Rest-redistribution thallium-201 scintigraphy to determine myocardial viability early after myocardial infarction.

OBJECTIVES: This study attempted to determine the utility of early rest-redistribution thallium-201 imaging in detecting residual myocardial viability after myocardial infarction. BACKGROUND: The early detection of myocardial viability after myocardial infarction would have clinical relevance. METHODS: Thirty-one patients with acute myocardial infarction had early (mean [+/- SD] 2 +/- 1 day) rest-redistribution thallium-201 imaging followed by radionuclide and coronary angiography. Late studies included stress-redistribution-reinjection thallium-201 imaging or radionuclide angiography, or both. Viability was defined by the rest thallium-201 scan as an initial mild rest defect or any defect that demonstrated redistribution. RESULTS: Group 1 (n = 15) was predicted to have viable and Group 2 (n = 16) nonviable myocardium in the infarct zone. Group 1 patients were more likely to have a patent infarct-related artery (15 of 15 vs. 10 of 16, p < 0.03), higher initial ejection fraction (61 +/- 12% vs. 53 +/- 9%, p < 0.05), higher infarct wall motion score (p < 0.0001) and fewer abnormal thallium-201 segments (p < 0.0001). On follow-up studies, ejection fraction improved in Group 1 (from 57 +/- 13% to 66 +/- 10%, p < 0.05, n = 9) and deteriorated in Group 2 (from 53 +/- 10% to 46 +/- 8%, p < 0.05, n = 13). On late stress testing with thallium-201 reinjection, Group 1 patients had fewer abnormal segments (p < 0.03) and higher infarct zone counts during exercise (p < 0.05) and after reinjection (p < 0.05) than Group 2 patients. CONCLUSIONS: If confirmed by larger studies, early rest-redistribution thallium-201 imaging may be a useful technique for identifying residual viability after myocardial infarction.

Mediastinal arteriovenous fistulae in the adult: case report and review of the literature.

An adult with an asymptomatic mediastinal arterio-venous fistula is presented. The diagnosis was established using angiography and oximetry after noninvasive imaging failed to identify the source of a continuous murmur. The literature is reviewed.

Direct measurement of myocardial free radical generation in an in vivo model: effects of postischemic reperfusion and treatment with human recombinant superoxide dismutase.

OBJECTIVES: The purpose of this study was to determine whether postischemic reperfusion of the heart in living rabbits induces a burst of oxygen free radical generation that can be attenuated by recombinant human superoxide dismutase administered at the moment of reflow. BACKGROUND: This phenomenon was previously demonstrated in crystalloid perfused, globally ischemic rabbit hearts. METHODS: Thirty-two open chest rabbits were assigned to one of four groups of eight animals each: Group I (control animals), no coronary artery occlusion; Group II, 30 min of circumflex marginal coronary artery occlusion without reperfusion; Group III, 30 min of coronary occlusion followed by 60 s of reperfusion, and Group IV, 30 min of coronary occlusion followed by treatment with recombinant human superoxide dismutase (a 20-mg/kg body weight bolus 90 s before reperfusion and a 0.17-mg/kg infusion during 60 s of reperfusion). Full thickness biopsy specimens taken from the ischemic region were then rapidly freeze clamped and electron paramagnetic resonance spectroscopy was performed at 77 degrees K. RESULTS: Three radical signals similar to those previously identified in the isolated, crystalloid perfused rabbit heart were observed: an isotropic signal with g = 2.004 suggestive of a semiquinone, an anisotropic signal with g parallel = 2.033 and g perpendicular = 2.005 suggestive of an oxygen-centered alkyl peroxy radical, and a triplet with g = 2.000 and aN = 24 G suggestive of a nitrogen-centered radical. In addition, a fourth signal consistent with an iron-sulfur center was seen. The oxygen-centered free radical concentration during normal perfusion (Group I) was 1.8 +/- 0.8 mumol compared with 4.4 +/- 0.9 mumol after 30 min of regional ischemia without reperfusion (Group II) and 13.0 +/- 2.5 mumol after 60 s of reperfusion (Group III) (p < 0.05 among all three groups). In contrast, superoxide dismutase treated-rabbits (Group IV) demonstrated a peak oxygen radical concentration of only 5.9 +/- 1.2 mumol (p < 0.05 vs. Group III). CONCLUSIONS: This study demonstrates that reperfusion after regional myocardial ischemia in the intact rabbit is associated with a burst of oxygen-centered free radicals. The magnitude of this burst is greater than that seen after a comparable duration of global ischemia in the isolated, buffer-perfused rabbit heart preparation and is significantly reduced by superoxide dismutase administration begun just before reflow.

Coronary artery pseudo-occlusion associated with the use of an active hemoperfusion system during PTCA.

