6 research outputs found
COVID-19 pneumonia in patients with chronic myocarditis (hbv-associated with infarct-like debute): specifics of the diseases course, the role of the basic therapy (Part II) [COVID-19 ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΡ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ Ρ Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ΠΈΡΠ°ΠΌΠΈ (HBV-Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΠΌ Ρ ΠΈΠ½ΡΠ°ΡΠΊΡΠΎΠΏΠΎΠ΄ΠΎΠ±Π½ΡΠΌ Π΄Π΅Π±ΡΡΠΎΠΌ): ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΡΠ΅ΡΠ΅Π½ΠΈΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ, ΡΠΎΠ»Ρ Π±Π°Π·ΠΈΡΠ½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ (Π§Π°ΡΡΡ II)]
Chronic infectious-immune myocarditis of severe course can potentially be considered as a factor that aggravates the course of new coronavirus disease (COVID-19) and increases the risk of adverse outcomes. The interaction of chronic myocarditis and COVID-19 during long-term immunosuppressive therapy has not been studied. We present a description of a 35-year-old female patient with chronic infectious-immune myocarditis (morphologically confirmed, with a history of infarction-like onset and thromboembolic complications), who had continuous immunosuppressive therapy with methylprednisolone and mycophenolate mofetil. The patient also received new oral anticoagulants and tenofovir (for chronic HBV infection). COVID-19 (SARS-Cov-2 RNA+) was diagnosed in May 2020. Risk factors for the adverse course of coronavirus infection included severe obesity, heart failure, and life-threatening ventricular arrhythmias. Correction of immunosuppressive therapy (withdrawal of the cytostatic agent, administration of hydroxychloroquine) and therapy with levofloxacin, an interleukin-17 inhibitor (netakimab) were performed. The severity of pneumonia and respiratory failure was moderate despite high fever and high levels of inflammatory markers in the blood (including interleukin-6). Signs of exacerbation of myocarditis, increased levels of troponin T and anticardial antibodies (compared with the initial ones) were not found. It can be assumed that supportive immunosuppressive therapy for myocarditis has a positive effect on the course of coronavirus pneumonia and avoids exacerbation of myocarditis. Careful continuation of immunosuppressive therapy with temporary withdrawal of aggressive cytostatics can be recommended in chronic myocarditis. Further study of the features of the course of previous myocarditis and COVID-19 pneumonia is necessary. Β© 2020 Stolichnaya Izdatelskaya Kompaniya. All rights reserved
COVID-19 pneumonia in patients with chronic myocarditis (recurrent infectious immune): Specifics of the diseases course, the role of basic therapy (Part 1) [COVID-19 ΠΏΠ½Π΅Π²ΠΌΠΎΠ½ΠΈΡ Ρ Π±ΠΎΠ»ΡΠ½ΡΡ Ρ Ρ ΡΠΎΠ½ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ΠΈΡΠ°ΠΌΠΈ (ΡΠ΅ΡΠΈΠ΄ΠΈΠ²ΠΈΡΡΡΡΠΈΠΉ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΎΠ½Π½ΠΎ-ΠΈΠΌΠΌΡΠ½Π½ΡΠΉ): ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΡΠ΅ΡΠ΅Π½ΠΈΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ, ΡΠΎΠ»Ρ Π±Π°Π·ΠΈΡΠ½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ (Π§Π°ΡΡΡ 1)]
