Abstract
Background
ST-segment elevation on an electrocardiogram (ECG) is a hallmark of acute ST-segment elevation myocardial infarction (STEMI). However, thoracic malignancies can produce electrocardiographic patterns identical to acute ischemia through direct myocardial invasion or extrinsic compression, creating a significant diagnostic dilemma.
Case Presentation
We present 2 patients with primary lung cancer who exhibited ECG findings strongly mimicking acute STEMI. Case 1 involves a 70-year-old man presenting with acute chest pain. His ECG demonstrated anterolateral ST-segment elevation with diffuse PR depression. Coronary angiography revealed nonobstructive disease with mildly elevated troponin. Multimodality imaging identified a hypermetabolic mass externally compressing the anterolateral myocardium. Case 2 describes an 80-year-old man presenting with dizziness and ST-segment elevation in leads V1 to V3. Imaging revealed a large thoracic mass compressing the right ventricular outflow tract and left pulmonary artery without coronary occlusion. After appropriate oncological treatment, the patient demonstrated partial tumor regression on follow-up positron emission tomography–computed tomography, which correlated with the complete resolution of the initial ECG abnormalities.
Conclusions
These cases demonstrate that ST-segment elevation in patients with advanced malignancy may arise from myocardial tumor invasion or extrinsic compression rather than acute coronary thrombosis, underscoring the importance of careful correlation between clinical findings and multimodality cardiac imaging.
Key words: acute coronary syndrome, cancer, electrocardiogram, imaging
Visual Summary
Visual Summary.
Diagnostic Pathway of Cancer Mimicking STEMI
CT = computed tomography; cTn = cardiac troponin; ECHO = echocardiography; STEMI = ST-segment elevation myocardial infarction.
Patients with lung cancer have a significantly increased risk of myocardial infarction compared to the general population, with the risk being highest in the first 6 to 12 months after cancer diagnosis and correlating with cancer stage and treatment intensity.1 ST-segment elevation myocardial infarction (STEMI) in the context of lung carcinoma can result from several mechanisms that differ from classic atherothrombotic STEMI: direct myocardial invasion, metastatic involvement of the heart, coronary artery embolization by tumor fragments, extrinsic compression of coronary arteries, or paraneoplastic hypercoagulability.1
We present 2 cases of ST-segment elevation caused by lung cancer, closely mimicking STEMI.
Case 1
A 70-year-old man presented to the emergency department with acute chest pain. His medical history included pulmonary fibrosis, ischemic heart disease with subsequent coronary artery bypass grafting, and stage IV non–small cell lung cancer diagnosed 2 years earlier, after several lines of therapy. A recent positron emission tomography–computed tomography (PET-CT) scan demonstrated disease progression with a hypermetabolic mediastinal mass invading the pericardium and adjacent cardiac structures (Figure 1).
Figure 1.
PET-CT Evidence of Disease Progression
(A) Noncontrast phase demonstrating a large, heterogeneous mass positioned in close proximity to the myocardium (red asterisk). (B) The hypermetabolic nature of this mediastinal mass is revealed with direct invasion into the pericardium. LV = left ventricle; PET-CT = positron emission tomography–computed tomography.
On admission, the patient's blood pressure was 110/77 mm Hg and heart rate was 105 beats/min. Physical examination was unremarkable. The electrocardiogram (ECG) showed diffuse ST-segment elevation in the anterolateral leads with diffuse PR depression (Figure 2). A diagnosis of STEMI was made, and the patient was transferred emergently for coronary angiography.
Figure 2.
Admission Electrocardiogram Mimicking STEMI
The ECG performed in the emergency department shows diffuse ST-segment elevation in the anterolateral leads (V1-V6, I, aVL) with diffuse PR depression. While these findings initially led to a presumptive diagnosis of a STEMI, this trace represents a “pseudo-STEMI” pattern caused by direct tumor-related myocardial involvement. ECG = electrocardiogram; STEMI = ST-segment elevation myocardial infarction.
Primary coronary angiography demonstrated nonobstructive coronary artery disease with patent bypass grafts. High-sensitivity troponin-T showed only mild elevation (44-68 ng/L) without a dynamic rise. Transthoracic echocardiography revealed focal myocardial thickening with regional hypokinesis and an adherent mobile echogenic mass involving the anterolateral myocardium, without pericardial effusion (Figure 3). Cardiac CT demonstrated a heterogeneous anterior mediastinal mass invading the pericardium and exerting mass effect on the anterolateral myocardium and coronary arteries, including the left anterior descending artery and left internal mammary artery (Figure 4).
