Angiographic no-reflow is defined as less than TIMI 3 flow or TIMI 3 flow with MBG 0 or 1 in the absence of angiographic evidence of mechanical vessel obstruction . Our study tested the impact of high-intensity statin loading before primary PCI on myocardial perfusion in patients presenting with STEMI, and the main findings were as follows.
We observed a significant improvement in TIMI flow, in MBG, and also in complete ST-segment resolution, but it did not have an impact on in-hospital MACE.
In our study, in the control group, there were 4 patients with TIMI I flow and MBG I, 13 with TIMI II flow and MBG II, and 68 with TIMI III flow and MBG III.
Meanwhile, in the cases group, there was 1 patient with TIMI I flow and MBG I, 3 with TIMI II flow and MBG II, and 81 with TIMI III flow and MBG III. This difference was statistically significant with a P value of 0.010 indicating that the TIMI flow grade improved with high-dose statin preloading.
Our results were indistinguishable as those of the STATIN-STEMI trial, which studied 171 patients with STEMI and randomized to either 80-mg atorvastatin (n = 86) or 10-mg atorvastatin (n = 85) arms for pre-PCI treatment. MBG after primary PCI was higher in the 80-mg atorvastatin arm (MBG, 2.2 ± 0.8 vs. 1.9 ± 0.8, P = 0.02); the post-procedural TIMI III flow grade was higher in the 80-mg atorvastatin arm, 83, vs. the 10-mg atorvastatin arm, 76, but it was not statistically significant with a P value of 0.07 . They also found that the corrected TIMI frame count (cTFC) was lower in the 80-mg atorvastatin arm (26.9 ± 12.3 vs. 34.1 ± 19.0, P = 0.01) which was not measured in our study .
Our results were not concordant with the NAPLES-II trial where 668 patients who were not on statin therapy were randomized to an atorvastatin 80 mg (atorvastatin group; n = 338) or no statin (control group; n = 330) the day before elective PCI, and results showed no significant difference in post-procedural TIMI flow grade (P value 0.68) . This could be explained by the fact that in the NAPLES-II trial, the patients were undergoing elective PCI, so they do not have an acute thrombotic occlusion thus having a lower risk of no-reflow.
In our study, there was no statistical significance when comparing the two groups regarding in-hospital death of all causes and stroke after primary PCI. This is in agreement with the results of the SECURE-PCI trial in which more than four thousand patients diagnosed with acute coronary syndromes were randomized to receive 2 loading doses of 80 mg of atorvastatin (n = 2087) or placebo (n = 2104) before and a day after the PCI. For the next 30 days, all patients received 40 mg of atorvastatin. At 30 days, MACE was not reduced as 6.2% of patients in the atorvastatin group and 7.1 % in the placebo group had an adverse event (P = .27) .
Our results were not concordant with the PROVE-IT trial where 4162 patients with ACS were recruited and randomized to high-intensity statin therapy (atorvastatin, 80 mg) or standard therapy (pravastatin, 40 mg). The composite end point of death, myocardial infarction, or rehospitalization for recurrent ACS was calculated in each group at 30 days. The composite end point at 30 days occurred in 3.0% of patients receiving atorvastatin 80 mg vs. 4.2% of patients receiving pravastatin 40 mg (hazard ratio [HR] = 0.72; 95% confidence interval [CI], 0.52 to 0.99; P = 0.046) which shows statistical significance .
This was also shown in the ARMYDA-ACS trial which included 171 non-ST-segment elevation ACS patients and randomized to loading 80 mg atorvastatin (n = 86) or placebo (n = 85). All patients received 40 mg atorvastatin treatment after hospitalization. The main end point of the trial was the incidence of major adverse cardiac events (death, myocardial infarction, or unplanned revascularization) within a 30-day follow-up. Major adverse cardiac events occurred in 5% of patients in the high-dose atorvastatin arm and in 17% of those who took the placebo (P = 0.01) which was statistically significant . This could be explained by the smaller number of patients in our study and the shorter duration of follow-up.
In our study, there were 34 patients in the cases group who showed complete ST-segment resolution (40%) vs. 19 patients (22.4%) in the control group which was statistically significant with a P value of 0.013.
This was similar to the results in the STATIN-STEMI trial where complete STR was significantly better in the 80-mg atorvastatin arm (34 patients [39.5%] vs. 19 patients [23.8%]; P = 0.03) .
Our study revealed that the echocardiography done the next day after primary PCI showed ejection fraction had values of mean ± SD of 45.91 ± 5.49 in the cases group vs. 43.01 ± 8.80 in the control group which was statistically significant with a P value of 0.011. This was not concordant with the results in the STATIN-STEMI trial where the mean LVEF was 47% in the whole patient population and there was no difference between the 2 groups . This difference could be explained by the fact that in our study, the control group did not receive a statin dose before PCI while in the STATIN-STEMI trial, the control group received 10 mg of atorvastatin.
In our study, statin preloading was done using either 80 mg of atorvastatin or 20 mg of rosuvastatin in STEMI patients before undergoing primary PCI, and the control group did not receive statin preloading. This was similar to the protocol used in the STATIN-STEMI trial where the STEMI patients received 80 mg of atorvastatin before undergoing PCI, but the control group also received a statin dose before PCI in the form of 10 mg of atorvastatin . In the SECURE-PCI trial, ACS patients were randomized to receive 2 loading doses of 80 mg of atorvastatin (n = 2087) or matching placebo (n = 2104) before and 24 h after a planned PCI, but only 25% of patients were presenting with STEMI . In the NAPLES-II, ARMYDA-ACS, and ARMYDA-RECAPTURE trials, no STEMI patients were included in the study [13, 16, 17].