Irregular coronary lesion morphology after thrombolysis predicts early clinical instability

Abstract

After successful thrombolytic treatment for acute myocardial infarction, recurrent ischemia and infarction may occur with little warning. Coronary lesion morphology was analyzed from angiograms performed in 72 consecutive patients at 1 to 8 days after streptokinase treatment for acute myocardial infarction and the data were evaluated in relation to the subsequent clinical course. All patients were clinically stable at the time of angiography and continued to receive heparin infusion for greater than or equal to 4 days after thrombolysis. The infarct-related artery was patent in 55 patients (76%). In the 10 days after angiography, 15 patients developed prolonged episodes of angina at rest; the condition of 4 stabilized with medical treatment, but 11 required urgent medical intervention (coronary angioplasty in 8 and bypass surgery in 3). There were no differences in age, gender, left ventricular function or extent of coronary artery disease between those patients who developed unstable angina and those who had a stable in-hospital course. However, the median plaque ulceration index of the infarct-related lesion was 6.7 (95% confidence limits 6.3, 10) in the 15 patients with an unstable course versus 3.3 (2, 4.4) in those with a stable course (p less than 0.001). There were no differences between the two patient groups in the severity of stenosis, length of diseased segment, symmetry/eccentricity, presence of a shoulder, location at branch point or bend, presence of globular or linear filling defects, contrast staining or collateral supply. These data show that after thrombolysis, the degree of irregularity of the infarct-related artery is a critical determinant of early clinical instability.(ABSTRACT TRUNCATED AT 250 WORDS)

Vertebral Artery Ostium Atherosclerotic Plaque as a Potential Source of Posterior Circulation Ischemic Stroke

“…First, morphological changes at the plaque level (including the severity of stenosis, concentric versus eccentric, smooth versus irregular, haziness, calcification, overhanging, and the presence or absence of a clot at the VAO or intracranially) were classified according to the definitions of these terms set out in coronary literature. [7][8][9][10][11][12] The second key feature noted was the hemodynamic situation of the posterior circulation blood supply, which included: bilateral VAO lesions, defined as any evidence of atherosclerotic stenosis at both VAO, including occlusion but independent of the severity; the presence of tandem lesion, defined as Ͼ50% stenosis at the ipsilateral vertebral artery; basilarization of the vertebral artery, defined as only 1 vertebral artery providing anterograde flow to the basilar artery, attributable to acquired or congenital occlusion of the other vertebral artery intracranially or extracranially; and status of the circle of Willis. Two authors (F.A.A., T.B.)…”

Physiopathology of the Acute Coronary Syndromes

“…Using their computer-assisted extracorporeal-perfusion system, Badimon et al 45 and Lassila et al 46 found that platelet deposition increased significantly with increased stenosis. Sudden coronary occlusion was often preceded by a period of plaque instability and thrombus formation, initiated days or weeks before the onset of symptoms [15][16][17][18] , and total coronary occlusion of the infarct-related artery always results from the growth of RMT 44, 47 -49 . Considering these reports and the histopathological findings of thrombi, PT was thought to be formed abruptly as a result of severe coronary stenosis due to sudden extrusion of atheromatous debris into vessel lumen in 43 group A patients with a SRA index less than 30 at hospitalization, and due to gradual growth of RMT in group B and C patients.…”

“…Meshwork of fibrin was observed in RMT, so RMT was thought not to be fragile. RMT predisposes patients to recurrent thrombotic vessel occulusion [15][16][17] , and plaque disruption, fissure or erosion with thrombus contributes to plaque development and progression 18 . Gradual growth of RMT plays an important role on the increased stenosis of coronary artery, and total occlusion of coronary artery by platelet thrombus.…”

“…Most of occlusive thrombi had a layered structure indicating an episodic growth by repeated mural deposits 13,14 . Morphological studies indicated that plaque complications remained clinically silent days or weeks before the fatal event [15][16][17][18] . A RMT predisposes patients to recurrent thrombotic vessel occlusion 15,16,17 , and plaque disruption, fissure or erosion with thrombus contributes to plaque development and progression 18 .…”

“…Morphological studies indicated that plaque complications remained clinically silent days or weeks before the fatal event [15][16][17][18] . A RMT predisposes patients to recurrent thrombotic vessel occlusion 15,16,17 , and plaque disruption, fissure or erosion with thrombus contributes to plaque development and progression 18 . Therefore, a marker that predicts disrupted, fissured or eroded plaque and the coronary thrombus may have practical clinical applications.…”