Angiographic patterns of myocardial reperfusion after primary angioplasty and ventricular remodeling.

BACKGROUND

No reflow after primary percutaneous coronary intervention is a dynamic process and its reversibility may affect left ventricular (LV) remodeling. We aimed at assessing in-hospital evolution of angiographic no reflow, predictors of its reversibility, and its impact on LV function at follow-up (FU).

METHODS

Fifty-three consecutive patients (age, 60±10 years; male sex, 79%) presenting with ST-elevation myocardial infarction and undergoing primary percutaneous coronary intervention within 12 h of symptom onset were enrolled. No reflow was defined as a final thrombolysis in myocardial infarction (TIMI) flow of 2 or final TIMI flow of 3 with myocardial blush grade (MBG) of less than 2. The evolution of angiographic no reflow was assessed by repeat in-hospital coronary angiography. Patients with no reflow found to have an improvement of TIMI and/or MBG leading to a final TIMI 3 and MBG of greater than or equal to 2 were classified as reversible no reflow; the remaining patients were classified as sustained no reflow. Variables predicting the patterns of no reflow, recorded on admission, were assessed among clinical, angiographic and laboratory data. FU echocardiographic data (at 6 months) were compared with those obtained in-hospital according to no reflow evolution.

RESULTS

Thirty-six patients (68%) exhibited myocardial reperfusion; 17 patients (32%) showed no reflow. Among these, six patients (age, 58±10 years; male sex, 83%) showed sustained no reflow, whereas 11 patients (age, 55±8 years; male sex, 82%) showed reversible no reflow. Patients with sustained no reflow had longer time to percutaneous coronary intervention (261±80 min) compared with those with myocardial reperfusion (216±94 min) or reversible no reflow (237±76 min; P=0.008 and 0.05, respectively). Moreover, patients with sustained no reflow had a higher peak troponin-T levels (14.5 ng/ml; range, 7.5-20.2 ng/ml) compared with those presenting with myocardial reperfusion (3.9 ng/ml; range, 3.3-9.1 ng/ml) and reversible no reflow (7.7 ng/ml; range, 3.6-29.9 ng/ml; P=0.03 and 0.07, respectively). At multivariate ordinal logistic regression, time pre-PCI retained its statistical significant association with angiographic no reflow evolution (odds ratio=2.54; 95% confidence interval: 1.45-6.53; P=0.04), with troponin T levels showing a borderline statistical significance (odds ratio=3.12; 95% confidence interval: 1.07-6.23; P=0.09). Finally, in patients with sustained no reflow only both end-diastolic and end-systolic volumes significantly increased at FU (P<0.001 and 0.001, respectively).

CONCLUSION

Sustained no reflow is associated with a longer ischemic time and predicts worse LV remodeling. No reflow, however, shows an in-hospital reversibility calling for therapeutic interventions when its prevention fails.