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Aims Whether pulmonary artery (PA) dimension and coronary artery calcium (CAC) score, as assessed by chest computed tomography (CT), are associated with myocardial injury in patients with coronavirus disease 2019 (COVID-19) is not known. The aim of this study was to explore the risk factors for myocardial injury and death and to investigate whether myocardial injury has an independent association with all-cause mortality in patients with COVID-19. Methods and Results This is a single-centre cohort study including consecutive patients with laboratory-confirmed COVID-19 undergoing chest CT on admission. Myocardial injury was defined as high-sensitivity troponin I >20 ng/L on admission. A total of 332 patients with a median follow-up of 12 days were included. There were 68 (20.5%) deaths; 123 (37%) patients had myocardial injury. PA diameter was higher in patients with myocardial injury compared with patients without myocardial injury [29.0 (25th–75th percentile, 27–32) mm vs. 27.7 (25–30) mm, P < 0.001). PA diameter was independently associated with an increased risk of myocardial injury [adjusted odds ratio 1.10, 95% confidence interval (CI) 1.02–1.19, P = 0.01] and death [adjusted hazard ratio (HR) 1.09, 95% CI 1.02–1.17, P = 0.01]. Compared with patients without myocardial injury, patients with myocardial injury had a lower prevalence of a CAC score of zero (25% vs. 55%, P < 0.001); however, the CAC score did not emerge as a predictor of myocardial injury by multivariable logistic regression. Myocardial injury was independently associated with an increased risk of death by multivariable Cox regression (adjusted HR 2.25, 95% CI 1.27–3.96, P = 0.005). Older age, lower estimated glomerular filtration rate, and lower PaO2/FiO2 ratio on admission were other independent predictors for both myocardial injury and death. Conclusions An increased PA diameter, as assessed by chest CT, is an independent risk factor for myocardial injury and mortality in patients with COVID-19. Myocardial injury is independently associated with an approximately two-fold increased risk of death.

Aims Mitral annulus disjunction (MAD) has been associated with sudden cardiac death in selected patients with arrhythmic presentation, while its clinical significance in unselected cohorts remains unknown. Our purpose was to assess the prevalence and clinical significance of MAD in consecutive patients referred to cardiovascular-magnetic-resonance (CMR). Methods and results Our population included 103 consecutive patients undergoing CMR at our Institution, between August and September 2021. MAD was defined as a ≥ 1 mm atrial displacement of the mitral leaflet hinge point in standard long-axis cine images during end-systole. MAD analysis was performed in 97 patients (feasibility = 94%) and resulted positive in 49 (51%). MAD—patients were more often males (75% vs. 57%; P = 0.045) and affected by ischaemic (35% vs. 12%, P = 0.01) and non-ischaemic cardiomyopathy (38% vs. 16%, P = 0.026) compared to MAD+ patients. No significant differences were found in terms of age, history of ventricular arrhythmias, bi-ventricular and bi-atrial volumes, bi-ventricular ejection fraction, native T1 and T2 mapping values, extracellular volume, and prevalence of late gadolinium enhancement (P > 0.05 for all) between MAD + vs. MAD—patients. MAD extent was higher in patients with mitral valve prolapse (MVP; n = 7), (3.5 ± 1.5 mm in MVP+ vs. 2.0 ± 1.0 mm in MVP– patients; P = 0.004). No significant differences were conversely found in MAD extent between patients with and without ventricular arrhythmias (2.5 ± 1.1 mm vs. 2.3 ± 1.1 mm; P = 0.815). Conclusions Our findings suggest a high prevalence of MAD in unselected cohorts of patients, with no clinical significance. Prospective studies are needed to further elucidate the interplay between MAD and malignant ventricular arrhythmias in unselected cohorts of patients.

