The washout rate of 123I-BMIPP and the evolution of left ventricular function in patients with successfully reperfused ST-segment elevation myocardial infarction: comparisons with the echocardiography

Abstract

The evolution of the oxidative metabolism of (11)C acetate parallels the recovery of left ventricular(LV) contraction following acute myocardial infarction(AMI). This study was designed to unravel, for the first time, the impact of the global washout rate(WR) of (123)I-beta-methyl-p-iodophenylpentadecanoic acid (BMIPP) on the recovery of LV function followingAMI, as evidenced from conventional echocardiography.Twenty consecutive patients (age: 58 +/- 13 years; 16 males and 4 females) with ST-segment elevation myocardial infarction (STEMI) were enrolled and all of them underwent successful percutaneous coronary intervention (PCI). (123)I-BMIPP cardiac scintigraphy was performed at 7 +/- 3 days after admission. The WR was calculated from the polar map and the regional BMIPP defect score was calculated using a 17 segment model. Echocardiography was performed within 24 h of admission and at 3 months to record the ejection fraction (EF), the wall motion score index (WMSI), the ratio of the mitralinflow velocity to the early diastolic velocity (E/E0)and the myocardial performance index (MPI). The mean global WR of the BMIPP was 22.12 +/- 7.22%, and it was significantly correlated with the improvement of the WMSI (r = 0.61, P\0.004). However,the relative changes of the EF, E/E0 and MPI were not correlated with the WR. The BMIPP defect score (18 +/- 10) was significantly correlated with the WMSI on admission (r = 0.74, P = 0.0002), but the defect score was not correlated with the relative changes of any of the echocardiographic parameters. We proved that the WR of the BMIPP is a promising indicator of improvement of the LV wall motion (WMSI) following ST-segment elevation myocardial infarction and successful reperfusion.

Metabolic Planar Imaging Using ¹²³I-<i>β</i>-Methyl-Iodophenyl Pentadecanoic Acid Identifies Myocardial Ischemic Memory After Intracoronary Acetylcholine Provocation Tests in Patients With Vasospastic Angina

“…Some investigators have noted that an increased WR of 123 I-BMIPP identifi es cardiac disease. [12][13][14]28,29) The severities of the H/M ratios and WR were associated with LVEF but BNP, respectively the present study. Delayed H/M ratios and WR of 123 I-BMIPP correlate with LVEF and BNP in patients with chronic heart failure.…”

“…[12][13][14] Regional tracer uptake was assessed using a 5-point scoring system (0, normal; 1, slightly reduced; 2, mildly reduced; 3, severely reduced; 4, no uptake) on the early and delayed SPECT images. 15) The left ventricular myocardium was divided into 17 segments corresponding to the vascular territories of the 3 major coronary arteries.…”

Fatty Acid Imaging of the Heart

“…The BMIPP washout rate was calculated using polar coordinate presentations as count at 20 min minus count at 4 h, divided by count at 20 min, times 100. There was no difference between the defect scores at 20 min and 4 h, whereas the mean overall washout rate was 22%±7% [26]. The BMIPP defect score was highly correlated with the LV myocardial performance index at baseline, with the wall motion score index at baseline and at 3 months, and with the LV ejection fraction at 3 months.…”

“…Biswas et al [26] assessed the washout rate of BMIPP in 20 patients successfully reperfused with percutaneous coronary intervention after presenting with ST-segment elevation myocardial infarction. Echocardiography was performed within 24 h of admission and again at 3 months.…”

“…The BMIPP washout rate did not correlate with any systolic or diastolic echocardiographic parameters assessed, but did correlate with the improvement in the wall motion score index. The authors concluded that the BMIPP washout rate following successful reperfusion after an ST-segment elevation myocardial infarction "has a great impact on the evolution of LV contractile function" [26]. They speculated that the supranormal BMIPP washout rate seen during the subacute phase of infarction, following reperfusion, is independent of blood flow and results due to the accelerated washout of FAs from the lipid pool into the bloodstream, in parallel to the drop in plasma free FA levels that occurs as systemic catecholamine levels fall following the acute event.…”