Timeto Peak

Time-to-peak (TTP) is the time the blood takes to reach the maximum intensity, from the start of the bolus injection to the peak concentration of contrast agent; it is defined as the time point of maximum intensity loss after the passage of the contrast agent. It is calculated in seconds and reveals any delays in transit time, enabling quick quantification of perfusion deficits. Ischaemic areas are characterized by a delay of tracer arrival and a TTP increase [6, 51, 52]. A study of patients with acute cerebral ischaemia postulated that TTP values of 0-3.5 s are related to normal perfusion, values ranging from 3.5 from 7 s may indicate a perfusion disorder, whereas values above 7 s indicate a high risk of ischaemic tissue injury and watershed infarcts in border zones [51].

Despite these difficulties in determining the absolute values of volume and flow, relative values of CBV and CBF are extremely useful in clinical practice, especially in stroke evaluation.

It is generally accepted that tissue with abnormalities on both perfusion and diffusion-weighted imaging has already undergone irreversible ischaemia.

However, tissue with perfusion abnormalities but normal diffusion is thought to be consistent with reversible ischaemia. This area of diffusion-perfusion mismatch, also called ischaemic penumbra, is a region of decreased perfusion that is potentially reversible because it is above the critical level for the maintenance of the Na+ K+-ATPase pump [1]. Exact evaluation of the tissue that can be rescued is critical in assessing the risk-benefit ratio of possible therapies, since patients with no mismatch are considered unlikely to benefit from thrombolytic therapy.

Time-dependent perfusion thresholds were first established using H215O PET to distinguish underper-fused tissue evolving towards infarction (<12 ml/min per 100 g) from penumbral flow with functionally compromised but viable tissue (12-20 ml/min per 100 g) [1-3].

The exact role of each haemodynamic parameter (CBV, CBF, MTT and TTP) in the correct evaluation of

Fig. 9.7. a, b Low grade astrocytoma: SE T1 after contrast agent administration (a) and CBV map (b); C, D glioblastoma: SE T1 after contrast administration (c) and CBV map (d). The CBV is reduced in the low grade astrocytoma (b) and in the cystic component of the glioblastoma (d), whereas it is increased in the solid part of the glioblastoma (d)

Fig. 9.7. a, b Low grade astrocytoma: SE T1 after contrast agent administration (a) and CBV map (b); C, D glioblastoma: SE T1 after contrast administration (c) and CBV map (d). The CBV is reduced in the low grade astrocytoma (b) and in the cystic component of the glioblastoma (d), whereas it is increased in the solid part of the glioblastoma (d)

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brain perfusion changes and which of them is more representative of salvageable tissue and predictive of final infarct size is still debated.

It appears that MTT maps generally show the largest area of abnormality and often overestimate final infarct size, while CBV maps tend to underestimate this size.

In one study comparing CBV maps, CBF maps, and MTT maps with change in size from initial infarct size to final infarct size, a mismatch between initial CBF maps and a diffusion abnormality predicted more often the growth of infarct than did a mismatch between initial CBV maps and diffusion abnormality [41]. In that study, however, CBV maps best correlated with change in infarct size from initial to follow-up imaging [41].

A recent study comparing TTP maps and thresholds in patients with acute ischaemia using CBF data acquired with PET, assumed as the gold standard, indicated that TTP is a useful estimate of ischaemic injury but entails considerable methodological limitations that have to be considered in routine use of MRI for stroke [52].

Relative TTP maps are only indirect surrogates of CBF and do not represent the best application of MRI perfusion imaging. They are used in clinical routine because they are simple, they clearly delineate haemody-namic alterations, yield satisfactory results compared with quantitative methods, and do not rely on deconvo-lution algorithms, calibration with PET data, or selection of adequate input functions [52].

However, TTP maps may be inappropriate, since simple visual analysis is more prone to errors related to individual subjectivity [52].

A quantitative observer-independent measure such as TTP thresholds has proved to be more indicative of

underperfusion stated by PET for a CBF value of < 20 ml/min per 100 g [52].

The best estimate of penumbral flow was found for a TTP delay of>4 s (sensitivity 84 %, specificity 77%); it best identifies the volume of penumbra and should be used to define the mismatch volume. The volume of a TTP delay of > 4 s correlated with clinical deficit, whereas the volume of a TTP delay between > 5 and >8 s was strongly associated with infarct growth [52].

The lack of a complete match between PET and TTP thresholds is partly explained by method-specific properties. TTP only yields a relative estimation of CBF as it indicates the time point of maximum signal intensity loss during the passage of the tracer within several seconds. H215O PET assesses the „true" CBF as the concentration of a partly diffusible tracer integrated over a scanning time of several minutes. TTP data are therefore more prone to movement artefacts, collateral flow or individual haemodynamic properties [1, 52].

However, even the TTP threshold with the best sensitivity and specificity seems to include a large portion of tissue with only modest haemodynamic damage; particularly in small ischaemia TTP tends to overestimate the true extent of the „tissue at risk" [52].

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