Figure 3.
Transthoracic Echocardiographic Assessment of the Cardiac Mass
Echocardiography 4-chamber view reveals a focal area of myocardial thickening and regional hypokinesis in the anterolateral wall. A distinct, adherent, and mobile echogenic mass is visualized externally compressing the anterolateral myocardium (red asterisk). Notably, there is no associated pericardial effusion, which helped differentiate this mass effect from acute inflammatory pericarditis or hemopericardium.
Figure 4.
Cardiac Computed Tomography Demonstrating Mechanical Compression
Multidetector cardiac CT scan confirms the presence of a heterogeneous anterior mediastinal mass invading the pericardial space (red asterisk). The mass exerts significant mechanical pressure on the anterolateral myocardium and is in direct contact with the LAD and the LIMA bypass graft. These anatomical details confirm that the ST-segment changes were likely due to external compression and direct infiltration rather than acute coronary artery occlusion. CT = computed tomography; LAD = left anterior descending artery; LIMA = left internal mammary artery.
Based on the discordance between ECG findings, coronary anatomy, biomarker profile, and multimodality imaging, ST-segment elevation was attributed to myocardial involvement by advanced lung cancer rather than acute coronary occlusion. The patient's clinical condition deteriorated, and he died 4 days later because of progression of his malignancy.
Case 2
An 80-year-old man presented to the emergency department with a report of dizziness, without associated chest pain or dyspnea. His past medical history included ischemic heart disease, prior percutaneous coronary intervention to the first diagonal artery, hypertension, and past smoking. A SPECT (single-photon emission computed tomography) myocardial perfusion scan performed 3 months before admission was negative for ischemia.
On admission, blood pressure was 120/66 mm Hg with a heart rate of 107 beats/min. Physical examination was unremarkable. The 12-lead ECG demonstrated ST-segment elevation in leads V1-V3 (Figure 5). Bedside echocardiography revealed no regional wall motion abnormalities, and aortic dimensions were within normal limits. Chest radiography demonstrated a widened mediastinum (Figure 6).
Figure 5.
Admission Electrocardiogram
The initial ECG demonstrates ST-segment elevation in leads V1 through V3 without evident reciprocal changes in the inferior leads. Notable T-wave inversion is present in lead III. These findings were carefully evaluated to differentiate between primary cardiac ischemia and secondary ST-segment changes related to noncardiac pathology. ECG = electrocardiogram.
Figure 6.
Initial Chest Radiograph in the Emergency Department
The baseline chest radiograph obtained upon presentation reveals significant mediastinal widening. This radiographic finding prompted further diagnostic work-up to evaluate for a mediastinal mass or vascular abnormalities, given the patient's presenting symptoms and electrocardiographic findings.
Emergency CT angiography ruled out obstructive coronary artery disease but revealed a anterior mediastinal mass extending from the anterior superior isthmus and involving the left upper lobe. The mass showed no cardiac invasion but was in contact with the right ventricular outflow tract and the left pulmonary artery without causing significant stenosis (Figure 7). Given the absence of clinical signs of acute ischemia and findings from multimodal imaging, the ST-segment elevation was attributed to the space-occupying lesion in the lung.
Figure 7.
Contrast-Enhanced Computed Tomography Angiography Findings
The CTA demonstrates a large, heterogeneous mass within the left upper lobe. The lesion is in direct anatomical contact with the right ventricular outflow tract and left pulmonary artery; however, there is no evidence of vascular invasion or significant luminal narrowing. CTA = computed tomography angiography; LPA = left pulmonary artery; MPA = main pulmonary artery.
Subsequently, a biopsy confirmed the diagnosis of small cell carcinoma; brain magnetic resonance imaging showed no evidence of metastasis. PET-CT imaging is presented in Figure 8. At the 1-year follow-up, after oncological treatment, partial regression of the carcinoma according PET-CT (Figure 9) and resolution of the ECG ST-segment elevation (Figure 10) were observed.
Figure 8.