Aims Repetitive Levosimendan treatment in advanced heart failure patients has not been investigated yet via myocardial work indices (MWI), which could more accurately detect the effects of this both inotropic and vasodilatory drug. The aims of this study were (1) to describe variations of myocardial work indices, as a consequence of repetitive Levosimendan infusions and (2) to assess the prognostic value of myocardial work parameters in these patients. Methods and results Fourteen patients with advanced heart failure treated with intermittent in-hospital levosimendan infusions were prospectively included. Clinical, laboratory, and echocardiographic assessment were performed before and after every Levosimendan infusion. The primary endpoint was a composite of any episode of decompensated HF, urgent HF rehospitalization, cardiogenic shock, cardiac arrest and cardiovascular death at 4–6 weeks follow-up after each planned infusion. During follow-up (mean: 150 ± 99 days) a total of 37 infusions were performed and a total of 11 cardiovascular events occurred. Global constructive work (GCW), global work efficiency (GWE), and global work index (GWI) increased after Levosimendan infusion in 62.2%, 73.0%, and 70.3% of cases, with significant differences between patients with and without outcomes [delta GCW: −7.36 mmHg% (134.12) vs. 113.81 mmHg% (204.41), P = 0.007; delta GWE: −3.27% (8.38) vs. 4.30% (5.58), P = 0.002]. Delta value of GWE showed the largest area under curve (AUC: 0.82, 95% CI: 0.64–1.00, P = 0.002) for outcome prediction with a cut-off point of 0.5%. Independent prognostic value of GWE variation was confirmed in multivariable regression models (OR: 0.825, 95% CI: 0.702–0.970, P = 0.02). Conclusions GWE and GCW provided incremental and independent prognostic value at short-term follow-up over traditional echocardiographic parameters. The differentiation of patients into ‘workers’, whose GWE improved after Levosimendan infusion, and ‘non-workers’, who failed to improve their GWE, permitted to identify patients at higher risk of forthcoming cardiovascular events. Monitoring these patients with MWI may have relevant clinical implications.

AIMS: Currently, there are few available data regarding a possible role for subclinical atherosclerosis as a risk factor for mortality in Coronavirus Disease 19 (COVID-19) patients. We used coronary artery calcium (CAC) score derived from chest computed tomography (CT) scan to assess the in-hospital prognostic role of CAC in patients affected by COVID-19 pneumonia. METHODS: Electronic medical records of patients with confirmed diagnosis of COVID-19 were retrospectively reviewed. Patients with known coronary artery disease (CAD) were excluded. A CAC score was calculated for each patient and was used to categorize them into one of four groups: 0, 1-299, 300-999 and at least 1000. The primary endpoint was in-hospital mortality for any cause. RESULTS: The final population consisted of 282 patients. Fifty-seven patients (20%) died over a follow-up time of 40 days. The presence of CAC was detected in 144 patients (51%). Higher CAC score values were observed in nonsurvivors [median: 87, interquartile range (IQR): 0.0-836] compared with survivors (median: 0, IQR: 0.0-136). The mortality rate in patients with a CAC score of at least 1000 was significantly higher than in patients without coronary calcifications (50 vs. 11%) and CAC score 1-299 (50 vs. 23%), P 

International audience; Background: Few data exist concerning genotype-phenotype relationships in left ventricular noncompaction (LVNC).Methods and results: From a multicenter French Registry, we report the genetic and clinical spectrum of 95 patients with LVNC, and their genotype-phenotype relationship. Among the 95 LVNC, 45 had at least 1 mutation, including 14 cases of mutation in ion channel genes. In a complementary analysis including 16 additional patients with ion channel gene mutations, for a total of 30 patients with ion channel gene mutation, we found that those patients had higher median LV ejection fraction (60% vs 40%; P < .001) and more biventricular noncompaction (53.1% vs 18.5%; P < .001) than the 81 other patients with LVNC. Among them, both the 19 patients with an HCN4 mutation and the 11 patients with an RYR2 mutation presented with a higher LV ejection fraction and more frequent biventricular noncompaction than the 81 patients with LVNC but with no mutation in the ion channel gene, but only patients with HCN4 mutation presented with a lower heart rate.Conclusions: Ion channel gene mutations should be searched systematically in patients with LVNC associated with either bradycardia or biventricular noncompaction, particularly when LV systolic function is preserved. Identifying causative mutations is of utmost importance for genetic counselling of at-risk relatives of patients affected by LVNC.

