Timi Myocardial Perfusion Grade

It has recently become apparent that epicardial flow does not necessarily imply tissue level or microvascular perfusion (21,22). This led to the recent development of a new angiographic measure of tissue level perfusion, the TIMI myocardial perfusion grade (TMPG) (4), as follows:

TMPG 3: Normal entry and exit of dye from the microvasculature. There is the ground glass appearance (blush) or opacification of the myocardium in the distribution of the culprit lesion that clears normally, and is either gone or only mildly/moderately persistent at the end of the washout phase (i.e., dye is gone or is mildly/moderately persistent after 3 cardiac cycles of the washout phase and noticeably diminishes in intensity during the washout phase), similar to that in an uninvolved artery. Blush that is of only mild intensity throughout the washout phase, but fades minimally, is also classified as grade 3.

TMPG 2: Delayed entry and exit of dye from the microvasculature. There is the ground glass appearance (blush) or opacification of the myocardium in the distribution of the culprit lesion that is strongly persistent at the end of the washout phase (i.e., dye is strongly persistent after three cardiac cycles of the washout phase and either does not or only minimally diminishes in intensity during washout).

TMPG 1: Dye slowly enters but fails to exit the microvasculature. There is the ground glass appearance (blush) or opacification of the myocardium in the distribution of the culprit lesion that fails to clear from the microvasculature, and dye staining is present on the next injection (approx 30 s between injections). TMPG 0: Dye fails to enter the microvasculature. There is either minimal or no ground glass appearance (blush) or opacification of the myocardium in the distribution of the culprit artery indicating lack of tissue level perfusion.

The TMPG has been shown to be a multivariate predictor of mortality in acute MI (Fig. 4) (4). The TMPG permits risk stratification even within epicardial TIMI grade 3 flow. Despite achieving epicardial patency with normal TIMI grade 3 flow, those patients whose microvasculature fails to open (TIMI myocardial perfusion grade 0/1) have a persistently elevated mortality of 5.4%. In contrast, those patients with both TIMI grade 3 flow in the epicardial artery and TIMI myocardial perfusion grade 3 have a mortality under 1% (4).

The TIMI flow grades and the TIMI myocardial perfusion grades can be combined to identify a group of patients at very low risk and alternatively very high risk for mortality. Those patients with both TIMI grade 3 flow and TIMI myocardial perfusion grade 3 flow had a mortality of 0.7% while those patients with both TIMI grade 0/1 and TIMI myocardial perfusion grade 0/1 flow had a mortality of 10.9% (4).

In order to quantitatively characterize the kinetics of dye entering the myocardium using the angiogram, digital subtraction angiography (DSA) was developed. DSA is performed at end diastole by aligning cineframes images before dye fills the myocardium with those at the peak of myocardial filling to subtract spine, ribs, diaphragm, and the epicardial artery (Fig. 5). A representative region of the myocardium is sampled that is free of overlap by epicardial arterial branches to determine the increase in the Gray scale brightness of the myocardium when it first reached its peak intensity. The circumference of the myocardial blush is measured using a handheld planimeter. The number of frames required for the myocardium to first reach its peak brightness is converted into time (s) by dividing the frame count by 30. In this way, the rate of rise in brightness (Gray/s) and the rate of growth of blush (cm/s) can be calculated.

Compared to normal patients, microvascular perfusion was reduced in acute MI patients on DSA as demonstrated by a reduction in peak Gray (brightness) (10.9 ± 5.7 vs 7.8 ± 8.9,p < 0.0001), the rate of rise in Gray/s (2.8 ± 1.4 vs 2.1 ± 2.5,p < 0.0001), the blush circumference (19.4 ± 5.4 vs 13.6 ± 10.7,p < 0.0001), and the rate of growth in circumference (cm/s)(5.2 ± 2.0 vs 3.7 ± 3.1,p < 0.0001) (23). However, while DSA perfusion was impaired overall in the setting of acute MI, TMPG grade 3 in the setting of acute MI did not differ from that in normal patients when studied quantitatively as shown by similar peak Gray (10.9 ± 5.7 vs 10.6 ± 6.1), rate of growth in Gray/s (2.8 ± 1.4 vs 3.1 ± 2.1), the blush circumference (19.4 ± 5.4 vs 18.0 ± 10.3), and the rate of growth in circumference (5.2 ± 2.0 vs 4.9 ± 2.4) (p = NS for all) (23).

