Graphical abstract

Background: Although severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) may cause an acute multiorgan syndrome (coronavirus disease 2019 (COVID-19)), data are emerging on mid- and long-term sequelae of COVID-19 pneumonia. Since no study has hitherto investigated the role of both cardiac and pulmonary ultrasound techniques in detecting such sequelae, this study aimed at evaluating these simple diagnostic tools to appraise the cardiopulmonary involvement after COVID-19 pneumonia. Methods: Twenty-nine patients fully recovered from COVID-19 pneumonia were considered at our centre. On admission, all patients underwent 12-lead electrocardiogram (ECG) and transthoracic echocardiography (TTE) evaluation. Compression ultrasound (CUS) and lung ultrasound (LUS) were also performed. Finally, in each patient, pathological findings detected on LUS were correlated with the pulmonary involvement occurring after COVID-19 pneumonia, as assessed on thoracic computed tomography (CT). Results: Out of 29 patients (mean age 70 ± 10 years; males 69%), prior cardiovascular and pulmonary comorbidities were recorded in 22 (76%). Twenty-seven patients (93%) were in sinus rhythm and two (7%) in atrial fibrillation. Persistence of ECG abnormalities from the acute phase was common, and nonspecific repolarisation abnormalities (93%) reflected the high prevalence of pericardial involvement on TTE (86%). Likewise, pleural abnormalities were frequently observed (66%). TTE signs of left and right ventricular dysfunction were reported in two patients, and values of systolic pulmonary artery pressure were abnormal in 16 (55%, despite the absence of prior comorbidities in 44% of them). Regarding LUS evaluation, most patients displayed abnormal values of diaphragmatic thickness and excursion (93%), which correlated well with the high prevalence (76%) of pathological findings on CT scan. CUS ruled out deep vein thrombosis in all patients. Conclusions: Data on cardiopulmonary involvement after COVID-19 pneumonia are scarce. In our study, simple diagnostic tools (TTE and LUS) proved clinically useful for the detection of cardiopulmonary complications after COVID-19 pneumonia.

Background: subclinical pulmonary and peripheral congestion is an emerging concept in heart failure, correlated with a worse prognosis. Very few studies have evaluated its prognostic impact in an outpatient setting and its relationship with right-ventricular dysfunction. The study aims to investigate subclinical congestion in chronic heart failure outpatients, exploring the close relationship between the right heart-pulmonary unit and peripheral congestion. Materials and methods: in this observational study, 104 chronic HF outpatients were enrolled. The degree of congestion and signs of elevated filling pressures of the right ventricle were evaluated by physical examination and a transthoracic ultrasound to define multiparametric right ventricular dysfunction, estimate the right atrial pressure and the pulmonary artery systolic pressure. Outcome data were obtained by scheduled visits and phone calls. Results: ultrasound signs of congestion were found in 26% of patients and, among this cohort, half of them presented as subclinical, affecting their prognosis, revealing a linear correlation between right ventricular/arterial coupling, the right-chambers size and ultrasound congestion. Right ventricular dysfunction, TAPSE/PAPS ratio, clinical and ultrasound signs of congestion have been confirmed to be useful predictors of outcome. Conclusions: subclinical congestion is widespread in the heart failure outpatient population, significantly affecting prognosis, especially when right ventricular dysfunction also occurs, suggesting a strict correlation between the heart-pulmonary unit and volume overload.

