Objective To investigate the effect of no-reflow phenomenon after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI).
Methods A total of 128 patients with the first AMI of the anterior wall were involved in this study. All patients underwent coronary angiography, PCI, and left ventriculography about 6 to 12 h after onset of AMI symptoms and were divided into two groups: the no-reflow group (0 to 1 grade) and reflow group (2 to 3 grade) identified by MBG. Equilibrium radionuclide angiography was performed 1 week after PCI to gain the parameters of left ventricular regional and global systolic function and systolic synchrony. All patients were reinvestigated at 6 months, and major adverse cardiac events were recorded during the 6 months after PCI.
Results At 6 months after AMI-PCI, the values of left ventricular end-systolic volume index, left ventricular end-diastolic volume index, wall motion score, and left ventricular end-diastolic volume pressure in the no-reflow group were significantly increased, whereas left ventricular ejection fraction, peak ejection rate, and peak filling rate of radionuclide angiography parameters were significantly decreased (p<0.05), respectively, compared with those in the reflow group. LrEF2-LrEF8 in the no-reflow group at 6 months after AMI-PCI were reduced (p<0.05) more than those in the reflow group, respectively. There was no improvement on the phase analysis in the no-reflow group at 6 months after AMI-PCI, and the values of PS FWHM and PSD were increased compared with those in the reflow group (p<0.05; respectively). Within the 6-month follow-up period, the incidence of major adverse cardiac events in the no-reflow group was significantly higher than in the reflow group.
Conculsion The infarct-related zone myocardium post-AMI still has no reperfusion status and directly causes the reduction of the regional and global left ventricular systolic performance with an increase of systolic asynchrony. It then progressively decreases the efficiency of ventricular blood ejection as well as causes ventricular remodelling with adverse long-term outcome in patients with AMI.