CT perfusion in acute ischemic stroke: a comparison of 2-second and 1-second temporal resolution.

BACKGROUND AND PURPOSE: CT perfusion data sets are commonly acquired using a temporal resolution of 1 image per second. To limit radiation dose and allow for increased spatial coverage, the reduction of temporal resolution is a possible strategy. The aim of this study was to evaluate the effect of reduced temporal resolution in CT perfusion scans with regard to color map quality, quantitative perfusion parameters, ischemic lesion extent, and clinical decision-making when using DC and MS algorithms. MATERIALS AND METHODS: CTP datasets from 50 patients with acute stroke were acquired with a TR of 1 second. Two-second TR datasets were created by removing every second image. Various perfusion parameters (CBF, CBV, MTT, TTP, TTD) and color maps were calculated by using identical data-processing settings for 2-second and 1-second TR. Color map quality, quantitative region-of-interest-based perfusion measurements, and TAR/NVT lesions (indicated by CBF/CBV mismatch) derived from the 2-second and 1-second processed data were statistically compared. RESULTS: Color map quality was similar for 2-second versus 1-second TR when using DC and was reduced when using MS. Regarding quantitative values, differences between 2-second and 1-second TR datasets were statistically significant by using both algorithms. Using DC, corresponding tissue-at-risk lesions were slightly smaller at 2-second versus 1-second TR (P < .05), whereas corresponding NVT lesions showed excellent agreement. With MS, corresponding tissue-at-risk lesions showed excellent agreement but more artifacts, whereas NVT lesions were larger (P < .001) compared with 1-second TR. Therapeutic decisions would have remained the same in all patients. CONCLUSIONS: CTP studies obtained with 2-second TR are typically still diagnostic, and the same therapy would have been provided. However, with regard to perfusion quantitation and image-quality-based confidence, our study indicates that 1-second TR is preferable to 2-second TR.

Perfusion CT in acute ischemic stroke: a qualitative and quantitative comparison of deconvolution and maximum slope approach.

BACKGROUND AND PURPOSE: PCT postprocessing commonly uses either the MS or a variant of the DC approach for modeling of voxel-based time-attenuation curves. There is an ongoing discussion about the respective merits and limitations of both methods, frequently on the basis of theoretic reasoning or simulated data. We performed a qualitative and quantitative comparison of DC and MS by using identical source datasets and preprocessing parameters. MATERIALS AND METHODS: From the PCT data of 50 patients with acute ischemic stroke, color maps of CBF, CBV, and various temporal parameters were calculated with software implementing both DC and MS algorithms. Color maps were qualitatively categorized. Quantitative region-of-interest-based measurements were made in nonischemic GM and WM, suspected penumbra, and suspected infarction core. Qualitative results, quantitative results, and PCT lesion sizes from DC and MS were statistically compared. RESULTS: CBF and CBV color maps based on DC and MS were of comparably high quality. Quantitative CBF and CBV values calculated by DC and MS were within the same range in nonischemic regions. In suspected penumbra regions, average CBF(DC) was lower than CBF(MS). In suspected infarction core regions, average CBV(DC) was similar to CBV(MS). Using adapted tissue-at-risk/nonviable-tissue thresholds, we found excellent correlation of DC and MS lesion sizes. CONCLUSIONS: DC and MS yielded comparable qualitative and quantitative results. Lesion sizes indicated by DC and MS showed excellent agreement when using adapted thresholds. In all cases, the same therapy decision would have been made.

Interaction between thromboxane A2 and angiotensin II in postischemic renal vasoconstriction in dogs.