Papillary muscle rupture is a rare complication of myocardial infarction. Here we describe a case of an apparently spontaneous rupture of papillary muscle, not associated with coronary obstruction. The patient was a 73-year-old man admitted to our hospital for diabetic ketoacidosis complicated by acute pulmonary edema and cardiogenic shock. Transthoracic and transesophageal echocardiography showed partial rupture of papillary muscle leading to severe mitral regurgitation. Urgent cardiac surgery with mitral valve replacement was performed.

The Eustachian valve was first described by Bartolomeo Eustachio (Italian anatomist) at 1552. It is an embryological remnant of the inferior vena cava valve that prenatally directs the oxygenated blood from inferior vena cava across the patent foramen ovale (PFO) into systemic circulation. Generally, following birth, after the closure of the foramen ovale it gradually regresses and not have a specific function, but it may persist in some patients as a floating membrane in the right atrium (RA), a nonpathological functionless structure.1 The prevalence of Eustachian valve in the normal population is unknown. Generally, it is an incidental finding without any significant pathophysiological consequences, but in some particular cases, unfortunately, it can become the site of thrombus formation and paradoxical embolic source.1 In our case report we describe a particular case of paradoxical systemic embolism due to a giant cauliflower thrombus on Eustachian valve, which caused ischemic stroke, pulmonary embolism and splenic infarction

Background Myocardial injury is frequent among patients hospitalized with coronavirus disease-2019 (COVID-19) and is associated with a poor prognosis. However, the mechanisms of myocardial...

Summary Background The incremental prognostic value of left atrial (LA) dysfunction, emerging in various clinical contexts, remains poorly explored in hypertrophic cardiomyopathy (HCM). Objective To assess LA strain correlation with outcome in HCM. Methods A cohort of all 307 consecutive patients presenting with HCM between 2007 and 2017 (54 ± 17 years; 34% women), with comprehensive echocardiography at diagnosis and LA peak longitudinal strain (PALS) and LA peak contraction strain (PACS) measurement, was enrolled and occurrence of HCM related cardiac events analysed. Results Clinically, atrial fibrillation (AF) was present in 13%, New York Heart Association functional class II–III in 54%, and B-type natriuretic peptide (BNP) concentration was 199 ± 278 pg/mL. By echocardiography, left ventricular (LV) ejection fraction (EF) was 67 ± 10%, LV thickness 21 ± 5 mm and European Society of Cardiology HCM risk score 3 ± 3%, with 109 patients (36%) presenting obstructive HCM (LV outflow gradient 21 ± 32 mmHg). LA diameter was 41 ± 8 mm [with 109 (36%) presenting LA diameter ≥ 40 mm], LA volume index 50 ± 26 mL/m2, PALS 24 ± 13%, PACS 11 ± 7% and LA peak systolic strain rate (LASRs) 1.7 ± 0.6 s−1. In addition to AF, age, BNP, LVEF and LV thickness were all independent determinants of lower PALS, with odd ratios almost unchanged after adjustment (all P ≤ 0.0004). At a mean follow-up of 21 (range 18–23) months, patients with adverse cardiac events (n = 65) presented with more impaired LA function (all P ≤ 0.0005), with a significant association between impaired PALS and worse outcome, hazard ratio 0.94 [95% confidence interval (CI) 0.92–0.97, P Conclusions The present study, by gathering a unique HCM cohort, suggests a strong link between LA dysfunction and poor outcome, to be further investigated.

Few data exist concerning genotype-phenotype relationships in left ventricular noncompaction (LVNC).From a multicenter French Registry, we report the genetic and clinical spectrum of 95 patients with LVNC, and their genotype-phenotype relationship. Among the 95 LVNC, 45 had at least 1 mutation, including 14 cases of mutation in ion channel genes. In a complementary analysis including 16 additional patients with ion channel gene mutations, for a total of 30 patients with ion channel gene mutation, we found that those patients had higher median LV ejection fraction (60% vs 40%; P.001) and more biventricular noncompaction (53.1% vs 18.5%; P.001) than the 81 other patients with LVNC. Among them, both the 19 patients with an HCN4 mutation and the 11 patients with an RYR2 mutation presented with a higher LV ejection fraction and more frequent biventricular noncompaction than the 81 patients with LVNC but with no mutation in the ion channel gene, but only patients with HCN4 mutation presented with a lower heart rate.Ion channel gene mutations should be searched systematically in patients with LVNC associated with either bradycardia or biventricular noncompaction, particularly when LV systolic function is preserved. Identifying causative mutations is of utmost importance for genetic counselling of at-risk relatives of patients affected by LVNC.

