Immediate angioplasty after acute myocardial infarction was associated with a higher rate of patency of the infarct-related artery, a less severe residual stenotic lesion, better left ventricular function, and less recurrent myocardial ischemia and infarction than was intravenous streptokinase.

Data from experimental, clinical, and pathologic studies have suggested that the process ofrestenosis begins very early after coronary angioplasty. The present study was performed to determine prospectively the incidence of restenosis with use of the four National Heart, Lung, and Blood Institute and the 50% or greater diameter stenosis criteria, as well as a criterion based on a decrease of 0.72 mm or more in minimal luminal diameter. Patients were recatheterized at 30, 60, 90, or 120 days after successful percutaneous transluminal coronary angioplasty (PTCA). After PTCA all patients received 10 mg nifedipine three to six times a day and aspirin once a day until repeat angiography. Of 400 consecutive patients in whom PTCA was successful (<50% diameter stenosis), 342 underwent quantitative angiographic follow-up (86%) by use of an automated edge-detection technique. A wide variation in the incidence of restenosis was found dependent on the criterion applied. The incidence of restenosis proved to be progressive to at least the third month for all except NHLBI criterion II. At 4 months a further increase in the incidence of restenosis was observed when defined as a decrease of 0.72 mm or more in minimal luminal diameter, whereas the criteria based on percentage diameter stenosis showed a variable response. The lack of overlap between the different restenosis criteria applied affirms the arbitrary nature of angiographic definitions currently in use. Restenosis should be assessed by repeat angiography, and preferably ascertained according to the change in absolute quantitative measurements of the luminal diameter.

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In vivo MRI provides a means to non-invasively image and assess the morphological features of atherosclerotic carotid arteries. To assess quantitatively the degree of vulnerability and the type of plaque, the contours of the lumen, outer boundary of the vessel wall and plaque components, need to be traced. Currently this is done manually, which is time-consuming and sensitive to inter- and intra-observer variability. The goal of this work was to develop an automated contour detection technique for tracing the lumen, outer boundary and plaque contours in carotid MR short-axis black-blood images. Seventeen patients with carotid atherosclerosis were imaged using high-resolution in vivo MRI, generating a total of 50 PD- and T1-weighted MR images. These images were automatically segmented using the algorithm presented in this work, which combines model-based segmentation and fuzzy clustering to detect the vessel wall, lumen and lipid core boundaries. The results demonstrate excellent correspondence between automatic and manual area measurements for lumen (r = 0.92) and outer (r = 0.91), and acceptable correspondence for fibrous cap thickness (r = 0.71). Though further optimization is required, our algorithm is a powerful tool for automatic detection of lumen and outer boundaries, and characterization of plaque in atherosclerotic vessels.

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