Aims Data regarding impact of COVID‐19 in chronic heart failure (CHF) patients and its potential to trigger acute heart failure (AHF) is lacking. The aim of this work was to study characteristics, cardiovascular outcomes and mortality in patients with confirmed COVID‐19 infection and prior diagnosis of HF. Also, to identify predictors and prognostic implications for AHF decompensations during hospital admission and to determine whether there was a correlation between withdrawal of HF guideline‐directed medical therapy (GDMT) and worse outcomes during hospitalization. Methods and results A total of 3080 consecutive patients with confirmed COVID‐19 infection and at least 30‐day follow‐up were analyzed. Patients with previous history of CHF (152, 4.9%), were more prone to develop AHF (11.2% vs 2.1%; p<0.001) and had higher levels of NT‐proBNP. Also, previous CHF group had higher mortality rates (48.7% vs 19.0%; p<0.001). In contrast, 77 patients (2.5%) were diagnosed of AHF and the vast majority (77.9%) developed in patients without history of HF. Arrhythmias during hospital admission and CHF were main predictors of AHF. Patients developing AHF had significantly higher mortality (46.8% vs 19.7%; p<0.001). Finally, withdrawal of beta‐blockers, mineralocorticoid antagonists and ACE/ARB inhibitors was associated with a significant increase of in‐hospital mortality. Conclusions Patients with COVID‐19 have a significant incidence of AHF, entity that carries within a very high mortality. Moreover, patients with history of CHF are prone to develop acute decompensation after COVID‐19 diagnosis. Withdrawal of GDMT was associated with higher mortality.

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Aims Extensive research regarding the association of troponin and prognosis in coronavirus disease 2019 (COVID‐19) has been performed. However, data regarding natriuretic peptides are scarce. N‐terminal pro B‐type natriuretic peptide (NT‐proBNP) reflects haemodynamic stress and has proven useful for risk stratification in heart failure (HF) and other conditions such as pulmonary embolism and pneumonia. We aimed to adequately characterize NT‐proBNP concentrations using a large cohort of patients with COVID‐19, and to investigate its association with prognosis. Methods and results Consecutive patients with confirmed severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection and available NT‐proBNP determinations, from March 1st to April 20th, 2020 who completed at least 1‐month follow‐up or died, were studied. Of 3080 screened patients, a total of 396 (mean age 71.8 ± 14.6 years, 61.1% male) fulfilled all the selection criteria and were finally included, with a median follow‐up of 53 (18–62) days. Of those, 192 (48.5%) presented NT‐proBNP levels above the recommended cut‐off for the identification of HF. However, only 47 fulfilled the clinical criteria for the diagnosis of HF. Patients with higher NT‐proBNP during admission experienced more frequent bleeding, arrhythmias and HF decompensations. NT‐proBNP was associated with mortality both in the whole study population and after excluding patients with HF. A multivariable Cox model confirmed that NT‐proBNP was independently associated with mortality after adjusting for all relevant confounders (hazard ratio 1.28, 95% confidence interval 1.13–1.44, per logarithmic unit). Conclusion NT‐proBNP is frequently elevated in COVID‐19. It is strongly and independently associated with mortality after adjusting for relevant confounders, including chronic HF and acute HF. Therefore, its use may improve early prognostic stratification in this condition.

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A 70-year-old man with no relevant family or medical history and normal electrocardiogram (ECG) presented at the emergency room with a 6-day history of cough, fever, and dyspnoea suggestive of COVID19 pneumonitis. The polymerase chain reaction for SARS-CoV2 was positive and he received 400 mg of hydroxychloroquine b.i.d. on hospital admission followed by 200 mg b.i.d. for four additional days. This treatment was complemented with 500 mg of azithromycin during these 5 days. On Day 14 from hospital admission, he developed bradycardia, diffuse T-wave inversion and severe QT (620 ms) and QTc (532-560 ms) interval prolongation (Panel A). Isoproterenol infusion quickly restored normal heart rate (70 b.p.m.) and new ECGs showed normal QTc interval with flat and inverted T waves in most ECG leads (Panel B). Electrolyte balance and renal function indicators were within normal values during the whole hospital stay but mild transient elevation of high-sensitive troponin I was demonstrated. A transthoracic echocardiogram showed normal systolic function and no ventricular segmental defects. Diffuse T-wave inversion and transient troponin elevation supports a significant role of myocardial inflammation on QT prolongation in this patient. This case emphasizes that QT prolongation may result from mechanisms other than or concurrent with drug toxicity in COVID patients.