BackgroundThere is emerging data of long-term effects of COVID-19 comprising a diversity of symptoms. The aim of this study was to systematically describe and measure pulmonary and extra- pulmonary post COVID-19 complications in relation to acute COVID-19 severity.MethodsPatients attending a standard of care 3-months post-hospitalisation follow-up visit, and those referred by their general practitioner because of persistent post-COVID-19 symptoms were included. Patients underwent symptomatic, quality of life, pulmonary (lung function and HRCT), cardiac (high resolution ECG), physical (1-MSTST, handgrip strength, CPET) and cognitive evaluations.ResultsAll 34 hospitalised and 22 out of 23 non-hospitalised patients had≥1 complaint or abnormal finding at follow-up. 67% of patients were symptomatic (MRC ≥2 or CAT ≥10), with no difference between hospitalised versus non-hospitalised patients. Pulmonary function (FEV1 or DLCO) <80% of predicted) was impaired in 68% of patients. DLCO was significantly lower in those hospitalised compared to non-hospitalised (70.1±18.0 versus 80.2±11.2% predicted, p=0.02). 53% had an abnormal HRCT (predominantly groundglass opacities) with higher composite CT-scores in hospitalised versus non-hospitalised patients (2.3 [0.1, 4.8] and 0.0 [0.0, 0.3], p<0.001). 1-MSTST was below the 25th percentile in almost half of patients, but no signs of cardiac dysfunction were found. Cognitive impairments were present in 59–66% of hospitalised and 31–44% of non-hospitalised patients (p=0.08).ConclusionThree months after COVID-19 infection, patients were still symptomatic and demonstrated objective respiratory, functional, radiological and cognitive abnormalities, which were more prominent in hospitalised patients. Our study underlines the importance of multidimensional management strategies in these patients.

Platelets are known to become activated in vivo by different stressful stimuli such as surgery and dynamic exercise. Mental stress has been shown to increase platelet aggregability. Platelet activation is thought to be of major importance in atherogenesis and cardiac fatalities. In order to clarify further stress-induced platelet activation with special reference to the period after the stress, we studied eight young, healthy volunteers during and for 1 h after a mental stress test (Stroops Colour Word Conflict Test). Using highly standardized techniques, we have measured platelet aggregability ex vivo and the platelet release products beta-thromboglobulin, platelet factor 4 and serotonin in plasma. As markers of the stress response we measured cyclic-AMP in plasma, heart rate, cardiac output and blood pressure. The stress test induced a significant cardiovascular response with increases in heart rate, blood pressure, and cardiac output and as a measure of adrenergic activity an increase in cyclic AMP in plasma during the test. Platelet aggregability was unaffected during the test but decreased following the stress. During the first hour following the test and release products beta-thromboglobulin and serotonin increased significantly in plasma. We conclude that platelets are activated during mental stress and that this activation involves a post-stress release of vasoactive compounds from platelets.

Central haemodynamics in the supine and head-up tilted positions were studied in 24 patients with severe postural hypotension with and without supine hypertension. Results were compared with those obtained in eight normotensive and eight untreated hypertensive controls. In the supine position the patients had higher vascular resistances, lower stroke volumes and longer left ventricular ejection time indexes compared to controls, whereas left ventricular ejection fractions did not differ significantly. The patients with supine hypertension had significantly higher vascular resistance compared to those with supine normotension. The highest supine blood pressure levels were found in patients with multiple system atrophy. During tilt, vascular resistance and heart rates were increased and stroke volumes and left ventricular ejection time indexes were decreased in the controls. The patients were unable to increase their vascular resistance, but increased their heart rate and decreased their left ventricular ejection time indexes to a degree similar to the controls. The reductions in stroke volume were smaller in the patients compared to the controls. Changes in haemodynamics in response to head-up tilting did not differ significantly between patients with supine hypertension and supine normotension. It is concluded that patients with postural hypotension have higher supine vascular resistance and are unable to contract peripheral arteries and arterioles during head-up tilting. Contractility of the left ventricle is preserved and the baroreceptors are partially intact. Postural hypotensive patients with supine hypertension differ from those with supine normotension only with respect to supine vascular resistances.

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