We report a 30-year-old woman who developed an acute myocardial infarction at 24 weeks of gestation. She did not undergo any kind of acute intervention. On the 8th hospital day, premature delivery was performed safely following premature rupture of membrane. Coronary angiogram was normal and no spasm was induced by provocative test with ergometrine maleate. The patient had abnormal values of fibrinogen, thrombin-antithrombin III complex and plasmin-α2-plasmin inhibitor complex. Thus, thrombus formation might have been associated with the onset of acute myocardial infarction. This is the first case of acute myocardial infarction during pregnancy, showing normal coronary angiogram and negative pharmacological provocation of coronary spasm.
We successfully performed cutting balloon angioplasty for a restenotic lesion involving the distal saphenous vein graft (SVG) anastomosis that had developed within 1 month after conventional balloon angioplasty. We considered that cutting balloon angioplasty, which has been considered to produce less vascular injury, could be a viable choice for the treatment of a lesion at the distal anastomosis of an SVG.
Coronary air embolism is one of the inadvertent complications of coronary angioplasty. We report two rare cases of complicating air embolism in the right coronary artery occurring during control left coronary angiography using a guiding catheter with a side hole, just prior to a coronary intervention procedure for a left coronary artery lesion. The air seemed to be injected into the right coronary artery through the side hole. When we use an angiographic or guiding catheter with a side hole, we should be aware that an air embolism can occur in the contralateral coronary artery and should carefully and repeatedly perform aspiration of the catheter. Cathet. Cardiovasc. Intervent. 49:331-334, 2000.
SummaryBackground: Although acceleration of plasma plasminogen activator inhibitor-1 (PAI-1) level after emergent coronary angioplasty in acute myocardial infarction (AMI) has been documented, its pathophysiologic role is still unknown.Hypothesis: This study was designed to elucidate the role of PAI-1 in the development of restenosis after primary coronary stenting in AMI.Methods: We selected for this study 66 patients with AMI, who underwent primary coronary stenting for infarct-related coronary artery lesions in an emergent situation. In all patients, plasma PAI-1 level was measured at admission, and at 3 h, 24 h, 48 h, and 1 month after coronary stenting.Results: At admission, the PAI-1 level was equivalent in 24 patients who experienced restenosis and in 42 patients without restenosis (28 ± 4 vs. 29 ± 4 ng/ml). In patients with restenosis, the levels did not change during the course after coronary stenting. In patients without restenosis, however, the level significantly increased at 3 h (48 ± 9 ng/ml, p < 0.001), 24 h (42 ± 9, p < 0.01), and 48 h (38 ± 7, p < 0.05) after coronary stenting, and was restored to the level equivalent to that at admission (27 ± 2 ng/ml) 1 month after coronary stenting. The PAI-1 level at 3 h after coronary stenting in patients without restenosis was significantly higher (p < 0.05) than the level (33 ± 6
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