Characteristics of ST-elevation myocardial infarction with failed thrombolysis

Abstract

Background Fibrinolytic therapy is an important reperfusion strategy, especially when primary percutaneous coronary interventions cannot be offered to ST-elevation myocardial infarction patients. Given that failed reperfusion after fibrinolytic therapy is common, it is pragmatic that the predictors, outcomes, and angiographic profiles of patients with failed thrombolysis are carefully scrutinized. Methods We prospectively studied clinical variables and outcomes over 30 months in 243 ST-elevation myocardial infarction patients who received fibrinolytics as primary treatment. Logistic regression analysis was used to identify predictors of failed thrombolysis. Results Failed thrombolysis occurred in 38.68% of patients with a mean window period of 6.58 ± 1.42 h, and 55.32% of patients with failed thrombolysis had Killip class >I on presentation. Risk factors such as diabetes mellitus (55.32%), dyslipidemia (60.64%) and obesity (77.66%) were frequently associated with failed thrombolysis; 73.40% of patients with failed thrombolysis had Thrombolysis in Myocardial Infarction flow grade 0/1 in the infarct-related artery, and 58.51% of such patients needed a rescue percutaneous coronary intervention. The mean Thrombolysis in Myocardial Infarction risk score was 5.46 ± 2.77 in failed thrombolysis patients, with mortality of 4.25% at the 6-month follow-up. Conclusion Non-resolution of presenting symptoms and ST changes on electrocardiography at 90 min served as the earliest indicators of failed thrombolysis, with a significant angiographic correlation. Clinical variables such as delayed presentation (>6 h), dyspnea, Killip class >I, cardiogenic shock, Thrombolysis in Myocardial Infarction score, and conventional risk factors including diabetes mellitus, dyslipidemia, and obesity represented cluster of predictors of failed thrombolysis.

Mortality outcomes and predictors of failed thrombolysis following STEMI thrombolysis in a non-PCI capable tertiary hospital: a 5-year analysis

“…The infarct-related artery in FT usually has persistent occlusion, where TIMI 3 flow (normal flow that fills the distal coronary bed) is not achieved. In one study, only 83.2% and 6.4% of STEMI patients with successful thrombolysis and FT, respectively, achieved the TIMI 3 flow [ 19 ]. In a meta-analysis, only TIMI 3 flow post thrombolysis is associated with a mortality benefit, with short-term mortality (in-hospital or 30-day mortality) of 3.7%, 7.0% and 8.8% among STEMI patients who achieved TIMI flow grade 3, 2, and 0/1, respectively [ 27 ].…”

“…We identified that STEMI patients with Killip II-IV at presentation to ED is a predictor of FT in the streptokinase arm but not in the tenecteplase arm, suggesting that tenecteplase is a better option in this population. Conversely, another Indian study has reported Killip II-IV as one of the predictors of FT in STEMI patients receiving either streptokinase or tenecteplase [ 19 ].…”

“…Most studies on STEMI FT did not report the anticoagulant used. However, two Indian studies using unfractionated heparin (UFH) have reported a higher FT of 32.7% and 38.7%, respectively [ 19 , 20 ]. In our setting, fondaparinux was the preferred anticoagulant for STEMI patients receiving thrombolytic therapy; enoxaparin is used only in patients with renal impairment.…”

“…Studies worldwide have reported inconsistent rates of FT in STEMI, ranging from 10 to 56.8%, for both fibrin-specific (alteplase, tenecteplase) and non-fibrin-specific (streptokinase) thrombolytic agents [ 11 – 26 ]. The predictors of FT (mainly on streptokinase) were identified in some studies: anterior location STEMI, higher Killip class, longer door-to-needle time, pre-existing diabetes and hypertension, higher total white cells count, longer symptoms-onset-to-thrombolysis time, hyperglycaemia, and higher thrombolysis in myocardial infarction (TIMI) score [ 18 , 19 , 21 ]. However, the small sample size in most studies is a major limitation.…”

Naringenin promotes angiogenesis of ischemic myocardium after myocardial infarction through miR-223-3p/IGF1R axis

“…Thrombolytic and interventional therapies based on the principle of vascular recanalization have been widely applied in clinical practice, in which great progress has been made [ 23 ]. However, severe ischemia-reperfusion injury, failure of myocardial cell regeneration, hypofunction of the heart, and even the immediate induction of heart failure are still vital factors for the high recurrence rate and mortality of MI, restricting the use of existing methods in the treatment of MI [ 18 ]. Based on the data of existing research, we found that the current therapy using bone marrow mesenchymal stem cell reduced the area of MI and improved heart function [ 13 ].…”