Anti-heart antibodies levels and their correlation with clinical symptoms and outcomes in patients with confirmed or suspected diagnosis COVID-19.

The aim of this study is to evaluate the blood level of anti-heart antibodies (AHA) and its correlation with clinical outcomes in patients with severe and moderate coronavirus disease 2019 (COVID-19). The study included 34 patients (23 males; mean age 60.2 ± 16.6 years) with COVID-19 pneumonia. Besides standard medical examination, the AHA blood levels were observed, including antinuclear antibodies, antiendothelial cell antibodies, anti-cardiomyocyte antibodies (AbC), anti-smooth muscle antibodies (ASMA), and cardiac conducting tissue antibodies. Median hospital length of stay was 14 [13; 18] days. AHA levels were increased in 25 (73.5%) patients. Significant correlation (p < 0.05) of AHA levels with cardiovascular manifestations (r = 0.459) was found. AbC levels correlated with pneumonia severity (r = 0.472), respiratory failure (r = 0.387), need for invasive ventilation (r = 0.469), chest pain (r = 0.374), low QRS voltage (r = 0.415), and levels of C-reactive protein (r = 0.360) and lactate dehydrogenase (r = 0.360). ASMA levels were found to correlate with atrial fibrillation (r = 0.414, p < 0.05). Antinuclear antibodies and AbC levels correlated with pericardial effusion (r = 0.721 and r = 0.745, respectively, p < 0.05). The lethality rate was 8.8%. AbC and ASMA levels correlated significantly with lethality (r = 0.363 and r = 0.426, respectively, p < 0.05) and were prognostically important. AHA can be considered as part of the systemic immune and inflammatory response in COVID-19. Its possible role in the inflammatory heart disease requires further investigation.

Previous and First Detected Cardiovascular Diseases in Patients with New Coronavirus Pneumonia: Possible Mechanisms and Place in a Unified Prognostic Model.

PURPOSE: The aim of this study is to evaluate the frequency of cardiac involvement in patients with coronavirus disease 2019 (COVID-19), possible immune mechanisms of myocardial injury, and the place of cardiovascular pathology among other prognostic factors. METHODS: The study included 86 patients (48 male, 60.2 ± 16.6 years) with COVID-19. In addition to common investigation, examination of troponin T (n = 18) and anti-heart antibodies (AHA, n = 34) were used. The average hospital period was 14 [12; 18] days. RESULTS: The incidence of cardiovascular disease and symptoms was 45.3%. Arrhythmias, heart failure, low-QRS voltage, repolarization disorders, and pericardial effusion were the typical for coronavirus cardiac injury. The level of AHA was increased in 73.5%. Significant (p < 0.05) correlations of AHA level with inflammatory activity, pneumonia, respiratory failure, cardiac symptoms, and death were found. D-dimer >0.5 µg/mL had a sensitivity of 79.2% and specificity of 60% in the prediction of cardiovascular manifestations. Cardiac failure was one of the causes of death in 3/8 patients (37.5%). Lethality in the presence of cardiovascular pathology was 17.9 versus 2.2% without it, p < 0.05. The most powerful prognostic model includes age, diabetes, oxygen therapy volume, maximum leukocyte level, C-reactive protein, and D-dimer (correlation coefficient 0.871, p < 0.001). The model with only age, diabetes, and cardiovascular disease included also had predictive power (correlation coefficient 0.568, p < 0.001). CONCLUSIONS: The cardiovascular pathology is frequent in patients with COVID-19 and strong correlates with the D-dimer. It indicates the high significance of prothrombotic and ischemic mechanisms. High AHA levels may reflect an inflammatory heart injury. The cardiovascular pathology is associated with higher lethality.

Post-COVID Myocarditis in Patients with Primary Cardiomyopathies: Diagnosis, Clinical Course and Outcomes.