The kidney responds to periods of ischemia with vasoconstriction and a decrease in glomerular filtration rate (GFR) on reperfusion. The mediators of this response have not been fully identified. In this study, we examined the contribution of angiotensin II (AII), thromboxane A2 (TXA2) and the interaction between them to this response. Anesthetized dogs were subjected to 30 min of clamping of both renal arteries. Renal hemodynamics and function were followed from 60 min before and for 105 min after clamping. Dogs were divided into salt-depleted (AII-stimulated) and captopril-treated (AII-inhibited) groups. Each group included dogs that received either the TXA2 synthase inhibitor CGS 13080 or its vehicle (controls) starting 30 min before renal artery clamping and lasting to the end of the experiment. In captopril-treated control dogs, 30 min of ischemia induced a 25% fall in renal blood flow (RBF). GFR initially fell by 75%, but recovered to 64% of base-line value 60 to 90 min after release of the clamp. In captopril-treated dogs, CGS 13080 prevented the fall in RBF, but the GFR response was similar to vehicle-treated dogs. In control dogs, both GFR and RBF responses were enhanced in salt-depleted compared with captopril-treated dogs; the decrease in RBF (44%) was greater, and the recovery in GFR, which fell by 89%, less. In salt-depleted, CGS 13080-treated dogs, the 30% fall in RBF was less than its control, but greater than dogs treated with captopril and CGS 13080. The change in GFR was similar to the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of the adenosine receptor antagonist, CGS 15943A, on renal function after reconstruction of chronic renal artery stenosis in the dog.

Surgical reconstruction of chronic renal artery stenosis may correct the anatomical defect but not result in an initial improvement in function of the revascularized kidney. The functional and hemodynamic changes associated with surgical correction of the one-clip, two-kidney, canine model of renovascular hypertension were studied. In 14 dogs, a surgical clip was placed across the proximal renal artery and tightened to decrease perfusion pressure (RPP) and blood flow (RBF). One month later, measurements were obtained distal to the constriction, before and 30 min after vascular reconstruction. Surgical reconstruction was associated with a rise in RPP (86%, P less than .001), renal vascular resistance (47%, P less than .001) and RBF (22%, P less than .05). Creatinine clearance (CCr) remained unchanged, but a significant negative association existed between initial CCr and change in CCr. The role of adenosine in mediating these changes was examined using the selective receptor antagonist, CGS 15943A (CGS), or its vehicle. After vascular reconstruction, vehicle dogs sustained a marked increase in renal vascular resistance, with a 60 +/- 8 mm Hg rise in RPP, but only an 18% rise in RBF. In contrast, renal vascular resistance was unchanged in the CGS group, with a 56 +/- 7 mm Hg increase in RPP and a 69% increase in RBF (P less than .0001). CCr was not changed by either vascular reconstruction or CGS 15943A. Vascular reconstruction was associated with increases in urinary flow rate and sodium excretion in both groups, but this change was significantly greater in the CGS group.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of renal vasoconstriction induced by intrarenal hypertonic saline by the nonxanthine adenosine antagonist CGS 15943A.

The hypothesis that intrarenal infusions of hypertonic saline induce endogenous release of adenosine to result in renal vasoconstriction has been investigated in salt-deplete dogs using the nonxanthine adenosine receptor antagonist, CGS 15943A. Intrarenal artery infusions of CGS 15943A induced dose-dependent reductions in the renal vasoconstrictor response to bolus doses of adenosine into the renal artery, without altering base-line blood pressure or renal blood flow. Infusion rates of 10 micrograms/min induced an approximate 50% reduction in response, whereas 100 micrograms/min produced a substantially greater response. There was no inhibition of the renal vasoconstrictor response to angiotensin II and norepinephrine by CGS 15943A at a rate of 100 micrograms/min. Changes in RBF after intrarenal infusion of hypertonic saline were compared between further series of salt-deplete dogs receiving intrarenal artery infusions of either vehicle or CGS 15943A (100 micrograms/min). An initial infusion of hypertonic saline to both groups of dogs induced renal vasodilation followed by vasoconstriction. In dogs subsequently infused with CGS 15943A (100 micrograms/min), the initial renal vasodilation response was similar, but there was an abolition of the later vasoconstrictor response. In contrast, the renal blood flow response to hypertonic saline was unchanged in the vehicle-infused dogs. We conclude that CGS 15943A can selectively block the renal blood flow response to exogenous adenosine without altering baseline renal vascular tone and that the ability of CGS 15943A to abolish the renal vasoconstrictor response to intrarenal hypertonic saline is consistent with the hypothesis that endogenous release of adenosine is involved in mediating the reduction in renal blood flow.