| Autor: |
Nordenswan HK; Heart and Lung Center University of Helsinki and Helsinki University Central Hospital Helsinki Finland., Lehtonen J; Heart and Lung Center University of Helsinki and Helsinki University Central Hospital Helsinki Finland., Ekström K; Heart and Lung Center University of Helsinki and Helsinki University Central Hospital Helsinki Finland., Räisänen-Sokolowski A; Department of Pathology University of Helsinki and Helsinki University Central Hospital Helsinki Finland., Mäyränpää MI; Department of Pathology University of Helsinki and Helsinki University Central Hospital Helsinki Finland., Vihinen T; Heart Center Turku University Hospital Turku Finland., Miettinen H; Heart Center Kuopio University Hospital Kuopio Finland., Kaikkonen K; Medical Research Center Oulu University and University Hospital of Oulu Oulu Finland., Haataja P; Heart HospitalTampere University Hospital Tampere Finland., Kerola T; Department of Internal Medicine Päijät-Häme Central Hospital Lahti Finland., Rissanen TT; Heart Center North Karelia Central Hospital Joensuu Finland., Kokkonen J; Central Finland Central Hospital Jyväskylä Finland., Alatalo A; South Ostrobothnia Central Hospital Seinäjoki Finland., Pietilä-Effati P; Vaasa Central Hospital Vaasa Finland., Utriainen S; South Karelia Central Hospital Lappeenranta Finland., Kupari M; Heart and Lung Center University of Helsinki and Helsinki University Central Hospital Helsinki Finland. |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of the American Heart Association [J Am Heart Assoc] 2021 Mar 16; Vol. 10 (6), pp. e019415. Date of Electronic Publication: 2021 Mar 04. |
| DOI: |
10.1161/JAHA.120.019415 |
| Abstrakt: |
Background Cardiac sarcoidosis (CS) and giant cell myocarditis (GCM) share many histopathologic and clinical features. Whether they are parts of a one-disease continuum has been discussed. Methods and Results We compared medical record data of 351 CS and 28 GCM cases diagnosed in Finland since the late 1980s and followed until February 2018 for a composite end point of cardiac death, aborted sudden death, and heart transplantation. Heart failure was the presenting manifestation in 50% versus 15% ( P <0.001), and high-grade atrioventricular block in 21% versus 43% ( P =0.044), of GCM and CS, respectively. At presentation, left ventricular ejection fraction was ≤50% in 81% of cases of GCM versus in 48% of CS ( P =0.004). The median (interquartile range) of plasma NT-proBNP (N-terminal pro-B-type natriuretic peptide) was 5273 (2782-11309) ng/L on admission in GCM versus 859 (290-1950) ng/L in CS ( P <0.001), and cardiac troponin T exceeded 50 ng/L in 17 of 19 cases of GCM versus in 48 of 239 cases of CS ( P <0.001). The 5-year estimate of event-free survival was 77% (95% CI, 72%-82%) in CS versus 27% (95% CI, 10%-45%) in GCM ( P <0.001). By Cox regression analysis, GCM predicted cardiac events with a hazard ratio of 5.16 (95% CI, 2.82-9.45), which, however, decreased to 1.58 (95% CI, 0.71-3.52) after inclusion of markers of myocardial injury and dysfunction in the model. Conclusions GCM differs from CS in presenting with more extensive myocardial injury and having worse long-term outcome. Yet the key determinant of prognosis appears to be the extent of myocardial injury rather than the histopathologic diagnosis. |
| Databáze: |
MEDLINE |
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