The myocardial perfusion reserve, defined as the ratio of hyperemic and basal myocardial blood flow, is a useful indicator of the functional significance of a coronary artery lesion. Rapid magnetic resonance (MR) imaging for the noninvasive detection of a bolus-injected contrast agent as a MR tracer is applied to the measurement of regional tissue perfusion during rest and hyperemia, in patients with microvascular dysfunction. A Fermi function model for the distribution of tracer residence times in the myocardium is used to fit the MR signal curves. The myocardial perfusion reserve is calculated from the impulse response amplitudes for rest and hyperemia. The assumptions of the model are tested with Monte Carlo simulations, using a multiple path, axially distributed mathematical model of blood tissue exchange, which allows for systematic variation of blood flow, vascular volume, and capillary permeability. For a contrast-to-noise ratio of 6:1, and over a range of flows from 0.5 to 4.0 ml/min per g of tissue, the ratio of the impulse response amplitudes for hyperemic and basal flows is linearly proportional to the ratio of model blood flows, if the mean transit time of the input function is shorter than approximately 9 s. The uncertainty in the blood flow reserve estimates grows both at low (< 1.0 ml/min/g) and high (> 3-4 ml/min/g) flows. The predictions of the Monte Carlo simulations agree with the results of MR first pass studies in patients without significant coronary artery lesions and microvascular dysfunction, where the perfusion reserve in the territory of the left anterior descending coronary artery (LAD) correlates linearly with the intracoronary Doppler ultrasound flow reserve in the LAD (r = 0.84), in agreement with previous PET studies.

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The myocardial perfusion reserve can be quantified with first-pass MR imaging. In patients with microvascular dysfunction, the myocardial perfusion reserve matches the reduced coronary flow reserve.

The authors represent a cooperative group of 15 institutions that examined the feasibility of using metabolic fea tures observed in vivo with 'H-magnetic resonance (MR) spectroscopy to characterize brain tumors of the glial type.The institutions provided blinded, centralized MR spectroscopy data processing along with independent central review of MR spectroscopy voxel placement, composition and contamination by brain, histopathological typing using current World Health Organization criteria, and clinical data, Proton 'H-MR spectroscopy was performed using a spin-echo technique to obtain spectra from 8-cc voxels in the tumor and when feasible in the contralateral brain. Eighty-six cases were assessable, 41 of which had contralateral brain spectra. Glial tumors had significantly elevated intensities of choline signals, decreased intensities of creatine signals, and decreased intensities of N-acetyl asp art ate compared to brain. Choline signal intensities were highest in astrocytomas and anaplastic astrocytomas, and creatine signal intensi ties were lowest in glioblastomas. However, whether expressed relative to brain or as intratumoral ratios, these meta bolic characteristics exhibited large variations within each subtype of glial tumor. The resulting overlaps precluded diagnostic accuracy in the distinction of low-and high-grade tumors. Although the extent of contamination of the ]H-MR spectroscopy voxel by brain had a marked effect on metabolite concentrations and ratios, selection of cases with minimal contamination did not reduce these overlaps. Thus, each type and grade of tumor is a metabolically hetero geneous group. Lactate occurred infrequently and in all grades. Mobile lipids, on the other hand, occurred in 41% of high-grade tumors with higher mean amounts found in glioblastomas. This result, coupled with the recent demonstra tion that intratumoral mobile lipids correlate with microscopic tumor cell necrosis, leads to the hypothesis that mobile lipids observed in vivo in E H-MR spectroscopy may correlate independently with prognosis of individual patients. W. G. Negendank, et ciL rylcholine), one primarily from creatines (creatine and phosphocreatine), and one primarily from acetyl aspar tate (NAA), In disease, signals from lactate and mobile lipids may also be observed.Studies of extracts of surgical specimens of human as trocytic tum ors using ]H -N M R spectroscopy indicated an increase in the ratio o f cholines to creatines, and a decrease in the ratio of N A A to creatines, with increas ing histopathological grades of m alignancy.16,45'61 Studies in patients using !H-N M R spectroscopy, referred to as MR spectroscopy, indicated sim ilar correlations betw een m etabolic features in vivo and the histopathological grades of astrocytic tum ors. 4'11'14'21,32,43'57'58'61 Other MR spectroscopy studies indicated that lactate is more likely to be present in high-than in low-grade tumors4, 14,15'20'21 and that the am ount of lactate may correlate with the extent of hyperm etabolic glucose consumption sho...

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Rapid MR imaging (MRI) during the first pass of an injected tracer is used to assess myocardial perfusion with a spatial resolution of 2-3 mm, and to detect any regional impairments of myocardial blood flow (MBF) that may lead to ischemia. The spatial resolution is sufficient to detect flow reductions that are limited to the subendocardial layer. The capacity of the coronary system to increase MBF severalfold in response to vasodilation can be quantified by analysis of the myocardial contrast enhancement. The myocardial perfusion reserve (MPR) is a useful concept for quantifying the vasodilator response. The perfusion reserve can be estimated from the ratio of MBFs during vasodilation and at baseline, in units identical to those used for invasive measurements with labeled microspheres, or from dimensionless flow indices normalized by their value for autoregulated flow at rest. The perfusion reserve can be reduced as a result of a blunted hyperemic response and/or an abnormal resting blood flow. The absolute quantification of MBF removes uncertainties in the evaluation of the vasodilator response, and can be achieved without the use of complex tracer kinetic models; therefore, its application to clinical studies is feasible.