Incomplete lysis of thrombus in the moderate underlying atherosclerotic lesion during intracoronary infusion of streptokinase for acute myocardial infarction: quantitative angiographic observations.

Abstract

Thrombolytic recanalization of the obstructed coronary lumen was studied in 32 patients receiving intracoronary streptokinase for 60 to 90 min during acute myocardial infarction. The process was viewed at high arteriographic magnification and was quantified with computer-assisted measurements from repeated single-plane views. The variability of the method for this application was 0.15 to 0.18 mm on minimum diameter estimates. Structural details were seen that are not commonly appreciated at conventional magnification. The recanalized lumen appears to form along an interface between the thrombus and the vessel wall, progressively enlarging its minimum arteriographic diameter to 0.65 +/- 0.24 mm (+/- 1 SD) at the end of the short-term infusion of streptokinase reflecting a final percent stenosis of 77 +/- 10%. In nine infarct lesions found patent 5 +/- 3 weeks later, the recanalized lumen further improved an average of 0.34 mm in minimum diameter (p less than .005) and 13% stenosis (p less than .01). A thin film of contrast medium surrounding the obstructing thrombus faintly defined the boundaries of the original atherosclerotic lumen in all but two cases. The "original stenosis" measured 1.25 +/- 0.32 mm in minimum diameter and 56 +/- 14% stenosis when first visualized; it was unchanged throughout the course of infusion of streptokinase. In five patients catheterized 10 +/- 12 weeks before their infarction, the original stenosis averaged 1.15 +/- 0.22 mm in the preinfarct angiogram, as compared with 1.17 +/- 0.23 mm in its faintly defined form during thrombolytic therapy (p = NS). In 10 cases, this original lesion was less than a 50% stenosis, and in 21 cases less than 60%.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracoronary Thrombus and Platelet Glycoprotein IIb/IIIa Receptor Blockade With Tirofiban in Unstable Angina or Non–Q-Wave Myocardial Infarction

“…16 Each culprit lesion was described qualitatively in terms of anatomic location, 17 perfusion characteristics, 18 morphological features, and intraluminal thrombus.…”

Can coronary angiography predict the site of a subsequent myocardial infarction in patients with mild-to-moderate coronary artery disease?

“…In every patient, at least some irregularity of the coronary wall was present on the first angiogram at the site of the subsequent coronary obstruction. In only 10 of the 29 (34%) did the infarction occur due to occlusion of the artery that previously contained the most severe stenosis. Furthermore, no correlation existed between the severity of the initial coronary stenosis and the time from the first catheterization until the infarction (r2 = 0.0005, p = NS).…”

Preparation and initial characterization of biodegradable particles containing gadolinium-DTPA contrast agent for enhanced MRI

“…Additionally, the financial burden of cardiovascular disease is more than double that of all cancers and is estimated at $430 billion in the United States in direct and indirect costs for 2007 (1). There have been many advances in identifying arterial stenosis, but the most common source of clinical events remains rupturing of vulnerable plaques in vessels with only 50-60% stenosis (2,3). In fact, only 30-40% of cases of myocardial infarction have a plaque that narrows the artery enough to limit flow (3,4).…”