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Left atrial pressure in patients with respiratory failure due to SARS-CoV-2 infection and supraventricular arrythmias

2022; Lippincott Williams & Wilkins; Volume: 23; Issue: 6 Linguagem: Inglês

10.2459/jcm.0000000000001291

1558-2035

Rita Pavasini, Gioele Fabbri, Luca Di Ienno, Maria Angela Deserio, Federico Sanguettoli, Nicola Bianchi, Ottavio Zucchetti, Emanuele D’Aniello, Alberto Papi, Savino Spadaro, Marco Contoli, Gianluca Campo,

COVID-19 Clinical Research Studies

To the Editor One of the most common complications of Coronavirus Disease 19 (COVID-19) is the development of supraventricular arrhythmias (SA).1–4 COVID-19 patients developing SA are at higher risk of worse prognosis, because of the development of hemodynamic instability, of the difficult management of the rhythm and rate control and of the related treatments (i.e. anticoagulants drugs) further causing adverse events (i.e. bleedings).3 The aim of this study was to detect clinical, and echocardiographic parameters useful for the identification of an increased risk of SA development in COVID-19 patients. Methods The 'Pro-thrombotic status in patients with severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection' (ATTAC-Co) study5–7 is an investigator-initiated single-center prospective study recruiting critically ill COVID-19 patients admitted to University Hospital of Ferrara, Italy for moderate-to-severe respiratory failure. The full protocol of the study has been previously reported (NCT04343053).6–8 All patients enrolled underwent comprehensive transthoracic echocardiogra-phy (TTE) within 96 h from the hospitalization.9,10 Dia-stolic disfunction (DD) was assessed following the last American Society of Echocardiography/European Association of Cardiovascular Imaging algorithm;10 normal left atrial pressure (LAP) was considered in case of DD grade 0 or 1, increased LAP in case of DD 2 or 3. Only patients with sinus rhythm detected at the hospital admission and at the time of TTE and without a previous history of atrial fibrillation/flutter were included in the study. TTE was performed with GE Vivid q with M4S-RS transducers. The main outcome of the study was to identify predictors of SA defined as the onset during hospitalization of atrial fibrillation, atrial flutter, atrial tachycardia, and any paroxysmal supraventricular tachycardia. Values were compared with the t-test, Mann-Whitney U test, and the two-tailed Fisher exact test as appropriate. Variables listed in Table 1 were evaluated by univariate logistic regression. Those with P < 0.05 were included in the multivariate model. The odds ratio (OR) with 95% confidence intervals (CIs) was used. All statistical analyses were performed using Stata/SE version 16 software (Stata Corp, College Station, Texas). Table 1 - Study population characteristics Supraventricular arrhythmia Total N = 76 No N = 58 Yes N = 18 P-value Age – years, mean ± sd 64.87 ± 10.42 63.69 ± 11.16 68.67 ± 6.69 0.075 Female sex, n (%) 20 (26) 12 (21) 8 (44) 0.046 BMI – kg/mq, mean ± sd 26.78 ± 4.19 26.88 ± 4.30 26.45 ± 4.05 0.706 SBP – mmHg, mean ± sd 133.49 ± 29.33 129.96 ± 20.97 144.44 ± 47.00 0.07 DBP – mmHg, mean ± sd 77.78 ± 11.77 75.75 ± 10.30 84.11 ± 14.35 0.007 History Hypertension, n (%) 36 (47) 22 (38) 14 (78) 0.003 Dyslipidemia, n (%) 10 (13) 6 (10) 4 (22) 0.193 Smoking habit, n (%) 22 (29) 12 (21) 10 (56) 0.004 Diabetes, n (%) 12 (16) 8 (14) 4 (22) 0.39 Chronic coronary syndrome, n (%) 2 (3) 2 (3) 0 (0) 0.42 Heart failure, n (%) 0 (0) 0 (0) 0 (0) Stroke, n (%) 0 (0) 0 (0) 0 (0) PAD, n (%) 6 (8) 6 (10) 0 (0) 0.15 COPD, n (%) 8 (11) 4 (7) 4 (22) 0.064 Medications RAAS inhibitors, n (%) 22 (33) 16 (30) 6 (50) 0.18 Diuretics, n (%) 6 (9) 4 (7) 2 (11) 0.31 B-blockers, n (%) 10 (15) 8 (15) 2 (11) 0.87 Aspirin, n (%) 4 (5) 4 (7) 0 (0) 0.33 p2y12 inhibitors, n (%) 4 (5) 4 (7) 0 (0) 0.33 Anticoagulant, n (%) 4 (5) 2 (4) 2 (11) 0.09 Respiratory drugs, n (%) 2 (3) 2 (4) 0 (0) 0.49 Inotropes, n (%) 24 (32) 20 (34) 4 (22) 0.32 Laboratory tests GFR – mL/min, mean ± SD 94.02 ± 66.42 100.16 ± 73.91 74.22 ± 26.59 0.15 PLT – 103/mmc, mean ± SD 254.63 ± 117.90 239.83 ± 108.84 302.33 ± 139.53 0.047 D-dimer – μg/mL, mean ± sd 2.33 ± 3.98 2.40 ± 4.61 2.12 ± 1.15 0.82 HS TnI – pg/mL, mean ± SD 67.64 ± 121.52 86.44 ± 150.54 33.80 ± 21.02 0.27 BNP – pg/mL, mean ± SD 146.29 ± 114.40 145.80 ± 107.81 147.50 ± 147.80 0.97 C-reactive protein – mg/mL, mean ± SD 15.50 ± 11.02 16.78 ± 10.91 11.66 ± 11.04 0.09 Echo EDV – mL/mq, mean ± SD 56.59 ± 12.31 54.85 ± 6.12 62.19 ± 22.87 0.025 LVEF – %, mean ± SD 59.30 ± 6.76 60.63 ± 5.15 55.04 ± 9.59 0.002 Increased filling pressure, n (%) 30 (26) 8 (15) 12 (67) <0.001 SVi – mL/mq, mean ± SD 35.76 ± 10.34 36.11 ± 8.54 34.81 ± 14.85 0.65 Dilated RA, n (%) 24 (32) 14 (24) 10 (56) 0.012 TAPSE – mm, mean ± SD 24.57 ± 3.70 24.50 ± 3.17 24.78 ± 5.26 0.78 sPAP – mmHg, mean ± SD 33.50 ± 6.82 32.57 ± 6.05 36.75 ± 8.71 0.028 Severe valve disease, n (%) 0 (0) 0 (0) 0 (0) Pericardial effusion, n (%) 2 (3) 2 (3) 0 (0) 0.57 Average LVGLS – %, mean ± SD −17.78 ± 2.72 −18.80 ± 1.78 −16.42 ± 3.29 0.44 Average RVS – %, mean ± SD −24.65 ± 8.69 −26.35 ± 9.63 −22.95 ± 8.15 0.84 Average PALS – %, mean ± SD 30.72 ± 12.51 35.20 ± 15.57 26.23 ± 7.03 0.05 Type of arrythmias developed Atrial fibrillation, n (%) 16 (21) – 16 (88) – Atrial flutter, n (%) 1 (1) – 1 (6) – Paroxysmal supraventricular tachycardia, n (%) 1 (1) – 1 (6) – BMI, body mass index; BNP, brain natriuretic peptide; COPD, chronic obstructive pulmonary disease; DBP, diastolic blood pressure; EDV, end-diastolic volume; GFR, glomerular filtration rate; HS TnI, troponin I high sensitivity; LVEF, left ventricle ejection fraction; LVGLS, left ventricle global longitudinal strain; MRA, mineralocorticoid receptor antagonists; PAD, peripheral artery disease; PALS, peak atrial longitudinal strain; PLT, platelets; RA, right atrium; RAAS, renin-angiotensin aldosterone system; RVS, rightventricle strain; SBP, systolicblood pressure; sPAP, systolic pulmonaryarterial pressure; SVi, strokevolumeindexed; TAPSE, tricuspid annularplane excursion. Results Overall, 76 patients were included in the analysis (mean age 64.8 ± 10 years, 26% female). SA occurred in 18 patients (24%). The median interval between TTE and onset SA was 4 (1–7) days. Patients who developed SA showed increased LAP (67% vs 15%, P < 0.001), lower left ventricle ejection fraction (LVEF) (55% vs 60%, P = 0.002), higher prevalence of dilated right atrium (56% vs 24%, P = 0.012), increased systolic pulmonary arterial pressure (36 ± 8vs32 ± 6 mmHg, P = 0.028) and increased prevalence of history of arterial hypertension and of smoking habit (Table 1). Considering serum biomarkers, the C-reactive protein levels and the platelet counts were higher in patients who developed SA (Table 1). At univariate analysis hypertension, smoking habit, LVEF, increased filling pressure, and dilated right atrium were significantly associated with SA (Table 2). After multivariate analysis only increased LAP (OR 5.61, 95% CI 1.35–23.31, P = 0.018) and hypertension (OR 6.32, 95% CI 1.22–32.7, P = 0.028) were shown to be independent predictors of SA (Table 2). Table 2 - Univariate and multivariate analysis for the occurrence of supraventricular arrythmias Univariate Multivariate OR (95% CI) P-value OR (95% CI) P-value Female 0.33 (0.11–1.01) 0.051 – – Diastolic blood pressure 1.07 (0.99–1.13) 0.052 – – Hypertension 5.73 (1.67–19.62) 0.005 6.32 (1.22–32.7) 0.028 Smoking habit 4.79 (1.55–14.77) 0.006 2.63 (0.60–11.59) 0.199 PLT 1 (0.99–1.01) 0.06 – – EDV 1.05 (0.99–1.09) 0.08 – – LVEF 0.88 (0.81–0.97) 0.006 0.90 (0.81–1.01) 0.057 Incremented filling pressure 12.5 (3.64–42.84) <0.001 5.61 (1.35–23.31) 0.018 Dilated RA 3.93 (1.29–11.89) 0.015 3.74 (0.86–16.27) 0.078 sPAP 1.09 (0.99–1.19) 0.055 – – EDV, end-diastolic volume; LVEF, left ventricle ejection fraction; PLT, platelets; RA, right atrium; sPAP, systolic pulmonary arterial pressure. Comment In this analysis, we found that LAP assessed at TTE together with a history of hypertension can predict SA development in patients with moderate-to-severe respiratory failure due to SARS-CoV-2 infection. Hypertensive patients had more DD.11,12 Increased LAP is closely associated with electro-anatomical remodeling of left atrium13,14 that progressively facilitate the development of arrythmias. In COVID-19 patients with history of hypertension, it seems to be of paramount importance to closely monitor LAP, aiming to reduce the burden of new-onset SA. Nevertheless, this study is based on a single-center experience, cases are very limited, and additional analyses are needed to confirm their consistence and transferability in clinical practice, defining which pharmacological or interventional strategy may reduce SA occurrence. Acknowledgements Funding: This work was conducted without a funding support. Conflicts of interest There are no conflicts of interest. The study was an investigator-driven clinical trial conducted by the University of Ferrara.