Myocardial injury determination improves risk stratification and predicts mortality in COVID-19 patients

Abstract

Background: Despite being associated with worse prognosis in patients with COVID-19, systematic determination of myocardial injury is not recommended. The aim of the study was to study the effect of myocardial injury assessment on risk stratification of COVID-19 patients. Methods: Seven hundred seven consecutive adult patients admitted to a large tertiary hospital with confirmed COVID-19 were included. Demographic data, comorbidities, laboratory results and clinical outcomes were recorded. Charlson comorbidity index (CCI) was calculated in order to quantify the degree of comorbidities. Independent association of cardiac troponin I (cTnI) increase with outcomes was evaluated by multivariate regression analyses and area under curve. In addition, propensity-score matching was performed to assemble a cohort of patients with similar baseline characteristics.Results: In the matched cohort (mean age 66.76 ± 15.7 years, 37.3% females), cTnI increase above the upper limit was present in 20.9% of the population and was associated with worse clinical outcomes, including all-cause mortality within 30 days (45.1% vs. 23.2%; p = 0.005). The addition of cTnI to a multivariate prediction model showed a significant improvement in the area under the time-dependent receiver operating characteristic curve (0.775 vs. 0.756, DC-statistic = 0.019; 95% confidence interval 0.001-0.037). Use of renin-angiotensin-aldosterone system inhibitors was not associated with mortality after adjusting by baseline risk factors. Conclusions: Myocardial injury is independently associated with adverse outcomes irrespective of baseline comorbidities and its addition to multivariate regression models significantly improves their performance in predicting mortality. The determination of myocardial injury biomarkers on hospital admission and its combination with CCI can classify patients in three risk groups (high, intermediate and low) with a clearly distinct 30-day mortality.

Prevalence and prognostic value of elevated troponins in patients hospitalised for coronavirus disease 2019: a systematic review and meta-analysis

“…We conducted a meta-analysis of 11 studies (13,889 patients) that reported multivariable-adjusted associations between admission troponins above the upper reference limit and mortality [ 13 – 15 , 26 , 27 , 32 , 37 , 45 , 46 , 55 , 67 ]. Elevated troponins on admission were associated with an increased risk of death (RR 2.68, 95% CI 2.08–3.46).…”

“…Thus, the detection of a normal troponin level at hospital admission may not be considered as a sign of very low mortality risk or criteria for early discharge. The combination of troponin with other clinical information might achieve more accurate prognostication than either alone [ 45 ].…”

The Role of Health Preconditions on COVID-19 Deaths in Portugal: Evidence from Surveillance Data of the First 20293 Infection Cases

“…The pathophysiological mechanisms behind this association may be multiple: from severe infection with SARS-CoV-2, precipitating myocardial infarction, myocarditis, heart failure, and arrhythmias as well as an acute respiratory distress syndrome and renal failure [ 33 , 34 ]; through the evolution along with multiorgan failure directly due to SARS-CoV-2-infected endothelial cells and resulting endothelitis [ 33 ]; to the potential impacts of therapies considering the likely increase in the number of ACE 2 receptors and the corresponding increase in the susceptibility [ 33 ]. Furthermore, the link between pneumonia and cardiovascular complications should be accounted for: recent studies explore/registered myocardial injury during SARS-CoV-2, secondary to type 2 myocardial infarction, a consequence of increased oxygen demand or reduced oxygen supply during respiratory failure [ 34 , 35 , 36 ]. In this scenario, cytokines microvascular activation can cause not only myocardial injury but also harm other systems involved in COVID-19 infections, including the kidneys [ 37 ].…”

Pre-symptomatic detection of COVID-19 from smartwatch data

“…Regardless, any illness onset information is valuable, especially during a pandemic, and can be followed up with appropriate testing. It is also likely that other types of physiological measurements that are obtainable from wearable devices (for example, heart rate variability, respiration rate, skin temperature, blood oxygen saturation and electrocardiogram readings) will be valuable for distinguishing illnesses caused by different infectious agents and could be used to increase diagnostic sensitivity and perhaps even predict illness severity and symptoms [24][25][26][27] . Data on reported respiratory rates and blood oxygen saturation are expected to be particularly useful in COVID-19 prediction 28 , although the disease is quite heterogeneous in its physiological presentation 29,30 , as observed in our study.…”