We describe the phenomenon of coronary artery "pseudo-occlusion," which may occur when active hemoperfusion devices are utilized during percutaneous transluminal coronary angioplasty (PTCA). In such cases, contrast injected via the guiding catheter fails to opacify the coronary artery distal to the tip of the dilating catheter, thereby giving the angiographic appearance of coronary occlusion. When active hemoperfusion is terminated, contrast opacifies the vessel in a normal fashion. The cause of this observation is likely multifactorial and includes obstruction to flow by the dilating catheter, high distal pressure delivered by the dilating catheter during hemoperfusion competing with the flow of contrast injected via the guiding catheter, and wash-out of contrast at the tip of the dilating catheter by non-contrast containing blood being pumped through the system. This phenomenon must be recognized if potentially deleterious repeat dilatations are to be avoided.

Contrast echocardiographic mapping of collateralized myocardium in humans before and after coronary angioplasty.

Conventional coronary arteriography is able to demonstrate the presence of coronary collateral vessels but cannot delineate the specific region of myocardium to which they supply blood. To test the hypothesis that contrast echocardiography can specifically identify collateralized myocardium, contrast echocardiographic perfusion "maps" were compared in patients with (n = 12) and without (n = 12) angiographic evidence of coronary collateral flow, both before and after coronary angioplasty. Contrast echocardiographic images of the mid-left ventricle in the short-axis view at end-diastole were obtained after separate injections of a sonicated contrast agent into both the right and the left coronary arteries. A computer-based contouring system was used to determine the individual areas of myocardium perfused by each of the two coronary arteries and then to superimpose the images of the two perfusion beds. The resulting area of overlapping perfusion represented myocardium receiving blood flow from both coronary systems and was defined as collateralized myocardium. To normalize for heart size, overlap area was expressed as a percent of total myocardial area, which was the area between endocardium and epicardium in the short-axis view. To adjust for differences in vascular distribution, overlap area was expressed as a percent of the perfusion area of the recipient vessel. In patients with angiographic collateral flow, the recipient vessel was that vessel receiving the collateral flow. In patients without angiographic collateral flow, the right coronary artery was considered the recipient vessel. Overlap area was 1.3 +/- 0.4% of total myocardial area and 6.6 +/- 1.7% of recipient vessel area in patients without angiographic evidence of collateral flow compared with 30.6 +/- 2.5% and 89.2 +/- 6.4%, respectively, in patients with angiographic collateral flow (p less than 0.001 for both). In four patients in whom angiographic collateral flow was abolished by angioplasty, overlap area decreased from 30.3 +/- 5.3% to 6.8 +/- 2.7% of total myocardial area and from 100% to 18.5 +/- 5.4% of recipient vessel area (p less than 0.05 for both). Thus, contrast echocardiography is able to map the specific myocardial territory perfused by coronary collateral flow and document an immediate reduction in perfusion in this territory when collateral flow is abolished by angioplasty.

Nonacute thrombolytic therapy: an adjunct to coronary angioplasty in patients with large intravascular thrombi.

The presence of intravascular thrombus can make coronary angioplasty difficult or impossible to perform. To determine if thrombolytic agents could lyse large, nonacute thrombi, we retrospectively analyzed the angiograms of all 14 patients with unstable angina and large intravascular thrombi (greater than 2 cm in length) who were treated with thrombolytic agents at The Johns Hopkins Hospital between October 1987 and April 1989. Twelve patients were treated with intracoronary streptokinase, and two with intravenous tissue plasminogen activator. Coronary arteriography was repeated immediately after treatment and a mean of 1.6 +/- 0.3 days later. The degree of thrombolysis and change in distal vessel perfusion was evaluated. Thrombolysis was graded as considerable if there was greater than 75% resolution of apparent thrombus, and as complete if no stenosis or only a discrete residual stenosis was apparent. Fifty-seven percent of patients ultimately achieved considerable or complete thrombolysis and were able to undergo successful angioplasty. Patients achieving considerable or complete thrombolysis had a 28 +/- 7% increase in luminal diameter and demonstrated normalization of initially absent distal perfusion, except for the one patient who had normal distal flow prior to treatment. A maximal thrombolytic effect was evident only at the time of "delayed" angiography in all patients who responded to treatment and underwent both follow-up arteriograms. We conclude that thrombolytic agents can effectively lyse large, nonacute intravascular thrombi, thereby facilitating coronary angioplasty. A full thrombolytic effect does not occur for hours to days after drug administration, and may not become evident unless delayed angiography is performed.

Late thrombotic occlusion of saphenous vein grafts: successful recanalization using thrombolytic therapy.

We report two cases in which thrombosis was the primary cause of vein graft occlusion many years after bypass surgery. Both displayed minimal thrombolysis immediately after a selective infusion of streptokinase but were patent when reimaged hours later. Such therapy may be helpful when graft occlusions are associated with a large volume of thrombus.