Acute myocardial infarction from paradoxical embolism in a case of massive pulmonary thromboembolism

Abstract

Objective-In the chronic phase of myocardial infarction, the relation between myocardial recovery and infarct related artery status remains unclear. The spontaneous changes in rest-redistribution thallium defect size were prospectively studied over six months in 52 patients with chronic Q wave myocardial infarction. Design-Changes in rest thallium defect size, thallium uptake in the infarct area, and radionuclide left ventricular ejection fraction were compared to the quantitative coronary angiogram data. Two groups of patients were considered: patients with a percentage of stenosis below 100% (group 1, n = 31); and patients with an occluded artery (group 2, n = 21). Results-In the overall population, the mean (SD) defect size decreased from 28.2 (17.2)% to 24.9 (19.3)% of the whole myocardium (p = 0.01), while, in this area, the thallium uptake increased from 62.9 (13.7)% to 66.9 (15.6)% (p < 0.001). At the time of inclusion, the defect size, thallium uptake, and ejection fraction were similar in both groups. In group 1 patients only, the reduction in defect size correlated with the improvement in ejection fraction (r = 0.41, p = 0.02) and was related to the percentage of coronary artery stenosis. TIMI 3 patients reduced the defect size while other patients increased this defect (−5.1 (7.0)% v +11.0 (14.4)%, p < 0.001). In contrast, no significant relations were found in group 2 patients. Conclusion-Late spontaneous recovery in thallium defect can occur in patients with a patent infarct related artery, depending on the TIMI flow grade and a low grade stenosis of the infarct related artery, and is associated with functional improvement. (Heart 1999;81:424-430)

Unique Case of ST-Segment–Elevation Myocardial Infarction Related to Paradoxical Embolization and Simultaneous Pulmonary Embolization

“…These reports also include cases deemed with air, tumor, and brain tissue embolization. [24][25][26][27][28][29][30][31][32] In 1988 Jungbluth et al identified 27 published cases of paradoxical coronary embolism, and 21 additional cases have been reported until 2004. 33,34 The unique subgroup particularly prone to experience paradoxical embolism comprises patients with PE and PFO.…”

Paradoxical Embolism Due to Open Foramen Ovale with Atrial Septal Aneurysm as a Cause of Myocardial Infarction in a Young Male

“…Additionally, pulmonary embolism, which already suggests the presence of venous thrombosis and causes an increase of the right heart pressure, enhancing right-to-left shunting in the presence of an interatrial connection, should raise the suspicion of paradoxical embolism when occuring simultaneously with systemic embolization. However, unless clear evidence is found, like a thrombus transiting from the right to the left atrium, it is often difficult to ascribe the occurence of a myocardial infarction to paradoxical thromboembolism [6][7][8].…”

Acute coronary syndrome of paradoxical origin

“…3 Pulmonary embolism (or any condition that raises right atrial pressure) is frequently implicated in the increased right heart pressures that set the stage for right-to-left shunting via a PFO. 4,7,9 TEE is crucial for accurate diagnosis and appropriate management when paradoxical embolism is suspected. 10 TEE study with color Doppler and contrast echocardiography is the most sensitive diagnostic technique for diagnosing PFO.…”