Clin Res Cardiol (2021)
DOI DOI https://doi.org/10.1007/s00392-021-01843-w
A comparative analysis of cardiac outcomes in COVID-19 pneumonias and pneumonias of other origin requiring mechanical ventilation
P. Jirak1, R. Larbig2, Z. Shomanova3, E. Fröb3, D. Dankl4, C. Torgersen4, N. Frank4, M. Mahringer1, D. Butkiene2, H. Haake2, H. Salzer5, T. Tschoellitsch6, M. Lichtenauer1, A. Egle4, B. Lamprecht5, H. Reinecke7, U. C. Hoppe1, L. J. Motloch1, R. Pistulli7
1Klinik für Innere Med. II, Kardiologie u. intern. Intensivmedizin, Universitätsklinik der Salzburger Landeskliniken, Salzburg, AT; 2Klinik für Kardiologie und Int. Intensivmedizin, Krankenhaus St. Franziskus, Kliniken Maria Hilf GmbH, Mönchengladbach; 3Department für Kardiologie und Angiologie, Universitätsklinikum Münster, Münster; 4Universitätsklinik der Salzburger Landeskliniken, Salzburg, AT; 5Pulmologie, Kepler Universitätsklinikum, Linz, AT; 6Kepler Uniklinikum, Linz, AT; 7Klinik für Kardiologie I: Koronare Herzkrankheit, Herzinsuffizienz und Angiologie, Universitätsklinikum Münster, Münster;

Objective:
COVID-19 represents a respiratory virus causing severe pneumonia, but involvement of other organs, predominantly the heart was reported. Whether this is a specific feature consisting of myocarditis, or simply a result of microvascular injury and systemic inflammation, is yet unclear and matter to debate. Given that myocardial injury is also common in other kinds of pneumonias, we investigated and compared such occurrence in severe pneumonias due to COVID-19 and other causes.

Methods and Results:
In total, 156 critically ill patients, 76 COVID-19 and 76 non-COVID patients requiring mechanical ventilation were included (82.9% intubated and 17.1% NIV respectively) in four European tertiary hospitals. Aetiology of pneumonia in the nonCOVID-19 group was bacterial in 67.1%, viral in 28.9% and toxic in 3.9% of patients respectively. Patients were matched for age, gender and ventilator therapy. ICU mortality (COVID-19=38.2% vs. nonCOVID-19=51.3%, p=0.142) was not significantly different between the two groups, while duration of ICU stay was significantly higher in COVID-19 patients (COVID-19=15d vs. nonCOVID-19=12d, p<0.033). Interestingly, myocardial injury (defined as CI hs-Tn above the 99th-percentile of the upper reference limit) was significantly more frequent in nonCOVID-19 (96.4% vs. 78.1%, p=0.004). Systolic function and radiographic signs of cardiomegaly were not significantly different between the two groups, while nonCOVID-19 patients showed a significant higher rate of pulmonary venous congestions (COVID-19=34.2% vs. nonCOVID-19=73.7%, p<0.001). Leukocytes and PCT were also significantly higher in nonCOVID-19 (COVID-19=14.82x109/L vs. nonCOVID-19=20.2x109/L, p<0.001; COVID-19=1,59ng/ml vs. nonCOVID-19=3.0ng/ml, p=0.003 respectively). D-dimer and thromboembolic incidence (COVID-19=23.7% vs. nonCOVID-19=5.3%, p=0.002) driven by pulmonary embolism rates (COVID-19=17.1% vs. nonCOVID-19=2.6%, p=0.005) were higher in COVID-19, while rates of therapeutic anticoagulation did not differ significantly.

Conclusions:
Myocardial injury was frequent in severe COVID-19 requiring mechanical ventilation, but still less frequent than in similarly severe pneumonias of other origin, indicating that  cardiac  involvement may not be a specific feature of COVID-19. While mortality was also similar, COVID-19  is  characterized with  increased thrombogenicity and high pulmonary embolism rates.

 
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