Percutaneous thrombectomy and right ventricular mechanical circulatory support for pulmonary embolism in a COVID-19 patient: Case report, one-year update, and echocardiographic findings

Background We previously described percutaneous thrombectomy and right ventricular mechanical support of a COVID-19 patient with a massive pulmonary embolism. Here we present a detailed echocardiographic and clinical timeline with 1 year follow-up. Case Summary A 57-year-old female with COVID-19 went into shock from a massive pulmonary embolism. After percutaneous removal of a large thrombus burden (AngioVac system; AngioDynamics Inc, Latham, NY, USA), she became severely hypotensive, requiring CPR, and was resuscitated with an Impella RP device (Abiomed, Danvers, MA, USA). A pediatric TEE probe monitored the procedure because an adult probe would not pass (S7-3t—Philips Medical Systems, Andover, MA, USA). Post thrombectomy, surface imaging documented gradual resolution of right ventricular dysfunction, tricuspid regurgitation, and elevated pulmonary artery pressure. Her course was complicated by renal failure requiring temporary dialysis. She was discharged home on apixaban. Hypercoagulability work-up was negative. Two months later, vocal cord surgery was performed for persistent stridor. Esophagoscopy at that time was prevented by osteophyte obstruction. At 10 months, she received the Pfizer-BioNTech vaccine. At one year, the patient remains healthy on apixaban, and her echocardiogram is normal. Discussion This case illustrates the pivotal role of echocardiography in the diagnosis, percutaneous treatment, and near- and long-term follow-up and management of a patient with massive pulmonary embolism due to COVID-19 with documentation of complete recovery from severe right ventricular dysfunction and hemodynamic collapse. A pediatric TEE probe was a crucial alternative to the adult probe because of possible osteophyte obstruction.

216 The ‘inflammatory perfect storm’: a case of COVID-19 pneumonia complicated by pulmonary embolism

Aims The inflammatory ‘cytokine storm’ that distinguishes COVID-19 pneumonia is associated with a state of systemic hypercoagulability, which leads to thrombotic complications on the venous, arterial, and microvascular side. Indeed, in patients with COVID-19, systemic inflammation, coagulation activation, hypoxemia, and immobilization expose a high risk of pulmonary embolism, which significantly worsens the prognosis of these patients. Methods and results In this report, we discuss the case of a 71-year-old female, with no prior medical history, admitted to the emergency department for syncope, dyspnoea, and fever started 48 h earlier. At presentation, ear temperature was 37 °C, oxygen saturation was 96% on oxygen therapy (6 l/min), the patient appeared hypertensive (160/80 mmHg) and tachycardic (114 b.p.m.). Laboratory tests revealed normal white blood cells count (10 000/μl) and increased C reactive protein (5.60 mg/dl), troponin I (0.417 ng/ml), and d-dimer levels (15743 ng/ml). Electrocardiogram showed sinus tachycardia at HR of 120/min, normal atrioventricular conduction time, new onset right bundle branch block, and inverted T waves on DIII. Considering the symptoms, CTPA was performed, revealing massive acute bilateral pulmonary embolism with peripheral ground glass opacities. Those findings were suggestive of COVID-19 pneumonia. Indeed, the patient was positive for SARS-CoV-2 infection, and a diagnosis of COVID-19 pneumonia complicated by pulmonary embolism was made. Treatments included oxygen, subcutaneous low molecular weight heparin (LWMH), and corticosteroids have been administrated according to current international guidelines. Since no haemodynamic instability was observed during hospitalization the patient was discharged on Warfarin therapy for 6 months. Conclusions In COVID-19 patients treated in a hospital the incidence of pulmonary embolism (PE) is very high. Patients with COVID-19 infection have respiratory symptoms, which often may not be distinguishable from pulmonary embolism symptoms. So, unexpected respiratory worsening, signs of right ventricular dysfunction on transthoracic echocardiogram, and ECG changes should lead to suspicion of the co-presence of pulmonary embolism. This case report shows how COVID-19 infection can be strongly associated with thrombotic complications. For this reason, the guidelines recommend anticoagulation at standard prophylactic doses in all patients admitted with COVID-19 infection.

