Presence Of Collateral Flow Research Articles

Residual flow to the infarct zone as a determinant of infarct size after direct angioplasty.

In acute myocardial infarction, residual flow to the infarct zone either through antegrade flow in the infarct-related coronary artery or collateral flow from the non-infarct-related arteries is often present before reperfusion therapy. The purpose of this study was to assess the influence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before successful direct angioplasty on infarct size and myocardial salvage in patients with acute evolving myocardial infarction. Sixty patients with acute evolving myocardial infarction underwent direct successful angioplasty without prior thrombolytic therapy. The myocardium at risk of infarction, the final infarct size, and myocardial salvage were measured by tomographic perfusion imaging with 99mTc sestamibi. Antegrade flow in the infarct-related artery before intervention was graded according to the Thrombolysis in Myocardial Infarction (TIMI) study group classification. Collateral flow to the infarct zone before angioplasty was also graded (0 through 3, 0 being no collateral flow). The presence of even minimal antegrade flow before angioplasty (TIMI grade 1) in the infarct-related artery compared with absent flow was associated with a significant reduction in final infarct size (9 +/- 17% versus 23 +/- 19% of left ventricle, P = .02) and a significant increase in myocardial salvage (23 +/- 16% versus 14 +/- 13% of left ventricle, P = .05) after angioplasty. When antegrade flow in the infarct-related artery was absent before angioplasty, the presence of collateral flow before angioplasty resulted in a significantly smaller final infarct size (P = .01) and more myocardial salvage (P = .05) after angioplasty. Both antegrade infarct-related artery flow and collateral flow to the infarct zone had significant independent ability to predict infarct size after angioplasty. When collateral grade and TIMI grade were added to provide an estimate of residual flow, a model including residual flow, myocardium at risk, and the interaction of residual flow and infarct site explained 83% of the variability in infarct size after angioplasty. The presence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before direct angioplasty in acute evolving infarction results in a smaller infarct size after direct successful angioplasty.

Intracranial vascular stenosis and occlusion: evaluation with three-dimensional time-of-flight MR angiography.

To assess the usefulness of magnetic resonance (MR) angiography in the characterization of intracranial arterial stenosis and occlusion, a three-dimensional time-of-flight method was compared with conventional angiography in 214 vessels in 29 patients. Studies were independently interpreted by two neuroradiologists who scored each vessel as normal, narrowed, or occluded. Overall, 97% of normal vessels and 100% of occlusions were correctly graded. Sixty-one percent of stenoses were graded correctly; the remainder were graded as normal. The portions of the intracranial vessels near the skull base and especially the paracavernous and supraclinoid segments of the internal carotid arteries were areas of frequent over- and underestimation of stenosis due to the presence of dephasing artifacts. In patients with stenosis or occlusion, MR angiography also provided information regarding the presence of collateral flow in the circle of Willis. When used in conjunction with MR imaging of the brain and MR angiography of the extracranial carotid arteries, intracranial MR angiography allows a more complete evaluation of the patient with symptoms of cerebral ischemia or infarction.

Reperfusion injury in dog hearts with permanent occlusion of a coronary artery, probably due to reperfusion via collateral vessels

To clarify whether or not reperfusion injury occurs in the permanent occlusion of a coronary artery, we analyzed quantitatively contraction band necrosis as an indicator of early recanalization, coagulation necrosis, infarct size and measured regional blood flow in dog hearts with collateral circulation. Fifty mongrel dogs were divided into four groups: 15 dogs with a 24-hour occlusion of the left anterior descending coronary artery just distal to the first diagonal branch (permanent occlusion group): 15 dogs a with 3-hour occlusion followed by 24-hour recanalization (recanalization group); 10 dogs with a 2-hour occlusion without recanalization (transient occlusion group); 10 dogs with a 4-hour occlusion without recanalization (transient occlusion group). The regional blood flow in the subepicardium and subendocardium determined by the generated hydrogen gas clearance method was greatly decreased 30 minutes after occlusion ( 14 + 8% 12 ± 9% ) and was relatively restored from 180 minutes ( 31 ± 21% 21 ± 14% ) to 24 hours later ( 41 + 19% 26 + 16% ) in spite of complete occlusion of the coronary artery. The percentage infarct area in the risk area was significantly greater in the permanent occlusion group (60 ± 26%) than in the recanalization group (35 ± 31%). Although most of the infarct was occupied by contraction band necrosis in the recanalization group (86 ± 12%), contraction band necrosis was diffusely seen even in the permanent occlusion group (54 ± 27%). In both the permanent and recanalization groups, contraction band necrosis was the main histological feature of small infarcts occupying less than 30% of the risk area, while coagulation necrosis was the main feature in very large infarcts occupying more than 80% of the risk area. In the occlusion groups without recanalization, the percentage area of contraction band necrosis in the risk area was 6 ± 8% after the 2-hour occlusion, 23 ± 17% after the 4-hour occlusion and 31 ± 21% after permanent occlusion; the difference between the 4-hour and permanent occlusion groups was not significant. In the permanent occlusion group, the percentage infarct area in the risk area was inversely correlated with regional blood flow during occlusion, an indicator of collateral flow. It was concluded that reperfusion injury occurs even in hearts without recanalization. The pathogenesis may involve reperfusion in the risk area via collateral circulation. Protection against reperfusion injury is important to minimize the infarct size even in hearts with permanent occlusion, although the presence of collateral flow is an important factor in limiting infarct size.

Surgical revascularization following unsuccessful percutaneous transluminal coronary angioplasty

From September, 1980, through August, 1981, 353 patients underwent attempted percutaneous transluminal coronary angioplasty (PTCA). Twenty-seven patients (7.6%) subsequently underwent elective myocardial revascularization without death or complicating PTCA. Surgical support in the first 2 months involved a fully-staffed operating room standing idle. During the last 10 months, patients requiring emergency revascularization were accommodated in the first operating room available. All 17 patients undergoing emergency revascularization had severe chest pain and 12 patients had ST-segment elevation on the electrocardiogram. The average time from onset of ischemia to revascularization was 135 minutes and did not change over the period of study. Improvement in the electrocardiogram and myocardial function were frequently noted with restoration of flow by the vein graft. Two patients (12%) required inotropic drug support following revascularization. All 12 patients with ST-segment elevation preoperatively had elevated myocardial enzyme levels postoperatively, including five patients (29%) with new Q waves on the electrocardiogram. Myocardial necrosis did not correlate with time to revascularization, number of diseased vessels, the artery being instrumented, the mechanism of ischemia, or the presence of collateral flow. There were no deaths. Because of the high incidence of myocardial infarction despite prompt revascularization, we now routinely insert the intra-aortic balloon pump in the catheterization laboratory in patients with refractory myocardial ischemia requiring emergency revascularization. Prompt safe revascularization for acute ischemia following PTCA can be achieved without expensive and inefficient standby of cardiac surgical facilities. Transmural myocardial ischemia following complicated PTCA is frequently associated with evidence of myocardial necrosis despite prompt surgical revascularization. Greater salvage of ischemic myocardium may be possible if the intra-aortic balloon pump is used in the interval between PTCA-induced injury and surgical revascularization.