International audience; Background: Diagnosis of left ventricular non-compaction (LVNC) is challenging, and different imaging techniques propose different criteria.Aim: To compare the value of two-dimensional transthoracic echocardiography (2D-TTE) and cardiac magnetic resonance (CMR) criteria in diagnosing LVNC, and to test a new trabecular quantification method obtained by 2D-TTE, exploring its relationship with CMR non-compacted mass quantification.Methods: From a multicentre French study, we selected 48 patients with LVNC and 20 with dilated cardiomyopathy (DCM) who underwent 2D-TTE and CMR. Current 2D-TTE (Jenni et al.) and CMR criteria (Petersen et al., Jacquier et al.), were tested. A new 2D-TTE method of trabecular quantification (percentage of trabecular area) was also proposed, and compared with current criteria.Results: The best cut-off values for the diagnosis of LVNC were a non-compacted/compacted ratio≥2.3 (Petersen et al.), a trabeculated left ventricular mass≥20% (Jacquier et al.) and a non-compacted/compacted ratio≥1.8 (Jenni et al.). Lowering the threshold for the criterion of Jenni et al. from>2 to ≥1.8 improved its sensitivity from 69% to 98%. The 2D-TTE percentage of trabecular area was 25.9±8% in the LVNC group vs. 9.9±4.4% in the DCM group (P2 to ≥1.8 is necessary to improve LVNC diagnosis in patients with left ventricular dysfunction. A new 2D-TTE trabecular quantification method improves TTE diagnosis of LVNC.

Background— Several cardiovascular diseases are characterized by an impaired O 2 kinetic during exercise. The lack of a linear increase of Δoxygen consumption (V O 2 )/ΔWork Rate (WR) relationship, as assessed by expired gas analysis, is considered an indicator of abnormal cardiovascular efficiency. We aimed at describing the frequency of ΔVO 2 /ΔWR flattening in a symptomatic population of cardiac patients, characterizing its functional profile, and testing the hypothesis that dynamic pulmonary hypertension and right ventricular contractile reserve play a major role as cardiac determinants. Methods and Results— We studied 136 patients, with different cardiovascular diseases, referred for exertional dyspnoea. Cardiopulmonary exercise test combined with simultaneous exercise echocardiography was performed using a symptom-limited protocol. ΔVO 2 /ΔWR flattening was observed in 36 patients (group A, 26.5% of population) and was associated with a globally worse functional profile (reduced peak V O 2 , anaerobic threshold, O 2 pulse, impaired VE/VCO 2 ). At univariate analysis, exercise ejection fraction, exercise mitral regurgitation, rest and exercise tricuspid annular plane systolic excursion, exercise systolic pulmonary artery pressure, and exercise cardiac output were all significantly ( P P =0.01) and exercise tricuspid annular plane systolic excursion (odds ratio, 0.88; confidence interval, 0.80–0.97; P =0.01) as main cardiac determinants of ΔVO 2 /ΔWR flattening; female sex was strongly associated (odds ratio, 6.10; confidence interval, 2.11–17.7; P Conclusions— In patients symptomatic for dyspnea, the occurrence of ΔVO 2 /ΔWR flattening reflects a significantly impaired functional phenotype whose main cardiac determinants are the excessive systolic pulmonary artery pressure increase and the reduced peak right ventricular longitudinal systolic function.