Patients with chronic myocarditis have a high risk of an unfavorable course of the novel coronavirus disease (COVID-19) due to the ability of the SARS-Cov-2 virus to independently cause acute myocarditis, to have a direct and cytokine-mediated cytopathic effect on the myocardium, as well as immunosuppressive therapy. At the same time, the features of the interaction of chronic myocarditis and COVID-19 have not been studied. The article describes a 31-year-old patient with a 10-year history of chronic recurrent infectious-immune myocarditis, who was on long-term immunosuppressive therapy (methylprednisolone and azathioprine in the past, then hydroxychloroquine). In May 2020, a serologically confirmed COVID-19 diagnosis was made. There were risk factors for the unfavorable course of coronavirus infection: heart failure and a history of persistent atrial fibrillation, male sex. Basic therapy with hydroxychloroquine (with an increase in its dose to 800-400 mg/day), ceftriaxone, and levofloxacin was carried out. The severity of pneumonia was moderate, despite febrile fever and severe intoxication. No relapses of arrhythmias, respiratory or heart failure were observed. Minimal laboratory (some increase in anticardial antibody titers) and echocardiographic signs of exacerbation of myocarditis without an increase in troponin T levels were revealed, which quickly regressed. It can be assumed that the maintenance immunosuppressive therapy of myocarditis with hydroxychloroquine had a positive effect on the course of coronavirus pneumonia and made it possible to avoid recurrence of myocarditis. Further study of the features of the course of the pre-existing myocarditis and pneumonia in COVID-19 is necessary. Β© 2020 Stolichnaya Izdatelskaya Kompaniya. All rights reserved
Π‘ΠΎΡΠ΅ΡΠ°Π½ΠΈΠ΅ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΠΏΡΠ°Π²ΠΎΠ³ΠΎ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠΊΠ° ΠΈ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΠΎΠ³ΠΎ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄Π° Π»Π΅Π²ΠΎΠ³ΠΎ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠΊΠ° ΠΊΠ°ΠΊ ΠΎΡΠΎΠ±Π°Ρ ΡΠΎΡΠΌΠ° ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠΈ: ΠΊΠ»ΠΈΠ½ΠΈΠΊΠ°, Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠ°, Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠ°Ρ ΠΏΡΠΈΡΠΎΠ΄Π°, ΡΠ΅ΡΠ΅Π½ΠΈΠ΅