Case description In November 2020, a 55-years-old female with no significant past medical history, was admitted to our Emergency Department for chest pain after acute stressful event. She had a significant family history of ischemic heart disease, and unclear comatose status of her sister. At admission, she was asymptomatic, blood pressure was 115/80 mmHg, and oxygen saturation was 96%. An electrocardiogram (ECG) showed biphasic T wave in anterolateral leads. Elevated levels of troponin I (hs-TnI of 900 ng/L) and B-type natriuretic peptide (BNP) of 864 pg/mL were detected. Transthoracic echocardiogram (TTE) revealed an ejection fraction (EF) of 30% with apical ballooning of mid and apical segments of the left ventricle (LV) along with a sizable apical thrombus. Aspirin, iv diuretics, iv nitrates and unfractioned heparin were started. After 13 hours, she suffered a sudden transient neurological sign of decreased level of consciousness. Cranial MRI revealed an ischemic lesion in the territory of the apex of basilar artery (thalamic region). After 7 days from stroke, the patients underwent coronary angiography demonstrating unobstructed coronaries. Thus, the diagnosis of takotsubo syndrome was confirmed. During hospitalization, ECG evolution showed T wave inversion in precordial and lateral leads. Hs-TnI declining within normal values. Of note, ventricular arrhythmias burden with polymorphic ventricular contraction (PVC) emerged on continuous ECG-monitoring. Despite resolution of apical balloning and apical thrombosis, there were persistent wall-motion abnormalities in infero-lateral walls and mild LV dysfunction. This was also confirmed by cardiac magnetic resonance (CMR). Further, CMR also showed an intense myocardial edema with elevated LV mass. The patients was discharged on Warfarin, Bisoprolol 2.5 mg/die, Ramipril 5 mg/die, Eplerenone 25 mg/die. A clinical documentation was required to further investigate history of her sister, and neurological sequelae after cardiac arrest at 28s related to ventricular fibrillation emerged. However, no deeply evaluation of underlining heart disease was available. Despite an early favorable follow-up of patient, after six months, she suffered from palpitations and heart failure requiring diuretic therapy. Persistent repolarization abnormalities in infero-lateral leads, and low-voltage in precordial leads were noted. An extensive wall-motion abnormalities and moderate LV dysfunction were detected. Importantly, significant arrhythmic burden with PVC (13%) at 24-hr ECG monitoring was recorded. CMR was requested to further investigate the possibility of underlining coexisting cardiomyopathy. Mild LV dilation, moderate dysfunction (LVEF 39%), wall motion abnormalities and thinning of the inferior wall middle segments were reported. Surprisingly, fibro-fatty replacement in infero-lateral of LV wall was detected, and unexpectedly, right ventricular (RV) fibro-fatty replacement and mild RV dysfunction were also described. Hence, diagnosis of arrhythmogenic cardiomyopathy was made. Since persistent arrhythmic burden despite optimized medical treatment, biventricular involvement, family history of SCD, an implantable cardioverter defibrillator in primary prevention was placed. Furthermore, genetic testing was required and extensive clinical family screening was suggested. Conclusion According to the clinical data collected, takotsubo and arrhytmogenic cardiomyopathy can coexist. A potential link between two myocardial heart disease may be identified in the future, especially among patients presenting takotsubo and long-term unfavorable outcome.

Background Arrhythmogenic cardiomyopathy is a genetically-inherited cardiomyopathy. PKP2 mutations are the most common cause of the disease, associated with conventional ARVC phenotype. Case presentation We presented a 14 years old sportswoman admitted to our emergency department for cardiac arrest-related to ventricular fibrillation. The patient was asymptomatic leading up to cardiac arrest. At admission, she met the diagnosis of AC with bi-ventricular involvement (T negative waves in V1-V6 and inferior leads; severe biventricular dysfunction with fibrofatty replacement involving both ventricles). Family history revealed that her cousin, a 15 years competitive athlete, received a recent diagnosis of ARVC, wherein pathogenetic variant p.Tyr857_Lys859 in heterozygosity in the PKP2 gene was found. As expected, the index case presented the same mutations in PKP2 gene, and no other mutations were found. Implanted cardioverter defibrillator (ICD) and strength follow-up, including heart failure management, was performed. Cascade screening of family members allowed us to identify 19 mutations carriers. Of these, 5 patients were identified to have disease expression. The first to be studied was her 9 years old sister, who involved in high level of sport activities. She presented abnormal ECG with negative T waves in V2-V4, significance burden of premature ventricular complex (PVC >500/24 h) with mild right ventricle dilatation. Of others family members, four patients presented early signs of myocardial disease and significant arrhythmias burden. Except for one patient, all these members were involved in amateur sport activities. Two members had signs of left ventricle (LV) involvement (inverted T waves in leads V4–V6 and inferior leads, LV wall motion abnormalities and late enhancement), whereas one patient (P3) showed a fulfilled ARVD. Three patients presented significant PVC on 24-hour ambulatory ECG monitoring (PVC >500/24 h) (P2, P3 and P5). The arrhythmic burden was more pronounced in two young patients having a sports activity (P2 and P3). This trend was also confirmed at exercise testing. Except for one patient, these findings appear to be related to sport activity, even if this is no high-intensity activity. Among other carriers of pathogenic mutation, three patients showed ECG abnormalities in infero-lateral leads and significance PVC at 24-hour ECG monitoring in absence of other findings related-cardiomyopathy. All family members carried PKP2 mutation were restricted in sports activities, and, in patients presented early disease and arrhythmogenic burden, treatment with beta-blockers was started. Conclusion In this family presenting PKP2 mutation, heterogenicity of disease expression and a close relationship with sport activity was found. This large family case encourages future ACM studies to better understand disease expression and their relationship with sports activity across the entire ACM phenotypic spectrum and ages. Also, this case underscores the importance of early familiar screening, including children involved high-level of sports activity.