We established that FDG-PET imaging can be used to assess the severity of inflammation in carotid plaques in patients. If subsequent natural history studies link increased FDG-PET activity in carotid arteries with clinical events, this noninvasive measure could be used to identify a subset of patients with carotid atherosclerosis in need of intensified medical therapy or carotid artery intervention to prevent stroke.

Adenosine stress CT can identify stress-induced myocardial perfusion defects with diagnostic accuracy comparable to SPECT, with similar radiation dose and with the advantage of providing information on coronary stenosis.

Angiographic severity of coronary artery stenosis has historically been the primary guide to revascularization or medical management of coronary artery disease. However, physiologic severity defined by coronary pressure and/or flow has resurged into clinical prominence as a potential, fundamental change from anatomically to physiologically guided management. This review addresses clinical coronary physiology-pressure and flow-as clinical tools for treating patients. We clarify the basic concepts that hold true for whatever technology measures coronary physiology directly and reliably, here focusing on positron emission tomography and its interplay with intracoronary measurements.

These data show that FDG accumulates in macrophage-rich atherosclerotic plaques and demonstrate that vascular macrophage activity can be quantified noninvasively with FDG-PET. As such, measurement of vascular FDG uptake with PET holds promise for the noninvasive characterization of vascular inflammation.

Radionuclide myocardial perfusion imaging (MPI) is among the most commonly performed diagnostic tests in cardiology. Although the diagnostic and prognostic applications of radionuclide MPI are supported by a wealth of observational and clinical trial data, its performance is limited by two fundamental drawbacks. First, conventional MPI by SPECT and PET measures relative perfusion, that

Measurement of Ado-stimulated absolute MBF is superior to relative measurement of myocardial tracer retention for identification of CAD and can be accomplished with a single MBFado measurement.

No abstract

This study tested the hypothesis that a reduction in blood viscosity by means of isovolumetric hemodilution will permit an increase in maximal oxygen delivery to myocardium distal to a moderate coronary arterial stenosis. It is known that blood viscosity is a determinent of resistance to blood flow at both the stenotic and the arteriolar levels. Accordingly, a reduction in blood viscosity could exert a favorable influence on maximal myocardial oxygen delivery in the setting of stenosis, provided that the oxygen-carrying capacity of the blood is not compromised excessively. Closed-chest, sedated domestic swine (n = 8) were instrumented with an artificial coronary arterial stenosis that reduced vessel diameter by 64%. Measurements of hemodynamics, regional myocardial blood flow (microspheres), lactate and oxygen metabolism, and whole blood viscosity were made at control and after two successive 10 min intracoronary infusions of adenosine (400 and 800 ,ug/min) distal to the stenosis. Next, albumin/saline solution was given intravenously to reduce the animal's hematocrit by approximately 50%. Repeat measurements of all experimental variables were then made at a second control and again after two successive 10 min intracoronary infusions of adenosine (400 and 800 gg/min) distal to the stenosis. Myocardial blood flow (ml/min/g) distal to the stenosis increased from 1.52 + 0.21 (mean 1 SD) to 4.10 0.86 in response to adenosine (peak dose) before hemodilution (p < .01) and from 2.07 + 0.59 to 4.08 + 0.93 (p < .01) after hemodilution. Minimum resistance (mm Hg/ml/min/g) distal to the stenosis, however, was approximately 33% lower (p < .05) during infusion of adenosine after hemodilution than it was before hemodilution (endocardium 15.8 6.3 vs 24.5 14.1 and epicardium 9.0 ± 2.3 vs 14.0 ± 8.0). Maximal oxygen delivery (ml/min/lOOg) to myocardium distal to the stenosis failed to improve and in fact was reduced (p < .01 vs before hemodilution) after hemodilution (34.6 ± 9.5 vs 19.9 ± 6.8 to endocardium and 65.5 ± 16.4 vs 38.0 + 10.5 to epicardium). Regional myocardial lactate metabolism, however, did not change vs initial control during the study. Finally, hematocrit was reduced from 32 3% to 17 + 3% (p < .01) and blood viscosity was reduced from 3.4 ± 0.2 to 2.4 ± 0.3 centipoise (p < .01) by hemodilution. The results of the study indicate that reducing blood viscosity by isovolumetric hemodilution may not enhance maximal myocardial oxygen delivery in the setting of a moderate coronary arterial stenosis. However, because minimal endocardial resistance is lowered by a reduction in blood viscosity, it is likely that maximal oxygen delivery could be improved by this intervention if hemodilution were accomplished with a fluid capable of transporting oxygen (e.g., perfluorocarbon emulsion). Circulation 74, No. 5, 1085No. 5, -1092No. 5, , 1986 DELIVERY OF OXYGENATED blood to the myocardium in the setting of a coronary arterial stenosis is influenced by a number of factors. Many of these (e.g., stenosis dimensions, heart...