Cardiac injury in COVID-19 patients linked with higher death rate

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Cardiac injury is common among hospitalised patients with COVID-19, and is associated with a higher risk of in-hospital mortality, a study from Wuhan, China, has shown. Although the exact mechanism of cardiac injury has not been defined, the researchers say it “highlights the need to consider this complication in COVID-19 management”.

The findings were published in JAMA: Cardiology, in which authors Shaobo Shi (Renmin Hospital of Wuhan University, Wuhan, China) et al write: “The present study demonstrates the statistically significant association between cardiac injury and mortality in patients with COVID-19. Cardiac injury, as a common complication (19.7%), was associated with an unexpected high risk of mortality during hospitalisation.”

The retrospective cohort study sought to explore the association between cardiac injury and mortality in patients with COVID-19. The researchers assessed consecutive patients admitted to Renmin Hospital with laboratory-confirmed COVID-19 from 20 January to 10 February 2020; the final date of follow-up was 15 February, 2020. Renmin Hospital was assigned responsibility for the treatment of patients with severe COVID-19 by the Wuhan government. Cases without cardiac biomarkers, including values of high-sensitivity troponin I (hs-TNI) and creatinine kinase–myocardial band (CK-MB), were excluded.

Clinical laboratory, radiological, and treatment data were collected and analysed. The clinical outcomes of discharge, mortality, and length of stay were monitored until the final date of follow-up, and compared between those with and without cardiac injury, with analysis of the association between cardiac injury and mortality. Cardiac injury was defined as blood levels of cardiac biomarkers (hs-TNI) above the 99th-percentile upper reference limit, regardless of new abnormalities in electrocardiography and echocardiography. Acute respiratory distress syndrome (ARDS) was defined according to the Berlin definition. Acute kidney injury was identified according to the Kidney Disease: Improving Global Outcomes definition.

The final analysis included 416 hospitalised patients with COVID-19; median age was 64 years (range, 21–95 years), and 211 (50.7%) were female. Common symptoms included fever (n=334, 80.3%), cough (n=144, 34.6%), and shortness of breath (n=117, 28.1%).

A total of 82 patients (19.7%) had cardiac injury, and compared with patients without cardiac injury, these patients were older (median age 74 [range 34–95] vs. 60 [range 21–90] years, p<0.001). They also had more comorbidities (for example, hypertension 59.8% vs. 23.4%, p<0.001), higher leucocyte counts, and higher levels of C-reactive protein and procalcitonin. Those with cardiac injury also had higher levels of creatinine kinase–myocardial band (median 3.2, interquartile range [IQR] 1.8–6.2 v.s 0.9, IQR 0.6–1.3ng/mL), myohaemoglobin (median 128, IQR 68–305 vs. 39, IQR 27–65μg/L), high-sensitivity troponin I (median 0.19, IQR 0.08–1.12 vs. <0.001) and invasive mechanical ventilation (22.0% vs. 4.2%, p<0.001) than those without cardiac injury. Complications were more common in patients with cardiac injury than those without cardiac injury, and included acute respiratory distress syndrome (58.5% vs. 14.7%, p<0.001), acute kidney injury (8.5% vs. 0.3%, p<0.001), electrolyte disturbances (15.9% vs. 5.1%, p=0.003), hypoproteinaemia (13.4% vs. 4.8%, p=0.01), and coagulation disorders (7.3% vs. 1.8%, p=0.02).

Patients with cardiac injury had shorter durations from symptom onset to follow-up compared to those without cardiac injury (mean 15.6, range 1–37 days vs. mean 16.9, range 3–37 days, p=0.001) and admission to follow-up (6.3, range 1–16 days vs. 7.8, range 1–23 days, p=0.039).

Patients with cardiac injury had higher mortality than those without cardiac injury (42 of 82, 51.2% vs. 15 of 334, 4.5%, p<0.001). The mortality rate increased in association with the magnitude of the reference value of hs-TNI. After adjusting for age, preexisting cardiovascular diseases (hypertension, coronary heart disease, and chronic heart failure), cerebrovascular diseases, diabetes mellitus, chronic obstructive pulmonary disease, renal failure, cancer, ARDS, creatinine levels greater than 133 μmol/L, and NT-proBNP levels greater than 900pg/mL, the multivariable adjusted Cox proportional hazard regression model showed a significantly higher risk of death in patients with cardiac injury than in those without cardiac injury, either during time from symptom onset (hazard ratio [HR] 4.26, 95% confidence interval [CI] 1.92–9.49) or time from admission to study end point (HR 3.41, 95% CI 1.62–7.16). Under this hazard regression model, ARDS was another independent risk factor for mortality with COVID-19.

The authors point out: “The present study lacks evidence from magnetic resonance imaging or echocardiography to determine the features of myocardial injury. On the basis of the present results of hs-TNI and ECG findings in a subset of patients, we can only estimate the severity of cardiac injury. Thus, because of the current limited evidence, the question of whether the SARS-CoV-2 virus can directly injure the heart requires further demonstration.”

Shi and colleagues hypothesise that “an intense inflammatory response superimposed on preexisting cardiovascular disease may precipitate cardiac injury” in patients with COVID-19 infections, and note: “Approximately 30% and 60% of patients with cardiac injury in the present study had a history of coronary heart disease and hypertension, respectively, which were significantly more prevalent than in those without cardiac injury.”

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