Elevated troponin spells worse outcomes in COVID-19

Elevated troponin T levels at hospital admission may be a harbinger of adverse outcomes in COVID-19 but could help risk-stratify patients, according to a new study. Those with cardiovascular disease (CVD) are also more vulnerable than those without, bolstering the suspected link between.

“Having pre-existing CVD or signs of myocardial injury (raised troponin) on admission is associated with an increased risk of both in-hospital death and major CV events,” said study author Dr Manan Pareek from Yale New Haven Hospital, New Haven, Connecticut, US at ESC 2020. His team systematically collected data on CVD and COVID-19 link from adult patients admitted to their hospital with a COVID-19 diagnosis.

Preliminary results from the first 485 patients showed that in patients hospitalized with COVID-19, 46 percent had a history of CVD. Over 40 percent had hypertension, hyperlipidaemia, and diabetes.

“One in 5 died in hospital, 1 in 3 were treated in the ICU, and 1 in 5 needed ventilation,” reported Pareek. “Two in 5 experienced a major adverse cardiovascular event [MACE], defined as an ischaemic event, arrhythmia, heart failure, or vascular outcome.”   

The main predictors of in-hospital death were a history of ventricular arrhythmia (odds ratio [OR], 9.87; p=0.004), which is a surrogate for previous serious CVD, and use of a P2Y12 inhibitor (OR, 4.58; p=0.04), a surrogate for underlying coronary heart disease.

Independent factors associated with MACE included use of diuretics and presence of atrial arrhythmias.

Virus or stress: The trigger

Pareek said it is unknown if SARS-CoV-2 is involved in the pathogenesis of CV events or it is physiological stress associated with the infection that is triggering the event. Increased troponin, he shared, often signals ongoing myocardial infarction.

Yet patients in the study were not having an acute cardiac event at baseline. “Chest pain was actually inversely associated with the CV event endpoint,” Pareek reported. “Hence, the elevated troponin may be suggestive of isolated myocardial injury.”

Cardiac injury was also a common finding among patients hospitalized for COVID-19 in Wuhan, China. Patients with cardiac injury had a three-fold increased risk of in-hospital mortality. More than half of the patients (51.2 percent) who suffered cardiac injury died compared to only 4.5 percent in those without cardiac injury (p<0.001). [JAMA Cardiol 2020;5:802-810]

So, does this finding warrant mandatory troponin testing for all patients hospitalized with COVID-9? “That would be useful for risk stratification,” said Pareek. “But while we know these patients may have worse outcomes, we don’t really know how to treat them differently.”

“What the study does tell us though is that the virus triggers CV events,” he added.

Raised troponin + BNP yields poor outcome in women

In a separate study of all patients hospitalized with COVID-19 between February and April in 24 hospitals in France, troponin and B-type natriuretic peptide (BNP) were both independent prognostic indicators of poor outcome in women hospitalized with COVID-19.

Of 2,878 patients in the cohort, 1,212 or 42 percent were women. Of these, 21.8 percent died.

Women in the study were older (average age 68 years vs 65 years in men) and had fewer CV comorbidities. They were also less likely than men to experience the primary outcome of intensive care unit (ICU) transfer or in-hospital death (OR, 0.63; p<0.001).  However, mortality rates were comparable between men and women.

Factors associated with ICU transfer or death in women included older age, higher BMI, hypertension, diabetes, heart failure, and chronic kidney disease.

CVD was also an independent predictor of adverse outcomes in these women, reported study author Dr Orianne Weizman from the Centre Hospitalier Régional Universitaire de Nancy, France at ESC 2020.

BNP and its N‐terminal fragment (NT‐proBNP) – both important markers of cardiac dysfunction and heart failure – were also increased in 33 percent of women who were transferred to the ICU or died. Elevated levels of these biomarkers doubled the risk of the primary endpoint (hazard ratio [HR], 1.96; p<0.001) after adjustment for heart failure.

Similar results were reported for troponin, which was increased in 35 percent of women (HR, 2.0; p<0.001).

Dr Martin Landray, session chair and Professor of Medicine and Epidemiology at the University of Oxford, UK, said “it is notable that prior CVD really plays a role in subsequent risk … that is something we might want to take forward when thinking about the epidemiology of COVID and the management of individual patients.”

Accurate instigation of cardiac biomarkers will also aid the assessment of cardiac function status in COVID-19 patients.