Can influenza B infection cause an elevation of cardiac troponin?

Can Influenza B Cause Troponin Elevation?

Yes, influenza B infection can cause troponin elevation, though it occurs less frequently than with influenza A and typically reflects either type 2 myocardial infarction from supply-demand mismatch, direct viral myocardial injury, or systemic inflammatory stress rather than acute coronary thrombosis.

Epidemiology and Frequency

• Troponin elevation occurs in approximately 0-33% of patients with influenza virus infections, with the frequency varying based on patient age, comorbidities, and disease severity 1
• During the 2017-2018 influenza season, only 2.9% of patients with laboratory-confirmed influenza had troponin levels >0.3 ng/mL, and among those with elevated troponin, 90.9% had influenza A rather than influenza B 2
• Influenza B accounts for a minority of troponin elevations compared to influenza A (especially H1N1 and H3N2 subtypes), making it a less common but documented cause of cardiac biomarker elevation 1, 2
• Approximately 31.8% of hospitalized influenza patients demonstrate elevated high-sensitivity troponin T at initial presentation, though this includes predominantly influenza A cases 3

Mechanisms of Troponin Elevation in Influenza

• Type 2 myocardial infarction from supply-demand mismatch is the primary mechanism, occurring when severe respiratory distress, hypoxemia, tachycardia, or fever creates an oxygen imbalance in the myocardium without coronary artery occlusion 4, 1
• Direct viral cytopathic effects can cause myocardial injury through cardiac invasion, particularly in cases progressing to viral myocarditis 4, 5
• Systemic inflammatory response and cytokine storm during severe influenza infection can trigger microinfarction and myocardial stress 4, 5
• Cardiac dysfunction develops in 75% of hospitalized influenza patients (predominantly influenza A), with left ventricular dysfunction being most common and right ventricular dysfunction observed in 20% 6

Clinical Presentation and Risk Factors

• Troponin elevation is more likely in elderly patients with significant cardiovascular or extra-cardiac comorbidities 1
• Patients with complicated influenza disease, acute respiratory distress syndrome, or cardiac dysfunction demonstrate higher rates of troponin elevation 1
• In most cases with modest troponin elevations, the phenomenon is self-limited, transient, and reversible 1
• In the minority of patients exhibiting abrupt cardiovascular symptoms (chest pain, dyspnea, diaphoresis) with concomitant troponin elevation, the biomarker reflects underlying cardiac injury—either myocarditis or an acute ischemic episode 1

Diagnostic Approach

• Obtain a 12-lead ECG immediately to assess for ST-segment elevation, depression ≥1 mm, new T-wave inversions, or conduction abnormalities suggesting type 1 myocardial infarction 4, 7
• Perform serial troponin measurements at 3-6 hour intervals; a ≥20% change with at least one value above the 99th percentile confirms acute myocardial necrosis 4, 7
• Mild troponin elevations (<2-3 times upper limit of normal) in influenza patients without ischemic symptoms or ECG changes generally do not require workup for type 1 MI 4, 7
• Marked elevations (>5 times upper limit of normal) warrant echocardiography and consideration of coronary angiography if clinical features suggest acute coronary syndrome 4, 7

Prognostic Significance

• Elevated troponin in influenza patients identifies those at higher risk of acute cardiac events, including myocardial infarction (45.5% of troponin-positive patients), left ventricular abnormalities (60.6%), and inpatient mortality (12.1%) 2
• A high-sensitivity troponin T cut-off of 46.4 ng/L demonstrates optimal discriminative potential (sensitivity 0.7, specificity 0.8) for identifying patients who will experience acute cardiac events 3
• Any troponin elevation carries independent prognostic significance with approximately three-fold increased mortality risk, independent of the underlying cause 4, 7
• Patients with acute cardiac events during influenza have significantly higher troponin and CRP levels compared to those without cardiac complications 3

Management Recommendations

• For influenza patients with elevated troponin but without symptoms or ECG changes suggestive of acute coronary syndrome, focus on treating the underlying viral infection and supportive care rather than invasive cardiac evaluation 4, 7
• Troponin measurement should be considered in all influenza patients developing acute cardiovascular symptoms, as well as those with cardiac or extra-cardiac comorbidities at higher risk of complications 1
• If ischemic symptoms and high-risk ECG features are present, initiate acute coronary syndrome protocols with dual antiplatelet therapy, anticoagulation, and urgent cardiology consultation 4, 7
• Echocardiography should be performed when marked troponin elevation occurs without clear type 1 MI indicators to assess for myocarditis, stress cardiomyopathy, or ventricular dysfunction 4, 6

Critical Clinical Pitfalls

• Do not dismiss troponin elevation in influenza patients as merely "inflammatory"—it reflects genuine myocardial injury with adverse prognostic implications 4, 1
• Avoid attributing troponin elevation solely to the viral infection without serial measurements and clinical correlation; 10-15% of patients with true myocardial injury may have initially normal troponin 4, 7
• Recognize that while influenza B can cause troponin elevation, it does so less frequently than influenza A, and most published data predominantly reflect influenza A experience 1, 2