PET-CT Imaging Findings
Integrated 3-dimensional PET-CT imaging shows a large, solid mass located in the left upper lobe of the lung. The lesion demonstrates intense fluorodeoxyglucose (FDG) uptake, consistent with a highly metabolically active malignancy, without signs of macroscopic direct invasion to the pericardium or myocardium. AO = aorta; LPA = left pulmonary artery; MPA = main pulmonary artery; PET-CT = positron emission tomography–computed tomography; RV = right ventricle; SVC = superior vena cava.
Figure 9.
PET-CT Follow-Up
At the end of the treatment course, a follow-up PET-CT scan was performed, showing low-grade FDG uptake associated with consolidation (arrow) without signs of disease progression based on the follow-up evaluation. FDG = fluorodeoxyglucose; LPA = left pulmonary artery; MPA = main pulmonary artery; PET-CT = positron emission tomography–computed tomography.
Figure 10.
Follow-Up Electrocardiogram After Chemotherapy Initiation
A subsequent ECG performed during the course of treatment shows complete resolution of the ST-segment elevation in leads V1-V3. This electrophysiological improvement correlates with the significant reduction in tumor volume observed on follow-up imaging, suggesting that the initial changes were associated with the primary lung lesion. ECG = electrocardiogram.
Discussion
Cardiac metastases are clinically underdiagnosed and are most frequently associated with lung cancer, melanoma, and hematologic malignancies.2,3 Epicardial and myocardial involvement are common sites of cardiac metastasis, often detected only postmortem, making early diagnosis particularly challenging.3
ST-segment elevation mimicking acute myocardial infarction in patients with cancer may result from direct myocardial invasion by tumor tissue, leading to local inflammation, myocardial injury, and disruption of normal electrical conduction. This mechanism can produce persistent ST-segment elevation without significant dynamic elevation of cardiac biomarkers and in the absence of acute coronary occlusion on angiography.4
The differential diagnosis of ST-segment elevation in oncology patients is broad and includes acute coronary syndromes, stress cardiomyopathy, myopericarditis, pulmonary embolism, electrolyte disturbances, and cardiac metastases.5 Persistence of ST-segment elevation without the typical temporal ECG evolution of infarction, combined with minimal biomarker elevation and nonobstructive coronary arteries, should raise suspicion for nonischemic myocardial involvement.
In case 1, upon re-evaluation of the ECG, diffuse ST-segment elevations and PR depressions suggest pericarditis as a possible cause of the pain and ECG changes.
In case 2, ST-segment elevation without obvious invasion may result from mechanical compression, as demonstrated in the case of a large mediastinal mass,6 or from local inflammation at the site of microinvasion, which cannot be detected by current CT scanners, followed by regression of ECG changes with tumor reduction.
Multimodality cardiac imaging plays a pivotal role in establishing the diagnosis. Transthoracic echocardiography is the initial modality for identifying pericardial effusion, myocardial thickening, or intracardiac masses. Cardiac CT provides superior spatial resolution and anatomical delineation of tumor extension and its relationship to coronary arteries, whereas fluorodeoxyglucose (FDG)-PET allows assessment of metabolic activity and systemic disease burden, aiding differentiation between malignant and benign processes.7,8
The prognosis of cardiac metastases remains poor and generally reflects advanced systemic malignancy. Management is typically palliative and requires a multidisciplinary approach involving cardiology, oncology, radiology, and, in selected cases, cardiothoracic surgery or radiotherapy.2,8
Current guidelines and expert consensus suggest that primary percutaneous coronary intervention should not be withheld in cancer patients presenting with suspected STEMI when life expectancy exceeds 6 months or when clinical instability is present, as invasive management has been associated with improved outcomes compared with conservative treatment.9 However, these cases demonstrate that ST-segment elevation in patients with advanced malignancy may arise from myocardial tumor invasion or tumor compression rather than acute coronary thrombosis, underscoring the importance of careful clinical and imaging correlation.
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Take-Home Messages
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Advanced lung cancer can mimic STEMI through mechanisms such as direct myocardial invasion or extrinsic compression, rather than classic thrombotic occlusion.
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Clinicians should suspect cardiac metastasis when there is a significant discordance between diffuse ST-segment elevation, nonobstructive coronary angiography, and only mild troponin elevation.
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Multimodality imaging, particularly cardiac CT and echocardiography, is essential to identify tumor infiltration and confirm the diagnosis in oncological patients presenting with chest pain.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
References
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