Title : The mirrored heart: Chronic troponin elevation beyond obstructive coronary disease in situs inversus totalis
Abstract:
Background
Situs inversus totalis is a rare congenital anomaly that poses unique challenges in electrocardiographic interpretation and the assessment of myocardial ischemia. While cardiac troponin elevation is commonly indicative of myocardial injury due to obstructive coronary artery disease, growing evidence suggests that chronic troponin elevation reflects ongoing myocardial injury in chronic heart failure and ventricular remodeling, independent of the severity of coronary stenosis.
Methods
We report the case of a female patient with situs inversus totalis and dextrocardia, presenting with chronic heart failure with reduced ejection fraction. The patient underwent standard electrocardiography, serial cardiac biomarker measurements, and invasive coronary angiography to evaluate the relationship between coronary artery disease severity and persistent troponin elevation.
Results
Electrocardiography demonstrated typical mirror-image patterns of dextrocardia, with reversed QRS complexes and electrical axis, necessitating careful adjustment in the interpretation of ST–T changes. Coronary angiography revealed two-vessel coronary artery disease with less than 70% stenosis, without flow-limiting lesions.
Despite this, cardiac troponin levels were persistently elevated, showing chronic fluctuations and consistently exceeding 1000 ng/L, in the absence of clinical or imaging evidence of acute coronary syndrome.
In the absence of significant obstructive coronary disease, chronic troponin elevation likely reflects ongoing myocardial injury related to the complex pathophysiology of progressive heart failure. Potential mechanisms include increased myocardial wall stress and chronic ventricular stretch, subendocardial ischemia due to oxygen supply–demand mismatch, coronary microvascular dysfunction, chronic neurohormonal activation, and low-grade but sustained cardiomyocyte injury.
In patients with anatomical variations such as dextrocardia, the risk of misinterpreting electrocardiographic changes and over-attributing findings to acute myocardial ischemia is heightened if anatomical, hemodynamic, and molecular data are not comprehensively integrated.
This case underscores the importance of differentiating “chronic myocardial injury” from “type 1 myocardial infarction,” highlighting the need for a pathophysiology-based approach and biomarker kinetics rather than reliance on absolute troponin thresholds alone.
Conclusion
“The heart in the mirror” not only challenges conventional imaging and electrocardiographic interpretation but also reflects the limitations of a paradigm centered solely on obstructive coronary artery disease. In patients with heart failure and situs inversus totalis, chronic troponin elevation may represent ongoing myocardial remodeling rather than acute coronary instability. An integrated approach incorporating anatomical, hemodynamic, and molecular insights is essential to avoid misdiagnosis and unnecessary interventions.
