Rethrombosis after reperfusion with streptokinase: importance of geometry of residual lesions.

We tested the hypothesis that lesion rethrombosis after streptokinase reperfusion is related to luminal size of the residual stenosis. Two independent techniques of analyzing coronary angiograms, quantitative coronary angiography and computer-based videodensitometry, were used to estimate the size of the residual lumen immediately after discontinuation of streptokinase. These techniques were selected because they provide independent estimates of cross-sectional area of a lesion with high degrees of reproducibility and minimal observer variability. Twenty-four patients who had undergone successful reperfusion with streptokinase were studied. Seven patients had lesion rethrombosis documented either on a repeat angiogram, at autopsy, or, in one case, by the fact that the patient had an acute transmural infarction resulting in death. Vessel patency was documented by repeat coronary angiography 8 to 14 days after initial streptokinase reperfusion in the other 17 patients. As assessed by quantitative coronary angiography, seven of 13 patients (54%) with minimal luminal cross-sectional areas of less than 0.4 mm2 had rethrombosis. None of the 11 patients with lumens greater than 0.4 mm2 had rethrombosis. In the 17 patients with vessels that remained patent the size of the residual lesion at repeat catheterization was compared with its size immediately after reperfusion with streptokinase. Over the intervening 8 to 14 day interval, an average percentage increase in minimal cross-sectional area of 116 +/- 34% was observed. In seven patients minimal luminal cross-sectional area more than doubled. Integrated optical density, an index of the severity of coronary stenosis derived from computer-based videodensitometry, was also useful in identifying a subgroup of patients at high risk for rethrombosis of lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

[1]  C. White,et al.  The value of lesion cross-sectional area determined by quantitative coronary angiography in assessing the physiologic significance of proximal left anterior descending coronary arterial stenoses. , 1984, Circulation.

[2]  R. C. Reeves,et al.  Prospective randomized trial of intravenous and intracoronary streptokinase in acute myocardial infarction. , 1983, Circulation.

[3]  P. Rentrop,et al.  Electrocardiographic changes after streptokinase-induced recanalization in patients with acute left anterior descending artery obstruction. , 1983, Circulation.

[4]  D. Ku Coronary vascular reactivity after acute myocardial ischemia. , 1982, Science.

[5]  R. Erbel,et al.  Percutaneous Transluminal Coronary Angioplasty Immediately After Intracoronary Streptolysis of Transmural Myocardial Infarction , 1982, Circulation.

[6]  G. Schuler,et al.  Thrombolysis in Acute Myocardial Infarction Using Intracoronary Streptokinase: Assessment by Thallium‐201 Scintigraphy , 1982, Circulation.

[7]  M. Claeys,et al.  Endothelium-dependent inhibitory effects of acetylcholine, adenosine triphosphate, thrombin and arachidonic acid in the canine femoral artery. , 1982, The Journal of pharmacology and experimental therapeutics.

[8]  E. Bolson,et al.  The Mechanisms of Nitroglycerin Action: Stenosis Vasodilatation as a Major Component of the Drug Response , 1981, Circulation.

[9]  D. Berman,et al.  Myocardial salvage by intracoronary thrombolysis in evolving acute myocardial infarction: evaluation using intracoronary injection of thallium-201. , 1981, American heart journal.

[10]  P. Rentrop,et al.  Selective Intracoronary Thrombolysis in Acute Myocardial Infarction and Unstable Angina Pectoris , 1981, Circulation.

[11]  R. Furchgott The requirement for endothelial cells in the relaxation of arteries by acetylcholine and some other vasodilators , 1981 .

[12]  W. Santamore,et al.  Altered coronary flow responses to vasoactive drugs in the presence of coronary arterial stenosis in the dog. , 1980, The American journal of cardiology.

[13]  J. Cohn,et al.  Effect of dilation of the distal coronary bed on flow and resistance in severely stenotic coronary arteries in the dog. , 1979, The American journal of cardiology.

[14]  K. Gould,et al.  Pressure‐Flow Characteristics of Coronary Stenoses in Unsedated Dogs at Rest and during Coronary Vasodilation , 1978, Circulation research.

[15]  G. Hutchins,et al.  The relationship between coronary artery lesions and myocardial infarcts: ulceration of atherosclerotic plaques precipitating coronary thrombosis. , 1977, American heart journal.

[16]  E. Bolson,et al.  Quantitative Coronary Arteriography: Estimation of Dimensions, Hemodynamic Resistance, and Atheroma Mass of Coronary Artery Lesions Using the Arteriogram and Digital Computation , 1977, Circulation.

[17]  J. Murray,et al.  Variability in the Analysis of Coronary Arteriograms , 1977, Circulation.

[18]  J. Folts,et al.  Platelet Aggregation in Partially Obstructed Vessels and its Elimination with Aspirin , 1976, Circulation.

[19]  R. Dinsmore,et al.  Interobserver Variability in Coronary Angiography , 1976, Circulation.

[20]  T. Takaro,et al.  Observer Agreement in Evaluating Coronary Angiograms , 1975, Circulation.

[21]  N R Cholvin,et al.  Pressure Drop across Artificially Induced Stenoses in the Femoral Arteries of Dogs , 1975, Circulation research.

[22]  Observer Agreement inEvaluating Coronary Angiograms , 1975 .

[23]  W. Roberts,et al.  The frequency and significance of coronary arterial thrombi and other observations in fatal acute myocardial infarction: a study of 107 necropsy patients. , 1972, The American journal of medicine.

[24]  C. Borchgrevink,et al.  Acute lesions of coronary arteries in anticoagulant-treated and in untreated patients. , 1971, Atherosclerosis.

[25]  M. Friedman,et al.  The pathogenesis of a coronary thrombus. , 1966, The American journal of pathology.

[26]  I. Chapman MORPHOGENESIS OF OCCLUDING CORONARY ARTERY THROMBOSIS. , 1965, Archives of pathology.

[27]  J. Ehrlich,et al.  LOW INCIDENCE OF CORONARY THROMBOSIS IN MYOCARDIAL INFARCTION. A RESTUDY BY SERIAL BLOCK TECHNIQUE. , 1964, Archives of pathology.

[28]  Beer Bestimmung der Absorption des rothen Lichts in farbigen Flüssigkeiten , 1852 .