Background. A few cases of combination of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC) with left ventricular noncompaction (LVNC) have been described. Aims to study the genetics, diagnostical features and clinical course of the combination of ARVC with LVNC. Methods. 58 patients with ARVC diagnosis (26 men; mean age 39.1 14.2 years; mean follow-up period 21.5 [6; 60] months) and 125 patients with LVNC (74 men; mean age 46.4 15.1 years; mean follow-up period 14 [3; 40] months). All patients underwent electrocardiogram (ECG), echocardiography, 24-h ECG monitoring. Heart MRI was performed in 53 (91.4%) patients with ARVC and 60 (48%) with LVNC, heart CT in 18 (31%) patients with ARVC and 89 (71.2%) with LVNC. For all patients with combination of ARVC and LVNC DNA-diagnostic was performed using both ARVC (PKP2, DSG2, DSP, DSC2, JUP, TMEM43, TGFB3, PLN, LMNA, DES, CTTNA3, EMD, SCN5A, LDB3, CRYAB, FLNC) and LVNC (MYH7, MYBPC3, TAZ, TPM1, LDB3, MYL2, MYL3, ACTC1, TNNT2, TNI3) gene panels. Results. Combination of ARVC and LVNC was found in 9 patients (15.5% of patients form ARVC cohort and 7.2% from LVNC cohort). These patients were distinguished from patients with isolated ARVC or LVNC by aggressive ventricular arrhythmias (frequent premature ventricular beats, sustained ventricular tachycardia, significantly worse antiarrhythmic therapy effect, appropriate shocks of implanted cardioverter-defibrillators (ICD) in all patients with ICD). Patients with combination of ARVC + LVNC were also distinguished from patients with isolated LVNC by the dilatation of RV, low QRS voltage on ECG, presence of AV block, absence of signs of LV hypertrophy on ECG. LV dilatation with reduction of its ejection fraction distinguished patients with mixed cardiomyopathy from patients with isolated ARVC. Potentially pathogenic variants (IVV classes of pathogenicity) and variants of unclear clinical significance (III class of pathogenicity) were found in both desmosomal and non-desmosomal genes in 78% of patients, including 3 (33%) in DSP gene. Conclusions. The combination of ARVC and LVNC can be caused by mutations in both desmosomal and non-desmosomal genes and has typical features: aggressive, resistant ventricular rhythm abnormalities leading to appropriate ICD shocks and a high risk of sudden cardiac death.ΠΠ±ΠΎΡΠ½ΠΎΠ²Π°Π½ΠΈΠ΅. Π Π»ΠΈΡΠ΅ΡΠ°ΡΡΡΠ΅ ΠΎΠΏΠΈΡΠ°Π½Ρ Π»ΠΈΡΡ Π΅Π΄ΠΈΠ½ΠΈΡΠ½ΡΠ΅ ΡΠ»ΡΡΠ°ΠΈ ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΡ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΠΏΡΠ°Π²ΠΎΠ³ΠΎ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠΊΠ° (ΠΠ) ΠΈ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΠΎΠ³ΠΎ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄Π° Π»Π΅Π²ΠΎΠ³ΠΎ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠΊΠ° (ΠΠ). Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΠΈΠ·ΡΡΠΈΡΡ Π³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΡΡ ΠΏΡΠΈΡΠΎΠ΄Ρ, Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΏΡΠΈΠ·Π½Π°ΠΊΠΈ ΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ΅ ΡΠ΅ΡΠ΅Π½ΠΈΠ΅ ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΡ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΠΠ ΠΈ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΠΎΠ³ΠΎ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄Π° ΠΠ. ΠΠ΅ΡΠΎΠ΄Ρ. 58 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π΄ΠΈΠ°Π³Π½ΠΎΠ·ΠΎΠΌ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½Π°Ρ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΡ ΠΠ (26 ΠΌΡΠΆΡΠΈΠ½; ΡΡΠ΅Π΄Π½ΠΈΠΉ Π²ΠΎΠ·ΡΠ°ΡΡ 39,1 14,2 Π³ΠΎΠ΄Π°; ΡΡΠ΅Π΄Π½ΠΈΠΉ ΡΡΠΎΠΊ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ 21,5 [6; 60] ΠΌΠ΅Ρ) ΠΈ 125 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π΄ΠΈΠ°Π³Π½ΠΎΠ·ΠΎΠΌ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΡΠΉ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ ΠΠ (74 ΠΌΡΠΆΡΠΈΠ½Ρ; ΡΡΠ΅Π΄Π½ΠΈΠΉ Π²ΠΎΠ·ΡΠ°ΡΡ 46,4 15,1 Π³ΠΎΠ΄Π°; ΡΡΠ΅Π΄Π½ΠΈΠΉ ΡΡΠΎΠΊ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ 14 [3; 40] ΠΌΠ΅Ρ). ΠΡΠ΅ΠΌ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°ΠΌ Π²ΡΠΏΠΎΠ»Π½Π΅Π½Ρ ΠΠΠ, ΡΡ
ΠΎΠΊΠ°ΡΠ΄ΠΈΠΎΠ³ΡΠ°ΡΠΈΡ, ΡΡΡΠΎΡΠ½ΠΎΠ΅ ΠΌΠΎΠ½ΠΈΡΠΎΡΠΈΡΠΎΠ²Π°Π½ΠΈΠ΅ ΠΠΠ ΠΏΠΎ Π₯ΠΎΠ»ΡΠ΅ΡΡ. ΠΠ Π’ ΡΠ΅ΡΠ΄ΡΠ° Π²ΡΠΏΠΎΠ»Π½Π΅Π½Π° 53 (91,4%) ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°ΠΌ Ρ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠ΅ΠΉ ΠΠ ΠΈ 60 (48%) Ρ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΡΠΌ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ΠΎΠΌ ΠΠ, ΠΠ‘ΠΠ’ ΡΠ΅ΡΠ΄ΡΠ° 18 (31%) ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°ΠΌ Ρ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠ΅ΠΉ ΠΠ ΠΈ 89 (71,2%) Ρ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΡΠΌ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ΠΎΠΌ ΠΠ. ΠΡΠ΅ΠΌ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠ°ΠΌ Ρ ΡΠΎΡΠ΅ΡΠ°Π½ΠΈΠ΅ΠΌ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΠΠ ΠΈ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΠΎΠ³ΠΎ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄Π° ΠΠ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ ΠΏΠΎΠΈΡΠΊ ΠΌΡΡΠ°ΡΠΈΠΉ Ρ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ΠΌ ΠΏΠ°Π½Π΅Π»Π΅ΠΉ Π³Π΅Π½ΠΎΠ² Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΠΠ (PKP2, DSG2, DSP, DSC2, JUP, TMEM43, TGFB3, PLN, LMNA, DES, CTTNA3, EMD, SCN5A, LDB3, CRYAB, FLNC) ΠΈ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΠΎΠ³ΠΎ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄Π° ΠΠ (MYH7, MYBPC3, TAZ, TPM1, LDB3, MYL2, MYL3, ACTC1, TNNT2, TNNI3). Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. Π‘ΠΎΡΠ΅ΡΠ°Π½ΠΈΠ΅ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΠΠ ΠΈ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΠΎΠ³ΠΎ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄Π° ΠΠ Π²ΡΡΠ²Π»Π΅Π½ΠΎ Ρ 9 Π±ΠΎΠ»ΡΠ½ΡΡ
, ΡΡΠΎ ΡΠΎΡΡΠ°Π²ΠΈΠ»ΠΎ 15,5% ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Π² ΠΊΠΎΠ³ΠΎΡΡΠ΅ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΠΠ ΠΈ 7,2% ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Π² ΠΊΠΎΠ³ΠΎΡΡΠ΅ Ρ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΡΠΌ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ΠΎΠΌ ΠΠ. ΠΡΠΈΡ
ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² ΠΎΡΠ»ΠΈΡΠ°ΡΡ ΠΎΡ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΠΈΠ·ΠΎΠ»ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠ΅ΠΉ ΠΠ ΠΈΠ»ΠΈ ΠΈΠ·ΠΎΠ»ΠΈΡΠΎΠ²Π°Π½Π½ΡΠΌ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΡΠΌ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ΠΎΠΌ ΠΠ Π°Π³ΡΠ΅ΡΡΠΈΠ²Π½ΡΠ΅ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠΊΠΎΠ²ΡΠ΅ Π½Π°ΡΡΡΠ΅Π½ΠΈΡ ΡΠΈΡΠΌΠ° (ΡΠ°ΡΡΠ°Ρ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠΊΠΎΠ²Π°Ρ ΡΠΊΡΡΡΠ°ΡΠΈΡΡΠΎΠ»ΠΈΡ, ΡΡΡΠΎΠΉΡΠΈΠ²Π°Ρ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠΊΠΎΠ²Π°Ρ ΡΠ°Ρ
ΠΈΠΊΠ°ΡΠ΄ΠΈΡ Ρ Π΄ΠΎΡΡΠΎΠ²Π΅ΡΠ½ΠΎ Ρ
ΡΠ΄ΡΠΈΠΌ ΡΡΡΠ΅ΠΊΡΠΎΠΌ Π°Π½ΡΠΈΠ°ΡΠΈΡΠΌΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ, Π°Π΄Π΅ΠΊΠ²Π°ΡΠ½ΡΠ΅ ΡΡΠ°Π±Π°ΡΡΠ²Π°Π½ΠΈΡ ΠΈΠΌΠΏΠ»Π°Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠ³ΠΎ ΠΊΠ°ΡΠ΄ΠΈΠΎΠ²Π΅ΡΡΠ΅ΡΠ°-Π΄Π΅ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΎΡΠ° ΠΎΡΠΌΠ΅ΡΠ΅Π½Ρ Ρ Π²ΡΠ΅Ρ
Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΠΈΠΌΠΏΠ»Π°Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΡΠΌ ΠΊΠ°ΡΠ΄ΠΈΠΎΠ²Π΅ΡΡΠ΅ΡΠΎΠΌ-Π΄Π΅ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΎΡΠΎΠΌ). ΠΡ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ ΠΈΠ·ΠΎΠ»ΠΈΡΠΎΠ²Π°Π½Π½ΡΠΌ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΡΠΌ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄ΠΎΠΌ ΠΠ Π±ΠΎΠ»ΡΠ½ΡΡ
ΡΠΎ ΡΠΌΠ΅ΡΠ°Π½Π½ΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠ΅ΠΉ ΠΎΡΠ»ΠΈΡΠ°Π»ΠΈ ΡΠ°ΠΊΠΆΠ΅ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΠ΅ ΠΠ ΠΏΠΎ Π΄Π°Π½Π½ΡΠΌ ΡΡ
ΠΎΠΊΠ°ΡΠ΄ΠΈΠΎΠ³ΡΠ°ΡΠΈΠΈ, ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ Π²ΠΎΠ»ΡΡΠ°ΠΆΠ° QRS Π½Π° ΠΠΠ, Π½Π°Π»ΠΈΡΠΈΠ΅ ΠΠ-Π±Π»ΠΎΠΊΠ°Π΄Ρ, ΠΎΡΡΡΡΡΡΠ²ΠΈΠ΅ ΠΏΡΠΈΠ·Π½Π°ΠΊΠΎΠ² Π³ΠΈΠΏΠ΅ΡΡΡΠΎΡΠΈΠΈ ΠΠ Π½Π° ΠΠΠ. ΠΠΈΠ»Π°ΡΠ°ΡΠΈΡ ΠΠ ΡΠΎ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ΠΌ Π΅Π³ΠΎ ΡΡΠ°ΠΊΡΠΈΠΈ Π²ΡΠ±ΡΠΎΡΠ° ΠΎΡΠ»ΠΈΡΠ°Π»Π° ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² ΡΠΎ ΡΠΌΠ΅ΡΠ°Π½Π½ΠΎΠΉ ΠΊΠ°ΡΠ΄ΠΈΠΎΠΌΠΈΠΎΠΏΠ°ΡΠΈΠ΅ΠΉ ΠΎΡ Π±ΠΎΠ»ΡΠ½ΡΡ
Ρ ΠΈΠ·ΠΎΠ»ΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠΉ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠ΅ΠΉ ΠΠ. ΠΠΎΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΡΠ΅ Π²Π°ΡΠΈΠ°Π½ΡΡ (IVV ΠΊΠ»Π°ΡΡΠΎΠ² ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ) ΠΈ Π²Π°ΡΠΈΠ°Π½ΡΡ Π½Π΅ΡΡΠ½ΠΎΠ³ΠΎ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π·Π½Π°ΡΠ΅Π½ΠΈΡ (III ΠΊΠ»Π°ΡΡ ΠΏΠ°ΡΠΎΠ³Π΅Π½Π½ΠΎΡΡΠΈ) ΠΎΠ±Π½Π°ΡΡΠΆΠ΅Π½Ρ ΠΊΠ°ΠΊ Π² Π΄Π΅ΡΠΌΠΎΡΠΎΠΌΠ½ΡΡ
, ΡΠ°ΠΊ ΠΈ Π² Π½Π΅Π΄Π΅ΡΠΌΠΎΡΠΎΠΌΠ½ΡΡ
Π³Π΅Π½Π°Ρ
Ρ 78% ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ², Π² ΡΠΎΠΌ ΡΠΈΡΠ»Π΅ Ρ 3 (33%) Π² Π³Π΅Π½Π΅ DSP. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. Π‘ΠΎΡΠ΅ΡΠ°Π½ΠΈΠ΅ Π°ΡΠΈΡΠΌΠΎΠ³Π΅Π½Π½ΠΎΠΉ Π΄ΠΈΡΠΏΠ»Π°Π·ΠΈΠΈ ΠΠ ΠΈ Π½Π΅ΠΊΠΎΠΌΠΏΠ°ΠΊΡΠ½ΠΎΠ³ΠΎ ΠΌΠΈΠΎΠΊΠ°ΡΠ΄Π° ΠΠ Π²ΡΡΡΠ΅ΡΠ°Π΅ΡΡΡ ΡΠ°ΡΠ΅, ΡΠ΅ΠΌ ΠΏΡΠΈΠ½ΡΡΠΎ ΡΡΠΈΡΠ°ΡΡ, ΠΌΠΎΠΆΠ΅Ρ Π±ΡΡΡ ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½ΠΎ ΠΌΡΡΠ°ΡΠΈΡΠΌΠΈ ΠΊΠ°ΠΊ Π² Π΄Π΅ΡΠΌΠΎΡΠΎΠΌΠ½ΡΡ