In myocardial contrast echocardiography (MCE) studies by Ito et al. (21,22), the culprit artery was patent after angioplasty or thrombolysis within 24 h of symptom onset in 126 patients with anterior MI. However, despite epicardial patency, one-fourth of

Timi Myocardial Perfusion Grade

Fig. 4. The TMPG assesses tissue level perfusion using the angiogram and is a multivariate predictor of mortality in acute MI. The TMPG permits risk stratification even within epicardial TIMI grade 3 flow. Despite achieving epicardial patency with normal TIMI grade 3 flow, those patients whose microvasculature fails to open (TMPG 0/1) have a persistently elevated mortality of 5.4%. In contrast, those patients with both TIMI grade 3 flow in the epicardial artery and TMPG 3 have a mortality under 1%.

Fig. 4. The TMPG assesses tissue level perfusion using the angiogram and is a multivariate predictor of mortality in acute MI. The TMPG permits risk stratification even within epicardial TIMI grade 3 flow. Despite achieving epicardial patency with normal TIMI grade 3 flow, those patients whose microvasculature fails to open (TMPG 0/1) have a persistently elevated mortality of 5.4%. In contrast, those patients with both TIMI grade 3 flow in the epicardial artery and TMPG 3 have a mortality under 1%.

patients had a lack of tissue level perfusion and the no reflow phenomenon, and these patients had a higher rate of adverse outcomes (sustained arrhythmias, pericardial effusion, cardiac tamponade, congestive heart failure, or death), and a lower rate of improvement in global (5 vs 11%) as well as regional left ventricle (LV) contractile function (standard deviations [SD]/chord) (-0.4 vs -0.9) (21,22).

Several mechanisms have been postulated in the development of the no reflow phenomenon following acute MI, such as a loss of microvasculature integrity and profound spasm of microvasculature, caused by the release of potent vasoconstrictors from activated platelets (e.g., serotonin) or neutrophil infiltration and platelet fibrin clots in the microvasculature (24-30). Adjunctive therapies such as superoxide dismutase, cata-lase, adenosine, verapamil, papaverine, ketanserine (a serotonin inhibitor), and other new therapies targeted at the microvasculature may warrant further investigations (31-33).

Unlike the epicardial artery, the microvasculature responds poorly to nitroglycerine due to impaired synthesis of endothelium-derived relaxing factor (EDRF) (27). Calcium channel blockers act directly on vascular smooth muscle rather than EDRF and may be of benefit in minimizing microvascular spasm. Indeed, in a prospective trial by Taniyama et al. (34), MCE has been used after primary angioplasty to demonstrate that the low reflow ratio (ratio of no flow zone plus low reflow zone to the risk area) decreased by 45% after the administration of 0.5 mg of intracoronary verapamil (from 0.39 ± 0.23 to 0.29 ± 0.17, p < 0.05) (34). Of note, the improvement in the regional

Digital Subtraction Angiography Dsa

Fig. 5. Digital subtraction angiography (DSA) was developed in order to quantitatively characterize the kinetics of dye entering the myocardium using the angiogram. DSA is performed at end diastole by aligning cineframes images before dye fills the myocardium with those at the peak of myocardial filling to subtract spine, ribs, diaphragm, and the epicardial artery. A representative region of the myocardium is sampled that is free of overlap by epicardial arterial branches to determine the increase in the Gray scale brightness of the myocardium when it first reached its peak intensity. The circumference of the myocardial blush is measured using a handheld planimeter. The number of frames required for the myocardium to first reach its peak brightness is converted into time (s) by dividing the frame count by 30. In this way the rate of rise in brightness (Gray/s) and the rate of growth of blush (cm/s) can be calculated.

Fig. 5. Digital subtraction angiography (DSA) was developed in order to quantitatively characterize the kinetics of dye entering the myocardium using the angiogram. DSA is performed at end diastole by aligning cineframes images before dye fills the myocardium with those at the peak of myocardial filling to subtract spine, ribs, diaphragm, and the epicardial artery. A representative region of the myocardium is sampled that is free of overlap by epicardial arterial branches to determine the increase in the Gray scale brightness of the myocardium when it first reached its peak intensity. The circumference of the myocardial blush is measured using a handheld planimeter. The number of frames required for the myocardium to first reach its peak brightness is converted into time (s) by dividing the frame count by 30. In this way the rate of rise in brightness (Gray/s) and the rate of growth of blush (cm/s) can be calculated.

wall motion score index from baseline to follow-up study at 24 d was higher in the ver-apamil-treated group than in the control group (0.7 ± 0.8 vs 0.2 ± 1.3, p < 0.05) (34). A major question has been whether microvascular spasm is an epiphenomenon in acute MI and if improving microvascular spasm will lead to improved clinical outcomes. This small preliminary study suggests that intracoronary verapamil can attenuate microvas-cular spasm and that it can in turn augment basal tissue level perfusion. It provides a critical link in relating these improvements in tissue perfusion to improved wall motion in patients with acute MI (34).

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