ABSTRACT
Post-coronavirus disease 19 (COVID-19) syndrome has substantial health and economic implications. It is multi-systemic, with prevalent autonomic symptoms. Understanding presentations and potential autonomic causes may help guide treatment strategies and recovery. All patients with a suspected or confirmed history of COVID-19 infection who underwent autonomic testing between May 2020 and October 2021 were reviewed retrospectively. We evaluated 62 patients (20 male, 42 female, mean age of 41.38 +/-11.52). COVID-19 was PCR confirmed in 15 patients (26%), and five (8%) required acute hospital intervention. Most common symptoms included palpitations (81%), lightheadedness/ dizziness (62%), dyspnoea (48%), fatigue (46%), or cognitive symptoms (33%) Autonomic testing showed normal blood pressure responses to pressor stimuli, a mean respiratory sinus arrhythmia of 18.89b/m, and Valsalva ratio of 2.09. Postural tachycardia syndrome (PoTS) was diagnosed in 12 patients, autonomically mediated syncope (AMS) in 11, neurogenic orthostatic hypotension (NOH) in two, and initial orthostatic hypotension (IOH) in seven. Normal supine and upright plasma noradrenaline levels were measured in 34 patients (mean 283.38 pg/ml supine;472.43pg/ml tilted). Autonomic testing was reassuring (PoTS and syncope) in the majority with abnormal testing (n=32, or 52%). Further phenotyping of PoTS to exclude neuropathic pathology may be needed. IOH and OH are important considerations.
ABSTRACT
A 76 year old woman was admitted to our hospital for self-limiting dyspnoea (NYHA class III) in oxygen dependence and frequent lipothymia following Valsalva manoeuvres. She was previously admitted to a Spoke Centre for heart failure (HF) with preserved ejection fraction (EF) and a new diagnosis of “pre-capillary pulmonary hypertension (PH)”. Despite a diagnosis of PH of unclear aetiology, she was started on macitentan without being reassessed for functional capacity due to Covid emergency;because of worsening symptoms, she was admitted to our Hub Centre. Resting ECG showed right axis deviation, right ventricle (RV) hypertrophy, first-degree atrioventricular block and right bundle branch block. Transthoracic echocardiography (TTE) showed reduced left ventricular (LV) volume with preserved EF (diastolic volume= 37 ml, EF=88%), severe right atrial and RV dilation with flattening of the interventricular septum, estimated pulmonary artery systolic pressure (PASP) of 124 mmHg, and moderate calcific aortic stenosis (peak aortic velocity 3.3 m/s, mean gradient 25 mmHg, valve area 1.1 cm2). Right and left heart catheterization showed severe pre-capillary PH (mean pulmonary pressure 60 mmHg, mean wedge 11 mmHg, pulmonary vascular resistance 14.41 WU), a severe aortic valve stenosis (aortic valve area 0.68 cmq and peak-to-peak gradient 25 mmHg, slight reduction of cardiac index 2.04 l/min/mq) and no significant coronary artery disease. The degree of aortic stenosis was considered as moderate-severe by integrating data of transesophageal echocardiography (planimetric area 1cm2) and assessment of calcium score (1615 Agatson units). Pneumological causes, chronic thromboembolic PH, rheumatologic diseases, HIV infection, paraneoplastic origin and veno-occlusive disease were all ruled out as potential PH causes and a diagnosis of Idiopathic pulmonary arterial hypertension (IPAH) was finally made. The Heart Team established the best therapeutic option was a transcatheter aortic valve replacement (TAVI) allowing better haemodynamic tolerability of PH therapy. The patient underwent TAVI and was started on PH therapy;a complete atrio-ventricular block developed after the procedure, requiring permanent pacemaker (PM) implantation. Unfortunately, few days later, the patient died following pacemaker's lead dislocation. Conclusion: PH has a diverse aetiology, and prognosis is generally poor, especially in patients with severe comorbidities. (Figure Presented).
ABSTRACT
Background: The pathophysiologic mechanisms leading to spontaneous pneumomediastinum (SP) in SARS-CoV-2 patients with severe pneumonia, during mechanical ventilation, are yet not fully elucidated. Case description: We report the case of a 21 years old man with positivity for COVID-19 infection. At admission in our department the patient had oxygen saturation of 95% in Venturi mask with FiO2 40%. Chest Computed Tomography (CT) showed extensive areas of increased density of “ground-glass” type with evolution towards crazy paving, involving of 50% of lung parenchyma. On day after admission, the condition of the patient worsened to required mechanical ventilation. Control CT highlighted severe pneumomediastinum and extensive subcutaneous emphysema. The patient was managed with conservative treatments and with high flow nasal cannula (HFNC). A week later chest CT showed almost complete resolution of subcutaneous emphysema and pneumomediastinum. The improvement of the blood gas parameters allowed weaning from the HFNC and suspension of oxygen therapy. Conclusions: Although the mechanism of the SP still remains unknown, the presumed cause is the combination of diffuse alveolar injuries due to SARS-CoV-2 and an increase intra-alveolar pressure with barotrauma due to coughing, Valsalva maneuvers or mechanical ventilation. Presumably in SARS-CoV-2 related SP lung frailty, due to crazy paving pattern, impairs compliance e reduces lung tolerance to pressure variations. HFNC could be a safe ventilatory support for critical COVID-19 pneumonia together antitussive and sedatives drugs.
ABSTRACT
Symptoms of autonomic dysfunction, particularly those of orthostatic intolerance, continue to represent a major component of the currently recognized post-acute sequelae of SARS-CoV-2 infections. Different pathophysiologic mechanisms can be involved in the development of orthostatic intolerance including hypovolemia due to gastrointestinal dysfunction, fatigue-associated deconditioning, and hyperadrenergic state due to pandemic-related anxiety. Additionally, there has been a well-established association of a common primary autonomic disorder like postural orthostatic tachycardia syndrome, a subtype of orthostatic intolerance, with antecedent viral infections. Here we report a case of neuropathic type postural orthostatic tachycardia syndrome as a form of autonomic neuropathy that developed following COVID-19 infection.