The aim of this study was to evaluate the clinical course and outcomes of post-COVID myocarditis in patients with cardiomyopathies (CMP). This case series includes 10 patients with different CMPs who had COVID-19 (seven men; 48.4 ± 11.4 yr.): left ventricular non-compaction (n = 2), arrhythmogenic right ventricular CMP in combination with a heterozygous form of hemochromatosis (n = 1, HFE), restrictive CMP (n = 1, MyBPC3), laminopathy (n = 1, LMNA), dilated cardiomyopathy (n = 1, MYH7 + MyBPC3), Danon's disease (n = 1, LAMP2) and AL cardiac amyloidosis (n = 3). Myocardial morphological examination with immunohistochemical staining and PCR for SARS-CoV-2 and cardiotropic viruses was performed in six patients, while cardiac MRI and anti-cardiac antibody titres were evaluated in all patients. Post-COVID lymphocytic myocarditis was confirmed morphologically in six patients (with LVNC, RCM, ARCV, Danon's disease, and AL amyloidosis). Spike and nucleocapsid coronavirus proteins were detected in cell infiltrates, endothelium and cardiomyocytes in all biopsies; SARS-CoV-2 RNA was found in five out of six. In four patients, the diagnosis of myocarditis was based on MRI, high titres of anti-cardiac antibodies and clinical data. The mean time from COVID-19 to the diagnosis of myocarditis was 7 (5; 10.5) months. Myocarditis manifested with the onset/increase of arrhythmias and heart failure. Immunosuppressive therapy with corticosteroids was administered to six patients and led to an increase in ejection fraction and improvement of heart failure symptoms in five of them. CMPs are a favourable background for the development of post-COVID myocarditis. The onset or deterioration of heart failure and/or arrhythmias in patients with CMPs after COVID-19 requires the exclusion of myocarditis and, if present, the administration of immunosuppressive therapy.

Chronic biopsy proven post-COVID myoendocarditis with SARS-Cov-2 persistence and high level of antiheart antibodies.

PURPOSE: To study the clinical signs and mechanisms (viral and autoimmune) of myoendocarditis in the long-term period after COronaVIrus Disease 2019 (COVID-19). METHODS: Fourteen patients (nine male, 50.1 ± 10.2 y.o.) with biopsy proven post-COVID myocarditis were observed. The diagnosis of COVID-19 was confirmed by IgG seroconversion. The average time of admission after COVID-19 was 5.5 [2; 10] months. An endomyocardial biopsy (EMB) of the right ventricle was obtained. The biopsy analysis included polymerase chain reaction diagnosis of viral infection, morphological, immunohistochemical (IHC) examination with antibodies to CD3, CD45, CD68, CD20, SARS-Cov-2 spike, and nucleocapsid antigens. Coronary atherosclerosis was ruled out in all patients over 40 years. RESULTS: The new cardiac symptoms (congestive heart failure 3-4 New York Heart Association class with severe right ventricular involvement, various rhythm, and conduction disturbances) appeared 1-5 months following COVID-19. Magnetic resonance imaging showed disseminated or focal subepicardial and intramyocardial late gadolinium enhancement, hyperemia, edema, and increased myocardial native T1 relaxation time. Antiheart antibodies levels were increased 3-4 times in 92.9% of patients. The mean left ventricular (LV) ejection fraction (EF) was 28% (24.5; 37.8). Active lymphocytic myocarditis was diagnosed in 12 patients, eosinophilic myocarditis in two patients. SARS-Cov-2 RNA was detected in 12 cases (85.7%), in association with parvovirus B19 DNA-in one. Three patients had also endocarditis (infective and nonbacterial, with parietal thrombosis). As a result of steroid and chronic heart failure therapy, the EF increased to 47% (37.5; 52.5). CONCLUSIONS: COVID-19 can lead to long-term severe post-COVID myoendocarditis, that is characterized by prolonged persistence of coronavirus in cardiomyocytes, endothelium, and macrophages (up to 18 months) in combination with high immune activity. Corticosteroids and anticoagulants should be considered as a treatment option of post-COVID myoendocarditis.