Clinical implications of the 'no reflow'phenomenon: a predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction

H Ito, A Maruyama, K Iwakura, S Takiuchi… - Circulation, 1996 - Am Heart Assoc
H Ito, A Maruyama, K Iwakura, S Takiuchi, T Masuyama, M Hori, Y Higashino, K Fujii…
Circulation, 1996Am Heart Assoc
Background Recent studies demonstrated that the “no reflow” phenomenon after coronary
reflow implies the presence of advanced myocardial damage. In this study, we verified the
prognostic value of the detection of this phenomenon by studying complications, left
ventricular morphology, and in-hospital survival after acute myocardial infarction (AMI).
Methods and Results The study population consisted of 126 patients with a first anterior AMI.
All patients received coronary reflow within 24 hours of onset of symptoms and underwent …
Background Recent studies demonstrated that the “no reflow” phenomenon after coronary reflow implies the presence of advanced myocardial damage. In this study, we verified the prognostic value of the detection of this phenomenon by studying complications, left ventricular morphology, and in-hospital survival after acute myocardial infarction (AMI).
Methods and Results The study population consisted of 126 patients with a first anterior AMI. All patients received coronary reflow within 24 hours of onset of symptoms and underwent myocardial contrast echocardiography (MCE) before and shortly after coronary reflow with an intracoronary injection of sonicated microbubbles. From contrast reperfusion patterns, patients were divided into two subsets: those with MCE no reflow (47 patients, 37%) and those with MCE reflow (79 patients). There was no difference in the frequency of arrhythmia or coronary events between the two subsets. Pericardial effusion and early congestive heart failure were observed more frequently in patients with MCE no reflow than in those with MCE reflow (26% versus 4%, P<.05; 45% versus 15%, P<.05, respectively). Congestive heart failure tended to be prolonged in those with MCE no reflow, and 3 patients (7%) of this subset died of pump failure. Left ventricular end-diastolic volume progressively increased in the convalescent stage in patients with MCE no reflow (early versus late, 145±43 versus 169±60 mL, P<.001), whereas it decreased in those with MCE reflow (154±42 versus 144±44 mL, P<.01).
Conclusions The substantial size of the MCE no reflow phenomenon at coronary reflow conveys useful information about an outcome of coronary intervention and left ventricular remodeling in individual patients with anterior wall AMI, although these are suggestive results in a limited number of patients.
Am Heart Assoc