B L Holman

Measuring Regional Myocardial Blood Flow with 133Xe and the Anger Camera

Regional myocardial blood flow was measured using the inert gas washout technique and the Anger scintillation camera following injection of 133Xe into the coronary artery. By applying compartmental analysis to 30-minute washout curves, three compartments were delineated, representing blood flow to fat (IIIF) and myocardium (IM and IIM). Regional heterogeneity of flow was a highly sensitive index of coronary artery disease. Functional images delineated areas of altered perfusion better than quadrantic flow values. Gamma camera images of initial xenon distribution identified patients with severely altered flow.

Regional myocardial blood flow in patients with chest pain syndromes and normal coronary arteriograms.

To evaluate possible disorders of regional myocardial blood flow in patients with chest pain syndromes and normal coronary arteriograms, we studied 21 patients with intracoronary injections of Xenon-133. Thirteen patients were restudied during an intervention: 6 patients received glyceryl trinitrate and 7 patients had contrast agent-induced hyperaemia. Patients were divided into 3 clinical groups: 7 patients had classic angina, 7 patients had a mixture of typical and atypical chest pain, and 7 patients had entirely atypical pain. A wide range of normal values for regional myocardial blood flow at rest was noted (41 to 128 ml/min per 100 g, with an average regional myocardial blood flow of 77 ml/min per 100 g ± 7 (mean ± SEM)). There were no significant differences between the 3 groups. With contrast hyperaemia, regional myocardial blood flow increased 164 per cent, while with glyceryl trinitrate, it decreased 31 per cent. Again, there was no statistical difference among the groups. Regional abnormalities offlow (> 15% difference between distal quadrants) were noted in 3 of 34 measurements. Two patients had heterogeneity of flow at rest by quadrant analysis but no focal perfusion abnormalities detected by functional imaging. Interestingly, both patients had positive exercise tests. Another patient had regional differences only during contrast-induced hyperaemia. Our findings suggest that most patients with chest pain syndromes and normal coronary arteriograms-even those with classic angina-do

Angiographic abnormalities associated with alterations in regional myocardial blood flow in coronary artery disease.

To evaluate the association between alterations in myocardial blood flow and angiographic findings, myocardial blood flow was compared in 26 patients with asymergy, 15 patients with a similar extent of coronary artery disease but without asynergy, and 10 patients without coronary artery disease or obvious myocardial or valvular disease. Myocardial blood flow was measured at rest with an Anger camera and PDP-11/20 computer after the intracoronary injection of 133xenon. In comparison with the normal subjects, whole heart blood flow was significantly reduced in patients with asynergy. In addition, myocardial blood flow in regions of anteroapical asynergy was reduced (85-7 +/- 7-0 ml/min per 100 g3 in controls to 65-4 +/- 4-5, P less than 0-05) and a similar reduction was noted in regions of posterolateral asymergy (91-5 +/- 8-8 in controls to 66-8 +/- 5-0, P less than 0-05). In general, regional myocardial blood flow was reduced distal to left anterior descending or left circumflex stenosis of less than 50 per cent, with a trend toward further reduction distal to less than 75 per cent stenosis. In these same patients, the presence of anteroapical or posterolateral asynergy resulted in a similar trend to even greater reduction of flow. The effect of collaterals was variable: 7 of 8 patients without asynergy but with less than 75 per cent left anterior descending stenosis and collateral circulation to the lower left anterior descending quadrant had minimally reduced flows. However, in the 17 patients with anteroapical asynergy, regional myocardial blood flow was very similar in the 9 patients with collaterals compared with the 8 patients without them. This study suggests that the degree of coronary artery stenosis and presence of asynergy are both important in evaluating alterations in myocardial blood flow in coronary artery disease, while the role of collaterals remains uncertain.

Platelet activation and aggregation after endothelial injury. Assessment with indium-111-labeled platelets and angiography.

Although platelet activation and aggregation after endothelial injury are well documented, the time course of platelet deposition and the relationship between platelet aggregation and the release of vasoactive products have not been fully clarified in vivo. To study the effect of platelet vasoactive products, a collateral blood supply was induced by ligating the superficial femoral artery in male New Zealand white rabbits. Two weeks later, endothelial injury to the distal abdominal aorta was produced by cytologic brush or mimicked with a metal coil embolus. Platelet aggregation was assessed with indium-111 (111In)-labeled platelets, and scintigraphy demonstrated significant, progressive platelet deposition up to 3 hours after injury and evidence of residual activity 24 hours later. Angiography showed that the time course of peripheral vasoconstriction matched closely that of platelet deposition, indicating release of vasoactive substances from the aggregating platelets. These pathophysiologic changes secondary to endothelial injury may have significant implications for intravascular interventional procedures.

Comparison of I-123 IMP cerebral uptake and MR spectroscopy following experimental carotid occlusion

Both I-123 IMP scintigraphy and MRI have been suggested as sensitive detectors of changes shortly after acute cerebral infarction. We compared the uptake of N-isopropyl I-123 p-iodoamphetamine (IMP) and MR spectroscopy of the brain after internal carotid artery ligation. Thirteen gerbils were lightly anesthetized with ether. After neck dissection, an internal carotid artery was occluded. After 2.8 hours, 100 muCi I-123 IMP was injected intravenously into the 13 experimental animals plus three controls. Seven gerbils remained asymptomatic while six developed hemiparesis. At 3 hours after ligation, the animals were killed. The brains were bisected and T1 and T2 relaxation times were determined for the right and left hemispheres by MR spectroscopy immediately after dissection. I-123 IMP uptake was then determined in the samples. Interhemispheric differences in uptake for I-123 IMP were 0.1 +/- 1.7% (SEM) in the control, 33.5 +/- 10% in the asymptomatic and 54.6 +/- 9.7% in the symptomatic animals. Significant differences were seen with I-123 IMP in 6/7 asymptomatic and 6/6 symptomatic animals. In conclusion, I-123 is more sensitive than T1 or T2 relaxation times for the detection of cerebral perfusion abnormalities. Prolongation in T1 and T2 relaxation times correlates closely with increased brain tissue water content and the development of symptoms, indicators of structural brain damage and probable infarction.

Embolization of platelets after endothelial injury to the aorta in rabbits. Assessment with 111indium-labeled platelets and angiography.

This study exploits the ability of a collateral arterial network to trap platelet aggregates in order to document the frequency of macroembolization in rabbits after endothelial damage. Two weeks after ligation of the right superficial femoral artery, endothelial injury was induced in the distal aorta; within 3 hours the rabbits were studied using either angiography or 111indium-labeled (111In) platelet scintigraphy. Angiography indicated visible aggregates in the thigh region in eight of 19 and arterial occlusion in three of 19 rabbits. The collateral-dependent thigh also showed more 111In-labeled platelet activity than the contralateral side (P less than .001), whether platelets were injected before or 2 hours after injury. Radioactivity in the limbs of rabbits with no injury was distributed symmetrically. Blood pool volume, assessed with technetium-99m-labeled red blood cells, was the same in both thighs, and could not account for these observations. The findings indicate that platelet activation and aggregation after endothelial injury lead to microembolization much more frequently than it leads to macroaggregate formation and visible artery occlusion.