264 Cardiac and pulmonary sequelae after COVID-19 pneumonia: a case series

Aims Although the new coronavirus (SARS-CoV-2) may cause an acute multiorgan syndrome (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 occurring after COVID-19 pneumonia. Methods and results 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). Out of 29 patients (mean age 70 ± 10 years old; M 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. ECG repolarization abnormalities were extremely common (93%) and 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 only, but values of systolic pulmonary artery pressure were abnormal in 16 (55%) despite absence of prior comorbidities in 44% of them. Regarding LUS evaluation, most patients displayed abnormal values of diaphragmatic thickness and excursion (93%) which well correlated with the high prevalence (76%) of on pathological findings on CT scan. CUS ruled out deep vein thrombosis in all patients. Conclusions Data on cardiopulmonary sequelae after COVID-19 pneumonia are scarce. In our study, simple diagnostic tools (TTE and LUS) proved clinically useful for detection of cardiopulmonary involvement after COVID-19 pneumonia.

535 Right ventricular dysfunction is independent predictor of in-hospital mortality in patients with low flow low gradient aortic stenosis

Aims Aim of the study is to assess the prevalence and in-hospital death in patients with low flow low gradient aortic stenosis (LFLG-AS) and right ventricular dysfunction (RVD) hospitalized for heart failure in a single referral centre. Methods and results Complete demographic, clinical characteristics, and imaging data were collected. Patients with LFLG AS hospitalized for heart failure were prospectively enrolled from 2013 to 2021. LFLG-AS was defined as indexed aortic valve area (iAVA) ≤0.6 cm2/m2, mean transaortic gradient < 40 mmHg, and stroke volume index <36 ml/m2. RVD was defined as tricuspid annular plane systolic excursion (TAPSE) < 16 mm at baseline in apical four chamber view according to current guidelines. Patients were divided into two subgroups according to the presence or absence of RVD. In hospitals all cause death has been considered as the primary outcome. A total of 130 patients [78 ± 10 yy; 67 (51%) male] with new diagnosis of LF-LG AS were included in the study. The most frequent comorbidities were hypertension (88.5%; n = 114), dyslipidaemia (74%; n = 96), and diabetes (38%; n = 49). Concomitant coronary artery disease and history of stroke were reported in 19% (n = 24) and 9% (n = 11), respectively. Society of thoracic surgeons score in overall population was 12.6 ± 4.5. Regarding echocardiographic evaluation, the mean transaortic gradient was 25.81 ± 7.42 mmHg and the mean iAVA was 0.42 ± 0.10 cm/m2. The mean left ventricular ejection fraction (LV EF) was 46 ± 13%. LFLG AS with a preserved LV EF was detected in 69 patients (53%) and the LFLG AS with a low LV EF was detected in 61 patients (47%). 26 patients (20%) underwent surgical valve replacement, 14 patients (11%) had aortic percutaneous valvuloplasty and 31 patients (24%) underwent TAVI. The remaining patients (45%, n = 59) were maintained under optimized medical therapy. In-hospital death occurred in 16 patients. When compared patients with RVD with those without a higher prevalence of atrial fibrillation/flutter (n = 21, 36%; P = 0.042) and in hospital death was observed (n = 8; 28%; n = 8, 8%; P = 0.026). In the overall population at multivariate regression analysis only RVD was a significant independent predictor of all-cause in-hospital death (P = 0.028; OR: 3.44; CI: 1.146–10.334). Conclusions RVD can be detected in more than one quarter of patient with new diagnosis of LFLG AS and is an independent predictor of all-cause in-hospital death. Quantification of right ventricular systolic function in these complex population give important information in identifying patients and higher risk requiring more aggressive therapy.