Effect of chronic pretreatment with beta-blockers on no-reflow phenomenon in diabetic patients with acute ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention

Abstract

BackgroundNo-reflow is an important factor as it predicts a poor outcome in patients undergoing primary angioplasty. In comparison with patients attaining TIMI 3 flow, patients with no-reflow have an increased incidence of ventricular arrhythmias, early congestive cardiac failure, cardiac rupture and cardiac death. As such, it is of paramount importance to consider strategies to prevent the occurrence of no-reflow phenomenon. Previous evidence suggests that Beta (β) blockers have multiple favorable effects on the vascular system not directly related to their effect on blood pressure. However, there are insufficient data regarding the effects of prior Beta blocker use on coronary blood flow after primary PCI in patients with AMI.AimThe aim of this study was to test the hypothesis that Beta blocker treatment before admission would have beneficial effects on the development of the no-reflow phenomenon after acute myocardial infarction.Methods and resultsThe study included 107 diabetic patients who had presented with acute STEMI within 12 h from the onset of chest pain. All of them have undergone primary angioplasty at Ain Shams University hospitals or National Heart institute. The incidence of no-reflow phenomenon was 21%. No-reflow phenomenon was significantly lower in patients on chronic B-blocker therapy (12% vs. 28%; P = 0.04). The heart rate was significantly lower in the normal reflow group than in the no-reflow group (P = 0.03). The study also showed that B-blocker pretreatment is an independent protective predictor for the no-reflow phenomenon (P = 0.045).ConclusionChronic pre-treatment with B-blocker in diabetic patients presenting with STEMI, is associated with lower rate of occurrence of no-reflow phenomenon after primary PCI.

Predictors of Suboptimal Reperfusion and Short Term Mortality in Patients Presented With Acute ST-Segment Elevation Myocardial Infarction and Treated With Primary Percutaneous Coronary Intervention

“…Both of Al-Jabari A et al 2017 [15] and Wang J et al 2014 [16] found that the no-reflow phenomenon was significantly lower in patients on chronic B-blocker therapy (12% vs. 28%; P = 0.04)&(13.6% vs. 21.2% P = 0.017); respectively which is concordant with our study finding. Similar to our study, Hu T et al 2013 [17] concluded that Chronic pretreatment of ARB is associated with the reduction of the no-reflow phenomenon in patients with reperfused AMI and could preserve microvascular integrity after AMI (p value 0.002).…”

The predictors of no reflow phenomenon after percutaneous coronary intervention in patients with ST elevation myocardial infarction: A meta-analysis

“…Our results found no association between infarct location and the risk of no reflow. While, higher heart rate (OR95%CI = 1.30 [1.07–1.57], p = 0.0080) of five studies 25 ,27,30,44,45 and lower LVEF (OR95%CI = 3.10 [2.02–4.80], p < 0.0001) of 11 studies 29 ,30,35,36,38,41,43,46, 47, 48,50 were associated with the risk of no reflow. Table 3 summarizes the association between electrocardiogram and echocardiography with the risk of no reflow.…”

“…Until now, the predictors of the no reflow phenomenon remain unclear. Although some studies 14 ,25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50 have reported no reflow risk factors, however they showed differences. Therefore, we aimed to perform a meta-analysis concerning the correlation between several factors and the risk of no reflow.…”

Platelet–Leucocyte Aggregates as Novel Biomarkers in Cardiovascular Diseases

“…It was observed that β-blockers, used chronically before AMI or in an early stage of the event improve the prognosis after STEMI [ 129 ]. Due to inhibition of corresponding receptors on leukocytes (and probably also platelets), the use of β-blockers was associated with reduced PLA-N and PLA-M formation, less inflammation, less microvascular obstruction, and accordingly smaller infarct size [ 106 , 130 ].…”