Primary angiosarcoma of the heart causing cardiac rupture.

5-FU was discontinued. Previous reports have identified angina1 symptoms as a rare symptom of 5-FU cardiac toxicity.1-5 Some of these patients had also undergone irradiation4 of the left ventricle or had coronary artery disease.‘s3 Underwood et a1.6 suggested coronary artery spasm as a possible mechanism of toxicity. Other proposed mechanisms have included an autoimmune response and inflammatory reaction.lm3 Unlike patients in previous reports our patient had profound left ventricular dysfunction associated with ischemic ECG changes. This episode of 5-FU toxicity is remarkable not only for the acuteness and severity of the myocardial depression but also for the rapid and complete recovery after the drug was discontinued. Furthermore, normal coronary anatomy was documented simultaneously with the severe myocardial failure. An endomyocardial biopsy in the recovery phase did not identify a specific pathologic process. Diffuse coronary artery spasm with subsequent myocardial “stunning” cannot be excluded. Although sluggish flow of dye could reflect low cardiac output and reduced perfusion pressure, arteriolar spasm must also be considered. Cardiac toxicity related to 5-FU therapy is rare but can be life threatening. Myocardial ischemia and profound hemodynamic compromise can occur. The diagnosis should be considered in patients with chest pain, profound hypotension, or congestive heart failure during 5-FU therapy. If suspected, the transient and reversible nature of this toxicity warrants aggressive cardiovascular support until recovery is achieved.