2007
DOI: 10.1536/ihj.48.399
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Misdiagnosis Cardiac Metastasis Presented as a Pseudo-Infarction on Electrocardiography

Abstract: SUMMARYMost tumor invasion into the heart is nonspecific and clinically silent. Myocardium metastasis rarely mimics a myocardial infarction. In this case, a cardiac metastasis from a squamous cell carcinoma presented with both persistent ST elevation and paroxysmal supraventricular tachycardia. The secondary lesion was located in the anterior wall and lateral wall of the left ventricle and induced electrocardiographic changes imitating an acute myocardial infarction. (Int Heart J 2007; 48: 399-405)

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Cited by 11 publications
(3 citation statements)
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“…The ST segment elevation was due to a metastatic tumor that invaded the pericardium and myocardium. Suggested mechanisms for these pseudo-infarction ECG patterns are continuous myocardial injury preventing formation of new cardiac cell membrane, stretched adjacent muscle fibers, inflammatory reaction, the ionic transfer of potassium from necrotic tissue to the adjacent myocardium, and transfer of potassium from damaged tissue to the adjacent myocardium producing electropotential differences 8 . A similar cardiac metastasis of bladder cancer, which ECG abnormality was reported by Na et al.…”
Section: Discussionmentioning
confidence: 67%
“…The ST segment elevation was due to a metastatic tumor that invaded the pericardium and myocardium. Suggested mechanisms for these pseudo-infarction ECG patterns are continuous myocardial injury preventing formation of new cardiac cell membrane, stretched adjacent muscle fibers, inflammatory reaction, the ionic transfer of potassium from necrotic tissue to the adjacent myocardium, and transfer of potassium from damaged tissue to the adjacent myocardium producing electropotential differences 8 . A similar cardiac metastasis of bladder cancer, which ECG abnormality was reported by Na et al.…”
Section: Discussionmentioning
confidence: 67%
“…El hallazgo de una elevación del segmento ST como forma de presentación de las tumoraciones cardíacas es muy infrecuente y puede deberse a la compresión tumoral de una arteria coronaria o a la invasión miocárdica. A nivel celular, varios son los mecanismos que podrían explicar una elevación persistente del segmento ST. Entre ellos pueden citarse el desarrollo de una corriente de injuria secundaria a una reacción inflamatoria peritumoral; la transferencia iónica de potasio desde el tejido necrótico al miocardio adyacente, lo que produce una diferencia de potencial eléctrico entre estas áreas y, finalmente, el estiramiento de las fibras musculares adyacentes que llevan a una corriente de injuria similar a la que ocurre en los aneuris-mas ventriculares (2,3) . En nuestro caso, la angiografía evidenció una disminución de calibre del ramo posterolateral, que podría corresponder a compresión tumoral extrínseca (figura 2).…”
Section: Discussionunclassified
“…Increased thoracic pressure may also interfere with the amount and type of matter between the heart and the chest wall [6]. Other mechanisms can be due to direct stretch and irritation of the cardiac myocytes and electrolyte abnormalities caused by a nearby hypermetabolic, damaged tissue [8]. The location and nature of this esophageal malignancy make the correlation possible ( Figure 2).…”
Section: Discussionmentioning
confidence: 99%