Background: Speckle tracking analysis is an emerging technique that can be useful to assess abnormalities in cardiac contractility before traditional echo parameters. Purpose: To investigate whether right ventricular (RV) 2D speckle tracking analysis at peak exercise could stratify a heart failure reduced ejection fraction (HFrEF) population in different functional phenotypes, with particular emphasis on RV to pulmonary circulation relationship. Methods: 36 HFrEF patients (mean age 69±12; male 69%; NYHA I-II-III-IV 19-17-25-5 %) underwent a maximal cardiopulmonary exercise testing evaluation (bike, incremental ramp protocol) combined with Echo-Doppler and off-line speckle tracking analysis. Study population was divided in two groups according to median value of 2D right ventricle longitudinal strain at peak exercise (Group A RVLG at peak < -16, 17 patients vs Group B ≥ -16, 19 patients). In all patients we performed traditional echo and 2D longitudinal speckle tracking analysis at rest and peak exercise. Results: Despite similar left ventricle ejection fraction (Group A 36± 9% vs Group B 32±9%, p=ns) and global right ventricle longitudinal strain (RVLG) at rest (Group A -18.6±5.6% vs Group B -14.5±8.2%, p=ns), Group B patients showed a similar exercise performance (Peak VO 2 Group A 31.6±7.4 vs Group B 11.6±3.4 mlO 2 /Kg/min, p=ns) but more impaired ventilation (VE/VCO2 slope Group A 31.6±7.4 vs Group B 37.4±8.8, p Conclusions: In HFrEF RV speckle tracking analysis at peak exercise seems a useful technique for unmasking RV to PC uncoupling and the unfavorable gas exchange and ventilatory phenotypes.

Exercise Ventilatory Power (EVP; peak systolic blood pressure/exercise ventilation to CO2 production slope) is a new powerful prognostic marker that combines ventilator abnormalities with systemic hemodynamic during exercise. The phenotype and clinical relevance of patients with a worse EVP is

Diabetes mellitus (DM) is a risk condition that may determine overall exercise limitation and reduced oxygen consumption (VO2). No study has addressed the cardiopulmonary exercise testing phenotype in diabetic subjects with normal left ventricular function. Their functional characterization by

Aortic stenosis (AS) is characterized by increased afterload and functional disability. Exercise intolerance may incur even without overt symptoms. Cardiopulmonary exercise testing (CPET) provides pathophysiological insights on mechanisms affecting exercise intolerance. Nonetheless, it has never

Group 2 pulmonary hypertension (PH) and exercise oscillatory ventilation (EOV) are prognostic signs in heart failure (HF). It is unknown what may characterize the exercise response of PH patients and EOV. Aim: To define the functional pattern in HF reduced ejection fraction (HFrEF) with PH according

Left ventricular (LV) diastolic pressure can be estimated by the echo-derived ratio of early diastolic transmitral velocity (E) and tissue septal velocity (e’). Cardiopulmonary exercise testing (CPET) provides indices of functional capacity such as peak oxygen consumption (VO2), which are related

Background There are limited data comparing ultrafiltration with standard medical therapy as first-line treatment in patients with severe congestive heart failure (HF). We compared ultrafiltration and conventional therapy in patients hospitalized for HF and overt fluid overload. Methods and Results Fifty-six patients with congestive HF were randomized to receive standard medical therapy (control group; n = 29) or ultrafiltration (ultrafiltration group; n = 27). The primary end point of the study was rehospitalizations for congestive HF during a 1-year follow-up. Despite similar body weight reduction at hospital discharge in the 2 groups (7.5 ± 5.5 and 7.9 ± 9.0 kg, respectively; P = .75), a lower incidence of rehospitalizations for HF was observed in the ultrafiltration-treated patients during the following year (hazard ratio 0.14, 95% confidence interval 0.04–0.48; P = .002). Ultrafiltration-induced benefit was associated with a more stable renal function, unchanged furosemide dose, and lower B-type natriuretic peptide levels. At 1 year, 7 deaths (30%) occurred in the ultrafiltration group and 11 (44%) in the control group (P = .33). Conclusions In HF patients with severe fluid overload, first-line treatment with ultrafiltration is associated with a prolonged clinical stabilization and a greater freedom from rehospitalization for congestive HF.