troponin T (cTn-T) in a mixture of patients with both acute and chronic congestive heart failure (CHF), simultaneously assessed and compared with neurohormonal factors, has not yet been thoroughly evaluated. Thus, we focused on the prognostic value of cTn-T in comparison with atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and plasma norepinephrine (PNE) in this population. METHODS: Prognostic correlates of elevation of cTn-T, ANP, BNP, PNE were analyzed in 63 acute and chronic CHF patients followed up to record worsening CHF and cardiac death. RESULTS: cTn-T (> or =0.03 microg/L) was found in 17.4% (11 of 63) of patients. cTn-T correlated with ANP, BNP, PNE. Acute CHF patients were more positive for cTn-T and BNP. In our cohort, neither cTn-T (> or =0.03 microg/L) nor PNE were associated with increased mortality and worsening HF in CHF patients. After adjustment, BNP was the only independent predictor of cardiac events (RR, 3.23; p=0.01). CONCLUSIONS: BNP emerged as the only independent predictor of cardiac events in a mixture of patients with both acute and chronic CHF, suggesting that it is the analyte that best reflects long-term prognosis in a diverse population enrolled to mirror the "real world" situation.

Atrial fibrillation and its determinants after radiofrequency ablation of chronic common atrial flutter.

AIM: Atrial fibrillation (AFib) is a major clinical issue and its occurrence is the main problem after catheter ablation of atrial flutter. The long-term occurrence of AFib after common atrial flutter ablation is still matter of debate as it may influence the therapeutic approach. So, the aim of our study was to analyze the determinants and the time course of AFib after radiofrequency catheter ablation of chronic common atrial flutter. METHODS AND RESULT: 89 consecutive patients (67.5 +/- 12.0 yrs) underwent RF ablation of chronic common atrial flutter. 38.2 % had previous history of paroxysmal AFib. 51% had no underlying structural heart disease. Over a mean follow-up of 38 +/- 13 months, the occurrence rate of AFib progressively increased up to 32.9% at the end of follow-up. The median occurrence time for AFib was 8 months. AFib occurrence was significantly associated with previous AFib history (P=0.01) but not with the presence of underlying heart disease (P=n.s.). Of particular interest, in our study, AFib never occurred in patients without previous AFib history. Palpitations after chronic common atrial flutter ablation was mostly related to AFib. CONCLUSION: In conclusion, after chronic common atrial flutter ablation, AFib incidence progressively increased over the follow-up in all patients. Patients with prior AFib history appeared to be a very high risk group. In these patients, closer monitoring is mandatory and the persistent risk of AFib recurrences may justify prolonged anticoagulation policy.