A Nomogram Based on Myocardial Damage and Novel Inflammatory Indexes for Post-Discharge Survival Rates of COVID-19.

BACKGROUND: In the course of SARS-CoV-2 infection, early prognostic evaluation is important since clinical symptoms may worsen rapidly and may be fatal. Inflammation plays an important role in the pathogenesis of COVID-19 and can cause myocardial damage which is common in severe COVID-19 patients. Therefore, novel inflammatory indexes and myocardial damage may be predictive of prognosis in patients with COVID-19. The aim of the study was to evaluate the role of cardiac troponin I (cTnI), modified Glasgow prognostic score (mGPS), systemic immune inflammation index (SII), prognostic nutritional index (PNI), and CRP to albumin ratio (CAR) in the outcome estimation of COVID-19 and to develop a risk model predicting the survival probability of COVID-19 survivors during early post-discharge. METHODS: This was a single-center, observational, retrospective cohort study. Laboratory confirmed COVID-19 patients (n = 265) were included and grouped according to in-hospital mortality. ROC curve analysis was performed and Youden's J index was used to obtain optimal cutoff values for inflammatory indexes in discriminating survivors and non-survivors. Cox regression analysis was performed to assess the possible predictors of in-hospital mortality. A nomogram was constructed based on the Cox regression model, to calculate 7- and 14-day survival. RESULTS: The area under the ROC curve (AUC) of the variables ranged between 0.79 and 0.92 with the three highest AUC values for albumin, PNI, and cTnI (0.919, 0.918, and 0.911, respectively). Optimal threshold value for cTnI was 9.7 pg/mL. Univariate analysis showed that gender, albumin, CRP, CAR, PNI, SII, cTnI, and mGPS were significantly related to in-hospital mortality. The Cox regression analysis indicated that mGPS (p = 0.001), CRP (p = 0.026), and cTnI (p = 0.001) were significant prognostic factors. CONCLUSIONS: cTnI should not be considered merely as an indicator of myocardial damage. It also reflects the inflammatory phase and, along with other inflammatory markers, it should be included in risk models as a prognostic factor for COVID-19.

Relationship of magnesemia with myocardial damage and mortality in patients with COVID-19.

Magnesium (Mg) is the second most abundant intracellular cation and plays a significant role in immune system and cardiac protection. Mg deficiency contributes to chronic low-grade inflammation leading to cardiovascular diseases, and low Mg level exacerbates virus-induced inflammation. The aim of the study was to investigate whether serum magnesium level is associated with myocardial damage and prognosis of COVID-19. This was a single-center, observational retrospective study of patients with COVID-19. The study population was divided into two groups according to in-hospital mortality: a survivor group (SG) and a non-survivor group (NSG). Myocardial damage was defined as blood levels of cardiac troponin I (cTnI) above the 99th percentile upper reference limit. Magnesium, variables regarding inflammation, and myocardial damage were compared between the groups. A total of 629 patients with COVID-19 were included. Mortality rate was 11.85% (n = 82). There were 61 (74.4%) and 294 male patients (53.7%) in NSG and SG, respectively (p = 0.001). The median age of NSG was 64.5 years (min-max: 37-93) and the median age of SG was 56.0 years (min-max: 22-92) (p < 0.001). Median serum magnesium levels of NSG and SG were 1.94 mg/dL (min-max: 1.04-2.87) and 2.03 mg/dL (min-max: 1.18-2.88), respectively (p = 0.027). Median cTnI levels of NSG and SG were 25.20 pg/mL (min-max: 2.10-2240.80) and 4.50 pg/mL (min-max: 0.50-984.3), respectively (p < 0.001). The cTnI levels were lower in those patients whose serum Mg levels were higher than 1.94. Although serum magnesium level was not a predictor for in-hospital mortality, there was a significant negative correlation between magnesemia and myocardial damage.