, ΡΠ°ΠΊ ΠΈ Π² Π½Π΅Π΄Π΅ΡΠΌΠΎΡΠΎΠΌΠ½ΡΡ
Π³Π΅Π½Π°Ρ
ΠΈ ΠΎΠ±Π»Π°Π΄Π°Π΅Ρ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠ½ΡΠΌΠΈ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΡΠΌΠΈ, ΡΠ°ΠΊΠΈΠΌΠΈ ΠΊΠ°ΠΊ Π°Π³ΡΠ΅ΡΡΠΈΠ²Π½ΡΠ΅, ΡΠ΅Π·ΠΈΡΡΠ΅Π½ΡΠ½ΡΠ΅ ΠΊ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠΊΠΎΠ²ΡΠ΅ Π½Π°ΡΡΡΠ΅Π½ΠΈΡ ΡΠΈΡΠΌΠ°, ΠΏΡΠΈΠ²ΠΎΠ΄ΡΡΠΈΠ΅ ΠΊ Π°Π΄Π΅ΠΊΠ²Π°ΡΠ½ΡΠΌ ΡΡΠ°Π±Π°ΡΡΠ²Π°Π½ΠΈΡΠΌ ΠΈΠΌΠΏΠ»Π°Π½ΡΠΈΡΠΎΠ²Π°Π½Π½ΠΎΠ³ΠΎ ΠΊΠ°ΡΠ΄ΠΈΠΎΠ²Π΅ΡΡΠ΅ΡΠ°-Π΄Π΅ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠΎΡΠ°, ΠΈ Π²ΡΡΠΎΠΊΠΈΠΉ ΡΠΈΡΠΊ Π²Π½Π΅Π·Π°ΠΏΠ½ΠΎΠΉ ΡΠ΅ΡΠ΄Π΅ΡΠ½ΠΎΠΉ ΡΠΌΠ΅ΡΡΠΈ
Arterial stiffness in the light of thromboembolic complications in elderly patients with atrial fibrillation
Clinical presentation, disease course, and outcome of COVID-19 in hospitalized patients with and without pre-existing cardiac disease: a cohort study across 18 countries
Aims Patients with cardiac disease are considered high risk for poor outcomes following hospitalization with COVID-19. The primary aim of this study was to evaluate heterogeneity in associations between various heart disease subtypes and in-hospital mortality.Methods and results We used data from the CAPACITY-COVID registry and LEOSS study. Multivariable Poisson regression models were fitted to assess the association between different types of pre-existing heart disease and in-hospital mortality. A total of 16 511 patients with COVID-19 were included (21.1% aged 66-75 years; 40.2% female) and 31.5% had a history of heart disease. Patients with heart disease were older, predominantly male, and often had other comorbid conditions when compared with those without. Mortality was higher in patients with cardiac disease (29.7%; n= 1545 vs. 15.9%; n= 1797). However, following multivariable adjustment, this difference was not significant [adjusted risk ratio (aRR) 1.08, 95% confidence interval (CI) 1.02-1.15; P = 0.12 (corrected for multiple testing)]. Associations with in-hospital mortality by heart disease subtypes differed considerably, with the strongest association for heart failure (aRR 1.19, 95% CI 1.10-1.30; P <0.018) particularly for severe (New York Heart Association class III/IV) heart failure (aRR 1.41, 95% CI 1.20-1.64; P < 0.018). None of the other heart disease subtypes, including ischaemic heart disease, remained significant after multivariable adjustment. Serious cardiac complications were diagnosed in <1% of patients.Conclusion Considerable heterogeneity exists in the strength of association between heart disease subtypes and in-hospital mortality. Of all patients with heart disease, those with heart failure are at greatest risk of death when hospitalized with COVID-19. Serious cardiac complications are rare during hospitalization.[GRAPHICS]